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Livestock Health
The Division of Animal Health maintains disease control programs to protect the health and well being of livestock in New Jersey. The division tracks information about emerging diseases around the world that may impact the Garden State, conducts epidemiological investigations of livestock diseases and drug residues, operates an animal health diagnostic laboratory and supports an aggressive Johne's disease control program.
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New Jersey Avian Influenza Infromation
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Click here to see a list of confirmations of Highly Pathogenic Avian Influenza in commercial and backyard flocks in the U.S.
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Synonyms: Lamziekte, Shaker Foal Syndrome, Loin Disease, Limberneck, Western Duck Sickness, Bulbar Paralysis
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Botulism is caused by botulinum toxin, a potent neurotoxin produced by Clostridium botulinum and a few strains of C. baratii and C. butyricum. Clostridium botulinum is an anaerobic, Gram-positive, spore-forming rod.
Botulism can result from the ingestion of preformed toxin or the growth of C. botulinum in anaerobic tissues. Seven types of botulinum toxin, designated A through G, have been identified. Types A, B, E and F cause illness in humans. Type C is the most common cause of botulism in animals. Type D is sometimes seen in cattle and dogs, and type B can occur in horses. Types A and E are found occasionally in mink and birds. Type G rarely causes disease, although a few cases have been seen in humans. All types of botulinum toxin produce the same disease; however, the toxin type is important if antiserum is used for treatment.
Geographic Distribution
C. botulinum is found worldwide and cases of botulism can be seen anywhere. In ruminants, botulism mainly occurs in areas where phosphorus or protein deficiencies are found. Botulism is seen regularly in cattle in South Africa and sheep in Australia. This disease is rare in ruminants in the United States, although a few cases have been reported in Texas and Montana.
Transmission
C. botulinum and its spores are widely distributed in soils, sediments in fresh and coastal waters, the intestinal tracts of fish and mammals, and the gills and viscera of shellfish. The bacteria can only grow under anaerobic conditions. Botulism occurs when animals ingest preformed toxins in food or C. botulinum spores germinate in anaerobic tissues and produce toxins as they grow.
Botulism in Humans
In humans, botulism is classified into three forms: foodborne, wound, and infant or intestinal botulism. Foodborne botulism is the most common form and occurs when humans ingest toxins in various foods. The foods associated with botulism are usually low acid (pH greater than 4.6) and may include home-canned foods, sausages, meat products, canned vegetables and seafood products. Commercial foods are occasionally implicated. Wound botulism occurs when an anaerobic wound is contaminated with C. botulinum, usually from the soil. Infant botulism is seen only in children less than a year of age. In this form, C. botulinum spores germinate in the intestinal tract and produce toxin. Honey has been associated with some cases of infant botulism but spores can also be found in many other sources. Adults with altered intestinal flora, secondary to gastrointestinal surgery or antibiotic therapy, may also be able to develop this form.
Botulism in Animals
Preformed toxins in a variety of sources, including decaying vegetable matter (grass, hay, grain, spoiled silage) and carcasses can cause botulism in animals. Carnivores, including mink and commercially raised foxes, usually ingest the toxins in contaminated meat such as chopped raw meat or fish. Cattle in phosphorus-deficient areas may chew bones and scraps of attached meat; a gram of dried flesh may have enough botulinum toxin to kill a cow. Similar cases occur in Australia, where protein-deficient sheep sometimes eat the carcasses of rabbits and other small animals. Ruminants may also be fed hay or silage contaminated by toxin-containing carcasses of birds or mammals. Horses usually ingest the toxin in contaminated forage. Birds can ingest the toxins in maggots that have fed on contaminated carcasses or in dead invertebrates from water with decaying vegetation. Cannibalism and contaminated feed can also result in cases in poultry.
The toxicoinfectious form of botulism corresponds to the wound and intestinal forms in humans. C. botulinum may grow in necrotic areas in the liver and GI tract, abscesses in the navel and lungs, or anaerobic wounds in the skin and muscles. This form of botulism appears to be responsible for shaker foal syndrome in horses. Toxicoinfectious botulism is also seen in chickens, when broilers are intensively reared on litter; the cause of this phenomenon is unknown.
Botulinum and Bioterrorism
In a bioterrorist attack, botulinum toxin could be delivered by aerosols, as well as food or water. After aerosol transmission, the clinical disease is expected to be similar to foodborne botulism.
Disinfection/ Inactivation
Botulinum toxins are large, easily denatured proteins. Toxins exposed to sunlight are inactivated within 1 to 3 hours. Botulinum can also be inactivated by 0.1% sodium hypochlorite, 0.1N NaOH, heating to 80°C for 30 minutes or 100°C for 10 minutes. Chlorine and other disinfectants can destroy the toxins in water.
The vegetative cells of Clostridium botulinum are susceptible to many disinfectants, including 1% sodium hypochlorite and 70% ethanol. The spores are resistant to environmental conditions but can be destroyed by moist heat (120°C for at least 15 min).
Incubation Period
The incubation period for foodborne infections is a few hours to 10 days; most cases become symptomatic after 18 to 36 hours. Wound infections may become evident within a few days to 2 weeks. The incubation period for intestinal or infant botulism is unknown. Inhalation botulism usually develops 12 to 36 hours after exposure, but in some cases the incubation period may be up to several days.
Clinical Signs
Foodborne Infections
In foodborne infections, gastrointestinal disturbances – including nausea, vomiting and abdominal pain - are often the first sign. Either diarrhea or constipation may occur. As the disease progresses, a symmetric, descending flaccid paralysis develops in the motor and autonomic nerves. The clinical signs may include blurred or double vision, photophobia, drooping eyelids, slurred speech, dysphagia, urine retention, a dry mouth and muscle weakness. In untreated progressive infections, descending paralysis of the respiratory muscles, arms and legs is seen. Fatal respiratory paralysis may occur within 24 hours in severe cases. Fever is not usually seen.
Wound Botulism
Wound botulism is very similar to foodborne infections; however, gastrointestinal signs are not usually present and patients may have a wound exudate or develop a fever.
Infant Botulism
Most cases of infant botulism occur in 2-week to 6-month-old babies. The first symptom is usually constipation. Other signs may include lethargy, weakness, excessively long sleep periods, diminished suck and gag reflexes and dysphagia with drooling. Some babies develop a weak or altered cry. In progressive cases, the infant may develop flaccid paralysis; a “floppy head” is typical. In severe cases, there may be respiratory arrest and death. The symptoms and severity of this disease vary considerably in different babies.
Intestinal botulism in adults
The initial symptoms of intestinal botulism in adults may include lassitude, weakness and vertigo. As the disease progresses, patients may experience double vision and have progressive difficulty speaking and swallowing. Other symptoms may include dyspnea, general muscle weakness, abdominal distention and constipation.
Communicability
No person-to-person transmission has been seen.
Diagnostic Tests
Botulism can tentatively diagnosed by the clinical signs and the exclusion of other neurologic diseases. The definitive diagnosis relies on identifying the toxin in feces, blood, vomitus, gastric aspirates, respiratory secretions or food samples. Feces are usually the most reliable clinical sample in foodborne or infant botulism; the toxin may be found for days or weeks in foodborne cases. Botulinum toxin is rarely found in the blood in adults but is occasionally detected in infants. The toxin can be identified by mouse inoculation studies (the mouse neutralization test), ELISAs or electrochemiluminescent (ECL) tests. Botulinum toxins can be typed with neutralization tests in mice. Serology is not useful for diagnosis, as small amounts of toxin are involved and survivors rarely develop antibodies.
C. botulinum can often be cultured from the feces in infant botulism or the wound in wound botulism. In foodborne cases, the food is usually cultured as well as tested for the toxin. C. botulinum is an anaerobic, Gram positive, spore-forming rod. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony. The iridescent zone around the colony is usually larger for C, D and E toxins.
Treatment and Vaccination
Supportive treatment, with respiratory support if necessary, is the cornerstone of treatment. Botulinum antitoxin, given early, may prevent the disease from progressing and decrease the duration of symptoms. In foodborne illness, the amount of toxin in the gastrointestinal tract can be reduced with stomach lavage and enemas. Antibiotics and debridement are used in cases of wound botulism. Antibiotics are also used occasionally in foodborne cases, but are not generally recommended in infant botulism as they may change the intestinal flora. Investigational vaccines may be available for humans who have a high risk of exposure.
Morbidity and Mortality
Outbreaks of botulism can occur worldwide. Approximately 10 to 30 outbreaks are seen annually in the United States. In 1999, 107 cases of infant botulism, 26 cases of foodborne botulism and 41 cases of wound botulism were reported in the United States.
The death rate is high in untreated cases, but has been decreasing with improvements in supportive care. Before 1950, the mortality rate was 60%; currently, it is less than 5%. Recovery may be slow and can take several months or longer. In some cases, survivors report fatigue and shortness of breath for years.
Botulinum toxins are known to have been weaponized by several countries and terrorist groups.
Species Affected
Many species of mammals and birds, as well as some fish, can be affected by botulism. Clinical disease is seen most often in wildfowl, poultry, mink, cattle, sheep, horses and some species of fish. Dogs, cats and pigs are resistant; botulism is seen occasionally in dogs and pigs but has not been reported from cats.
Incubation Period
The incubation period can be 2 hours to 2 weeks; in most cases, the symptoms appear after 12 to 24 hours. Mink are often found dead within 24 hours of ingesting the toxin.
Clinical Signs
Botulism is characterized by progressive motor paralysis. Typical clinical signs may include muscle paralysis, difficulty chewing and swallowing, visual disturbances and generalized weakness. Death usually results from paralysis of the respiratory or cardiac muscles.
Ruminants
In cattle, the symptoms may include drooling, restlessness, incoordination, urine retention, dysphagia and sternal recumbency. Lateral recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur.
Horses
The clinical signs in horses are similar to cattle. The symptoms may include restlessness, knuckling, incoordination, paralysis of the tongue, drooling and sternal recumbency. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, head and neck.
The shaker foal syndrome is usually seen in animals less than 4 weeks old. The most characteristic signs are a stilted gait, muscle tremors and the inability to stand for more than 4 to 5 minutes. Other symptoms may include dysphagia, constipation, mydriasis and frequent urination. In the later stages, foals usually develop tachycardia and dyspnea. Death generally occurs 24 to 72 hours after the initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.
Pigs
Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation and muscle paralysis.
Foxes and Mink
During outbreaks of botulism, many animals are typically found dead, while others have various degrees of paralysis and dyspnea. The clinical picture is similar in commercially raised foxes.
Birds
In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck and eyelids. Wildfowl with paralyzed necks may drown. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess urates.
Communicability
Botulism is not communicable by casual contact but, in some cases, tissues from dead animals can be toxic if ingested by other animals.
Diagnostic Tests
Botulism can be difficult to diagnose, as the toxin is not always found in clinical samples or the feed. Diagnosis is often a matter of excluding other diseases. A definitive diagnosis can be made if botulinum toxin is identified in the feed, stomach or intestinal contents, vomitus or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice.
In toxicoinfectious botulism, the organism can be cultured from tissues. C. botulinum is an anaerobic, Gram positive, spore-forming rod. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony. The iridescent zone around the colony is usually larger for C, D and E toxins.
Treatment and Vaccination
The treatment is usually supportive and may include gastric lavage to remove some of the toxin. Botulinum antitoxin is sometimes used in animals; the success rate may depend on the type of toxin causing the disease and the species of animal. Type C antitoxins have been effective in some outbreaks in birds and mink. There are also some reports of success with guanidine hydrochloride. Antibiotics are used in the toxicoinfectious form, but are not always successful in birds.
In endemic areas, vaccines can be used in horses, cattle, sheep, goats, mink and pheasants. In chickens, they may not be cost-effective.
Morbidity and Mortality
Botulism is common in wild waterfowl; an estimated 10 to 50 thousand wild birds are killed annually. In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. Botulism also affects commercially raised poultry. In chickens, the mortality rate varies from a few birds to 40% of the flock. Some affected birds may recover without treatment.
Botulism seems to be relatively uncommon in most domestic mammals; however, in some parts of the world, epidemics with up to 65% morbidity are seen in cattle. The prognosis is poor in large animals that are recumbent. In cattle, death generally occurs within 6 to 72 hours after sternal recumbency. Most dogs with botulism recover within 2 weeks.
Post-Mortem Lesions
There are no pathognomonic lesions; the lesions are usually the result of general muscle paralysis. Respiratory paralysis may cause nonspecific signs in the lungs. In shaker foal syndrome, the most consist lesions are excess pericardial fluid with strands of fibrin, pulmonary edema and congestion. Foreign material in the fore-stomachs or stomach may suggest botulism.
“Botulinum.” In Medical Management of Biological Casualties Handbook, 4 th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 10 Dec 2002 <http://www.vnh.org/BIOCASU/17.html>.
“Botulism.” Centers for Disease Control and Prevention (CDC), June 2002. 10 Dec 2002 <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/botulism_t.htm>.
“Botulism.” In Control of Communicable Diseases Manual, 17 th ed. Edited by J. Chin. Washington, D.C.: American Public Health Association, 2000, pp. 70-75.
“Botulism.” In The Merck Veterinary Manual, 8 th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 442-444; 916 1315; 1362; 1969-70.
“Clostridium botulinum.” In Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. U.S. Food & Drug Administration, Center for Food Safety & Applied Nutrition, Feb 2002. 12 Dec 2002
<http://www.cfsan.fda.gov/~mow/chap2.html>
Herenda, D., P.G. Chambers, A. Ettriqui, P. Seneviratna, and T.J.P. da Silva. “Botulism.” In Manual on meat inspection for developing countries. FAO Animal Production and Health Paper 119. 1994 Publishing and Multimedia Service, Information Division, FAO, 12 Dec 2002
<http://www.fao.org/docrep/003/t0756e/T0756E03.htm#ch3.3.2>.
“Material Safety Data Sheet –Clostridium botulinum.” January 2001 Canadian Laboratory Centre for Disease Control. 10 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds35e.html>.
Solomon H.M. and T. Lilly, Jr. “Clostridium botulinum.” In Bacteriological Analytical Manual Online, 8 th ed. U.S. Food and Drug Administration, January 2001. 12 Dec 2002
<http://vm.cfsan.fda.gov/~ebam/bam-17.html>.
Wells C.L. and T.D. Wilkins. “Clostridia: sporeforming anaerobic bacilli.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 10 Dec 2002
<http://www.gsbs.utmb.edu/microbook/ch018.htm>.
Weber, J.T., C.L. Hatheway and M.E. St. Louis. “Botulism” In Infectious Diseases, 5 th ed. Edited by P.D. Hoeprich, M.C. Jordan, and A.R. Ronald. Philadelphia: J. B. Lippincott Company, 1994, pp. 1185-1194.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Facts about Brucellosis
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What is brucellosis?
It is a contagious, costly disease of ruminant animals that also affects humans. Although brucellosis can attack other animals, its main threat is to cattle, bison, and swine. The disease is also known as contagious abortion or Bang's disease. In humans, it's known as undulant fever because of the severe intermittent fever accompanying human infection or Malta fever because it was first recognized as a human disease on the island of Malta. -
How serious is brucellosis?
Considering the damage done by the infection in animals-decreased milk production, weight loss in animals, loss of young, infertility, and lameness, it is one of the most serious diseases of livestock. The rapidity with which it spreads and the fact that it is transmissible to humans makes it all the more serious. -
What disease agents cause brucellosis?
The disease is caused by a group of bacteria known scientifically as the genus Brucella. Three species of Brucella cause the most concern: B. abortus, principally affecting cattle and bison; B. suis, principally affecting swine and reindeer but also cattle and bison; and B. melitensis, principally affecting goats but not present in the United States. In cattle and bison, the disease currently localizes in the reproductive organs and/or the udder. Bacteria are shed in milk or via the aborted fetus, afterbirth, or other reproductive tract discharges. -
What are the signs of brucellosis?
There is no effective way to detect infected animals by their appearance. The most obvious signs in pregnant animals are abortion or birth of weak calves. Milk production may be reduced from changes in the normal lactation period caused by abortions and delayed conceptions. Not all infected cows abort, but those that do usually abort between the fifth and seventh month of pregnancy. Infected cows usually abort once, but a percentage will abort during additional pregnancies, and calves born from later pregnancies may be weak and unhealthy. Even though their calves may appear healthy, infected cows continue to harbor and discharge infectious organisms and should be regarded as dangerous sources of the disease. Other signs of brucellosis include an apparent lowering of fertility with poor conception rates, retained afterbirths with resulting uterine infections, and (occasionally) enlarged, arthritic joints. -
How is brucellosis spread?
Brucellosis is commonly transmitted to susceptible animals by direct contact with infected animals or with an environment that has been contaminated with discharges from infected animals. Aborted fetuses, placental membranes or fluids, and other vaginal discharges present after an infected animal has aborted or calved are all highly contaminated with infectious Brucellaorganisms. Cows may lick those materials or the genital area of other cows or ingest the disease-causing organisms with contaminated food or water. Despite occasional exceptions, the general rule is that brucellosis is carried from one herd to another by an infected or exposed animal. This mode of transmission occurs when a herd owner buys replacement cattle or bison that are infected or have been exposed to infection prior to purchase. The disease may also be spread when wild animals or animals from an affected herd mingle with brucellosis-free herds. -
What is being done to fight brucellosis?
Before 1934, control of brucellosis was limited mainly to individual herds. Today, there is a Cooperative State Federal Brucellosis Eradication Program to eliminate the disease from the country. Like other animal disease-eradication efforts, success of the program depends on the support and participation of livestock producers. The program's Uniform Methods and Rules set forth the minimum standards for States to achieve eradication. States are designated brucellosis free when none of their cattle or bison are found to be infected for 12 consecutive months under an active surveillance program. As of June 30, 2000, 44 States, plus Puerto Rico and the U.S. Virgin Islands, were free of brucellosis. Six States currently have a herd infection rate of less than 0.25 percent and are considered to be in Class A status. There are no States in Class B (herd infection rate between 0.26 percent and 1.5 percent) or Class C status (herd infection rate greater than 1.5 percent). -
What about free-ranging bison herds?
The presence of brucellosis in free-ranging bison in Yellowstone National Park and Grand Teton National Park threatens the brucellosis status of the surrounding States and the health of their livestock herds, which are free of the disease. Reintroduction of the disease into a brucellosis-free State could have a serious economic impact on domestic livestock markets and potentially threaten export markets. The U.S. Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS) is working cooperatively with other State and Federal agencies toward containing the spread of brucellosis from bison to domestic livestock and eliminating the disease from the Yellowstone and Teton herds while maintaining viable free-roaming bison herds in the Parks. -
How do epidemiologists help fight brucellosis?
Epidemiologists are specially trained veterinarians who investigate disease sources and the means of eliminating infection in affected herds and areas. Epidemiologists are concerned with disease in a group or population of animals and evaluate circumstances connected with the occurrence of disease. These veterinarians help eliminate brucellosis by identifying factors essential to its control and prevention. -
How costly is brucellosis to the livestock industry?
The livestock and dairy industries and the American consumer have realized great financial savings from the success of the Cooperative State Federal Brucellosis Eradication Program. Annual losses from lowered milk production, aborted calves and pigs, and reduced breeding efficiency have decreased from more than $400 million in 1952 to less than $1 million today. Studies have shown that, if brucellosis eradication program efforts were stopped, the costs of producing beef and milk would increase by an estimated $80 million annually in less than 10 years. -
How effective is the Brucellosis Eradication Program?
At the beginning of the program, brucellosis was widespread throughout U.S. livestock, but eradication efforts have had dramatic results. In 1956, there were 124,000 affected herds found by testing in the United States. By 1992, this number had dropped to 700 herds, and as of June 30, 2000, there were only 6 known affected herds remaining in the entire United States. USDA, APHIS expects the Cooperative State Federal Program to achieve the goal of nationwide eradication of brucellosis from domestic cattle and bison in the very near future. -
What is the basic approach to eradication?
The basic approach has always been to test cattle for infection and send infected animals to slaughter. Identification of market animals for tracing, surveillance to find infected animals, investigation of affected herds, and vaccination of replacement calves in high-risk areas are important features of the current program. -
How is infection found in cattle?
Two primary surveillance procedures are used to locate infection without having to test each animal in every herd. Milk from dairy herds is checked two to four times a year by testing a small sample obtained from creameries or farm milk tank for evidence of brucellosis. Bison herds and cattle herds that do not produce milk for sale are routinely checked for brucellosis by blood-testing animals sold from these herds at livestock markets or at slaughter. In addition, some States require adult cattle and bison to be subjected to blood tests for brucellosis upon change of ownership even if sold directly from one farm to another. The cattle and bison remaining in the herds from which such animals originated are not tested unless evidence of brucellosis is disclosed among the market animals. -
What happens when evidence of disease is found by surveillance testing?
Once an infected herd is located, the infection is contained by quarantining all infected and exposed cattle and bison and limiting their movement to slaughter only, until the disease can be eliminated from the herd. Diagnostic tests are used to find all infected cattle and bison. Also, Federal and State animal health officials check neighboring herds and others that may have received animals from the infected herd. All possible leads to additional infection are traced. -
How does the brucellosis ring test (BRT) surveillance work?
The BRT procedure makes it possible to do surveillance on whole dairy herds quickly and economically. Milk or cream from each cow in the herd is pooled, and a sample is taken for testing. A suspension of stained, killed Brucella organisms is added to a small quantity of milk. If the milk from one or more infected animals is present in the sample, a bluish ring forms at the cream line as the cream rises. -
How does market cattle identification (MCI) work?
Numbered tags, called backtags, are placed on the shoulders of adult breeding animals being marketed from beef, dairy, and bison herds. Blood samples are collected from the animals at livestock markets or slaughtering plants and tested for brucellosis. If a sample reacts to a diagnostic test, it is traced by the backtag number to the herd of origin. The herd owner is contacted by a State or Federal animal health official to arrange for testing of his or her herd. Once the animals have been gathered, all of the eligible animals in the herd are tested at no cost to the owner. -
Which animals are eligible for MCI testing?
At slaughter, all cattle and bison 2 years of age or older are tested, except steers and spayed heifers. At market, all beef cattle and bison over 24 months of age and all dairy cattle over 20 months of age are tested except steers and spayed heifers. Pregnant or postparturient heifers are also eligible for testing regardless of their age. Herd tests must include all cattle and bison over 6 months of age except steers and spayed heifers. -
Why is identification of market cattle important?
The key to the MCI program is proper identification of all animals so they can be traced to their herds of origin. Most livestock markets identify cattle and bison with numbered USDA-approved backtags. Backtags, as well as eartags and other identification devices, are collected and sent to the diagnostic laboratory along with the matching blood samples to aid in identifying ownership of test-positive animals. -
What are the advantages of MCI?
MCI provides a means of determining the brucellosis status of animals marketed from a large area and eliminates the need to round up cattle and bison in all herds for routine testing. MCI, along with other preliminary testing procedures, is effective in locating infection so control measures can be taken to contain the disease and eliminate it. -
What is a blood agglutination test?
It is an effective method of diagnosing brucellosis. To pinpoint infection within a herd, a blood sample is taken from each animal and tested in the field or at a laboratory. The blood serum is mixed with a test fluid or antigen containing dead Brucella organisms. When the organisms in the test fluid clump together in a reaction known as agglutination, the test is positive. -
What is the brucellosis card test?
It is a rapid, sensitive, and reliable procedure for diagnosing brucellosis infection. It is similar to the blood agglutination test but employs disposable materials contained in compact kits. Brucella antigen is added to the blood serum on a white card. Results of the test are read 4 minutes after the blood serum and antigen are mixed. -
Are there any other tests for brucellosis?
There are a number of supplemental tests based on various characteristics of antibodies found in the blood and milk of infected animals. These tests are especially useful in identifying infected animals in problem herds herds in which chronic brucellosis infection exists and from which infection is difficult to eliminate. Another diagnostic method involves culturing Brucella organisms from infected tissues, milk, or other body fluids, from aborted calves or fetal fluids and membranes. -
What animals are eligible for testing?
With certain exceptions, herd tests must include all cattle and bison over 6 months of age except steers and spayed heifers. -
What is the incubation period of brucellosis?
An incubation period is the interval of time between exposure to an infectious dose of organism and the first appearance of disease signs. The incubation period of brucellosis in cattle, bison, and other animals is quite variable ranging from about 2 weeks to 1 year and even longer in certain instances. When abortion is the first sign observed, the minimum incubation period is about 30 days. Some animals abort before developing a positive reaction to the diagnostic test. Other infected animals may never abort. Generally, infected animals that do not abort develop a positive reaction to the diagnostic test within 30 to 60 days after infection, although some may not develop a positive reaction for several months to over a year. -
Can brucellosis in animals be cured?
No. Repeated attempts to develop a cure for brucellosis in animals have failed. Occasionally, animals may recover after a period of time. More commonly, however, only the signs disappear and the animals remain diseased. Such animals are dangerous sources of infection for other animals with which they associate. -
Can brucellosis be prevented?
The disease may be avoided by employing good sanitation and management practices. Replacement animals should be tested when purchased and retested after a 30- to 60-day isolation period during which they are kept separate from the remainder of the herd. These practices will allow detection of animals that were in the incubation period of the disease when acquired. -
What about vaccination?
For cattle and bison in heavily infected areas or replacement animals added to such herds, officials recommend vaccinating heifers with an approved Brucella vaccine. The vaccine is a live product and must be administered only by an accredited veterinarian or State or Federal animal health official. For best results, female calves should be vaccinated when they are 4 to 6 months old. At the time of vaccination, a tattoo is applied in the ear; that tattoo identifies the animal as an "official vaccinate." The tattoo identifies the year in which vaccination took place. -
How does the vaccine work?
Brucella abortus vaccine produces a bodily response that increases the animal's resistance to the disease. However, vaccination is not 100-percent effective in preventing brucellosis; it typically protects about 65 percent of the vaccinated cattle from becoming infected by an average exposure to Brucella. -
Is Strain 19 the only approved Brucella vaccine?
No. USDA recently licensed a new Brucella vaccine, called Strain RB51, for use in cattle. Strain RB51 is as efficacious as Strain 19 vaccine but virtually eliminates adverse postvaccination reactions in cattle, such as abortions and localized inflammation at the vaccine injection site. Most importantly, unlike Strain 19, Strain RB51 does not stimulate the same type of antibodies that can be confused on standard diagnostic tests with those antibodies produced by actual infection. -
Is Strain RB51 vaccine approved for use in bison?
As of June 2000, B. abortus Strain RB51 had not yet been approved for use in bison. Preliminary studies indicate that RB51 is safe and efficacious in bison calves. However, in order for RB51 to be conditionally licensed in bison, additional safety and efficacy trials must be completed. -
Where or when is calfhood vaccination most important?
Owners whose herds are located in areas of relatively heavy infection or who ship replacement cattle or bison to, or receive animals from, such areas should carry out a vigorous calfhood vaccination program. Every cattle or bison owner, regardless of location, should discuss the advantages and disadvantages of vaccination with his or her veterinarian. Some States do not allow cattle and bison to be imported for breeding if they are not official vaccinates and they are beyond the age at which they should have been vaccinated. -
Where is vaccination less important?
In many areas of the country, low herd infection rates coupled with improvement in the detection of early infection through BRT, MCI, and other surveillance systems have lessened the need to continue calfhood vaccination. Vaccination should be reduced in such areas, provided that adequate regulatory measures are in effect to prevent reintroduction of the disease. -
How does brucellosis affect humans?
People infected with the brucellosis organism usually develop symptoms similar to a severe influenza, but this disease, called undulant fever, persists for several weeks or months and may get progressively worse. Farmers, ranchers, veterinarians, and packing plant workers are infected most frequently because they come into direct contact with infected animals. The initial symptoms are fatigue and headaches, followed by high fever, chills, drenching sweats, joint pains, backache, and loss of weight and appetite. Undulant fever does not often kill its victims, but the disease is too serious to be dealt with lightly. -
What are the main sources of human infection?
In years past, prior to pasteurization, raw milk was considered the prime source of brucellosis in humans. Today, most humans contract the disease by coming in direct contact with aborted fetuses, afterbirth, and uterine discharges of diseased animals or with infected carcasses at slaughter. However, one 1994 study suggests that human brucellosis in California is most likely to be a food-borne illness (unpasteurized milk or cheese products) acquired in Mexico or from Mexican products consumed in California. Rarely, if ever, does a human contract the disease from another human. -
How common is human brucellosis in this country?
Fortunately, the combination of pasteurization of milk and progress in the eradication of the disease in livestock has resulted in substantially fewer human cases than in the past. Ninety eight cases of human brucellosis were reported in 1997, a fraction of the 6,400 cases reported in 1947. Sixty two (62) cases of brucellosis in humans have been reported to the Centers for Disease Control and Prevention for 1998 (provisional data). -
Can people get brucellosis by eating meat?
There is no danger from eating cooked meat products because the disease-causing bacteria are not normally found in muscle tissue and they are killed by normal cooking temperatures. The disease may be transmitted to humans when slaughtering infected animals or when processing contaminated organs from freshly killed animals. -
How can people be protected from brucellosis?
Ranchers, farmers, or animal managers should clean and disinfect calving areas and other places likely to become contaminated with infective material. All individuals should wear sturdy rubber or plastic gloves when assisting calving or aborting animals, and scrub well with soap and water afterward. Precautions against drinking raw milk or eating unpasteurized milk byproducts are also important. Ultimately, the best prevention is to eliminate brucellosis from all animals in the area.
For additional information, contact:
USDA, APHIS, Veterinary Services
National Animal Health Programs
4700 River Road, Unit 43
Riverdale, MD 20737-1231
Telephone (301) 734-7708
Synonyms: Campylobacter enteritis, Vibrionic enteritis, Vibriosis
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Campylobacter are Gram negative, microaerophilic, curved or spiral rods in the family Campylobacteriaceae. Campylobacter jejuni (formerly known as C. fetus subsp. jejuni) and C. coli are associated with enteritis in domestic animals and humans. Some strains of C. jejuni, C. fetus subsp. venerealis, and C. fetus subsp. fetus (also known as C fetus subsp. intestinalis and Vibrio fetus var intestinalis) cause infertility and abortions in sheep and cattle. C. fetus subsp. fetus is occasionally isolated from humans with septicemia.
Other species of Campylobacter including C. lari, C. hyointestinalis and C. upsaliensis can cause disease but seem to be of minor importance in domestic animals. Uncharacterized Campylobacter species may be involved in proliferative ileitis of hamsters, porcine proliferative enteritis and proliferative colitis of ferrets.
Geographic Distribution
C. jejuni, C. coli and C. fetus infections are found worldwide.
Transmission
Campylobacter jejuni and C coli are transmitted by the fecal-oral route; they can be spread by direct contact and on fomites including food or water. C. jejuni may also be present in the vaginal discharges, aborted fetuses and fetal membranes of aborting sheep. Undercooked poultry and other meats are sources of infection for pets and commercially raised mink. Houseflies are mechanical vectors. Humans can be infected after ingesting undercooked poultry and other meats, raw milk, raw clams, contaminated foodstuffs or unchlorinated water, and after contact with infected pets or livestock. Asymptomatic carriers are seen in many species of domestic animals; humans do not usually become carriers.
Campylobacter fetus subsp. fetus is transmitted by ingestion in cattle, sheep and goats. Animals can become infected after contact with feces, vaginal discharges, aborted fetuses and fetal membranes. This organism and C. fetus subsp. venerealis are also transmitted venereally in cattle. Genital C. fetus infections can be spread on fomites including contaminated semen, contaminated instruments and bedding. Bulls may transmit C. fetus for several hours after being bred to an infected cow; some bulls can become permanent carriers. Cows can also become carriers for years.
Campylobacter species do not tolerate drying or heating but can often survive for a time in moist environments: C. jejuni may remain viable for up to 9 days in feces, 3 days in milk and 2 to 5 days in water. C. jejuni and C. coli can remain infective in moist poultry litter for prolonged periods. C fetus can survive in liquid manure for 24 hours and soil for up to 20 days.
Disinfection
Campylobacter species are susceptible to many disinfectants, including 1% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde, iodine-based disinfectants, phenolic disinfectants and formaldehyde. Common disinfectants used to treat drinking water can also kill C. jejuni. C. jejuni and fetus are inactivated by moist heat (121°C for at least 15 min) or dry heat (160-170°C for at least 1 hour). Campylobacter is also sensitive to gamma irradiation and UV radiation.
Incubation Period
In humans, the incubation period for C. jejuni gastroenteritis is 1 to 10 days and most often 2 to 5 days. The incubation period for human C. fetus infections is usually 3 to 5 days.
Clinical Signs
C. jejuni and occasionally C. coli cause enteritis; disease varies from mild gastrointestinal distress that resolves within 24 hours to a fulminating or relapsing colitis. The clinical signs may include watery or sticky diarrhea, fever, nausea, vomiting, abdominal pain, headache and muscle pain. The feces may contain blood. Complications are not common; however, reactive arthritis, hemolytic uremic syndrome and septicemia are occasionally seen. Rare complications include meningitis, recurrent colitis, acute cholecystitis and Guillain-Barré syndrome (an acute, rapidly progressive polyneuropathy). Cases of C. jejuni abortion have been seen in humans, but are extremely rare.
C. fetus is an opportunistic human pathogen and mainly causes systemic infections. Infections tend to occur in people with debilitating illnesses such as diabetes, cancer or cirrhosis. Intestinal symptoms may be mild. Fever is the only consistent symptom, but abdominal pain, splenomegaly and hepatomegaly are common. Subacute endocarditis, septic arthritis, meningitis or fever of unknown origin are also seen. Complications may include endocarditis, pericarditis, pneumonia, thrombophlebitis, peritonitis or meningoencephalitis.
Communicability
Yes. C. jejuni is found in the feces and can be shed for as long as 2 to 7 weeks in untreated infections; however, humans rarely become chronic carriers. C. fetus subsp. fetus is communicable for several days to several weeks.
Diagnostic Tests
Feces or (rarely) blood cultures are used for diagnosis. A presumptive diagnosis can be made by detecting the characteristic darting motility of the organism with dark-field or phase-contrast microscopy. Gram negative, curved or spiral rods are seen in Gram stained preparations. Definitive diagnosis is by isolation of the causative organism; however, Campylobacter is fragile and cannot always be found. Selective media or filtration techniques improve the chance of isolation. Forty-eight to 72 hour colonies are raised, round, translucent and sometimes mucoid. Biochemical testing, antigen testing and restriction endonuclease DNA analyses are used for species and strain identification.
Polymerase chain reaction (PCR)-based techniques for rapid detection or culture confirmation are also available. Serology is currently used only in research.
Treatment and Vaccination
Treatment is often limited to fluid and electrolyte replacement therapy. Antibiotics are occasionally given, particularly when the symptoms are severe or prolonged; however, their efficacy is not proven for mild infections. Individuals with Guillain-Barré syndrome usually require intensive care. Antibiotics can reduce the shedding of infectious organisms. Vaccines are not available.
Morbidity and Mortality
C. jejuni is the most common cause of bacterial diarrhea in the United States; roughly 20 cases per 100,000 population are seen yearly. Infections are particularly common in young children, and in young adults from age 18 to 29. Asymptomatic human carriers are very rare in the United States or Europe.
C. jejuni or C. coli diarrhea is usually self-limiting and generally resolves after 7-10 days; relapses can occur in approximately 10-25% of cases. Immunosuppressed individuals are at a high risk for severe or recurrent infections or for septicemia. Deaths are rare in C. jejuni infections and are seen mainly in patients with cancer or other debilitating diseases. The estimated case/fatality ratio for C. jejuni infections is one in 1,000.
Guillain-Barré syndrome is seen after approximately 1 in 1000 diagnosed infections; up to 5% of these patients may die and 30% or more may have residual weakness or other neurologic defects.
Species Affected
C. jejuni and C. coli can infect cattle, sheep, chickens, turkeys, dogs, cats, mink, ferrets, pigs, non-human primates and other species. C. fetus subsp. fetus is found in cattle, sheep and goats. C. fetus subsp. venerealis is found in cattle. Animals can be infected asymptomatically with any of these organisms.
Incubation Period
The incubation period for Campylobacter infections is generally short. Symptoms of enteritis appear within 3 days in gnotobiotic puppies and rapidly in chicks and poults.
Clinical Signs
Campylobacter species cause enteritis, abortions and infertility in various species.
Enteritis
C. jejuni and occasionally C. coli cause enteritis in dogs, cats, calves, sheep, mink, ferrets, poultry and some species of laboratory animals. The clinical signs may be more severe in young animals. In dogs, symptoms can include diarrhea, decreased appetite, vomiting and sometimes fever. The feces are usually watery or bile-streaked, with mucus and sometimes blood. Symptoms generally last 3 to 7 days, but some animals may have intermittent diarrhea for weeks and occasionally for months. Calves typically have a thick, mucoid diarrhea with occasional flecks of blood, either with or without a fever. Mucoid, watery and sometimes bloody diarrhea is also seen in cats, primates, mink and ferrets. Newly hatched chicks and poults develop acute enteritis, with rapid onset of diarrhea and death.
Reproductive symptoms
In cattle, C. fetus subsp. venerealis and C. fetus subsp. fetus can cause bovine genital campylobacteriosis; this disease is characterized by infertility, early embryonic death and a prolonged calving season. Abortions are uncommon but are occasionally seen. Infected cows may develop a mucopurulent endometritis but do not usually have other systemic signs. Bulls are asymptomatic.
C. fetus subsp. fetus and C. jejuni can cause late term abortions, stillbirths and weak lambs in sheep. Infections in sheep are sometimes followed by metritis and occasionally deaths. Recovery, with immunity to reinfection, is typical. Sheep can become persistently infected and continue to shed bacteria in the feces.
Other Campylobacter infections
Other species of Campylobacter including C. lari, C. hyointestinalis and C. upsaliensis can cause disease but seem to be of minor importance. Uncharacterized Campylobacter species may be involved in proliferative ileitis of hamsters, porcine proliferative enteritis, and proliferative colitis of ferrets.
Communicability
Yes. Campylobacter species are readily transmitted between animals or from animals to humans. Organisms are present in feces, vaginal discharges and the products of abortions and can be spread by direct contact, on fomites and by arthropods acting as mechanical vectors. Contaminated food and water is often the source of infections.
Diagnostic Tests
Enteritis can be diagnosed by isolating the causative organism in fresh fecal samples; however, Campylobacter is fragile and cannot always be found. Forty-eight to 72 hour colonies are raised, round, translucent and sometimes mucoid. Biochemical testing, antigen testing and restriction endonuclease DNA analyses are used for species and strain identification. A presumptive diagnosis can also be made by observing the characteristic darting motility in darkfield or phase contrast preparations. Gram negative, curved or spiral rods are seen in Gram stained preparations. Serology on paired titers may be helpful in some cases.
Darkfield and phase contrast preparations of samples from the placenta, fetal abomasum and uterine discharge are used to diagnose Campylobacter abortions in sheep. Campylobacter antigens can also be detected by immunofluorescence.
Bovine genital campylobacteriosis can be diagnosed by detecting specific IgA in the cervical mucus; these antibodies are present for several months in half of all infected cows. Tests include a vaginal mucus agglutination test (VMAT) and enzyme-linked immunosorbent assays (ELISAs). Individual responses in the VMAT are variable; for this test, a minimum of 10 cows or 10% of the herd should be sampled. Sheath washings taken twice from bulls, approximately one week apart, can be submitted for culture or immunofluorescent testing. Vaginal cultures can also be collected immediately after abortion or infection, but this method may be unreliable: Campylobacter fetus is fragile and usually present in low numbers. Systemic antibody responses are not useful in genital campylobacteriosis, as they can be directed against nonpathogenic species.
Treatment and Vaccination
Antibiotics may be useful for some cases of enteritis; however, information on efficacy is limited. Antibiotics may also prevent exposed sheep from aborting during an outbreak. Bulls with bovine genital campylobacteriosis are sometimes treated; cows usually are not, due to practical considerations.
Vaccines are not available for enteritis, but can prevent abortions in sheep. They are also useful for both prophylaxis and treatment in bovine genital campylobacteriosis; however, vaccinated cows may remain carriers. Artificial insemination can control or prevent bovine genital campylobacteriosis.
Morbidity and Mortality
Gastrointestinal campylobacteriosis is usually self-limiting in mammals; however, up to 32% mortality may be seen with highly pathogenic isolates in chicks. Mortality is also low in adult sheep and cattle affected by abortions and infertility. Morbidity may be up to 90% in outbreaks in sheep but is usually around 5 to 50%.
Post-Mortem Lesions
In dogs, the colon may be congested and edematous. In calves, the lesions may include mild to severe hemorrhagic colitis and edematous mesenteric lymph nodes. In chicks, distention of the jejunum, disseminated hemorrhagic enteritis and focal hepatitis may be seen.
Aborted cattle fetuses may have bronchopneumonia, mild fibrinous pleuritis or peritonitis. Placentitis is usually mild; the cotyledons may be hemorrhagic and the intercotyledonary area edematous. In sheep, the fetus is usually autolyzed after C. fetus abortions; 1 to 2 cm orange/ yellow necrotic foci can sometimes be found in the liver. Placentitis may be evident, with hemorrhagic necrotic cotyledons and edematous or leathery areas between the cotyledons.
“Abortion in large animals.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 988-997.
“Avian Campylobacter infection.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 1902-3.
“Bovine genital campylobacteriosis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 997-8.
“Campylobacter infections.” Centers for Disease Control (CDC), Dec 2001. 24 Oct 2002
<http://www.cdc.gov/ncidod/dbmd/diseaseinfo/campylobacter_t.htm>.
“Campylobacter jejuni.” In Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. Food and Drug Administration (FDA), Feb 2002. 26 Oct 2002 <http://www.cfsan.fda.gov/~mow/chap4.html>.
“Campylobacteriosis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 117-9.
“Campylobacteriosis.” Organic Livestock Research Group, VEERU, The University of Reading, March 2000. 29 Oct 2002
<http://www.organic-vet.reading.ac.uk/Sheepweb/disease/campyl/campyl1.htm>.
“Guillain- Barré Syndrome.” In The Merck Manual, 16th ed. Edited by R. Berkow and A.J. Fletcher. Rahway, NJ: Merck and Co., 1992, pp. 1521-2.
“Infectious diseases caused by Gram negative bacilli. Campylobacter Infections.” In The Merck Manual, 17th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 28 Oct 2002 <http://www.merck.com/pubs/mmanual/section13/chapter157/157d.htm>.
Perez-Perez, G.I. and M.J. Blaser. “Campylobacter and Helicobacter.” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 23 Oct 2002
<http://www.gsbs.utmb.edu/microbook/ch023.htm>.
“Material Safety Data Sheet – Campylobacter fetus ssp. fetus.” Canadian Laboratory Centre for Disease Control, 1999. 25 October 2002
<1999 http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds28e.html>.
“Material Safety Data Sheet – Campylobacter jejuni, C. coli, C. fetus subsp. jejuni.” Canadian Laboratory Centre for Disease Control, 1999. 25 October 2002 <http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds29e.html>.
Spronk, G.D. “Practitioner's approach to ovine abortion.” Pipestone Veterinary Supply, 2000. 29 Oct 2002 <http://www.pipevet.com/articles/Practioners_Approach_to_Ovine_Abortion.htm>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Canine influenza virus is a highly contagious type A influenza virus that causes respiratory disease in dogs. The virus was first identified in racing greyhounds and appears to have been the cause of significant respiratory disease on canine tracks throughout the US for the last 2-3 years. The most recent cases have occurred in dog breeds other than greyhounds in shelters, boarding facilities and veterinary clinics in Florida. All dogs are susceptible to infection and do not have naturally acquired immunity to the virus.
The Virology Lab at Cornell isolated the first influenza virus from a dog that died from the infection. The virus was sequenced at the CDC as subtype H3N8 and was found to be closely related to equine influenza virus. Researchers at the CDC suspect that a change of 8 to 10 amino acids in the Hemagglutinin gene (the H in the H3N8) may be responsible for the ability of the virus to infect dogs.
The clinical signs of canine influenza virus infection closely resemble a common respiratory syndrome known as Kennel Cough, and may include nasal discharge, high fever and a soft gagging cough of 10-14 days. While some dogs can be infected with the virus and not show clinical signs, a small percentage will develop more severe complications such as pneumonia. Canine influenza virus is characterized as a high morbidity low mortality virus. The mortality rate for dogs suffering from complications associated with canine influenza infection is 1 to 5 percent. Canine influenza should be a differential diagnosis for any dog presenting with respiratory disease. No vaccine is currently available.
Rapid identification and isolation of suspected cases of canine influenza in veterinary clinics, shelters and boarding facilities are recommended.
Researchers have indicated that this influenza virus subtype has circulated in horses for over 40 years and has never infected humans. However, the CDC will be monitoring for human exposure to the virus.
The New Jersey Department of Agriculture Animal Health Diagnostic Laboratory can provide preliminary screening for canine influenza. Samples suspect or positive on this preliminary screen will be forwarded to the appropriate veterinary diagnostic laboratory for additional testing.
If you have a suspect case of canine influenza and would like to submit samples for preliminary screening, please call the New Jersey Department of Agriculture Diagnostic Laboratory at (609) 671-6400.
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Cholera results from infection by Vibrio cholerae, a Gram negative, facultatively anaerobic rod in the family Vibrionaceae. Two serogroups, 01 and 0139 ("Bengal"), can cause disease. Serogroup O1 contains two serologically indistinguishable biotypes, classical and El Tor. Mild or asymptomatic infections are seen more often with the El Tor biotype. Cholera caused by serogroup 0139 emerged in 1992, in epidemics in India and Bangladesh.
Geographic Distribution
Cholera is endemic in the Middle East, Africa, Central and South America, parts of Asia and the Gulf Coast of the United States but outbreaks can occur in any country. Major epidemics occur periodically in less developed countries; outbreaks in developed countries are usually localized due to better sanitation.
Transmission
Transmission is by the fecal-oral route. Infections are particularly common after ingesting contaminated water or food. Cases are occasionally seen in people who have eaten raw or undercooked shellfish, particularly oysters, from contaminated waters.
V. cholerae is excreted in the feces and vomitus. Viable organisms can be found in feces for up to 50 days, on glass for up to a month, on coins for a week, in soil or dust for up to 16 days and on fingertips for 1 to 2 hours. Bacteria survive well in water and may remain viable in shellfish, algae or plankton in coastal regions.
Disinfection
V. cholerae is susceptible to many disinfectants, including 0.05% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde, 8% formaldehyde, 10% hydrogen peroxide and iodine-based disinfectants. Organisms are tolerant of alkaline conditions but are sensitive to acids and cold temperatures.
Incubation Period
The incubation period is a few hours to 5 days. Most infections become apparent after 2 to 3 days.
Clinical Signs
Cholera appears abruptly with painless, watery diarrhea, sometimes accompanied by vomiting. Infections may be subclinical, mild and self-limiting, or fulminant and severe. Severe fluid loss can be seen in more serious cases; thirst, oliguria, severe dehydration, acidosis, muscle cramps and shock may result. Most cases last approximately 2 to 7 days but death may occur within a few hours if the fluid loss is high. A self-limiting gastroenteritis is seen after infection with pathogenic non O1/O139 strains.
Communicability
Yes. Most people excrete V. cholerae while diarrhea is present and for a few days after recovery. A few individuals carry the organism in the gall bladder for several months. Rare long-term carriers have been reported; one woman was an asymptomatic carrier for 12 years before her infection spontaneously resolved.
Diagnostic Tests
Cholera can be diagnosed by observing the organism’s characteristic motility during direct, bright-field or dark-field microscopic examination of the feces; the addition of specific antibodies to V. cholerae stops the movement. Bacteria can also be identified in the feces by immunofluorescence. A polymerase chain reaction (PCR) assay or other genetic tests may be available in some laboratories.
V. cholerae can be isolated from feces or rectal swabs. Distinctive yellow colonies are seen on selective thiosulfate-citrate-bile salts-sucrose (TCBS) agar. Other selective and nonselective media, including nutrient agar and bile salts agar, can also be used. Enrichment procedures and selective media may be necessary to identify carriers. Identification is by rapid slide agglutination test or immunofluorescence. Biochemical tests may also be helpful, particularly for non-O group 1 (nonagglutinable) vibrios. The "string test" - the development of a mucoid string when a colony is emulsified in 0.5% aqueous sodium deoxycholate - may also be useful. The classic and El Tor biotypes can be differentiated by chicken cell hemagglutination, hemolysis, polymyxin sensitivity or susceptibility to bacteriophages.
A rising titer is also diagnostic. Serologic tests include agglutination tests, complement fixation and tests to detect antitoxic antibodies. Enzyme -linked immunosorbent assays (ELISAs) and passive hemagglutination may also be available.
Treatment and Vaccination
Treatment relies on fluid replacement and the restoration of electrolyte balance. Antibiotics reduce the stool volume, decrease shedding of organism and shorten the course of the disease but may not be effective alone.
Vaccines have been developed but their efficacy is limited; some vaccines are effective for only short periods of time, particularly in children.
Morbidity and Mortality
Endemic cholera and epidemics are seen periodically in susceptible populations where sanitation and environmental conditions favor the spread of V. cholerae. In developed countries with good sanitation, outbreaks are usually limited. Approximately 0 to 5 cases occur annually in the United States.
Cholera is rarely fatal if the lost fluids and electrolytes are adequately replaced. The mortality rate with proper treatment is less than 1% and most patients recover within 3 to 7 days. In untreated cases, the case fatality rate is greater than 50%. Death may occur within a few hours if the diarrhea is severe.
Humans appear to be the only natural host for V. cholerae. Diarrhea can be induced in experimentally infected rabbits, mice and chinchillas by bacteria or their toxins. Dogs are susceptible if massive doses of bacteria are given.
“Bacterial infections caused by Gram-negative bacilli.” In The Merck Manual, 17 th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 8 Nov 2002
<http://www.merck.com/pubs/mmanual/section13/chapter157/157d.htm>.
“Cholera.” Centers for Disease Control and Prevention, July 2002. 8 Dec 2002 <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/cholera_t.htm>.
Finkelstein R.A. “Cholera, Vibrio cholerae O1 and O139, and other pathogenic vibrios.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 8 Dec 2002
<http://www.gsbs.utmb.edu/microbook/ch024.htm>.
“Material Safety Data Sheet – Vibrio cholerae, serogroup O1, serogoup O139 (Bengal).” Canadian Laboratory Centre for Disease Control, February 2001. 8 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds164e.html>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: Enterohemorrhagic Escherichia coli (EHEC), Verotoxin producing Escherichia coli (VTEC), Shiga toxin producing Escherichia coli (STEC)
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Escherichia coli 0157:H7 is a pathogenic, verotoxin-producing serotype of E. coli. This Gram negative motile rod belongs to the family Enterobacteriaceae and is responsible for many cases of hemorrhagic colitis in humans.
Geographic Distribution
Escherichia coli 0157:H7 infections occur worldwide.
Transmission
Transmission is by the fecal-oral route. Humans can be infected by direct contact with animal or human carriers; transmission by fomites, including water and food, is also common. Birds are potential vectors. Human outbreaks are often associated with eating improperly cooked or prepared animal products, particularly ground beef but also unpasteurized milk and processed meats (including acidic meats such as salami). Cider, alfalfa sprouts and other contaminated vegetable products have also been sources of epidemics.
Escherichia coli 0157:H7 remains viable for more than 2 months in feces and soil, and survives well in ground beef. It remains infectious for weeks to months in acidic foods such as mayonnaise, sausage, apple cider and cheddar at refrigeration temperatures. It is destroyed fairly quickly in slurry systems; in one experiment, organisms could no longer be recovered after 9 days.
Disinfection/ Inactivation
E. coli 0157:H7 can be killed by numerous disinfectants including 1% sodium hypochlorite, 70% ethanol, phenolic or iodine-based disinfectants, glutaraldehyde and formaldehyde. It can be inactivated by moist heat (121° C for at least 15 min) or dry heat (160-170° C for at least 1 hour). Foods can be made safe by cooking them to a minimum temperature of 160°F/71°C. The infective dose is very low; washed vegetables may contain enough organisms to cause disease.
Incubation Period
The incubation period ranges from one to eight days in humans; one to two days is most common.
Clinical Signs
Human infection results in hemorrhagic colitis; this infection is characterized by cramps, abdominal pain, and watery diarrhea followed by bloody diarrhea. A low-grade fever may be present or absent in the initial stages. Dehydration is possible. In healthy adults, infections are usually self-limiting and last about a week.
Serious complications can develop in a small percentage of cases. Hemolytic uremic syndrome (HUS) occurs in 2-10% of patients, usually a week after the diarrhea begins. HUS is characterized by kidney failure, which may result in permanent damage, and hemolytic anemia. Seizures, strokes, pancreatitis, colonic perforation, hypertension and coma may also be seen. Some patients develop permanent insulin-dependent diabetes. HUS can affect all ages but is most common in children under 10 years old.
Thrombotic thrombocytopenic purpura (TTP) is usually seen in adults, particularly the elderly. This disease resembles HUS and some sources consider it to be the same syndrome; there is typically less kidney damage but neurologic signs including stroke, seizures and CNS deterioration are more common.
Communicability
Yes, by the fecal oral route. Most people shed E coli 0157:H7 infections for approximately 7 to 9 days; a third of infected children can excrete this organism for as long as 3 weeks. Transmission is particularly common among children still in diapers.
Diagnostic Tests
E coli 0157:H7 infections are diagnosed by isolating the organism from fecal samples. This serotype is not detected in routine cultures but can be recognized by incubation on sorbitol-MacConkey agar. Antiserum can rapidly identify sorbitol-negative cultures as E coli 0157:H7. Fecal samples may be negative after one week. Another method of diagnosis is to test the feces for E coli verotoxin. Hemorrhagic colitis agar is used to isolate bacteria from food samples.
Treatment and Vaccination
Treatment of hemorrhagic colitis is supportive and may include fluids and a bland diet. Antibiotics are not typically used: they do not seem to reduce symptoms, prevent complications or decrease shedding and do appear to increase the risk of HUS. Patients with complications may require intensive care, including dialysis. Vaccines are not available.
Morbidity and Mortality
In the United States, approximately 73,000 infections are thought to occur yearly. Hemorrhagic colitis is generally self-limiting and illness usually lasts about a week. HUS develops in 2-10%. Complications and deaths are particularly common in young children, the elderly, and those with debilitating illnesses. HUS is fatal in 3-5% of patients and TTP in up to 50% of the elderly. Death can occur even in cases of uncomplicated colitis.
E. coli 0157:H7 has been found in cattle, sheep, goats, pigs, deer, dogs and poultry. The major reservoir of this organism is cattle; young animals are most likely to shed bacteria in the feces. Fecal shedding may last only weeks to months and can be intermittent.
Currently, there is no published evidence that E coli 0157:H7 causes disease in animals; however, B. Fenwick and colleagues have suggested that this organism may be linked to Idiopathic Cutaneous and Renal Glomerular Vasculopathy of Greyhounds (CRGV). Experimental infection of calves results in no clinical signs. Sheep also appear to carry the organism asymptomatically.
Buchanan, R.L. and M.P. Doyle. “Foodborne disease significance of Escherichia coli 0157:H7 and other enterohemorrhagic E coli.” The Institute of Food Technologists’ Expert Panel on Food Safety and Nutrition. Food Technology 51, no. 10 (Oct 1997): 69-76.
“E. coli 0111, 0157.” Animal Health Australia. The National Animal Health Information System (NAHIS). 8 Oct 2002
<http://www.brs.gov.au/usr-bin/aphb/ahsq?dislist=alpha>.
“Escherichia coli O157:H7.” Centers for Disease Control (CDC), July 2002. 12 Nov 2002 <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/escherichiacoli_t.htm>.
“Escherichia coli O157:H7.” In Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. U.S. Food & Drug Administration, Center for Food Safety & Applied Nutrition, Feb 2002. 12 Nov 2002
<http://www.cfsan.fda.gov/~mow/chap15.html>.
“Escherichia coli O157:H7 infection.” In The Merck Manual, 17th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 12 Nov 2002 <http://www.merck.com/pubs/mmanual/section3/chapter28/28b.htm>.
Fenwick, B. “E. coli O157 food poisoning/HUS in Dogs.”1996. 12 Nov 2002 <http://hayato.med.osaka-u.ac.jp/o-157-HUS.html>.
Guentzel, M.N. “Escherichia, Klebsiella, Enterobacter, Serratia, Citrobacter and Proteus.” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 12 Nov 2002
<http://www.gsbs.utmb.edu/microbook/ch026.htm>.
“Material Safety Data Sheet –Escherichia coli, enterohemorrhagic.” January 2001 Canadian Laboratory Centre for Disease Control. 8 October 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds63e.html>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: : “Sleeping Sickness”
Eastern Equine Encephalomyelitis – EEE, Eastern equine encephalitis, Eastern encephalitis
Western Equine Encephalomyelitis – WEE,
Western equine encephalitis
Venezuelan Equine Encephalomyelitis – VEE, VE, Peste loca, Venezuelan equine encephalitis, Venezuelan encephalitis, Venezuelan equine fever
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Eastern, Western and Venezuelan equine encephalomyelitis result from infection by the respectively named viruses in the genus Alphavirus (family Togaviridae). In the human literature, the disease is usually called Eastern, Western or Venezuelan equine encephalitis.
Eastern Equine Encephalomyelitis Virus
There are two variants of the Eastern equine encephalomyelitis (EEE) virus. The virus found in North America is more pathogenic than the variant that occurs in South and Central America. The Eastern equine encephalitis virus can cause disease in humans, horses and some species of birds.
Western Equine Encephalomyelitis Viruses
The Western equine encephalomyelitis (WEE) virus group includes the Western equine encephalitis (WEE), Sindbis, Ft. Morgan, Aura and Y 61-33 viruses. The Western equine encephalitis virus can cause disease in humans, horses and some species of birds. A related virus, the Highlands J virus, is sometimes isolated in the eastern United States. The Highlands J virus can cause disease in turkeys. It has also been linked to a single case of encephalitis in a horse.
Venezuelan Equine Encephalomyelitis Viruses
The Venezuelan equine encephalomyelitis (VEE) complex contains at least 8 viral subtypes; these viruses are divided into epizootic and enzootic groups. The epizootic subtypes are responsible for most epidemics. They are highly pathogenic for horses and also cause illness in humans. Enzootic (sylvatic) subtypes are generally found in limited geographic areas, where they occur in natural cycles between rodents and mosquitoes. The enzootic subtypes can cause human disease. They are usually nonpathogenic for horses; however, in 1993 an enzootic variant was responsible for an outbreak of VEE among horses in Mexico.
Geographic Distribution
The Western, Eastern and Venezuelan encephalomyelitis viruses are found in North, Central and South America. The WEE viruses occur in western Canada, Mexico, parts of South America, and west of the Mississippi in the United States. The EEE virus is found in eastern Canada, all states east of the Mississippi, Arkansas, Minnesota, South Dakota and Texas. It also occurs in the Caribbean and regions of Central and South America, particularly along the Gulf coast. VEE viruses are endemic in South and Central America and Trinidad. Enzootic subtypes of VEE are also found in Florida, the Rocky Mountains and northern plains of the United States. Most epidemics of VEE occur in northern and western South America, but some may spread into adjacent countries, including the United States.
Transmission
Eastern and Western Equine Encephalomyelitis
The Eastern and Western encephalomyelitis viruses are transmitted mainly by mosquitoes. Normally, these two viruses cycle between birds and mosquitoes. Humans and horses are incidental, dead end hosts.
The EEE virus can be isolated from 27 species of mosquitoes in the United States. Culiseta melanura, a mosquito that primarily feeds on birds, is the most important vector in the enzootic cycle. During some years, the virus is spread to mammalian hosts by bridge vectors (mosquitoes that feed on both birds and mammals) such as Coquilletidia perturbans, Aedes canadensis, Aedes sollicitans, Aedes vexans and Culex nigripalpus. WEE cycles between passerine birds and culicine mosquitoes. Culex tarsalis appears to be the most important vector; other significant vectors include Aedes melanimon, Aedes dorsalis and Aedes campestris. The EEE and WEE viruses may be transmitted vertically in mosquitoes.
In birds, EEE and WEE are occasionally spread by non-arthropod-borne routes. During outbreaks of disease in game birds, infections are introduced by mosquitoes but spread in the flock mainly by feather picking and cannibalism. EEE and WEE viruses do not survive outside the host.
Venezuelan Equine Encephalomyelitis
The Venezuelan equine encephalomyelitis viruses are also spread mainly by mosquitoes. The enzootic subtypes of VEE cycle between rodents and mosquitoes, mainly Culex species. Birds may also be involved in some cycles. Humans and horses are incidental hosts.
The natural host for the epizootic subtypes, between epidemics, is unknown. Horses infected with the epizootic subtypes can infect mosquitoes and are the main amplifiers for VEE during epidemics. Other mammals, including cattle, pigs and dogs, can be infected but do not usually become ill or spread the virus. Many different species of mosquitoes and other hematogenous insects can transmit epizootic VEE. Efficient vectors include arthropods in the genera Aedes, Anopheles, Culex, Deinocerites, Mansonia, Haemogogus, Sabethes and Psorophora.
In some cases, humans have also developed VEE after being exposed to debris from the cages of infected laboratory rodents. Person-to-person transmission has not been reported; however, the VEE virus can be found in pharyngeal secretions in humans and is stable when aerosolized. The virus can also occur in dried blood and exudates.
Disinfection
EEE and WEE viruses do not persist in the environment but the VEE virus may be found in dried blood and exudates. VEE, EEE and WEE are susceptible to many disinfectants including 1% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde and formaldehyde. They can also be destroyed by moist or dry heat, as well as drying.
Incubation Period
In humans, the incubation period is usually 1 to 6 days for VEE and 4 to 15 days for WEE and EEE.
Clinical Signs
Eastern and Western Equine Encephalitis
Eastern equine encephalitis usually begins abruptly, with fever, myalgia and headache and sometimes nausea and vomiting. This prodrome is often followed by neurologic signs; the symptoms may include confusion, focal neurologic deficits, somnolence, neck stiffness, stupor, disorientation, coma, tremors, seizures and paralysis. Abdominal pain, diarrhea and a sore throat can also occur. The mortality rate for EEE is high.
Western equine encephalitis resembles EEE but is usually asymptomatic or mild in adults, with nonspecific signs of illness and few deaths. The symptoms usually appear abruptly and may include fever, headache, nausea, vomiting, anorexia and malaise. Many adults do not develop other symptoms. In more severe cases, neurologic symptoms, similar to those seen in EEE, can develop. WEE can be severe in children, particularly infants under a year of age.
Venezuelan Equine Encephalitis
In humans, VEE is usually an acute, often mild, systemic illness. The clinical signs may include fever, generalized malaise, severe headache, photophobia and myalgia, particularly in the legs and lumbosacral region. These symptoms usually last for 24 to 72 hours and may be followed by a cough, sore throat, nausea, vomiting and diarrhea. The disease usually lasts 1 to 2 weeks. In pregnant women, VEE can affect the fetus; fetal encephalitis, placental damage, abortion or severe congenital neurologic anomalies may be seen.
Encephalitis usually develops in 4% of children and less than 1% of adults. In mild cases, the symptoms may include lethargy, somnolence, or mild confusion. Severe infections are characterized by seizures, ataxia, paralysis or coma. An increased incidence of encephalitis would be expected after a biological attack with aerosolized viruses.
Communicability
WEE and EEE viruses are not found in the blood or cerebrospinal fluid after the symptoms appear, and only low titers develop during the viremic phase. These viruses do not seem to be spread directly from person to person. Humans do not transmit EEE or WEE viruses to mosquitoes.
Person-to-person transmission is theoretically possible for VEE, but has not been reported in natural cases. Humans with VEE can infect mosquitoes for approximately 72 hours.
Diagnostic Tests
Eastern, Western and Venezuelan equine encephalitis can be diagnosed by virus isolation, serology or other tests. In humans, VEE virus can be isolated from blood, cerebrospinal fluid or throat swabs. Serology is also useful; a rise in titer or the presence of specific IgM is diagnostic. A variety of serologic tests may be available, including virus neutralization, ELISA, hemagglutination inhibition and complement fixation. Indirect immunofluorescence assays have been developed for VEE. Polymerase chain reaction (PCR) or immunohistochemistry may be available at some laboratories.
During the febrile stage of the illness, antigen-capture ELISAs can often detect VEE antigens in the blood. This test is generally not useful during the encephalitic stage. PCR assays may also be available.
Treatment and Vaccination
Treatment consists of supportive care. Investigational VEE, EEE and WEE vaccines may be available for humans at high risk of infection. The VEE vaccine may not be effective for all of the VEE complex viruses.
Morbidity and Mortality
Eastern Equine Encephalitis
In the United States, approximately 12 to 17 cases of EEE are reported to the Centers for Disease Control and Prevention (CDC) each year. The infection rate is approximately 33% and the morbidity rate 90%. Most cases are seen in people over 55 and children younger than 15. Eastern equine encephalitis is often severe in humans. Estimates of the case fatality rate vary from 33 to 70% and permanent neurologic deficits can occur in survivors.
Western Equine Encephalitis
The annual incidence of WEE is highly variable; during an epidemic in 1941, over 3000 human cases occurred in the United States and Canada. The case-infection ratio is approximately 1:1000 in adults, 1:58 in children from 1 to 4 years old and 1:1 in infants up to a year of age. The overall mortality rate is 3 to 4%. Most infections in adults are asymptomatic or mild, without neurologic disease. Infections in children, particularly infants under one year old, can be severe. Approximately 5 to 30% of young patients have permanent neurologic damage.
Venezuelan Equine Encephalomyelitis
In natural epidemics of VEE, human cases are usually preceded by an epidemic in horses. After an attack by a biological weapon, cases would be expected simultaneously in both species or first in humans. Caution should be used in interpreting such patterns of infection, as VEE may be missed in wild or free-ranging equines.
Humans are highly susceptible to VEE; approximately 90 to 100% of exposed individuals become infected and nearly 100% of these infections are symptomatic. However, most infections are mild. Less than 1% of adults develop encephalitis and approximately 10% of these cases are fatal. The overall case fatality is less than 1%. Very young or elderly patients are more likely to develop severe infections. Encephalitis occurs in approximately 4% of children less than 15 years old; the case fatality rate in children with neurologic disease is 35%. A higher incidence of neurologic disease could be seen in adults as well as children after a biological attack with aerosolized virus; mortality rates would be expected to be correspondingly higher.
Species Affected
The equine encephalomyelitis viruses usually cause illness only in equine species and humans. These viruses can also infect a variety of other animals, often asymptomatically.
Eastern and Western Equine Encephalomyelitis
Eastern equine encephalitis virus infects horses, pigs, birds, bats, reptiles, amphibians, forest-dwelling marsupials and rodents. WEE virus can infect birds, horses and a variety of mammals. Most WEE and EEE infections in birds are asymptomatic; however, disease can be seen in chukar partridges, pheasants, psittacine birds, ratites and whooping cranes.
Venezuelan Equine Encephalomyelitis
Rodents seem to be the natural hosts for the enzootic subtypes of VEE but, in some cases, birds may also be involved. VEE virus can cause serious disease in horses, mules, burros and donkeys. Cattle, pigs and dogs can be infected asymptomatically. VEE can also infect a wide variety of laboratory animals.
Incubation Period
The incubation period for WEE or EEE is 5 to 14 days. The clinical signs of VEE are usually seen 1 to 5 days after infection.
Clinical Signs
Eastern and Western Equine Encephalomyelitis in Horses
Eastern and Western equine encephalomyelitis are very similar in horses. The initial clinical signs are usually fever, anorexia and depression. In severe cases, this prodromal stage is followed by neurologic signs; the symptoms may include involuntary muscle movements, impaired vision, aimless wandering, head pressing, circling, an inability to swallow, ataxia, paresis, paralysis and convulsions. Periods of excitement or intense pruritus can also be seen. Laterally recumbent animals may develop a characteristic “paddling” motion. Both EEE and WEE can also cause asymptomatic infections or mild disease without neurologic signs. Occasional cases of encephalitis have been seen in pigs.
Venezuelan Equine Encephalomyelitis in Horses
The enzootic subtypes usually infect horses subclinically. The epizootic subtypes can cause asymptomatic infections or two clinical syndromes. One syndrome resembles EEE and WEE; in this form, a febrile prodrome is followed by neurologic signs and sometimes diarrhea and colic. Death can occur within hours after the onset of neurologic signs or after protracted disease. Animals that recover may have permanent neurologic signs. The second form of VEE is a generalized acute febrile disease without neurologic signs. The symptoms may include fever, weakness, depression, anorexia, colic and diarrhea.
Western and Eastern Equine Encephalitis Viruses in Birds
Western and Eastern equine encephalomyelitis virus infections are asymptomatic in most species of birds, but fatal infections can occur in some species. Most reported outbreaks have been caused by EEE. Chukar infected with the EEE virus are usually dull and listless, with ruffled feathers. The birds are typically found sitting on their hocks with the beak on the ground. In pheasants, the symptoms may include incoordination, weakness and progressive paralysis. In the late stages of the disease, the birds cannot stand but can still move their wings. Whooping cranes may develop lethargy, ataxia and paresis of the legs and neck. The EEE virus has also been isolated from psittacine birds with viral serositis.
Both EEE and WEE viruses can cause fatal hemorrhagic enteritis in ratites; the characteristic clinical signs include depression, hemorrhagic diarrhea, and vomiting of bloodstained material. Highlands J and EEE infections can also cause depression, somnolence, decreased egg production and increased mortality in turkeys.
Communicability
Birds can amplify the Western and Eastern equine encephalomyelitis viruses and are infectious for mosquitoes. Horses are dead-end hosts for these viruses. Direct transmission has been seen only between birds.
Both horses and birds infected with the VEE virus are infectious for mosquitoes. In horses, the virus can be found in bodily fluids. Some authorities suggest that transmission may be possible by direct contact or aerosols but natural transmission between horses or from horses to humans has not been seen. Humans can be infected by laboratory rodents.
Diagnostic Tests
Eastern and Western Equine Encephalomyelitis
In horses, Eastern and Western equine encephalomyelitis can be diagnosed by serology. Tests include plaque reduction neutralization (PRN), hemagglutination inhibition, antibody-capture enzyme linked immunosorbent assay (ELISA) and complement fixation. Cross-reactions may occur between EEE and WEE antibodies in the complement fixation and hemagglutination inhibition tests.
Clinical infections in birds are usually diagnosed by virus isolation. In horses, virus isolation is useful in cases of EEE; it is rarely successful in WEE. The EEE virus can usually be recovered from the brain of infected horses; other tissues such as the liver or spleen may also be positive. EEE and WEE viruses can be isolated in newborn mice, embryonating chicken eggs, newly hatched chicks or cell cultures including primary chicken or duck embryo fibroblasts, African green monkey kidney (Vero), rabbit kidney (RK-13), and baby hamster kidney (BHK-21) cells. Virus identity can be confirmed by complement fixation, immunofluorescence or plaque reduction neutralization (PRN) tests. EEE viruses can also be detected in the brain with immunohistochemistry or an antigen-capture ELISA.
Venezuelan Equine Encephalomyelitis
VEE can be diagnosed by virus isolation or serology. VEE virus can often be recovered from the blood during the febrile stage and is sometimes isolated from the brain of animals with encephalitis. Virus is also found occasionally in the pancreas or other tissues. Animals with neurologic signs are not usually viremic. VEE virus can be isolated in guinea pigs, hamsters, mice, embryonated chicken eggs or cell lines including Vero, RK-13, BHK-21 and duck or chicken embryo fibroblasts. The virus can be identified by complement fixation, hemagglutination inhibition, plaque reduction neutralization (PRN) or immunofluorescence assays. Subtypes can be characterized by immunofluorescence, differential PRN tests or nucleic acid sequencing.
VEE can also be diagnosed by serology. Serologic tests include the PRN test, complement fixation, hemagglutination inhibition and ELISAs. Cross-reactions can occur between VEE, EEE and WEE viruses in the hemagglutination inhibition test. Animals may have pre-existing antibodies to enzootic variants of VEE.
Treatment and Vaccination
Treatment consists of supportive care. Equine vaccines are available for EEE, WEE and VEE. EEE vaccines are also available for susceptible birds, but do not always prevent disease.
Morbidity and Mortality
Eastern and Western Equine Encephalomyelitis
WEE often occurs as sporadic cases of encephalitis in horses, scattered over a wide area. Clinical cases of EEE are usually more clustered. EEE is often fatal in horses; the mortality rate is 50 to 90%. WEE is more likely to be asymptomatic or mild, with mortality rates of approximately 20 to 30%. Significant morbidity and mortality can also occur in poultry, game birds and ratites. In pheasants and other susceptible species of birds, both the morbidity and mortality rates may be up to 90%. The morbidity and mortality rates for emus with hemorrhagic enteritis can be greater than 85%.
Venezuelan Equine Encephalomyelitis
Most enzootic VEE subtypes do not result in serious disease or deaths in horses. Epizootic subtypes can cause significant morbidity and mortality; the morbidity rate can be as high as 90% and the mortality rate varies from 30 to 90%.
Post-Mortem Lesions
The gross lesions are usually nonspecific. In horses with VEE, the lesions in the central nervous system vary from no lesions to extensive necrosis with hemorrhages. Necrotic foci are sometimes seen in the pancreas, liver and heart of horses with VEE. Congestion of the brain and meninges is found in some cases of EEE and WEE. Antemortem trauma can result in ecchymotic hemorrhages.
Microscopic analysis of the brain tissue is often diagnostic. The typical lesion is severe inflammation of the gray matter; neuronal degeneration, infiltration by inflammatory cells, gliosis, perivascular cuffing and hemorrhages may be seen. WEE, EEE and VEE can sometimes be differentiated by the location and pattern of the lesions in the brain.
“Arthropod-Borne Viral Diseases.” In Control of Communicable Diseases Manual, 17th ed. Edited by James Chin. Washington, D.C.: American Public Health Association, 2000, pp. 28-47.
“Eastern Encephalitis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 1970-1.
“Eastern Encephalomyelitis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 931-4.
“Equine Encephalomyelitis (Eastern and Western).” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000. 16 Dec 2002
<http://www.oie.int/eng/normes/mmanual/A_00071.htm>.
“Equine Viral Encephalomyelitis.” In Manual for the Recognition of Exotic Diseases of Livestock: A Reference Guide for Animal Health Staff. Food and Agriculture Organization of the United Nations, 1998. 16 Dec 2002 <http://panis.spc.int/RefStuff/Manual/Equine/EQUINE%20VIRAL%20ENCEPH.HTML>.
“Information on Arboviral Encephalitides.” Centers for Disease Control and Prevention (CDC), 2001. 16 Dec 2002
<http://www.cdc.gov/ncidod/dvbid/arbor/arbdet.htm>.
Leake, Colin J. “Mosquito-Borne Arboviruses.” In Zoonoses. Edited by S.R. Palmer, E.J.L. Soulsby and D.I.H Simpson. New York: Oxford University Press, 1998, pp. 401-413.
“Material Safety Data Sheet –Eastern equine encephalitis virus, Western equine encephalitis virus.” March 2001 Canadian Laboratory Centre for Disease Control. 4 October 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds52e.html>.
“Material Safety Data Sheet –Venezuelan equine encephalitis virus.” Canadian Laboratory Centre for Disease Control, September 2001. 10 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds162e.html>.
Nandalur M. and A.W. Urban. “Eastern Equine Encephalitis.” eMedicine, Sept 2002. 16 Dec 2002
<http://www.emedicine.com/med/topic3155.htm>.
Nandalur M. and A.W. Urban. “Western Equine Encephalitis.” eMedicine, June 2002. 16 Dec 2002
<http://www.emedicine.com/MED/topic3156.htm>.
Schmaljohn A.L. and D. McClain. “Alphaviruses (Togaviridae) and Flaviviruses (Flaviviridae).” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 16 Dec 2002 <http://www.gsbs.utmb.edu/microbook/ch054.htm>.
“Venezuelan Equine Encephalitis.” In Medical Management of Biological Casualties Handbook, 4th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 10 Dec 2002
<http://www.vnh.org/BIOCASU/14.html>.
“Venezuelan Equine Encephalomyelitis.” USDA Animal and Plant Health Inspection Service (APHIS), Sept 2002. 16 Dec 2000 <http://www.aphis.usda.gov:80/oa/pubs/fsvee.html>.
“Venezuelan Equine Encephalomyelitis.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000. 16 Dec 2002 <http://www.oie.int/eng/normes/mmanual/A_00078.htm>.
Walton, T.E. “Venezuelan Equine Encephalomyelitis.” In Foreign Animal Diseases. Richmond, VA: United States Animal Health Association, 1998, pp 406-414.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: Farcy, Malleus, Droes
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Glanders results from infection by Burkholderia mallei, a Gram negative, aerobic, nonmotile rod (family Pseudomonadaceae). This organism was formerly known as Pseudomonas mallei and is closely related to the agent of melioidosis, Burkholderia pseudomallei.
Geographic Distribution
Glanders is seen in some Middle Eastern countries, the Indian subcontinent, Southeast Asia, parts of China and Mongolia, and Africa. Sporadic cases are also seen in South America. Cross-reactions with B. pseudomallei may interfere with serologic estimates of the prevalence and distribution of B. mallei.
Transmission
Infectious organisms are found in skin exudates and respiratory secretions. Latently infected horses can also spread the disease. Transmission is usually by ingestion in horses and related species; the infection can also be spread by inhalation or through skin abrasions and the conjunctiva. Carnivores can become infected after eating contaminated meat. B. mallei is spread on fomites, including harnesses, grooming tools, food and water troughs. This organism can survive in room temperature water for as long as 30 days and may be able to survive for a few months in other favorable environments. It is susceptible to heat, light, drying and a variety of chemicals.
Humans can become infected after contact with sick animals or infectious materials. Transmission is typically through small wounds and abrasions in the skin; ingestion or inhalation, with invasion through the mucous membranes, is also possible. Cases are usually seen in people who handle laboratory samples or have frequent close contact with horses, mules and donkeys. Natural human infections are rare even when infection rates in horses are 5-30%. Weaponization of B. mallei has been attempted by some countries.
Disinfection
Burkholderia mallei is susceptible to numerous disinfectants including benzalkonium chloride, iodine, mercuric chloride in alcohol, potassium permanganate, 1% sodium hypochlorite, 70% ethanol and 2% glutaraldehyde. It is less susceptible to phenolic disinfectants. This organism can also be destroyed by heating to 55°C for 10 min or by ultraviolet irradiation.
Incubation Period
In natural infections, the incubation period is 1 to 14 days. Infections from aerosolized forms in biological weapons are expected to have an incubation period of 10-14 days.
Clinical Signs
Humans can develop four forms of disease: septicemia, pulmonary infection, acute localized infection or chronic infection. Combinations of syndromes can occur.
In the septicemic form, fever, chills, myalgia, and pleuritic chest pain develop acutely. Other symptoms may include generalized erythroderma, jaundice, photophobia, lacrimation, diarrhea and granulomatous or necrotizing lesions. Tachycardia, cervical adenopathy and mild hepatomegaly or splenomegaly may also be seen. Death usually occurs in 7 to 10 days.
The pulmonary form is characterized by symptoms of pneumonia, pulmonary abscesses and pleural infusions. A cough, fever, dyspnea and mucopurulent discharge may be seen. Skin abscesses sometimes develop after several months.
Localized infections are characterized by nodules, abscesses and ulcers in the mucous membranes, skin, lymphatic vessels and/or subcutaneous tissues. A mucopurulent, blood-tinged discharge may be seen from the mucous membranes. The lymph nodes may be swollen. Mucosal or skin infections can disseminate; symptoms of disseminated infections include a papular or pustular rash, abscesses in the internal organs (particularly the liver and spleen) and pulmonary lesions. Disseminated infections are associated with septic shock and high mortality.
In the chronic form, multiple abscesses, nodules or ulcers can be seen in the skin, liver, spleen or muscles.
Communicability
Person to person transmission has been reported, but appears to be uncommon. Human epidemics have not been seen.
Diagnostic Tests
Glanders can be diagnosed by isolation and identification of Burkholderia mallei. In the septicemic form, blood cultures may be negative until just before death. B. mallei is a nonmotile Gram negative rod; organisms from young cultures and clinical samples are rods with bipolar staining, while bacteria from older cultures can be pleomorphic. Few bacteria may be found in clinical samples. On blood agar or Loeffler’s serum agar, colonies are approximately 1 mm, white, semitranslucent and viscid. Older colonies turn yellow. On glycerin-potato media, a clear honey-like layer is seen by day 3; this eventually darkens to reddish-brown or brown. B. mallei can also be isolated by inoculation into guinea pigs. A polymerase chain reaction can differentiate B. mallei DNA from B. pseudomallei.
Serology is sometimes helpful; serologic tests include agglutination tests and complement fixation. High background titers can be found in normal serum and cross-reactions may occur with Burkholderia mallei, the causative agent of glanders. Positive reactions in agglutination tests develop only after 7 to 10 days.
Treatment and Vaccination
B. mallei is variably susceptible to antibiotics. Long-term treatment or multiple drugs may be necessary. Treatment may be ineffective, particularly in cases of septicemia; the bacteria produce toxins. No vaccine is available.
Morbidity and Mortality
In most parts of the world, naturally acquired cases of glanders are rare and sporadic. Infections are typically seen in people who work with clinical samples or have frequent, close contact with horses. Human epidemics have not been seen.
The septicemic form of glanders has a high mortality rate in humans: the case fatality rate is 95% in untreated cases and more than 50% when the infection is treated. The mortality rate for localized disease is 20% when treated. The overall mortality rate is 40%.
Species Affected
The major hosts are horses, mules and donkeys. Infections can also occur in dogs, cats, goats and camels; cats may be particularly susceptible. Hamsters and guinea pigs can be infected in the laboratory.
Incubation Period
In natural infections, the incubation period varies from 6 days to many months; 2 to 6 weeks is typical. Experimental infections can result in clinical signs after 3 days.
Clinical Signs
Acute, chronic and latent forms of glanders are seen in horses, mules and donkeys.
The clinical signs in the acute form may include a high fever, cough, inspiratory dyspnea, a thick nasal discharge, and deep, rapidly spreading ulcers on the nasal mucosa. Healed ulcers become star-shaped scars. The submaxillary lymph nodes are usually swollen and painful, and the lymphatic vessels on the face may be thickened. Secondary skin infections, with nodules, ulcers and abscesses may be seen. Affected animals usually die within 1 to 2 weeks.
The chronic form develops insidiously. The symptoms may include coughing, malaise, unthriftiness, weight loss and an intermittent fever. A chronic purulent nasal discharge may be seen, often only from one nostril. Other symptoms may include ulcers and nodules on the nasal mucosa, enlarged submaxillary lymph nodes, chronic enlargement and induration of lymphatics and lymph nodes, swelling of the joints and painful edema of the legs. The skin may contain nodules, particularly on the legs, that rupture and ulcerate. This form is slowly progressive and may be fatal.
In the latent form, there may be few symptoms other than a nasal discharge and occasional labored breathing. Lesions may be found only in the lungs.
Communicability
Yes. Horses, donkeys and mules can transmit the disease to other animals and humans; nasal discharges and wound exudates are infectious. Laboratory samples are highly infectious to humans.
Natural transmission from infected animals to humans appears to be inefficient; despite infection rates of 30% in horses in China during World War II and 5-25% in Mongolia, few or no human cases occurred.
Diagnostic Tests
Glanders can be diagnosed by bacteriologic isolation of B. mallei, animal inoculation into guinea pigs, the mallein test or serology.
In live animals, B. mallei is isolated from skin lesions or blood samples. Organisms are much easier to find in fresh than in old lesions, where they may be scant. At necropsy, bacteria can also be isolated from exudates in the nasal passages and the upper respiratory tract. B. mallei is a nonmotile Gram negative rod; bacteria from young cultures and clinical samples are rods with bipolar staining while organisms from older cultures may be pleomorphic. On blood agar or Loeffler’s serum agar, colonies are approximately 1 mm, white, semitranslucent and viscid. Older colonies turn yellow. On glycerin-potato media, a clear honey-like layer is seen by day 3; this eventually darkens to reddish-brown or brown. A polymerase chain reaction can differentiate B. mallei DNA from B. pseudomallei.
In the mallein test, a positive reaction is indicated by eyelid swelling 1 to 2 days after intrapalpebral injection of a protein fraction of B. mallei, or by conjunctivitis after administration in eyedrops.
A variety of serologic tests are available, including complement fixation, enzyme-linked immunosorbent assay (ELISA), indirect hemagglutination, counter- immunoelectrophoresis and immunofluorescence. The most accurate and reliable tests in horses are complement fixation and ELISA. Agglutination and precipitin tests are unreliable for horses with chronic glanders and animals in poor condition. Complement fixation tests cannot be used with donkey or mule serum.
Treatment and Vaccination
Antibiotics may be effective; however, treatment is not generally recommended, as infections can be spread to humans and other animals, and treated animals may become asymptomatic carriers. Vaccines are not available.
Morbidity and Mortality
Glanders can spread widely when large numbers of animals are in close contact; in China, 30% of horses were infected when large numbers of animals were gathered together in World War II. Acute infections are usually fatal within 1 to 2 weeks. Animals with the chronic form can sometimes survive for years.
Post-Mortem Lesions
At necropsy, there may be ulcers, nodules and stellate scars in the nasal cavity, trachea, pharynx, larynx, skin and subcutaneous tissues. Catarrhal bronchopneumonia with enlarged bronchial lymph nodes may be evident. The lungs, liver, spleen and kidneys may contain firm, rounded, encapsulated miliary gray nodules similar to tubercles. The lymphatic vessels may be swollen; the lymph nodes are typically enlarged and fibrotic and contain focal abscesses. In addition, necrosis may be noted in the internal organs and testes.
Batts-Osborne D., P.P. Rega, A.H. Hall and T.W. McGovern. “CBRNE - Glanders and Melioidosis.” eMedicine, Oct 2001. 17 Nov 2002 <http://www.emedicine.com/emerg/topic884.htm>.
Bauernfeind A., Roller C., Meyer D., Jungwirth R., and Schneider I. “Molecular procedure for rapid detection of Burkholderia mallei and Burkholderia pseudomallei.” J. Clin. Microbiol. 36 (1998): 2737-2741.
Gilbert, R.O. “Glanders” In Foreign Animal Diseases. Richmond, VA: United States Animal Health Association, 1998. 14 Nov 2002 <http://www.vet.uga.edu/vpp/gray_book/FAD/gla.htm>.
“Glanders.” Animal Health Australia. The National Animal Health Information System (NAHIS). 4 Oct 2002
<http://www.brs.gov.au/usr-bin/aphb/ahsq?dislist=alpha>.
“Glanders (Burkholderia mallei)” Centers for Disease Control and Prevention (CDC), July 2002. 8 Oct 2002
< http://www.cdc.gov/ncidod/dbmd/diseaseinfo/glanders_t.htm>.
“Glanders.” In Herenda, D., P.G. Chambers, A. Ettriqui, P. Seneviratna, and T.J.P. da Silva. “Manual on meat inspection for developing countries. FAO Animal Production and Health Paper 119.” 1994 Publishing and Multimedia Service, Information Division, FAO, 14 Nov 2002
< http://www.fao.org/docrep/003/t0756e/T0756E07.htm#ch6.2.3>.
“Glanders.” In Manual for the Recognition of Exotic Diseases of Livestock: A Reference Guide for Animal Health Staff. Food and Agriculture Organization of the United Nations, 1998. 14 Nov 2002
<http://panis.spc.int/RefStuff/Manual/Equine/GLANDERS.HTML>.
“Glanders.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000. 14 Nov 2002 <http://www.oie.int/eng/normes/mmanual/A_00076.htm>.
“Glanders.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 502-3.
“Glanders and Melioidosis.” In Medical Management of Biological Casualties Handbook, 4th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 14 Nov 2002
<http://www.vnh.org/BIOCASU/8.html>.
“Material Safety Data Sheet –Burkholderia (Pseudomonas) mallei.” Canadian Laboratory Centre for Disease Control, January 2001. 14 Nov 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds25e.html>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: hemorrhagic fever with renal syndrome, HFRS, hantavirus pulmonary syndrome, HPS, hemorrhagic nephrosonephritis, epidemic hemorrhagic fever, Korean hemorrhagic fever,
nephropathia endemica, NE.
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Hantaviruses (genus Hantavirus, family Bunyaviridae) are a group of at least 25 antigenically distinct viruses carried in rodents. Some of these viruses can cause hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome in humans.
Hemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar diseases that occur throughout Eurasia. HFRS includes several diseases that formerly had other names, including Korean hemorrhagic fever, epidemic hemorrhagic fever and nephropathia epidemica. Hantaviruses that can cause HFRS include Hantaan virus, Puumala virus, Dobrava virus and Seoul virus.
Hantavirus pulmonary syndrome (HPS) is a clinical syndrome caused by a number of hantaviruses in North and South America. In the United States, the Sin Nombre virus causes most cases. HPS can also result from infection by the New York, Black Creek, Bayou, Andes, Oran, Lechiguanas, Bermejo, Laguna Negra, Choclo, Araraquara and Castelo dos Sonhos viruses, as well as other unnamed hantaviruses.
Hantaviruses that have not been linked to human disease include the Isla Vista, Bloodland Lake, Muleshoe, Prospect Hill and El Moro Canyon viruses in North America, the Rio Segundo virus in Costa Rica and the Rio Mamore virus in Bolivia. European and Asian hantaviruses that have not been implicated in any human disease include Thailand virus in Thailand, Khabarovsk virus in Russia, Thottapalayam virus in India, Tula virus in Europe and Topografov virus in Siberia.
Geographic Distribution
Hantaviruses are found worldwide in rodents. The viruses that cause hantavirus pulmonary syndrome seem to occur only in North, Central and South America. Confirmed human cases have been seen in the United States, Argentina, Bolivia, Brazil, Chile, Paraguay, Panama and Uruguay. Viruses associated with HPS in the United States include the Sin Nombre, New York, Black Creek and Bayou viruses. The Sin Nombre virus has also been found in Canada. In South America, HPS is caused by the Andes virus in Argentina and Chile, the Bermejo virus in Bolivia and Argentina, the Oran and Lechiguanas viruses in Argentina, the Laguna Negra virus in Paraguay and Bolivia, the Choclo virus in Panama, and the Araraquara and Castelo dos Sonhos viruses in Brazil.
HFRS is mainly seen in Europe and Asia; however, one causative agent, the Seoul virus, can be found worldwide and has been associated with cases of HFRS in the United States. HFRS is also caused by the Hantaan virus in China, Russia and Korea, the Puumala virus in Europe, Russia and Scandinavia, and the Dobrava virus in the Balkans.
Transmission
Rodents are the reservoir host for hantaviruses; infections can be spread among the natural hosts by aerosols and bites. Virus is found in rodent saliva, feces and urine. Humans can become incidental hosts when they come into contact with infected rodents or their excretions. Often, rodent urine, droppings or nests are disturbed in enclosed areas; the viruses are then inhaled in aerosolized dust. Hantaviruses can also be transmitted through broken skin, the conjunctiva and other mucous membranes, by rodent bites and possibly by ingestion. Arthropod vectors do not seem to exist. Vertical transmission also appears to be negligible or nonexistent. Person to person spread has not been seen in HPS cases in North America or HFRS in Eurasia but may occur with the Andes virus in Argentina.
Hantaviruses are sensitive to drying but have been found in neutral solutions for several hours at 37° C and for several days in colder temperatures. Infectious viruses have also been detected in dried cell cultures for up to 2 days.
Disinfection
Hantaviruses are susceptible to 1% sodium hypochlorite, 2% glutaraldehyde and 70% ethanol. A 10% sodium hypochlorite solution has been recommended for heavily soiled areas. Hantaviruses are also susceptible to acid (pH 5) conditions and can be inactivated by heating to 60° C for 1 hour.
Incubation Period
The incubation period varies from 3 to 60 days; most often, the symptoms appear after 14 to 30 days.
Clinical Signs
Hemorrhagic Fever with Renal Syndrome
The onset of HFRS is usually abrupt; the initial clinical signs may include fever, chills, prostration, headache and backache. Patients may also develop injected mucous membranes, a flushed face and conjunctivae, or a petechial rash, usually on the palate and axillae. The fever typically lasts for 3 to 8 days and is followed by a proteinuric stage. Hypotension may develop during this phase of the disease and can last for hours or days. Nausea and vomiting often occur and death may result from acute shock. This stage is typically followed by an oliguric phase then a diuretic phase as kidney function improves. Death can occur at any point, but is particularly common during the hypotensive or oliguric phases. In severe cases, kidney failure, pulmonary edema or disseminated intravascular coagulation may be seen. Convalescence can take weeks or months.
The severity of disease varies with the causative agent. Hantaan virus and Dobrava virus infections usually cause severe symptoms. Seoul virus generally results in more moderate disease and Puumala infections are typically mild.
Hantavirus Pulmonary Syndrome
Hantavirus pulmonary syndrome is usually characterized by pulmonary rather than kidney disease. The initial phase usually lasts for 3 to 5 days; the clinical signs during this period may include fever, myalgia, headache, chills, dizziness, malaise, lightheadedness, nausea, vomiting and sometimes diarrhea. Arthralgia, back pain and abdominal pain are occasionally seen. Respiratory distress and hypotension usually appear abruptly, with cough and tachypnea followed by pulmonary edema and evidence of hypoxia. Cardiac abnormalities may be seen, including bradycardia, ventricular tachycardia or fibrillation. After the onset of the cardiopulmonary phase, the disease usually progresses rapidly; patients may be hospitalized and require mechanical ventilation within 24 hours. Kidney disease develops occasionally, but is most often mild; kidney damage occurs more often with the Andes, Bayou and Black Creek viruses. Although recovery is rapid, convalescence may last for weeks or months. Asymptomatic or mild infections appear to be rare.
Communicability
Although viruses can be found in the blood and urine of HFRS patients, no person-to-person transmission has been seen in cases of HPS in North America or HFRS in Eurasia. Person-to-person transmission has been reported during an outbreak of Andes virus in South America: a physician apparently contracted an infection after exposure to a patient’s blood and an adolescent seems to have contracted the disease from her parents. These cases remain to be confirmed by laboratory investigation.
Diagnostic Tests
Hantavirus infections are often diagnosed by serology. IgM in acute phase sera or a rise in IgG titer is diagnostic. Enzyme-linked immunosorbent assay (ELISA) assays are available for the Sin Nombre virus as well as other hantaviruses. Immunoblotting (Western blotting) and neutralizing plaque assays may also be used. A rapid immunoblot strip assay (RIBA) that detects antibodies to Sin Nombre and other hantaviruses is being developed.
Infections can also be diagnosed by finding antigens in tissues with immunohistochemistry or RNA with reverse transcriptase- polymerase chain reaction assays (RT-PCR). Virus isolation is rarely used, as hantaviruses are difficult to isolate from humans.
Treatment and Vaccination
Supportive care is the mainstay of treatment. Intensive care may be required. Ribavirin may be helpful in early cases of HFRS, but has not been effective for HPS to date. Vaccines are not available.
Morbidity and Mortality
Hantavirus outbreaks are often associated with increased rodent populations or environmental factors that lead to increased human exposure to rodents. Worldwide, approximately 150,000 to 200,000 people are hospitalized with HFRS each year. Different hantaviruses tend to cause mild, moderate or severe cases of HFRS; the mortality rate can vary from 0.1 to 3% for Puumala virus infections, to approximately 5% to 15% for Hantaan and Dobrava virus infections. Seoul virus tends to cause moderate disease with mortality rates of approximately 1%. Sin Nombre and New York virus infections are often fatal; the mortality rate is estimated to be 40 to 50%. The renal variant form of HPS caused by the Andes, Bayou and Black Creek viruses also has a high mortality rate. Convalescence from either HFRS or HPS can take weeks or months, but patients usually recover full lung function.
Hantaviruses are found naturally in various species of rodents. Infections do not appear to be pathogenic to their rodent hosts and may be carried lifelong.
Hantavirus-associated diseases have not been reported in domestic animals. Antibodies have been found in cats and dogs in the United States and western Canada and cats in Europe. In one study, 9.6% of healthy cats in the United Kingdom and 23% of cats with chronic diseases were seropositive. Horses, cattle and coyotes were seronegative in one U.S. survey.
|
“All about hantavirus. Technical information index.” Centers for Disease Control and Prevention, Sept 2000. 11 Dec 2002
<http://www.cdc.gov/ncidod/diseases/hanta/hps/noframes/phys/
technicalinfoindex.htm>.
Bennett M., G. Lloyd, N. Jones, A. Brown, A.J. Trees, C. McCracken, N.R. Smyth, C.J. Gaskell and R.M. Gaskell. "Hantavirus in some cat populations in Britain" Vet. Rec. 127 (1990): 548-549.
Leighton F.A., H.A. Artsob, M.C. Chu and J.G. Olson. “A serological survey of rural dogs and cats on the southwestern Canadian prairie for zoonotic pathogens.” Can. J. Public Health 92, no. 1 (Jan-Feb 2001): 67-71.
Malecki T.M., G.P. Jillson, J.P. Thilsted JP, J. Elrod, N. Torrez-Martinez and B. Hjelle. “Serologic survey for hantavirus infection in domestic animals and coyotes from New Mexico and northeastern Arizona.” J. Am. Vet. Med. Assoc. 212, no. 7 (April 1998): 970-3.
“Material Safety Data Sheet – Hantavirus.” Canadian Laboratory Centre for Disease Control, Sept 2002. 11 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds74e.html>.
Nowotny N. “The domestic cat: a possible transmitter of viruses from rodents to man." Lancet 343 (1994): 921.
Schmaljohn C. and B. Hjelle. “Hantaviruses: A global disease problem.” Emerg. Infect. Dis. 3, no. 2 (April-June 1997):95-104. 11 Dec 2002
<http://www.cdc.gov/ncidod/EID/vol3no2/schmaljo.htm>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: Pseudoglanders, Whitmore Disease
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Melioidosis results from infection by Burkholderia pseudomallei, a motile Gram negative bacillus (family Pseudomonadaceae). This organism was formerly known as Pseudomonas pseudomallei.
Geographic Distribution
Melioidosis is endemic in Southeast Asia, Africa, Australia, the Middle East, India and China. This infection is mainly associated with tropical and subtropical regions; however, B. pseudomallei has also been isolated from the temperate regions of southwest Australia and France. Isolated cases have occurred in South America and in the states of Hawaii and Georgia in the United States. B. pseudomallei is generally found in water or moist soil.
Transmission
New infections are primarily acquired from organisms in the environment. Contaminated swamps, muddy water and rodents are important sources of infection. Soil-borne infections are generally associated with heavy rainfall or flooding in areas with high humidity or temperatures. Infection can occur by ingestion, inhalation, or through wounds and abrasions. The role of insect bites is uncertain. Direct human-to-human and animal-to-human transmission is rare but can occur after contact with blood or body fluids. Depending on the site of the infection, contaminated body fluids may include urine, nasal secretions and milk. Shed organisms can survive for months in soil and water.
Disinfection/ Inactivation
B. pseudomallei can survive for months to years in soil and water, but can be readily destroyed by heat. Moist heat of 121°C for at least 15 min or dry heat of 160-170°C for at least 1 hour is recommended for disinfection. The organism is also susceptible to numerous disinfectants, including 1% sodium hypochlorite, 70% ethanol, glutaraldehyde and formaldehyde.
Incubation Period
In natural infections, the incubation period can vary from two days to months or years. Infections may remain latent for years. Infections from aerosolized forms in biological weapons are expected to have an incubation period of 10-14 days.
Clinical Signs
B. pseudomallei infections may be inapparent or can result in pulmonary infections, disseminated septicemia, acute nondisseminated septicemia or localized chronic suppurative infections.
The most serious form is disseminated septicemic infection. In natural infections, this form is most common in people with pre-existing debilitating diseases such as AIDS, cancer, diabetes and kidney failure. Its onset may be acute. The clinical signs may include severe headache, severe dyspnea, disorientation, pharyngitis, upper abdominal pain, diarrhea, pustular skin lesions and notable muscle tenderness. Pulmonary signs and symptoms of arthritis or meningitis are sometimes seen. This form is often accompanied by septic shock.
Pulmonary infections vary in severity, from mild bronchitis to severe necrotizing pneumonia. Symptoms can appear suddenly or gradually and may include fever, headache, cough, tachypnea, rales, blood-tinged sputum, anorexia, generalized myalgia and dull aching or pleuritic chest pain.
Localized chronic suppurative infections are characterized by abscesses in the skin, lymph nodes or other organs including the brain. Osteomyelitis is common with this form. Fever may or may not be present. Acute nondisseminated septicemic infection also occurs, involves a single organ and is relatively rare.
In cases with acute infection of the oral, nasal or conjunctival mucosa, the clinical signs may include mucopurulent, blood streaked nasal discharge from the nose, as well as nodules and ulcerations in the septum and turbinates.
Communicability
Yes. Direct transmission between humans or from humans to animals is rare but can occur after contact with blood or body fluids. Depending on the site of the infection, contaminated body fluids may include urine, nasal secretions and milk. Human carriers have not been seen.
Diagnostic Tests
Melioidosis can be diagnosed by isolation and identification of Burkholderia pseudomallei. Bacteria may be found in blood, sputum, tissues and wound exudates. In the septicemic form, blood cultures may be negative until just before death.
The organism has a wrinkled colony form, which may be mixed with smooth colonies. A characteristic odor has been described. (Due to the risk of infection, directly sniffing the plates is not recommended.) Organisms are oval, Gram negative bacilli, with bipolar staining in young cultures. A polymerase chain reaction can differentiate B. mallei DNA from B. pseudomallei.
Serologic tests on paired sera may be helpful. High single titers in the presence of clinical signs may also be used for diagnosis. Serologic tests include agglutination tests, indirect hemagglutination, complement fixation, immunofluorescence assays and enzyme immunoassays. Cross-reactions may occur in serologic tests with Burkholderia mallei, the causative agent of glanders.
Treatment and Vaccination
B. pseudomallei is variably susceptible to antibiotics. Long-term treatment may be necessary and multiple drugs may be needed. Pulmonary resection or draining of abscesses is sometimes necessary for chronic cases. No vaccine is available.
Morbidity and Mortality
In natural infections, the mortality rate is usually less than 10%, except in disseminated septicemic infections; mortality rates as high as 90% may be seen in this form. Localized lesions may be progressive or disseminate. Fatal infections are more common in patients who are immunosuppressed or have concurrent disease.
Exposure to biological weapons containing aerosolized forms is expected to result in septicemia or severe pulmonary infections, with high mortality rates in spite of treatment.
Species Affected
Infection with B. pseudomallei is seen most often in pigs, goats and sheep. It occurs less often in cattle, horses, dogs, rodents, birds, dolphins, tropical fish, primates and various wild animals. Hamsters, guinea pigs and rabbits can be infected in the laboratory.
Incubation Period
The incubation period can vary from days to months or years. Abscesses may be carried without symptoms.
Clinical Signs
B. pseudomallei infection results in suppurating or caseous lesions in lymph nodes or other organs. Infections may be asymptomatic and abscesses may be found in clinically normal goats, sheep and pigs. Symptomatic melioidosis mimics other diseases; the clinical signs vary with the site of the lesion. They may include fever, loss of appetite, and lymphadenopathy, often involving the submandibular nodes in pigs. Lameness or posterior paresis, nasal discharge, encephalitis, gastrointestinal symptoms or respiratory signs may also be seen in some species. Extensive abscesses and infections of vital organs can be fatal.
In sheep and goats, lung abscesses and pneumonia are common. Other common symptoms in sheep include high fever, coughing, ocular and nasal discharge, lameness with swollen joints, neurologic disease, and gradual emaciation. Some animals may display only weakness and fever. Mastitis is sometimes seen in goats and the superficial lymph nodes and udder may contain palpable abscesses. Pulmonary lesions in goats are usually less severe than in sheep and coughing is not prominent. In horses, neurologic disease, respiratory symptoms, or colic and diarrhea have been described. Infections in pigs are usually chronic and asymptomatic. Acute infections in this species may result in septicemia with fever, anorexia, coughing and nasal and ocular discharges. Abortions and stillbirths may occur but are rare, and orchitis may occur in boars. Cattle are rarely affected, but may develop pneumonia or neurologic signs.
Communicability
Yes. Direct transmission between animals or from animals to humans is rare but can occur after contact with blood or body fluids. Depending on the site of the infection, contaminated body fluids may include urine, nasal secretions and milk. Animals may become carriers.
Diagnostic Tests
Swabs of nasal discharges and samples collected from lesions should be submitted for culture. Organisms may be isolated from the sputum, blood, wound exudates or tissues. In some species, serum may also be collected for serologic tests.
Melioidosis is diagnosed by isolation and identification of Burkholderia pseudomallei. This organism has a wrinkled colony form, which may be mixed with smooth colonies. A characteristic odor has been described. (Due to the risk of infection, directly sniffing the plates is not recommended.) Organisms are oval, Gram negative bacilli, with bipolar staining in young cultures. A polymerase chain reaction can differentiate B. mallei DNA from B. pseudomallei.
In some species, agglutination tests, indirect hemagglutination, immunofluorescence, and enzyme immunoassays can be used for diagnosis. Cross-reactions may occur in serologic tests with Burkholderia mallei, the causative agent of glanders.
Treatment and Vaccination
B. pseudomallei is susceptible to various antibiotics, but relapses can occur when treatment is stopped. Vaccines are available in some countries but are not effective against large challenge doses.
Morbidity and Mortality
Mortality varies with the site of the lesions, but can be high in sheep. Extensive abscesses and infections of vital organs can be fatal. Disseminated septicemic infections have a high mortality rate, but are less common in animals than humans. Infections may be progressive.
Post-Mortem Lesions
At necropsy, the major findings are multiple abscesses containing thick, caseous greenish-yellow or off-white material. These abscesses are generally not calcified. The regional lymph nodes, spleen, lung, liver and subcutaneous tissues are most often involved, but abscesses can occur in most organs. In acute cases, pneumonic changes in the lungs, meningoencephalitis and suppurative polyarthritis may be found. In cases with suppurative arthritis, the joints may contain fluid and large masses of greenish-yellow purulent material.
In sheep, common findings include abscesses and suppuration in the nasal mucosa. Splenic abscesses are often found in pigs at slaughter.
Bauernfeind A., Roller C., Meyer D., Jungwirth R., and Schneider I. “Molecular procedure for rapid detection of Burkholderia mallei and Burkholderia pseudomallei.” J. Clin. Microbiol. 36 (1998): 2737-2741.
Bogle, R.B. “Bioterrorism: Hype or Hazard?” Cactus Chronicle (Arizona Society for Clinical Laboratory Science) 23, no. 1 (January/February 2000): 7 Oct 2002 <http://pw1.netcom.com/~aguldo/agga/txt/cactusbt.htm>.
Gilbert, R.O. “Glanders” In Foreign Animal Diseases. Richmond, VA: United States Animal Health Association, 1998. 7 Oct 2002 <http://www.vet.uga.edu/vpp/gray_book/FAD/gla.htm>.
“Glanders and Melioidosis.” In Medical Management of Biological Casualties Handbook, 4th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 26 Oct 2002
<http://www.usdpi.org/glanders_and_m__-_dod_medical_guide.htm>.
Herenda, D., P.G. Chambers, A. Ettriqui, P. Seneviratna, and T.J.P. da Silva. “Manual on meat inspection for developing countries. FAO Animal Production and Health Paper 119.” 1994 Publishing and Multimedia Service, Information Division, FAO, 8 Oct 2002
<http://www.fao.org/docrep/003/t0756e/t0756e00.htm>.
Jesudason M.V., W.S. Anandaraj and B. Malathi. “An indirect ELISA for the diagnosis of melioidosis.” J. Med. Res. 114 (Aug 2001):51-3.
“Material Safety Data Sheet –Burkholderia (Pseudomonas) pseudomallei.” January 2001 Canadian Laboratory Centre for Disease Control. 4 October 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds26e.html>.
“Melioidosis.” Animal Health Australia. The National Animal Health Information System (NAHIS). 4 Oct 2002
<http://www.brs.gov.au/usr-bin/aphb/ahsq?dislist=alpha>.
“Melioidosis.” In Manual for the Recognition of Exotic Diseases of Livestock: A Reference Guide for Animal Health Staff. Food and Agriculture Organization of the United Nations, 1998. 8 Oct 2002
<http://panis.spc.int/RefStuff/Manual/Multiple%20Species/MELIOIDOSIS.HTML>.
“Melioidosis.” In The Merck Manual, 17th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 7 Oct 2002 <http://www.merck.com/pubs/mmanual/section13/chapter157/157d.htm>.
“Melioidosis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 481-2.
“Melioidosis (Burkholderia pseudomallei)” Centers for Disease Control and Prevention (CDC). 8 Oct 2002 <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/melioidosis_g.htm>.
Vadivelu, J. and S.D. Puthucheary. “Diagnostic and prognostic value of an immunofluorescent assay for melioidosis.” The American Journal of Tropical Medicine & Hygiene 62, no. 2 (2000): 297–300.
Synonyms: Paratyphoid
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Salmonella are Gram negative, facultatively anaerobic bacilli (family Enterobacteriaceae). Over 1800 serovars are known and are currently considered to be separate species. Standardized classification schemes for Salmonella have not been completely adopted and several synonyms may be used for the same serovar.
Non-typhoidal salmonellosis can result from infection by numerous Salmonella serovars. Common serovars in domestic animals include S. typhimurium, S. dublin and S newport in cattle; S. typhimurium, S. dublin, S. anatum and S montevideo in sheep; S typhimurium and S. choleraesuis in pigs; and S. typhimurium, S. anatum, S. newport, S. enteritidis and S. arizonae in horses. Pullorum disease (caused by S. pullorum) and fowl typhoid (caused by S. gallinarum) are found in chickens. Avian paratyphoid can be caused by a number of different species of Salmonella, including S. typhimurium, S. enteritidis and S. heidelberg. Some serovars tend to produce a particular syndrome: for example, in pigs S. choleraesuis is usually associated with septicemia and S. typhimurium with enteric salmonellosis.
Geographic Distribution
Salmonella can be found worldwide, although the distribution of serovars may vary. Salmonellosis seems to be more common where livestock are intensively farmed.
Transmission
Transmission usually occurs by the fecal-oral route; bacteria are shed in the feces. Animals can become infected through contaminated feed, pasture, water or close contact with an infected host. Carnivores, including humans, are also infected through meat, milk, eggs and other animal products that are not thoroughly cooked. Salmonella can be spread by fomites, rodents and wild birds, but vectors are not required. Animals may become carriers for months to years.
Some Salmonella can persist for months or years in the environment, particularly in wet, warm environments. S. typhimurium remains viable for seven months in soil, water or feces or on pasture. S. dublin can remain infective for more than a year. S. choleraesuis can survive in pig meat for up to 450 days and for several months in feces or slurry. Salmonella survives for less than one week in composted cattle manure.
Disinfection/ Inactivation
Salmonella are susceptible to a variety of disinfectants including 1% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde, iodine-based disinfectants, phenolic disinfectants and formaldehyde. The organism can also be inactivated by moist heat (121° C for a minimum of 15 min) or dry heat (160-170° C for at least an hour).
Incubation Period
Symptoms of gastroenteritis usually begin 6 to 72 hours after the ingestion of bacteria.
Clinical Signs
Salmonella species can cause gastroenteritis, enteric fevers, septicemia and focal infections in humans. Host factors and the virulence of the isolate influence both the severity of the disease and the form it takes. More severe disease is seen in infants, the elderly, and individuals with debilitating illnesses.
More than 2000 serovars can cause gastroenteritis in humans. Approximately half of all cases are caused by S. enteritidis and S. typhimurium. In humans, Salmonella infections most often result in self-limiting gastroenteritis, characterized by nausea, diarrhea (sometimes bloody), vomiting, abdominal cramps and sometimes fever and chills.
Enteric fevers can be caused by S. typhi (typhoid fever) or other Salmonella species. These life-threatening illnesses are characterized by fever, anorexia, headache, myalgia and constipation, and may be preceded by gastroenteritis. Septicemia can also occur without intestinal symptoms or bacteria in the feces. Occasionally, localized infections such as septic arthritis develop. Asymptomatic carriers also occur.
Communicability
Yes. Salmonella are shed through the course of infection, for several days to several weeks. Humans can become temporary carriers for several months after recovery; 1% of adults and 5% of children shed bacteria for more than a year. Antibiotics can prolong shedding.
Diagnostic Tests
Salmonellosis is diagnosed by isolating the causative organism from feces, blood or other specimens. Salmonella species are identified by culture and biochemical testing. Under the microscope, they are Gram negative short rods. Colonies on nutrient agar are grayish, moist, translucent to opaque, and smooth. Broth cultures are turbid and may contain a pellicle or sediment. Selective media are available. Identification can be confirmed by serologic analysis of O and H antigens.
Treatment and Vaccination
Salmonella is susceptible to a variety of antibiotics; resistance is sometimes seen. Antibiotics are given for enteric fevers, septicemia and focal infections. They are not generally recommended for uncomplicated gastroenteritis as they prolong shedding of bacteria without shortening the illness. Supportive therapy, including fluid replacement, is sometimes necessary. Vaccines are not available for non-typhoidal salmonellosis.
Morbidity and Mortality
An estimated 1.4-3 million cases and more than 500 deaths occur yearly in the United States. Salmonellosis is particularly common in infants and young children. Large outbreaks are sometimes seen in restaurants as well as hospitals, nursing homes and other institutions. Most cases of gastroenteritis in healthy adults are self-limiting and resolve without complications; infections may be more serious in young children, the elderly and those with debilitating illnesses.
Species Affected
Clinical salmonellosis can occur in all species of domestic animals. It is most common in cattle, sheep, pigs and horses, with infrequent disease in dogs and cats. Reservoirs include poultry, pigs, cattle, sheep, rodents, horses, tortoises, turtles, cats and dogs. Some serovars are associated with specific animal reservoirs, including poultry with S. enteritidis and pigs with S. choleraesuis. Other serovars infect a wide variety of animals as well as humans. Carriers can occur in all species.
Incubation Period
The incubation period for Salmonella gastroenteritis varies with the dose of bacteria and the form of the disease. In horses, severe infections can develop acutely, with diarrhea appearing after 6 to 24 hours. Similarly, humans develop symptoms of gastroenteritis 6 to 72 hours after ingesting bacteria. Long incubation periods are also seen; animals with asymptomatic infections can develop overt disease when stressed.
Clinical Signs
Infections in Large Animals
Infections in healthy animals may be asymptomatic. Symptomatic infections are often precipitated by stressors such as transport, drought, malnutrition or food deprivation, crowding and some drugs. Clinical disease is common in horses after major surgery. Symptomatic infections may result in several syndromes: acute septicemia, acute enteritis, subacute or chronic salmonellosis, and abortion.
Acute septicemia is usually seen in newborn calves, lambs and foals. It also occurs in pigs up to 6 months of age. Typically, a high fever and severe depression develop acutely, often followed by death within 24 to 48 hours. Pigs and calves may have pneumonia or neurologic signs including nystagmus and incoordination. Pigs often develop a dark red or purple skin discoloration, most often on the ears and abdomen. Animals can be found dead without signs of diarrhea.
Acute enteritis is the most common form in adult animals and older calves. Symptoms may include fever, diarrhea, dehydration, tenesmus, abdominal pain, a drop in milk production and sometimes dysentery. The fever may disappear before diarrhea appears. The feces are foul smelling and contain mucus, shreds of mucus membrane or casts of intestinal mucosa, and sometimes large blood clots. Horses often have abdominal pain and severe dehydration and may die within 24 to 48 hours. Sheep sometimes develop “snoring” respiratory sounds associated with regurgitation of the ruminal contents. Surviving animals may become emaciated and remain unthrifty. Calves can develop other complications including joint infections, pneumonia, and gangrene at the tips of the ears and tail or below the fetlock.
Subacute enteritis occurs in adult sheep, horses and cattle. Symptoms may include a mild fever, inappetence, soft feces and dehydration. In cattle, fever and abortion may be seen, followed by diarrhea several days later. Chronic enteritis is mainly seen in older calves, adult cattle and growing pigs. Infected animals have persistent diarrhea, with progressive emaciation, a low-grade intermittent fever and anorexia. The feces are typically scant and may be normal or contain mucus, casts or spots of blood. Rectal strictures sometimes develop in growing pigs. This form of salmonellosis may follow an episode of acute enteritis.
Abortions can occur after acute or chronic enteritis, or without other clinical signs. S. dublin is often associated with abortions in cattle and Salmonella abortus ovis with abortions in sheep. These two infections can occur without enteritis. Abortions in pregnant ewes may be followed by a fetid, dark red vaginal discharge and sometimes death.
Infections in Small Animals and Birds
Salmonellosis is relatively rare in dogs and cats. In these species, acute diarrhea is typical, either with or without septicemia. Pneumonia or abortion may be seen and cats sometimes develop conjunctivitis. Rats and mice may also develop enteritis or septicemia. The clinical signs in rodents include anorexia, weight loss, conjunctivitis and a rough coat, with sporadic deaths. Avian paratyphoid mainly occurs in hatchling chickens, turkeys and other birds, and is rare in older birds. Symptoms may include somnolence, anorexia, watery diarrhea and increased thirst.
Communicability
Yes. Organisms are shed in the feces and animals may become carriers for months to years.
Diagnostic Tests
Enteric infections are diagnosed by clinical signs and the isolation of Salmonella from the feces. Isolation alone is unreliable; Salmonella can be found in the feces of healthy animals and in animals ill from other causes. Blood may be cultured from animals with septicemia, egg contents from poultry, and fetal stomach contents, fresh placenta and vaginal swabs after abortions. Heart blood, bile, liver, spleen and mesenteric lymph nodes are usually sampled at necropsy. Environmental samples, including feed, water, and feces from wild rodents and birds, may be helpful.
Salmonella species are identified by culture and biochemical testing. Under the microscope, they are Gram negative short rods. Colonies on nutrient agar are grayish, moist, translucent to opaque, and smooth. Broth cultures are turbid and may contain a pellicle or sediment. Selective media are available. Identification can be confirmed by serologic analysis of O and H antigens.
Serology on acutely ill animals is rarely diagnostic; agglutinins do not appear until 2 weeks after an infection. However, herd sampling may be helpful. Serologic tests include the whole blood test for the rapid diagnosis of S. pullorum and S. gallinarum in poultry and the tube agglutination test for all species of farm animals. Enzyme-linked immunosorbent assays (ELISAs) are also available for some serovars.
Treatment and Vaccination
Septicemia can be treated with a variety of antibiotics; treatment of gastroenteritis is controversial as these drugs may prolong fecal shedding and alter the intestinal flora. Fluid therapy and other supportive care may be indicated. Commercial killed vaccines or autogenous bacterins are sometimes used in outbreaks, particularly when pregnant cattle are involved.
Morbidity and Mortality
Acute septicemia in very young animals can result in morbidity and mortality rates up to 100%. Mortality in horses may also be very high. Enteric infections are often self-limiting, although animals can become chronically infected or remain unthrifty.
Post-Mortem Lesions
Post-mortem lesions usually include signs of necrotizing fibrinous enteritis or septicemia. In animals with enteritis, the intestine contains mucosal erosions; these lesions are most apparent in the lower ileum and colon. Hemorrhages and fibrin strands are common and the lumen may contain blood. Similar lesions may be seen in the abomasum. Extensive diphtheritic membranes are sometimes found in the intestines and inflammation may be noted in the wall of the gall bladder. The mesenteric lymph nodes are usually edematous and hemorrhagic. Other lesions may include fatty degeneration in the liver, bloodstained fluid in the serous cavities, and petechial hemorrhages under the epicardium or other serous membranes. In animals with acute septicemia, there are usually extensive submucous and subserous petechial hemorrhages.
In cattle with chronic salmonellosis, discrete areas of necrosis are usually found in the cecal and colonic mucosa. The lesions are characterized by necrotic material over a red granular surface, in a thickened intestinal wall.
“Bacterial infections caused by Gram-negative bacilli. Enterobacteriaceae.” In The Merck Manual, 17th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 8 Nov 2002 <http://www.merck.com/pubs/mmanual/section13/chapter157/157d.htm>.
Euzéby, J.P. “List of bacterial names with standing in nomenclature. Salmonella nomenclature.” July 2000. 24 October 2002 <http://www.bacterio.cict.fr/Salmonellanom.html>.
Giannella, R.A. “Salmonella.” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 23 Oct 2002 <http://www.gsbs.utmb.edu/microbook/ch021.htm>.
“Material Safety Data Sheet – Salmonella choleraesuis.” Canadian Laboratory Centre for Disease Control, May 2001. 15 October 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds132e.html>.
“Material Safety Data Sheet – Salmonella spp. (excluding S. typhi, S. choleraesuis, and S. paratyphi).” Canadian Laboratory Centre for Disease Control, March 2001. 15 October 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds135e.html>.
“Salmonella.” Animal Health Australia. The National Animal Health Information System (NAHIS), 1996. 18 Oct 2002
<http://www.brs.gov.au/usr-bin/aphb/ahsq?dislist=alpha>.
“Salmonellosis.” Centers for Disease Control (CDC), Dec 2001. 24 Oct 2002 <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/salmonellosis_t.htm>.
“Salmonella.” In Schnierson’s Atlas of Diagnostic Microbiology, 9th ed. Abbott Park, IL: Abbott Laboratories, 1984, pp. 24-5.
“Salmonellosis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 120-3;241-3;251-2;1321;1947-9.
“Salmonellosis” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000. 25 Oct 2002 <http://www.oie.int/eng/normes/mmanual/A_00114.htm>.
“Salmonellosis (Avian).”Animal Health Australia. The National Animal Health Information System (NAHIS). 18 Oct 2002
<http://www.brs.gov.au/usr-bin/aphb/ahsq?dislist=alpha>.
“Salmonellosis (Pigs).” Animal Health Australia. The National Animal Health Information System (NAHIS). 18 Oct 2002
<http://www.brs.gov.au/usr-bin/aphb/ahsq?dislist=alpha>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
What is the link between H1N1 flu and agriculture?
Many domestic species, including some of our agricultural animals (i.e., pigs, horses, birds), and even ferrets, could become infected with influenza viruses, including the current H1N1 virus circulating in humans. This new strain differs from previously identified human viruses and consists of a mixture of genetic material from human, swine, and avian influenza viruses.
Can I get this new strain of virus from eating pork or pork products?
No. H1N1 is a respiratory disease and pork is safe to eat. There has been no known transmission of the H1N1 virus through the consumption or handling of pork or pork products. Pork should always be properly handled and cooked to an internal temperature of at least 160 degrees Fahrenheit to kill food-borne pathogens that might be present.
For more information about safe food handling visit www.befoodsafe.gov.
Have any swine in the U.S. been infected with the H1N1 flu virus?
Swine herds are being monitored and there is no evidence that this strain of the virus has infected any swine herds in the United States. On October 19, 2009 - Agriculture Secretary Tom Vilsack announced that USDA's National Veterinary Services Laboratories (NVSL) has confirmed the presence of 2009 pandemic H1N1 influenza virus in a pig sample collected at the Minnesota State Fair. The infection of the fair pig does not suggest infection of commercial herds. The main reason is that show pigs and commercially raised pigs are in separate segments of the swine industry that do not typically interchange personnel or animal stock. Good hygiene, biosecurity and other management practices are essential to maintain swine herds free of H1N1.
Can humans transmit the H1N1 virus to swine or vice versa?
The United States Department of Agriculture's (U.S.D.A.) National Animal Disease Center in Ames, Iowa is conducting studies to determine how infective this virus is in swine. From the information available from this outbreak and from scientific studies, we can assume that the disease can pass from human to pig and from pig to pig. However, the specific conditions required for the virus to infect other people or animals are still being determined.
Can you get H1N1 from being around or touching swine?
Possibly. An infected human may be able to pass the virus to pigs. However, the most likely way for a person to become infected with the H1N1 virus is through contact with a person who has the influenza. Influenza spreads from person-to-person mainly through coughing or sneezing by infected people.
They found H1N1 in pigs in Canada, are pigs passing the disease to people?
No, the Canadian Food Inspection Agency (C.F.I.A.) announced the occurrence of H1N1 virus in a swine herd in Alberta. The C.F.I.A. believes that the swine became ill after exposure to a Canadian farm worker, exhibiting flu-like symptoms, who had recently returned from Mexico.
What are the clinical signs of H1N1 in swine?
Signs of influenza in swine are similar to those in humans, sudden onset of fever, depression, coughing, sneezing, runny nose, breathing difficulties, watery red eyes, and lack of appetite. If your pigs are showing any of these signs, call your veterinarian.
Is there anyone monitoring swine for H1N1?
Veterinarians are on constant alert for the signs of influenza in swine. Private practitioners, state and federal veterinarians and animal health officials are monitoring swine herds for signs of disease. U.S.D.A. has put U.S. pork producers on a high alert for safety. To date, the U.S. swine herd is free of H1N1 influenza.
How can I protect my swine herd?
- Practice, enforce and intensify your biosecurity measures.
- Avoid new introductions to the herd.
- Buy animals from trusted sources.
- Avoid using farm equipment from other farms and disinfect it prior to use if borrowed equipment is necessary. Disinfect equipment prior to returning it back to the loaning farm.
- Only healthy essential workers should be allowed to enter the farm. Workers should disinfect shoes, clothes and hands before entering the farm.
- Train workers to recognize influenza signs in swine and to report sick animals promptly.
For more information on biosecurity measures, visit: www.nj.gov/agriculture/divisions/ah/news/biosecurity.shtml
Are pet pigs susceptible to H1N1 flu? Can I get infected from my pet pig?
Yes, pet pigs are susceptible to H1N1; however it is not likely that you will get it from your pet pig. On the contrary, it is more likely that your pet pig will get it from you.
What can I do to protect both myself and my pet pig?
Practice biosecurity measures and proper hygiene, including washing your hands frequently, especially after handling your pet pig. Clean and disinfect shoes and clothes if you have been around other animals or people with influenza symptoms before touching your pet pig. If you become ill, do not have contact with your pig for at least 24 hours after the fever (temperature above 100 degrees Fahrenheit) is gone, without the use of fever-reducing medication.
What measures then can I take to prevent the spread of H1N1?
- Vaccination – The human H1N1 vaccine is expected to be available in the fall of 2009. Although annual seasonal influenza vaccines do not confer immunity to H1N1, annual influenza vaccination is strongly encouraged.
- Practice good hygiene:
- Cover your nose and mouth when you cough or sneeze. Use a tissue when possible and throw the tissue in the trash after you use it.
- Wash your hands with soap and water, especially after you cough or sneeze.
- Avoid touching your eyes, nose or mouth.
- Avoid close contact (within 6 feet) with sick people.
- Stay home if you are sick for at least 24 hours after the fever (temperature above 100 degrees Fahrenheit) is gone, without the use of fever-reducing medication. This is to keep you from infecting others and spreading the virus.
- Stay informed. Health officials will provide additional information as it becomes available.
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Plague results from infection by Yersinia pestis, a non-motile, facultatively intracellular, Gram negative rod (family Enterobacteriaceae).
Geographic Distribution
Plague is seen in parts of North and South America, Africa, the Middle East, Central and Southeast Asia and Indonesia. Foci of infection are found in the former Soviet Union. This disease does not occur in Europe, Australia or Japan.
Transmission
Plague is usually spread between rodents or humans by the bites of infected fleas. Vectors include a variety of rodent fleas, particularly the oriental rat flea (Xenopsylla cheopis). In the U.S., the most common vector is Oropsylla montana, a flea often found on California ground squirrels, rock squirrels, and sometimes other rodents including prairie dogs. Human fleas (Pulex irritans) may also carry Y. pestis. Y. pestis is also present in the tissues and body fluids of infected animals; these bacteria can be transmitted directly through mucous membranes and broken skin. Aerosols from people or animals with the pneumonic form are infectious and animals may transmit bacteria in bites. Carnivores often become infected when they eat diseased rodents.
In the wild, Y. pestis is maintained in cycles between wild rodents and fleas; sporadic cases occur in humans and domestic animals when they come into contact with infected animals or fleas. Infection of rodents in urban areas, particularly the Roof rat or Norway rat, can result in epizootic and epidemic plague in humans. Direct person-to-person transmission can occur in pneumonic plague.
Y. pestis can survive for long periods of time in organic material; it may remain viable for up to 100 days in blood and for as long as 9 months in human bodies. Infectious bacteria can also be found in water, moist soil and grains for several weeks. Y. pestis is not resistant to desiccation or heat: it is destroyed by exposure to 55°C for 15 minutes or several hours in sunlight.
Disinfection
Y. pestis is susceptible to a number of disinfectants including 1% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde, formaldehyde and iodine-based and phenolic disinfectants. It can also be inactivated by moist heat (121° C for at least 15 min) or dry heat (160-170° C for at least 1 hour).
Incubation Period
The incubation period for pneumonic plague is 1 to 3 days. The symptoms of bubonic plague appear after 2 to 6 days.
Clinical Signs
Three major forms of plague are seen in humans: bubonic plague, septicemic plague, pneumonic plague.
Bubonic plague appears acutely; the initial symptoms may include fever, headache, malaise and myalgia. Vomiting, nausea, abdominal pain, hepatomegaly and splenomegaly are sometimes seen. Patients with bubonic plague typically develop an infected, swollen, and very painful draining lymph node, called a bubo; the bubo is often one of the femoral or inguinal lymph nodes. Other lymph nodes, or multiple nodes, may also be involved. In some cases, a pustule, vesicle, eschar or papule occurs at the site of the flea bite.
Bubonic plague can develop into septicemic plague. Bacteremia is present in most cases of bubonic plague but the symptoms of septicemia – including high fever, chills, malaise, nausea, vomiting, abdominal pain, diarrhea and hypotension – do not always develop. Meningitis is relatively rare; it occurs in approximately 6% of people with the septicemic or pneumonic forms. Thromboses in blood vessels can cause necrosis and gangrene of the extremities or disseminated intravascular coagulation (DIC).
Pneumonic plague occurs after inhalation of bacteria or after blood-borne spread to the lungs. Pneumonic plague is expected to be the predominant form in a bioterrorist attack. The symptoms of pneumonic plague develop acutely and include high fever, chills, headache, myalgia and malaise. Nausea, vomiting, diarrhea and abdominal pain may be seen. Within 24 hours, a cough with bloody sputum develops; the sputum contains only specks of blood at first but eventually becomes foamy and pink or red. Cervical buboes occur rarely. Pneumonic plague is rapidly fatal, with dyspnea, stridor and cyanosis ending in respiratory failure and circulatory collapse.
Pestis minor is a benign form of bubonic plague, usually seen only in regions where plague is endemic. Pestis minor is characterized by fever, lymphadenitis, headache and prostration. These symptoms resolve spontaneously within a week.
Communicability
In the United States, person-to-person transmission of bubonic plague has not occurred since 1924; however, person-to-person transmission is seen in epidemics in some countries. Pneumonic plague can be highly contagious, particularly under crowded conditions.
Diagnostic Tests
A presumptive diagnosis can be made by identifying the characteristic organisms in sputum, blood, lymph node (bubo) aspirates or cerebrospinal fluid; Y. pestis is a Gram negative, non-motile, facultative intracellular coccobacillus with bipolar staining. Organisms can be identified by immunofluorescence. Immunoassays can also detect Y. pestis antigens in serum. Polymerase chain reaction (PCR) assays are used in research. Bacteriophage typing can be helpful in tracing outbreaks.
Plague can also be diagnosed by isolation of Y. pestis. Organisms can be recovered from sputum, blood or aspirates of lymph nodes and may be cultured on ordinary media including blood agar, MacConkey agar or infusion broth. Automated systems may misidentify this bacterium, as it grows slowly and biochemical reactions may be delayed. Guinea pig inoculation can also be used.
Serology is occasionally helpful. A fourfold rise in titer is diagnostic. Latex agglutination is most often used, but passive hemagglutination tests and complement fixation are also available.
Treatment and Vaccination
Antibiotics are effective in the early stages of bubonic or pneumonic plague; in pneumonic plague, their efficacy is often limited after 24 hours. Buboes are occasionally drained but usually resolve with antibiotic treatment.
Vaccines may be available for people with occupational risk factors; these vaccines are not wholly protective, particularly against the pneumonic form. A whole cell vaccine was marketed until November 1998 but appears to have been taken off the market. A new vaccine is in development and may be more effective against both forms of plague.
Morbidity and Mortality
The mortality rate is approximately 50 to 60% for untreated bubonic plague and nearly 100% for untreated pneumonic plague. The pneumonic form is often fatal within 48 hours after it becomes symptomatic. Early treatment reduces the mortality rate to less than 5%; however, treatment for the pneumonic form must be started during the first 24 hours after symptoms begin.
Worldwide, approximately 1,000 to 2,000 cases of plague are seen annually; epidemics occur regularly in Africa and Asia. Sporadic cases also occur in North and South America after exposure to wild rodents and fleas. In the United States, approximately 18 cases of plague were seen yearly during the 1980s; the mortality rate for these cases was approximately 14%.
Species Affected
More than 200 species of mammals can be infected with Y. pestis. Rodents are the reservoir hosts. Many rodents, including prairie dogs, chipmunks, wood rats, ground squirrels, deer mice and voles suffer occasional epidemics or maintain the virus in natural cycles. Rock squirrels and the California ground squirrel are often the sources of human infections in the United States. Rats are usually the carriers for epidemics in humans. Rabbits, wild carnivores, domestic cats and dogs can develop plague when they are exposed to infected rodents or their fleas; among carnivores, cats are particularly susceptible.
Incubation Period
Clinical signs develop can develop within 3-4 days in experimentally infected cats.
Clinical Signs
Asymptomatic infections and mild illness are typical in some reservoir hosts. Wild carnivores including coyotes, skunks and raccoons can also seroconvert without clinical disease. Other animals may have fever, lymphadenitis, abscesses in internal organs, or sudden death from sepsis.
In cats, clinical signs can include fever, anorexia, dehydration and depression. Infected cats may develop enlarged lymph nodes near the site of infection: the submandibular or cervical lymph nodes are most often involved. Infected lymph nodes can develop abscesses, ulcerate and drain. Swellings may also be seen around the head, neck and eyes. Sneezing, hemoptysis, incoordination, quadriplegia, necrotic tonsillitis and symptoms of pneumonia may occur.
Dogs seem to be relatively resistant to plague and animals may seroconvert without symptoms. High fevers and lymphadenopathy, with occasional deaths, have also been seen. Ten experimentally infected dogs developed a fever and other signs of illness but recovered spontaneously during the next week.
Communicability
Yes. Bacteria can be transmitted in aerosols, by direct contact with tissues and body fluids, and in bites. Infected fleas can transmit bacteria for months.
Diagnostic Tests
Plague can be diagnosed by isolation of Y. pestis; bacteria may be found in blood, nasal swabs, lymph node aspirates, transtracheal aspirates and tissue samples. If neurologic signs are present, cerebrospinal fluid (CSF) may yield bacteria. Y. pestis is a Gram negative, non-motile, facultative intracellular coccobacillus with bipolar staining. The organism can be identified by immunofluorescence or antigen-capture enzyme linked immunosorbent assays (ELISAs).
Organisms can also be cultured; Y. pestis will grow on ordinary media including blood agar, MacConkey agar or infusion broth. Automated systems may misidentify this bacterium, as it grows slowly and biochemical reactions may be delayed. Guinea pig inoculation can also be used. A rise in titer in paired serum samples is diagnostic, if the animal survives; the latex hemagglutination and passive hemagglutination tests (PHA) are often used.
Treatment and Vaccination
Early treatment with antibiotics can be successful.
Morbidity and Mortality
In endemic areas, many rodents - including chipmunks, wood rats, ground squirrels, deer mice and voles - suffer occasional epidemics. Mortality in some rodent species can be high; infections are fatal in nearly 100% of prairie dogs. Between outbreaks, bacteria seem to cycle in reservoir populations without causing high mortality
The mortality rate is 50% in cats fed plague-infected mice; sick cats may die within 1 to 2 days or after several weeks. Dogs, coyotes, raccoons, skunks and other carnivores often seroconvert without symptoms; clinical infections and deaths are relatively rare in these species. Ten experimentally infected dogs recovered spontaneously.
Post-Mortem Lesions
Post mortem lesions vary with the type of infection. Signs can include lymphadenopathy, bacterial pneumonia with lung hemorrhages, and necrosis in the liver, spleen and other internal organs.
Biberstein, E.L. and J. Holzworth. “Bacterial Diseases. Plague.” In Diseases of the Cat. Edited by J. Holzworth. Philadelphia, PA: W.B. Saunders, 1987, p. 294; 660.
Collins, F.M. “Pasteurella, Yersinia, and Francisella.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 20 November 2002 <http://www.gsbs.utmb.edu/microbook/ch029.htm>.
“Bacterial infections caused by Gram-negative bacilli. Enterobacteriaceae.” In The Merck Manual, 17 th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 8 Nov 2002 <http://www.merck.com/pubs/mmanual/section13/chapter157/157d.htm>.
Butler, T. In Zoonoses. Edited by S.R. Palmer, E.J.L. Soulsby and D.I.H Simpson. New York: Oxford University Press, 1998, pp. 286-292.
“Control of Communicable Diseases.” Edited by J. Chin. American Public Health Association, 2000, pp.532-535.
“Information on plague.” Centers for Disease Control and Prevention (CDC), June 2001. 19 Nov 2002
<http://www.cdc.gov/ncidod/dvbid/plague/info.htm>.
Macy, D.W. “Plague.” In Infectious Diseases of the Dog and Cat. Edited by C.E. Greene. Philadelphia: W.B. Saunders, 1998, pp. 295-300.
Macy, D.W. “Plague.” In Current Veterinary Therapy X. Small Animal Practice. Edited by R.W. Kirk and J.D. Bonagura. Philadelphia: W.B. Saunders, 1989, pp. 1088-91.
“Material Safety Data Sheet –Yersinia pestis.” Canadian Laboratory Centre for Disease Control, March 2001. 20 November 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds169e.html>.
“Plague.” In Medical Management of Biological Casualties Handbook, 4 th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 19 Nov 2002 <http://www.vnh.org/BIOCASU/9.html>.
“Plague.” In The Merck Veterinary Manual, 8 th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 485-6.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: Avian Chlamydiosis, Ornithosis, Parrot Fever
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
In birds, chlamydiosis results from infection by Chlamydophila psittaci (order Chlamydiales, family Chlamydiaceae). This organism, previously known as Chlamydia psittaci, is a Gram negative, coccoid, obligate intracellular bacterium. There are at least six avian serotypes.
Geographic Distribution
Avian chlamydiosis can be found worldwide. C. psittaci is particularly common in psittacine birds in tropical and subtropical regions. This disease is present in the United States. In a 1982 survey, C. psittaci was isolated from 20-50% of necropsied pet birds in California and Florida.
Transmission
Among birds, C. psittaci is transmitted frequently by inhalation of infectious dust and occasionally by ingestion. Fomites can also spread chlamydiosis, and biting insects, mites, and lice may be important in mechanical transmission. Birds can be asymptomatic carriers; carriers shed C. psittaci intermittently, particularly when stressed. One form of the organism, the elementary body, can survive in dried feces for months.
Humans usually become infected after inhaling contaminated dust from feathers or bird droppings. Direct contact with infected birds and bites can also spread the disease. Person-to-person transmission is rare but can occur by aerosol or venereal spread.
Disinfection/ Inactivation
C. psittaci is susceptible to quaternary ammonium compounds, chlorophenols, iodophore disinfectants, formaldehyde, 80% isopropyl alcohol or a 1:100 dilution of household bleach.
Incubation Period
The incubation period in humans is 1 to 4 weeks; most infections become symptomatic after 10 days.
Clinical Signs
Human chlamydiosis can be acute or insidious in onset. The disease varies from a mild, flu-like infection with a fever, chills, headaches, anorexia, malaise, sore throat and photophobia to a serious atypical pneumonia with dyspnea. There may be a dry cough, which sometimes becomes mucopurulent. In uncomplicated infections, the fever lasts for approximately 2 to 3 weeks then resolves. More rarely, a severe systemic illness with endocarditis, myocarditis and renal complications can develop. Hepatitis and neurologic complications including encephalitis, meningitis and myelitis have also been seen.
Communicability
Person-to-person transmission is rare; the agent is occasionally spread in aerosols during paroxysmal coughing. Venereal transmission has also been reported.
Diagnostic Tests
Chlamydiosis can be diagnosed by isolation of C. psittaci or by serology. C. psittaci can be isolated in embryonated eggs, laboratory animals, or cell cultures of buffalo green monkey (BGM), African green monkey (Vero), McCoy or L cells. Iodine staining of inclusion bodies or immunofluorescence can differentiate C. psittaci from C. trachomatis. DNA restriction endonuclease analysis can also distinguish these two organisms in tissue samples. Serologic tests include complement fixation or immunofluorescent tests; individuals treated with antibiotics may not develop antibodies. A presumptive diagnosis is sometimes made, based on exposure to birds and clinical signs.
Treatment and Vaccination
Antibiotics (tetracycline) combined with supportive care are effective. There is no vaccine.
Morbidity and Mortality
Currently, fewer than 50 confirmed cases are reported annually in the United States; additional undiagnosed or unreported cases are thought to occur. The disease may be mild or severe, depending on age and health of the individual and the extent of pneumonia; more serious disease is usually seen in the elderly and those who are debilitated. The mortality rate can be as high as 30% in severe infections left untreated; treated cases are rarely fatal. Convalescence may be slow after severe disease.
Species Affected
Avian chlamydiosis occurs in most birds, but is particularly common in psittacine birds, pigeons, doves, and mynah birds. This disease is sometimes seen in ducks and turkeys but only rarely in chickens.
Incubation Period
The incubation period in cage birds is usually three days to several weeks. However, in latent infections, active disease may be seen years after infection.
Clinical Signs
In turkeys, ducks, and pigeons, the clinical signs can include depression, ruffled feathers, weakness, inappetence, weight loss, nasal discharge, respiratory distress, yellowish-green or green diarrhea, and unilateral or bilateral conjunctivitis. Egg production is decreased. Nervous signs may be seen, including transient ataxia in pigeons and trembling or gait abnormalities in ducks.
In pet birds, common symptoms include anorexia, weight loss, diarrhea, yellowish droppings, sinusitis, respiratory distress, nervous signs, and conjunctivitis. Asymptomatic infections and mild infections with diarrhea or mild respiratory signs may also be seen. Residual disturbances in feathering may be apparent in survivors.
Communicability
Yes. Infected birds can shed C. psittaci for weeks to months. Shedding may be continuous or intermittent.
Diagnostic Tests
In live birds, chlamydiosis is usually diagnosed by isolating C. psittaci from pharyngeal or nasal swabs, feces, cloacal swabs, conjunctival scrapings or peritoneal exudate. At necropsy, the organism may be isolated from blood, ocular or nasal exudates, inflammatory exudates, or tissue samples from the lung, kidney, spleen, liver, and pericardium. If diarrhea is present, organisms may be found in the colonic contents or feces.
C. psittaci is isolated in embryonated eggs, laboratory animals or cell cultures of buffalo green monkey (BGM), African green monkey (Vero), McCoy or L cells. The organisms can be identified by direct immunofluorescence or other staining techniques. A single negative culture may be misleading, as carrier birds may shed C. psittaci only intermittently. Treatment with antibiotics during the 2 to 3 weeks before testing may also lead to false negatives.
Chlamydiosis can also be diagnosed by demonstrating C. psittaci in tissues, feces, or exudates by histochemical or immunohistochemical staining. Antigen capture enzyme-linked immunosorbent assays (ELISAs) are also used, but may lack sensitivity or cross-react with other Gram negative bacteria. Polymerase chain reaction (PCR) and polymerase chain reaction/ restriction fragment length polymorphism (PCR-RFLP) assays have been described.
Serology is occasionally helpful. At least a four-fold rise in titer should be seen in paired samples. Complement fixation is the standard test. Other assays include ELISA, latex agglutination (LA), elementary body agglutination (EBA), micro-immunofluorescence (MIFT), and agar gel immunodiffusion tests. The EBA test detects IgM only and can be used to diagnose current infections.
Treatment and Vaccination
Antibiotics are effective in treating the symptoms of chlamydiosis, but some birds may remain infected.
Morbidity and Mortality
Morbidity and mortality vary with the host species and pathogenicity of the serotype. Young birds tend to be more susceptible than older birds. In turkeys, serovar D strains cause 50-80% morbidity and 10-30% mortality. In broiler turkeys, up to 80% of infections with this serovar may be fatal. Other serovars in turkeys usually result in 5-20% morbidity, with mortality under 50%. In ducks, morbidity may be up to 80% and mortality 0-40%. Concurrent infections or stress increase the severity of the disease.
Post-Mortem Lesions
Post-mortem lesions in birds can include pneumonia, airsacculitis, hepatitis, myocarditis, epicarditis, nephritis, peritonitis, and splenitis. In turkeys, an enlarged and congested spleen may be the only lesion. Wasting, vascular congestion, fibrinous airsacculitis, fibrinous pericarditis, fibrinous pneumonia with congestion of the lungs, or fibrinous perihepatitis may also be seen. In pigeons, common lesions include hepatomegaly, airsacculitis, enteritis, and conjunctivitis with swollen and encrusted eyelids. The spleen may rupture. In cage birds, the liver may be enlarged and yellow with focal necrosis. The spleen is often enlarged, with white foci. Airsacculitis, pericarditis, and congestion of the intestinal tract can also be seen.
“Avian Chlamydiosis.” In Whiteman and Bickford’s Avian Disease Manual, 4th ed. Edited by B.R. Charlton et al. Kennett Square, Pa: American Association of Avian Pathologists, 1996, pp. 68-71.
“Avian Chlamydiosis.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000, pp. 679-90.
Becker, Y. “Chlamydia.” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 14 Nov 2002 <http://www.gsbs.utmb.edu/microbook/ch039.htm>.
“Chlamydiosis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 1300-01.
“Chlamydiosis.” In Poultry Diseases, 4th ed. Edited by F.T.W. Jordan and M. Pattison. London: W.B. Saunders, 1996, pp. 94-99.
Gerlach, H. “Chlamydia.” In Clinical Avian Medicine and Surgery. Edited by G.J. Harrison and L. Harrison. Philadelphia: W.B. Saunders, 1986, pp. 457-63.
Johnston W.B., M. Eidson, K.A. Smith, and M.G. Stobierski. “Compendium of chlamydiosis (psittacosis) control, 1999.” Psittacosis Compendium Committee, National Association of State Public Health Veterinarians. Journal of the American Veterinary Medical Association 214, no. 5 (1999): 640-6.
“Material Safety Data Sheet –Chlamydia psittaci.” January 2001 Canadian Laboratory Centre for Disease Control. 1 November 2001
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds31e.html>.
“Psittacosis.” Centers for Disease Control and Prevention (CDC), July 2002. 14 Nov 2002 <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/psittacosis_t.htm>.
“Psittacosis.” In The Merck Manual, 17th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 14 Nov 2002 <http://www.merck.com/pubs/mmanual/section6/chapter73/73j.htm>.
Vanrompay D., R. Ducatelle, and F. Haesebrouck. “Chlamydia psittaci infections: a review with emphasis on avian chlamydiosis.” Veterinary Microbiology 45, no. 2-3 (1995): 93-119.
.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Q fever results from infection by Coxiella burnetii. This organism is an obligate intracellular pathogen and has been traditionally placed in the family Rickettsiaceae; however, recent phylogenetic studies have demonstrated that C. burnetii is more closely related to Legionella, Francisella and Rickettsiella in the gamma subdivision of Proteobacteria.
C. burnetii forms unusual spore-like structures that are highly resistant to environmental conditions. The organism also has two distinct antigenic phases. Phase I is pathogenic and is found in infected animals or in nature; phase II is less pathogenic and is recovered after bacteria are passaged repeatedly in cell cultures or eggs.
Geographic Distribution
Q fever has been found worldwide, except in New Zealand.
Transmission
C. burnetii can be transmitted by aerosols or direct contact; it is also spread by ingestion of an infected placenta, other reproductive discharges or milk. Organisms localize in the mammary glands, supramammary lymph nodes, uterus and placenta in domestic ruminants and other susceptible species; bacteria can be shed in milk, the placenta and reproductive discharges during subsequent pregnancies and lactations. C. burnetii can also be found in the feces and urine. Ticks seem to spread infections among ruminants and sometimes people. Transmission has occurred in blood transfusions and by sexual contact in humans. Organisms have also been found in the semen of bulls. Vertical transmission is possible but rare.
C. burnetii is highly resistant to environmental conditions and is easily spread by aerosols; infectious airborne particles can travel a half-mile or more. Viable organisms can be found for up to 30 days in dried sputum, 120 days in dust, 49 days in dried urine from infected guinea pigs, and for at least 19 months in tick feces. At 4-6°C, organisms can survive for 42 months in milk and 12 to 16 months in wool.
Disinfection
C. burnetii is highly resistant to physical and chemical agents. Variable susceptibility has been reported for hypochlorite, formalin and phenolic disinfectants; a 0.05% hypochlorite, 5% peroxide or 1:100 solution of Lysol® may be effective. C. burnetii is also susceptible to glutaraldehyde, ethanol, gaseous formaldehyde, gamma irradiation or temperatures of 130°C for 60 min. High temperature pasteurization destroys the organism.
Incubation Period
In humans, the incubation period varies from 2 to 40 days; the typical incubation period is approximately 2 to 5 weeks.
Clinical Signs
The symptoms of Q fever appear acutely and can include fever, chills, a severe headache, fatigue, malaise, myalgia and chest pains. The illness generally lasts from a week to more than 3 weeks. A nonproductive cough, with pneumonitis on X-ray, sometimes develops during the second week. In severe cases, lobar consolidation and pneumonia may occur; severe infections are particularly common in elderly or debilitated patients. Hepatitis is seen in approximately one third of patients with prolonged disease; the clinical signs may include fever, malaise, right upper abdominal pain, hepatomegaly and sometimes jaundice. In pregnant women, infections can result in premature delivery, abortion and placentitis.
Complications are not common but may include chronic hepatitis, aseptic meningitis, encephalitis, osteomyelitis, vasculitis and endocarditis. Endocarditis usually occurs in people who have pre-existing damage to the heart valves. The symptoms are similar to subacute bacterial endocarditis.
Communicability
Person to person spread is very rare but has been seen in people with pneumonia.
Diagnostic Tests
In humans, Q fever is usually diagnosed by serology. Serologic tests can be done as early as the second week of illness; they may include immunofluorescence, ELISA, agglutination or complement fixation. Antibodies to the protein antigens found in phase II organisms appear in acute Q fever; antibodies to the lipopolysaccharide of phase I organisms indicate chronic Q fever. Organisms are occasionally found in stained tissue samples but this test is not routinely used in humans.
Isolation of C. burnetii is dangerous to laboratory personnel and is rarely done. Organisms can be recovered from blood samples; bacteria are isolated in cell cultures, embryonated chicken eggs or laboratory animals including mice, hamsters and guinea pigs. Blood cultures from patients with endocarditis are usually negative.
Treatment and Vaccination
Antibiotics can shorten the course of acute illness and reduce the risk of complications. Treatment of chronic cases is more difficult and may require long-term antibiotic therapy. Surgical replacement is sometimes necessary for damaged valves.
Effective vaccines may be available for people who are occupationally exposed. A licensed vaccine is available in Australia. In the United States, an investigational vaccine can be obtained from special laboratories such as the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID).
Morbidity and Mortality
Most cases of Q fever occur in people occupationally exposed to farm animals or their products: farmers, abattoir workers, researchers, laboratory personnel, dairy workers and woolsorters have an increased risk of infection. Approximately 60% of cases are thought to be asymptomatic. An additional 38% of infected people experience mild illness, while 2% develop severe disease and require hospitalization.
Q fever is usually a self-limiting illness; most cases resolve spontaneously within 2 days to 2 weeks. The mortality rate is 1% in untreated cases and lower in those who are treated. A biological attack with aerosolized organisms is expected to be similar to a natural outbreak.
Species Affected
Sheep, goats and cattle are the most common domestic animal reservoirs. Dogs, cats, rabbits, horses, pigs, camels, buffalo, rodents, pigeons, geese and other fowl may carry C. burnetii. Antibodies to C. burnetii have been found in badgers, coyotes, raccoons, opossums, badgers, jackrabbits, feral pigs, black bears and musk ox. Ticks and wild birds can also harbor this organism.
Incubation Period
The incubation period is variable; reproductive failure is usually the only symptom in animals. Abortions generally occur late in pregnancy.
Clinical Signs
Abortion, stillbirth, retained placenta, endometritis, infertility and small or weak offspring can be seen in ruminants, cats, dogs, rabbits and other species. Most abortions occur near term. Several abortions may be followed by uncomplicated recovery, particularly in small ruminants; in other cases, the disease may recur yearly.
With the exception of reproductive disease, animals are usually asymptomatic. Goats sometimes have a poor appetite and are depressed for 1 to 2 days before an abortion. Clinical signs including fever, anorexia, mild coughing, rhinitis and increased respiratory rates occur in experimentally infected sheep but have not been reported in natural infections. Experimentally infected cats develop fever and lethargy.
Communicability
Yes. Large numbers of organisms are found in the placenta, fetal fluids, aborted fetus, milk, urine and feces. Serologically negative animals may shed organisms.
Diagnostic Tests
C. burnetii can be detected in vaginal discharges, the placenta, placental fluids and aborted fetuses, as well as milk, urine and feces. Organisms are not shed continuously in milk and colostrum. In the placenta, organisms can be identified in exudates or areas of inflammation with a modified Ziehl-Neelsen or Gimenez stain; C. burnetii is an acid-fast, pleomorphic, small coccoid or filamentous organism. This organism is not usually detected by Gram stains. Bacterial identity can be confirmed by immunohistochemistry. Polymerase chain reaction techniques are also available in some laboratories. Fresh, frozen or paraffin-embedded samples of serum, buffy coat, milk, feces, vaginal exudates, cerebrospinal fluid, bone marrow, placenta, liver, cardiac valve, fetal tissue and other tissues can be tested by PCR.
A number of serologic tests are available; the most commonly used tests include indirect immunofluorescence, enzyme-linked immunosorbent assay (ELISA) and complement fixation. Cross-reactions have been seen between some strains of C. burnetii and Chlamydia in ELISA and immunoblot assays.
C. burnetii can be isolated in cell cultures, embryonated chicken eggs or laboratory animals including mice, hamsters and guinea pigs; however, isolation is dangerous to laboratory personnel and is rarely used for diagnosis.
Treatment and Vaccination
Little is known about the efficacy of antibiotic treatment in ruminants or other domestic animals. Treatment is sometimes recommended to reduce the risk of abortion. Antibiotics may in some cases suppress rather than eliminate infections. Isolating infected pregnant animals and burning or burying the reproductive membranes and placenta can decrease transmission.
Vaccines are not available for domestic ruminants in the United States but are used in other countries. Vaccines may prevent infections in calves, decrease shedding of organisms and improve fertility in infected animals. They do not eliminate shedding of the organism.
Morbidity and Mortality
Information on the prevalence of infection is limited. In an endemic region in California, 18 to 55% of sheep had antibodies to C. burnetii; the number of seropositive sheep varied seasonally and was highest soon after lambing. In other surveys, 82% of cows in some California dairies were seropositive, as well as 78% of coyotes, 55% of foxes, 53% of brush rabbits and 22% of deer in Northern California. In Ontario, Canada, infections were found in 33 to 82% of cattle herds and 0 to 35% of sheep flocks. Close contact with sheep appears to increase the risk of infection in dogs.
Significant morbidity can be seen in some species. In sheep, abortions can affect 5 to 50% of the flock. In one California study, Q fever may have been responsible for 9% of all abortions in goats. Deaths are rare in natural infections.
Post-Mortem Lesions
Placentitis is the most characteristic sign in ruminants. The placenta is typically leathery and thickened and may contain large quantities of white-yellow, creamy exudate at the edges of the cotyledons and in the intercotyledonary areas. In some cases, the exudate may be reddish- brown and fluid. Severe vasculitis is uncommon, but thrombi and some degree of vascular inflammation may be noted. Fetal pneumonia has been seen in goats and cattle and may occur in sheep; however, the lesions in aborted fetuses are usually non-specific.
“Control of Communicable Diseases.” Edited by J. Chin. American Public Health Association, 2000, pp.407-411.
De la Concha-Bermejillo, A., E.M. Kasari, K.E. Russell, L.E. Cron, E.J. Browder, R. Callicott and R.W. Ermel1. “Q Fever: An Overview. United States Animal Health Association. 4 Dec 2002
<http://www.usaha.org/speeches/speech01/s01conch.html>.
Marrie, T.J. “Q Fever.” Edited by S.R. Palmer, E.J.L. Soulsby and D.I.H Simpson. New York: Oxford University Press, 1998, pp. 171-185.
Martin J. and P. Innes. “Q Fever.” Ontario Ministry of Agriculture and Food, Sept 2002. 4 Dec 2002 <http://www.gov.on.ca/OMAFRA/english/livestock/vet/facts/info_qfever.htm>.
“Material Safety Data Sheet –Coxiella burnetii.” Canadian Laboratory Centre for Disease Control, January 2001. 2 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds43e.html>.
“Q Fever.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000, pp. 822-831.
“Q Fever.” In Medical Management of Biological Casualties Handbook, 4 th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 2 Dec 2002 <http://www.vnh.org/BIOCASU/10.html>.
“Q Fever.” In The Merck Manual, 17 th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 7 Oct 2002
<http://www.merck.com/pubs/mmanual/section13/chapter159/159i.htm>.
“Q Fever.” In The Merck Veterinary Manual, 8 th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 486-7.
Van der Lugt, J, B. van der Lugt and E. Lane. “An approach to the diagnosis of bovine abortion.” Paper presented at the mini-congress of the Mpumalanga branch of the SAVA, 11 March 2000. Pathology for the practicing veterinarian, Large Animal Section, no. 1 (April 2000). 2 December 2002 <http://vetpath.vetspecialists.co.za/large1.htm>.
Walker, D.H. “Rickettsiae.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 3 December 2002 <http://www.gsbs.utmb.edu/microbook/ch038.htm>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: Infectious enzootic hepatitis of sheep and cattle
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Rift Valley fever results from infection by the Rift Valley fever virus, an RNA virus in the genus Phlebovirus (family Bunyaviridae).
Geographic Distribution
Rift Valley fever is found throughout most of Africa. Outbreaks occur at irregular intervals in southern and eastern Africa, as well as in Egypt.
Transmission
Rift Valley fever is transmitted by mosquitoes and is usually amplified in ruminant hosts. The virus appears to survive in the dried eggs of Aedes mosquitoes; when these mosquitoes hatch during wet years, epidemics can occur. Aedes and other species of mosquitoes can transmit infections from the amplifying hosts. Ticks and biting midges may also be able to spread the virus. Humans do not seem to be infected by contact with live hosts, but can be infected by aerosols or direct contact with tissues during parturition, necropsy, slaughter, laboratory procedures or meat preparation for cooking. The Rift Valley fever virus can be found in raw milk. It is also likely to be present in semen; therefore, sexual transmission may be possible.
Under optimal conditions, the Rift Valley fever virus remains viable in aerosols for more than an hour at 25° C. In a neutral or alkaline pH, mixed with serum or other proteins, the virus can survive for as long as 4 months at 4° C and 8 years below 0° C. It is quickly destroyed in decomposing carcasses by pH changes.
Disinfection/ Inactivation
The Rift Valley fever virus is susceptible to low pH, lipid solvents and detergents, ether, chloroform and solutions of sodium or calcium hypochlorite with a residual chlorine content greater than 5000 ppm.
Incubation Period
In humans, the incubation period is 2 to 6 days.
Clinical Signs
Infection with the Rift Valley fever virus usually results in an asymptomatic infection or a relatively mild illness with fever and liver abnormalities. The symptoms of uncomplicated infections may include fever, headache, generalized weakness, dizziness, weight loss, myalgia and back pain. Some patients also have stiffness of the neck, photophobia and vomiting. Most people recover spontaneously within 2 days to a week.
Complications - hemorrhagic fever, meningoencephalitis or ocular disease - occur in a small percentage of patients. Hemorrhagic fever usually develops 2 to 4 days after the initial symptoms. The symptoms may include jaundice, hematemesis, melena, a purpuric rash, petechiae and bleeding from the gums. Hemorrhagic fever may progress to frank hemorrhages, shock and death.
Ocular disease and meningoencephalitis are usually seen one to three weeks after the initial symptoms. The ocular form is characterized by retinal lesions and may result in some degree of permanent visual impairment. Death is rare in cases of ocular disease or meningoencephalitis.
Communicability
Virus titers in infected humans are high enough to infect mosquitoes and introduce Rift Valley fever into new areas. Virus can be found in the blood and tissues.
Diagnostic Tests
The Rift Valley fever virus can be isolated from the blood, brain, liver or other tissues; in living hosts, viremia is usually seen only during the first three days of fever. The virus can be grown in numerous cell lines including baby hamster kidney cells, monkey kidney (Vero) cells, chicken embryo reticulum, and primary cultures from cattle or sheep. Hamsters, adult or suckling mice, embryonated chicken eggs or 2-day-old lambs can also be used.
Virus antigens can be detected in blood and tissue samples by various tests including reverse transcription polymerase chain reaction (RT-PCR) testing. Enzyme-linked immunoassay (ELISA) and other serologic assays can detect specific IgM or rising titers.
Treatment and Vaccination
No specific treatment, other than supportive care, is available; however, ribavirin has been promising in animal studies. Interferon, immune modulators and convalescent-phase plasma may also prove to be helpful. Most cases of Rift Valley fever are relatively brief and mild illnesses and may not require treatment.
A human vaccine has been developed and other vaccines are in earlier stages of investigation. None of these vaccines are sold commercially, but one may be available from government sources for people who are occupationally exposed.
Morbidity and Mortality
Humans are highly susceptible to Rift Valley fever. Most cases develop in veterinarians, abattoir workers and others who work closely with blood and tissue samples of animals. During outbreaks in animals, mosquitoes may spread the virus to humans and cause epidemics. In Egypt, approximately 200,000 human cases and 598 deaths occurred during a 1977 epidemic.
Most people with Rift Valley fever recover spontaneously within a week. Ocular disease is seen in approximately 0.5 to 2% and meningoencephalitis and haemorrhagic fever in less than 1%. The case fatality rate for hemorrhagic fever is about 50%. Deaths rarely occur in cases of eye disease or meningoencephalitis but 1 to 10% of patients with ocular disease have some permanent visual impairment. The overall case fatality rate for all patients with Rift Valley fever is less than 1%.
Species Affected
Rift Valley fever can affect many species, including sheep, cattle, goats, buffalo, camels, monkeys, gray squirrels and other rodents. The primary amplifying hosts are sheep and cattle. Viremia without severe disease may be seen in adult cats, dogs, horses and some monkeys, but severe disease can occur in newborn puppies and kittens. Rabbits, pigs, guinea pigs, chickens and hedgehogs do not become viremic.
Incubation Period
The incubation period can be as long as 3 days in sheep, cattle, goats and dogs. In newborn lambs, it is 12 to 36 hours. Experimental infections usually become evident after 12 hours in newborn lambs, calves, kids and puppies.
Clinical Signs
The clinical signs vary with the age, species and breed of the animal. In endemic regions, epidemics of Rift Valley fever can be recognized by the high mortality in newborn animals and abortions in adults.
Rift Valley fever is usually most severe in young animals. In young lambs, a biphasic fever, anorexia and lymphadenopathy may be followed by weakness and death within 36 hours; hemorrhagic diarrhea or abdominal pain can also occur. The mortality rate may reach 90 to 100% in neonates. Disease is similar in young calves: fever, anorexia and depression are typical, with mortality rates of 10 to 70%.
The symptoms in adult sheep may include fever, a mucopurulent nasal discharge (sometimes bloodstained), hemorrhagic or foul-smelling diarrhea, vomiting, jaundice, abortion and an unsteady gait. In adult cattle, fever, anorexia, weakness, excessive salivation, fetid diarrhea, abortion and decreased milk production may be seen. In some cases, abortion can be the only sign of infection in these two species. Similar but milder infections occur in goats. Adult camels do not develop symptoms other than abortion but young animals may have more severe disease.
Communicability
Infections are typically transmitted by mosquitoes and not by direct contact; however, during parturition, necropsy or slaughter, viruses in the tissues can be spread by aerosols and enter the skin through abrasions. The Rift Valley fever virus has also been found in raw milk and may be present in semen.
Diagnostic Tests
Rift Valley fever can be diagnosed by virus isolation. The virus can be isolated from the blood of febrile animals. It can also be recovered from the tissues from dead animals and aborted fetuses; the liver, spleen and brain are generally used. Virus can be grown in numerous cell lines including baby hamster kidney cells, monkey kidney (Vero) cells, chicken embryo reticulum and primary cultures from cattle or sheep. Hamsters, adult or suckling mice, embryonated chicken eggs or 2-day-old lambs can also be used.
Virus titers in tissues are often high; a rapid diagnosis can sometimes be made with complement fixation, neutralization and agar gel diffusion tests on tissue suspensions. Rapid tests may need to be confirmed by virus isolation. Virus antigens can also be detected by immunofluorescent staining of the liver, spleen or brain. Enzyme immunoassays and immunodiffusion tests can identify virus in the blood.
Serologic tests are helpful in epidemiologic studies but may be of limited use in diagnosis. Available tests include virus neutralization, enzyme-linked immunosorbent assay (ELISA), hemagglutination inhibition, immunofluorescence, complement fixation and immunodiffusion assays. Cross-reactions may occur with other phleboviruses.
Treatment and Vaccination
The only treatment is supportive care. Vaccines are available in some countries.
Morbidity and Mortality
Epidemics of Rift Valley fever tend to occur at intervals, when heavy rainfalls cause infected mosquitoes to hatch and a susceptible animal population has developed. Outbreaks are characterized by large numbers of abortions and high mortality in neonates. Indigenous cattle may have asymptomatic infections, while more severe disease is seen in exotic species.
The mortality rate can be very high in young animals, with fatalities decreasing in older age groups. Deaths are common in neonatal lambs, calves, kids, puppies and kittens. The mortality rate is 90 to 100% in newborn lambs, 40 to 60% in weaners and 15 to 30% in adult sheep. Ewes that abort are more likely to have a fatal infection. In calves, mortality rates range from 10 to 70%. Fewer than 10% of infections in adult cattle are fatal. Abortion rates range from 5 to almost 100% in ewes but are usually less than 10% in cattle.
Post-Mortem Lesions
The most consistent lesion is hepatic necrosis; the necrosis is more extensive and severe in younger animals. In aborted fetuses and newborn lambs, the liver may be very large, yellowish-brown to dark reddish-brown, soft and friable, with patchy congestion. Multiple gray to white necrotic foci are usually present, but may only be visible microscopically. The liver lesions are usually less severe in adult animals and may consist of numerous pinpoint necrotic foci.
Additional lesions may include jaundice, widespread cutaneous hemorrhages and fluid in the body cavities. The peripheral lymph nodes and spleen may be enlarged and edematous and often contain petechiae. The walls of the gallbladder are often edematous, with visible hemorrhages. A variable degree of inflammation or hemorrhagic enteritis can sometimes be found in the intestines. In lambs, many small hemorrhages are usually seen in the abomasal mucosa and the small intestine and abomasum may contain dark chocolate-brown contents, with partially digested blood. In addition, petechial and ecchymotic hemorrhages may be seen on the surface of other internal organs.
Mebus, C.A. “Rift Valley Fever.” In Foreign Animal Diseases. Richmond, VA: United States Animal Health Association, 1998, pp. 353-61. 16 Nov 2002 <http://www.vet.uga.edu/vpp/gray_book/FAD/RVF.htm>.
“Rift Valley Fever.” Centers for Disease Control and Prevention, May 2002. 3 Dec 2002 <http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/rvf.htm>.
“Rift Valley Fever. WHO information fact sheet no. 207.” World Health Organization, September 2000. 3 Dec 2002 <http://www.who.int/inf-fs/en/fact207.html>.
“Rift Valley Fever.” In Manual for the Recognition of Exotic Diseases of Livestock: A Reference Guide for Animal Health Staff. Food and Agriculture Organization of the United Nations, 1998. 27 November 2002 <http://panis.spc.int/RefStuff/Manual/Multiple%20Species/RIFTVALLEY%20FEVER.HTML>.
“Rift Valley Fever.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000, pp. 144-152.
“Rift Valley Fever.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 541-2.
Shope, R.E. “Bunyaviruses.” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 20 November 2002 <http://www.gsbs.utmb.edu/microbook/ch056.htm>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: Variola major, Variola minor
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Smallpox results from infection by variola virus (genus Orthopoxvirus, family Poxviridae). At least two strains of virus exist: the more virulent strain causes variola major and the less virulent strain causes variola minor.
The Orthopoxvirus genus also includes the vaccinia, monkeypox, cowpox, camelpox and ectromelia viruses; these agents resemble each other in electron micrographs and in many culture systems. They are also serologically cross-reactive. Monkeypox, which is seen in Africa, closely resembles smallpox; in monkeypox infections, the mortality rate is lower and the cervical and inguinal lymph nodes are highly enlarged.
Geographic Distribution
The last naturally acquired case of smallpox occurred in 1977 and the last two laboratory-acquired infections in 1978. In 1980, the World Health Organization (WHO) declared that endemic smallpox had been eradicated. Currently, the only known stocks of virus are stored at the Centers for Disease Control and Prevention (CDC) in Atlanta and the Institute for Viral Preparations in Moscow. Other countries may have clandestine stores of virus.
Transmission
The smallpox virus must be continuously transmitted from human to human to survive; humans do not become long-term carriers and animal reservoirs do not exist. Virus is spread by direct contact or inhalation of aerosols; infectious virus is present in oronasal secretions and in scabs from the skin. (The virus in scabs may be tightly bound and spread in this form may be less efficient.) Close contact is usually required for efficient virus transmission; therefore, smallpox mainly spreads to household members and others in close contact. Variola viruses can also be transmitted by individuals who maintain the virus in the throat without clinical signs. The potential for long-distance aerosol spread is controversial but has been demonstrated under certain conditions such as in hospitals. Transmission on fomites such as contaminated clothing or bedclothes is possible for short periods of time; however, variola does not remain viable for more than 2 days outside a human host. It is sensitive to heat and humidity; most natural epidemics occurred in the winter and spring.
Disinfection
Variola virus is susceptible to various disinfectants including 1% sodium hypochlorite, 0.1N sodium hydroxide, 1% peracetic acid, formaldehyde, ethylene oxide and others. The virus can also be destroyed by autoclaving or boiling for 10 minutes.
Incubation Period
The incubation period is 7 to 19 days; 12 to 14 days is average.
Clinical Signs
Smallpox has an acute onset; the initial clinical signs may include fever, malaise, rigors, vomiting, headache, backache and occasionally delirium. Some people develop an erythematous rash during this prodromal phase. The characteristic skin lesions usually appear 2 to 3 days later; the first signs are macules, which develop into papules and eventually pustular vesicles. These lesions are most common on the face and extremities and develop in synchronous “crops.” Approximately 8 to 14 days after the first symptoms appeared, the pustules develop scabs and heal, leaving depressed, depigmented scars. Severe scarring may occur.
Two forms of smallpox may be seen. Variola minor is characterized by milder clinical signs, smaller skin lesions and a low mortality rate; variola major is characterized by more severe disease and scarring and a higher mortality rate.
Approximately 5 to 10% of individuals develop flat-type or hemorrhagic variants of variola major. The hemorrhagic form is more common in pregnant women. Patients with this form have more severe initial symptoms, which are followed by generalized erythema and hemorrhages in the skin and mucosa. The initial symptoms are similar in the malignant or ‘flat’ form; in this form, confluent, flat nonpustular lesions develop and the epidermis often peels in survivors. The hemorrhagic and malignant forms are usually fatal.
Communicability
Yes. Patients are known to be infectious from the time the rash appears and remain infectious until the time the scabs have separated (approximately 7 to 10 days). Some sources recommend quarantine for all contacts for 17 days post-exposure.
Diagnostic Tests
Smallpox is usually diagnosed by finding the characteristic viruses in skin scrapings examined by electron microscopy. Aggregations of virus particles called Guarnieri bodies are found under the light microscope. Gispen’s modified silver stain can demonstrate Guarnieri bodies in vesicular scrapings; this test is rapid but relatively insensitive.
Differentiation of variola from vaccinia, monkeypox or cowpox requires virus isolation and identification. Variola, vaccinia, monkeypox and cowpox viruses look similar in most cell culture systems but can be distinguished by their characteristic lesions on the chorioallantoic membranes of 10 to 12 day old chick embryos. Other biological tests are occasionally necessary for confirmation. A new polymerase chain reaction technique is expected to be an easier and more accurate method to identify closely related viruses as well as viral strains. In a confirmed outbreak, most cases are diagnosed clinically.
During recovery, patients develop high titers of hemagglutinin-inhibiting, neutralizing and complement fixing antibodies; antibodies to related viruses can be identified by cross-absorption studies.
Treatment and Vaccination
No effective treatment other than supportive therapy is known; cidofovir and other antiviral agents are under investigation.
An effective human vaccine is available and appears to be protective for at least 3 years. Vaccination after exposure can prevent disease or reduce clinical signs and the risk of death; vaccination is most effective if it is given within a few days after exposure. Vaccinia Immune Globulin (VIG) may also be helpful in post-exposure prophylaxis. Vaccines are contraindicated in immunosuppressed persons, those infected with HIV, and persons with eczema. Rare vaccine complications may include generalized vaccinia, progressive vaccinia, and postvaccinial encephalitis (which has a 25% fatality rate).
Morbidity and Mortality
Natural smallpox infections spread slowly, with infections transmitted mainly to family members and other close personal contacts. Aerosolized virus in biological weapons would be expected to infect large numbers of individuals; younger people have no immunity against this disease and the resistance of those vaccinated more than 10 years ago is unknown.
Variola minor is a milder disease; the mortality rate is approximately 1% in unvaccinated persons. The overall mortality rate for variola major is 3% in vaccinated individuals and 30% in unvaccinated; mortality is generally higher with the Asian form than African form and in children under a year old. The malignant and hemorrhagic forms of variola major develop in approximately 5 to 10% of infected people. These forms are almost always fatal; the mortality rate in the malignant form is 95%.
Serious vaccine complications occur in approximately 100 per million primary vaccinations. The risk of complications is higher in people with eczema, HIV or other immunosuppressive diseases, pregnant women, and those receiving cancer chemotherapy or radiation.
Humans are the only mammals that are naturally susceptible to infection. Recently, Peter Jahrling’s group at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) was able to infect cynomolgus monkeys with variola virus. Monkeys were infected with extremely high doses by either injection alone or both injection and aerosols. All of the research animals became ill and 12 of 14 animals died. Virus was found in skin pustules. Details of this experiment have not been published.
Baxby, D. “Poxviruses.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 19 Nov 2002
<http://www.gsbs.utmb.edu/microbook/ch069.htm>.
Enserink M. and R. Stone. “Dead Virus Walking.” Science 295, no.5562 (15 Mar 2002): 2001-5.
Henderson, D.A. “Smallpox: clinical and epidemiologic features.” Emerg. Infect. Dis. 5, no. 4 (July-Aug 1999): 537-9.
Henderson, D.A. and B. Moss. “Smallpox and Vaccinia.” In Vaccines, 3 rd ed. Edited by S. Plotkin and W. Orenstein. Philadelphia, PA; W.B. Saunders Co, 1999. 19 Nov 2002 <http://www.ncbi.nlm.nih.gov/books/bv.fcgi?
call=bv.View..ShowSection&rid=vacc.chapter.d1e2084>.
“Medical treatment and response to suspected smallpox: Information for health care providers during biologic emergencies.” New York City Department of Health Bureau of Communicable Disease, July 2000. 20 Nov 2002
<http://www.nyc.gov/html/doh/html/cd/smallmd.html>.
“Smallpox.” In Medical Management of Biological Casualties Handbook, 4 th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 26 Oct 2002
<http://www.vnh.org/BIOCASU/13.html>.
“Smallpox.” In The Merck Manual, 17 th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 7 Oct 2002 <http://www.merck.com/pubs/mmanual/section13/chapter162/162f.htm>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Staphylococcal enterotoxin B (SEB) is an exotoxin produced by Staphylococcus aureus. It is one of the toxins responsible for staphylococcal food poisoning in humans and has been produced by some countries as a biological weapon. SEB is a superantigen; it acts by stimulating cytokine release and inflammation.
Transmission
Staphylococcal enterotoxin B is toxic by inhalation and ingestion. In a biological attack, it could be administered in food, water or as an aerosol.
Inactivation/ Decontamination
Staphylococcal enterotoxin B is moderately stable in the environment, including foods. It can be inactivated by heating to 100°C for a few minutes. Soap and water is also recommended for decontamination. Contaminated foods should be discarded.
Incubation Period
After ingestion, the incubation period is usually 4 to 10 hours. After an aerosol exposure, the symptoms usually appear after 3 to 12 hours.
Clinical Signs
The clinical signs include nonspecific flu-like symptoms, including fever, chills, headache, myalgia and varying degrees of prostration. Additional symptoms are specific to the route of exposure. Ingestion results in gastrointestinal signs; nausea, vomiting and diarrhea may occur. Inhalation causes respiratory signs, including a nonproductive cough, chest pain and dyspnea. In severe cases, there may be pulmonary edema and respiratory failure. Gastrointestinal signs may also be seen after an aerosol exposure, as the toxin is swallowed during mucociliary clearance. SEB can cause toxic shock syndrome when it occurs systemically, or erythema and induration after skin contact.
Communicability
Toxins are not usually transmitted from person to person. Staphylococcal enterotoxin B is not dermally active. Secondary aerosols are not expected to be a hazard from infected patients.
Diagnostic Tests
Staphylococcal food poisoning is usually diagnosed by the clinical signs and epidemiology. Staphylococcal enterotoxin B may be found in the blood, urine, respiratory secretions or nasal swabs for a short period of time. The toxin is detected by enzyme-linked immunosorbent assays (ELISAs) and chemiluminescence (ECL). A reverse passive latex agglutination test may be able to identify SEB rapidly in food. Polymerase chain reaction (PCR) assays can sometimes find Staphylococcus aureus genes in environmental samples.
Serology may be useful for a retrospective diagnosis. Most patients develop significant antibody titers to SEB.
Treatment and Vaccination
The treatment is symptomatic; respiratory support may be necessary after aerosol exposure. Vaccines and antisera are not currently available, but have been promising in animal studies. A protective mask is currently the best method of prophylaxis.
Morbidity and Mortality
Staphylococcal enterotoxin B, produced naturally by Staphylococcus aureus in food, is a very common cause of food poisoning. Respiratory symptoms might differentiate a natural outbreak from a biological attack.
Significant morbidity occurs after either ingestion or aerosol exposure. The estimated morbidity rate after inhalation could be 50 to 80% or greater. The clinical signs and outcome depend on the dose of toxin and route of exposure. High mortality rates are not expected to occur after ingestion; in natural cases of food poisoning, death is very rare but may be seen in infants, the elderly or those who are severely debilitated. Most treated patients are also expected to survive aerosol exposure, although deaths may occur in severe cases. After respiratory exposure, fever can persist for up to 5 days and a cough for up to 4 weeks.
Although Staphylococcus aureus is associated with numerous diseases in animals, there is little information about it as a source of gastroenteritis. Administration of Staphylococcal enterotoxin B in food or water would presumably result in diarrhea or other gastrointestinal signs in some species.
Aerosolized SEB appears to have been studied mainly in mice and nonhuman primates. In rhesus monkeys, inhalation of toxin caused diarrhea and vomiting within 24 hours, followed by depression, dyspnea and shock. Three of 6 animals died within 3 days. Diffuse severe pulmonary edema was the most prominent postmortem lesion.
Antisera and vaccines have been promising in mouse models.
Casadevall A. “Passive antibody administration (immediate immunity) as a specific defense against biological weapons.” Emerg. Infect. Dis. 8, no. 8 (Aug 2002):833-41. 19 Dec 2002
<http://www.cdc.gov/ncidod/EID/vol8no8/01-0516.htm>.
Foster T. “Staphylococcus.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 20 Dec 2002 <http://www.gsbs.utmb.edu/microbook/ch012.htm>.
Lowell G.H., R.W. Kaminski, S. Grate, R.E. Hunt, C. Charney, S. Zimmer and C. Colleton. “Intranasal and intramuscular proteosome-staphylococcal enterotoxin B (SEB) toxoid vaccines: Immunogenicity and efficacy against lethal SEB intoxication in mice.” Infect. Immun. 64, no. 5: 1706-13.
Mattix M.E., R.E. Hunt, C.L. Wilhelmsen, A.J. Johnson and W.B. Baze. “Aerosolized staphylococcal enterotoxin B-induced pulmonary lesions in rhesus monkeys (Macaca mulatta).” Toxicol. Pathol. 23, no. 3 (May-June 1995):262-8.
Schmitt C.K., K.C. Meysick and A.D. O'Brien. “Bacterial Toxins: Friends or Foes?” Emerg. Infect. Dis. 5, no. 2 (March- April 1999):224-34. 19 Dec 2002 <http://www.cdc.gov/ncidod/eid/vol5no2/schmitt.htm>.
“Staphylococcal Enterotoxin B.” In Medical Management of Biological Casualties Handbook, 4 th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 19 Dec 2002
<http://www.vnh.org/BIOCASU/19.html>.
“Staphylococcus aureus.” In Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. U.S. Food & Drug Administration, Center for Food Safety & Applied Nutrition, January 1992. 19 Dec 2002
<http://www.cfsan.fda.gov/~mow/chap3.html>.
Strange P., L. Skov, S. Lisby, P.L. Neilson and O. Baadsgaard. “Staphylococcal enterotoxin B applied on intact normal and intact atopic skin induces dermatitis.” Arch. Dermatol. 132, no. 1 (1996):27-33.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: TSE, BSE, FSE, vCJD
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Bovine spongiform encephalopathy (BSE) feline spongiform encephalopathy (FSE), variant Creutzfeldt-Jakob disease (vCJD) and spongiform encephalopathy of exotic ruminants appear to be related diseases. All four diseases appeared at the same time, during an epidemic of BSE in the United Kingdom. The causative agent(s) are generally thought to be prions; a minority opinion is that they may be virinos or retroviruses.
Geographic Distribution
BSE
BSE appears to have originated in the United Kingdom in 1985. Infected cattle have since been found in numerous European countries, including Portugal, Ireland, Switzerland, Belgium, Spain, Germany, France, Slovakia, Italy, the Netherlands, Denmark, Slovenia, Greece, the Czech Republic, Finland, Austria and Poland. Albania, Bulgaria, Croatia, Cyprus Republic, Estonia, Hungary, Latvia, Lithuania, Luxembourg, Romania, San Marino Republic and Turkey are also likely or confirmed to have BSE. Israel and Japan reported their first cases in 2002. Cases have also been seen in imported cattle in Liechtenstein, the Falkland Islands and Canada. BSE has not been detected in Australia, New Zealand, the United States or South America. As a result of control measures, the current epidemics in the United Kingdom and Switzerland appear to be diminishing.
FSE and Spongiform Encephalopathy of Exotic Ruminants
FSE has been found almost exclusively in the United Kingdom, with a single isolated case in a cat in Norway. Spongiform encephalopathy of exotic ruminants has been detected only in captive ruminants in the United Kingdom. These two diseases have been declining in parallel with the BSE epidemic.
Variant Creutzfeldt-Jakob disease
The vast majority of cases of vCJD have occurred in the United Kingdom. Six cases have been reported from France and one each from Ireland, Italy and the United States. The patient in the United States lived in the United Kingdom from 1979 to 1992 and was probably infected there during the BSE epidemic.
Transmission
BSE
BSE, FSE, vCJD and spongiform encephalopathy of exotic ruminants all seem to be transmitted orally. BSE is thought to have mutated from the scrapie agent, found in sheep. The first cases of BSE appeared in the U.K. in 1985 and have been linked to changes in the rendering practices for livestock feed. These changes may have allowed infectious meat or bone meal from scrapie-infected sheep to be fed to cattle. Rendering of contaminated cattle carcasses and wastes seems to have amplified the agent. A minority of researchers believes that BSE has always existed in cattle but was unrecognized until the outbreak in the U.K.
The BSE agent is found mainly in nervous tissues. In naturally infected cattle, it has been detected only in the brain, spinal cord, and retina. In experimentally infected calves, it is also seen in the distal ileum. This agent has never been found in muscle, blood, or milk, and natural infections do not seem to spread laterally between cattle. The offspring of BSE-infected cattle have an increased risk of developing BSE, but it is not known whether this is due to vertical transmission.
Spongiform Encephalopathy of Exotic Ruminants
The outbreak of spongiform encephalopathy of exotic ruminants paralleled the BSE epidemic, and may have been due to the same agent. Experimentally, this spongiform encephalopathy can be transmitted both orally and parenterally. Vertical transmission is uncertain: two offspring of affected animals developed the disease, but vertical transmission has not been seen in experimental infections.
FSE
The BSE agent or a related agent may also have been the source of FSE. In domestic cats, the source of infection was thought to be pet food that contained cattle offal. Wild cats in zoos may have been infected when they were fed cattle carcasses.
Variant Creutzfeldt-Jakob disease
The first cases of vCJD in humans appeared almost 10 years after the first cases of BSE in cattle. The source of vCJD has not been definitively identified but appears to be beef, most likely products contaminated by nervous system tissue. Genetic factors may play a role in infection: to this date, all patients with clinical disease have been homozygous for methionine at codon 129 of the prion protein gene.
Disinfection
The prototype agent, scrapie, is highly resistant to disinfectants, heat, ultraviolet radiation, ionizing radiation and formalin. Effective disinfection is possible with a single porous load autoclave cycle of 134-138°C for 18 minutes. Infectious tissues should either be autoclaved under the same conditions or incinerated. A 4% sodium hydroxide or 10% sodium hypochlorite solution is effective if it is applied for more than 1 hour at 20°C. Overnight disinfection is recommended for equipment.
Incubation Period
The incubation period in humans has not been established, but appears to be at least several years. The first case of vCJD appeared in 1994, almost a decade after BSE first appeared in cattle.
Clinical Signs
Variant CJD is similar to the classic (genetic) form of CJD, but the clinical signs usually appear in younger patients; the median age of onset is 26 years of age for vCJD, and 68 years for classical CJD.
The first signs are usually psychiatric symptoms, including anxiety, depression, and social withdrawal. Some patients also develop persistent painful sensory symptoms. Frank neurologic signs, including gait disturbances, ataxia, incoordination, slurring of speech and tremor usually appear several months later. Chorea, dystonia, myoclonus and dementia typically develop late in the course of disease. Variant CJD usually progresses over years, compared to months for classic CJD.
Communicability
Person to person transmission of either vCJD or classic CJD has not been seen during casual contact. In rare cases, classic CJD has been transmitted during medical procedures such as corneal and dura mater grafts. It may be possible to spread CJD by liver transplants, blood transfusions, pituitary-derived human growth hormone injections and contaminated brain electrodes.
Diagnostic Tests
The definitive diagnosis of vCJD is by microscopic examination of brain tissue, usually at necropsy. Numerous amyloid plaques surrounded by vacuoles are found; such plaques are seen in only 5 to 10% of cases of classic CJD. Large amounts of prion protein can be found around the plaques by immunohistochemistry.
A tentative diagnosis can be made before death by the history, clinical signs and cortical atrophy on magnetic resonance imaging (MRI) of the brain. The abnormal prion protein may be found in tonsil biopsies by Western blot and immunohistochemistry. The electroencephalogram (EEG) is sometimes normal during the early stages of disease, but later develops characteristic abnormalities.
Treatment and Vaccination
No treatment or vaccine is available. The possible benefits of quinacrine are being investigated.
Morbidity and Mortality
From 1993 to October 2002, 138 cases of vCJD were reported worldwide. Only small increases were seen in vCJD cases during the first 6 years. The full extent of the outbreak is not yet known; mathematical models predict from fewer than one hundred to hundreds of thousands of cases, depending on the exact length of the incubation period and other factors.
Most cases of vCJD have occurred in the United Kingdom. One case has been confirmed in a resident of the United States who lived in the United Kingdom from 1979 to 1992. Genetic factors may play a role in infection: to this date, all patients with clinical disease have been homozygous for methionine at codon 129 of the prion protein gene. The mortality rate is 100%.
Species Affected
BSE is seen in cattle and can be experimentally transmitted to cats, mink, mice, pigs, sheep, goats, marmosets and cynomolgus monkeys. FSE has been found in domestic cats and captive wild cats, including tigers, a puma, an ocelot and a cheetah. Spongiform encephalopathy of exotic ruminants has been seen in captive nyala, gemsbok, Arabian oryx, eland, kudu, scimitar-horned oryx, ankole and bison. Variant Creutzfeldt-Jakob disease is a disease of humans.
Incubation Period
All spongiform encephalopathies have incubation periods of months or years. The incubation period of BSE is more than a year and often several years. The peak incidence of disease occurs in 4 to 5 year old cattle.
Clinical Signs
Spongiform encephalopathies are usually insidious in onset and tend to progress slowly. The clinical signs are usually neurologic. Once the symptoms appear, these diseases are relentlessly progressive and fatal.
BSE
The clinical signs of BSE may include hyperesthesia, hindlimb ataxia, pelvic swaying, hypermetria, tremors, falling, recumbency, and behavioral changes such as apprehension, nervousness, and occasionally frenzy. Intense pruritus is not usually seen. Nonspecific symptoms include loss of condition, weight loss, and decreased milk production. Decreased rumination, bradycardia, and altered heart rhythms have also been reported. The disease progresses to recumbency and coma, and death occurs from weeks to months later. Rare cases may develop acutely and progress rapidly within days.
Spongiform encephalopathy of exotic ruminants
In exotic ruminants, the clinical signs may include loss of condition, unsteadiness, incoordination, and self-mutilation by biting. Asymptomatic cases have been described. This disease appears to progress more rapidly than most spongiform encephalopathies; the mean period from the onset of symptoms to euthanasia is 13.5 days.
FSE
The clinical signs of FSE can include behavioral changes, tremors, and ataxia. Cats may become aggressive or tend to creep aimlessly around their home and hide. In later stages, somnolence is common and convulsions may occur. Excessive salivation, hyper-responsiveness to loud noises, and dilated pupils have also been seen. Death occurs in approximately 6 to 8 weeks.
Communicability
There is no evidence that BSE or FSE is communicable during casual contact.
Diagnostic Tests
Spongiform encephalopathies can be diagnosed by histopathology or by detecting PrPSc (a disease-specific isoform of the membrane protein PrP) in the brain. Accumulations of PrPSc can be found in unfixed brain extracts by immunoblotting and in fixed brains by immunohistochemistry. The diagnosis can also be confirmed by finding characteristic fibrils of PrPSc (scrapie-associated fibrils) with electron microscopy in brain extracts. Some of these tests can be used on frozen or autolyzed brains.
BSE can also be diagnosed by transmission tests in mice. However, an incubation period of several months often makes this technique impractical. New commercial tests to detect BSE (PrPSc) in cattle brain samples include a modified immunoblot, a chemiluminescent ELISA test, a sandwich immunoassay and a two-site noncompetitive immunometric procedure.
Serology is not useful for diagnosis, as antibodies are not made against the agents of spongiform encephalopathies.
Treatment and Vaccination
No treatment or vaccination is available. Spongiform encephalopathies are uniformly fatal once the symptoms appear.
Morbidity and Mortality
In 1992, the annual incidence of BSE in United Kingdom cattle was 1%; however, the number of cases has been decreasing in recent years. The incidence of FSE is unknown. This disease was seen in a total of 81 domestic cats (as well as a few wild felids) in the United Kingdom, but many cases may have been missed. Spongiform encephalopathies are always fatal once the symptoms appear.
Post-Mortem Lesions
No gross lesions are found in spongiform encephalopathies, except emaciation or wasting of the carcass in some cases.
The typical histopathologic lesions are confined to the central nervous system. Neuronal vacuolation and non-inflammatory spongiform changes in the gray matter are pathognomonic. Astrocytosis is prominent in some diseases but not others. Amyloid plaques are seen in some spongiform encephalopathies but are rare in BSE and not found in FSE. These lesions are usually but not always bilaterally symmetrical.
“Bovine Spongiform Encephalopathy.” Animal Health Australia. The National Animal Health Information System (NAHIS). 7 November 2001
<http://www.brs.gov.au/usr-bin/aphb/ahsq?dislist=alpha>.
“Bovine Spongiform Encephalopathy.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000, pp.
“Bovine Spongiform Encephalopathy.” In The Merck Veterinary Manual, 8 th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 897-8.
Brown P., R.G. Will, R. Bradley, D.M. Asher and L. Detwiler. “Bovine Spongiform Encephalopathy and variant Creutzfeldt-Jakob disease: background, evolution, and current concerns.” Emerg. Infect. Dis. 7, no. 1 (Jan–Feb 2001):6-16. 10 Dec 2002 <http://www.cdc.gov/ncidod/EID/vol7no1/brown.htm>.
“Central nervous system. Viral diseases. Prion diseases (Transmissible spongiform encephalopathies).” In The Merck Manual, 17 th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 10 Dec 2002 <http://www.merck.com/pubs/mmanual/section13/chapter162/162d.htm>.
Irani, D.N. “Bovine Spongiform Encephalopathy.” Johns Hopkins Department of Neurology. Resource on Prion Diseases. 7 November 2001
<http://www.jhu-prion.org/animal/ani-bse-hist.shtml>.
Irani, D.N. “Feline Spongiform Encephalopathy.” Johns Hopkins Department of Neurology. Resource on Prion Diseases. 7 November 2001
<http://www.jhu-prion.org/animal/ani-fse-hist.shtml>.
Irani, D.N. “Spongiform Encephalopathy of Exotic Ruminants.” Johns Hopkins Department of Neurology. Resource on Prion Diseases. 7 November 2001 <http://www.jhu-prion.org/animal/ani-seoer-hist.shtml>.
“New variant CJD: Fact Sheet.” Centers for Disease Control and Prevention, April 2002. 10 Dec 2002
<http://www.cdc.gov/ncidod/diseases/cjd/cjd_fact_sheet.htm>.
“Prions and Transmissible Spongiform Encephalopathies.” In Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. U.S. Food & Drug Administration, Center for Food Safety & Applied Nutrition, Feb 2002. 8 Dec 2002 <http://www.cfsan.fda.gov/~mow/prion.html>.
“Probable variant Creutzfeldt-Jakob disease in a U.S. Resident --- Florida, 2002.” Morbidity and Mortality Weekly Report 51, no. 41 (Oct 18, 2002):927-929. 10 Dec 2002 <http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5141a3.htm>.
“Questions and answers regarding Bovine Spongiform Encephalopathy (BSE) and Creutzfeldt-Jakob disease (CJD).” Centers for Disease Control and Prevention, January 2001. 10 Dec 2002
<http://www.cdc.gov/ncidod/diseases/cjd/bse_cjd_qa.htm>.
“Transmissible Spongiform Encephalopathies.” July 2000 United States Department of Agriculture Animal and Plant Health Inspection Service. 7 November 2001 <http://www.aphis.usda.gov/oa/pubs/fsspongiform encephalopathy.html>.
“Update 2002: Bovine Spongiform Encephalopathy and variant Creutzfeldt-Jakob disease.” Centers for Disease Control and Prevention, Sept 2002. 10 Dec 2002 <http://www.cdc.gov/ncidod/diseases/cjd/bse_cjd.htm>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: rabbit fever, deerfly fever, Ohara's disease, Francis disease
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Tularemia results from infection by Francisella tularensis (formerly known as Pasteurella tularensis), a Gram negative, non-motile coccobacillus. Two subspecies exist: F. tularensis tularensis (also known as Jellison type A) and F. tularensis holarctica (Jellison type B). F. tularensis tularensis is found in lagomorphs in North America and is highly virulent for humans and domestic rabbits; F. tularensis holarctica is less virulent and occurs in beaver, muskrats and voles in North America and in hares and small rodents in Eurasia.
Geographic Distribution
Tularemia occurs in North America, continental Europe, Russia, China and Japan. The subspecies F. tularensis tularensis is found in North America; F. tularensis holarctica is seen in North America and Eurasia.
Transmission
F. tularensis can be transmitted by ingestion, inhalation, arthropod-borne transfer or direct contact through the skin and mucous membranes. Organisms are found in the blood and tissues of infected animals and can survive for long periods on fomites including food and water. Aquatic animals may develop tularemia after being immersed in contaminated water. Carnivores sometimes become infected after ingesting a contaminated carcass. Vectors for F. tularensis tularensis include ticks (including Dermacentor andersoni, D. variabilis and Amblyomma americanum) and biting flies (particularly deerflies). F. tularensis holarctica is also transmitted by mosquitoes in Russia. Rarely, the organism is spread by animal bites.
F. tularensis can survive for long periods of time in arthropod vectors and in the environment. Individual flies may carry the organism for 2 weeks and ticks throughout their lifetimes. Viable bacteria can also be found for weeks to months in the carcasses and hides of infected animals and in fomites including grain dust, straw, water, soil and bedbugs. This organism is highly resistant to freezing; live organisms have been found after 3 years in rabbit meat stored at -15° C. F. tularensis has been weaponized.
Disinfection
F. tularensis is easily killed by disinfectants including 1% hypochlorite, 70% ethanol, glutaraldehyde and formaldehyde. It can also be inactivated by moist heat (121° C for at least 15 min) and dry heat (160-170° C for at least 1 hour). This bacterium remains viable at freezing temperatures for months to years.
Incubation Period
The incubation period in humans is 3 to 15 days; clinical signs usually appear after 3 to 5 days.
Clinical Signs
Six forms of tularemia are seen in humans: typhoidal, ulceroglandular, glandular, oculoglandular, oropharyngeal and pneumonic. The form of the disease depends on the inoculation site.
Typhoidal tularemia usually occurs after inhalation but can also develop after skin inoculation or ingestion. The clinical signs may include fever, prostration, headache, nausea and weight loss. Some patients become extremely weak and develop recurring chills and drenching sweats. A nonspecific rash may be seen but lymphadenopathy is usually absent. Pneumonia is particularly common in the typhoidal form and can be severe.
Ulceroglandular tularemia usually occurs after infection through the skin or mucous membranes. The clinical signs may include fever, chills, headache and malaise. The regional lymph nodes are typically enlarged and painful; they may suppurate and drain profusely. An inflamed papule usually develops where the initial transmission occurred; it quickly turns into a pustule then ulcerates. On the extremities, single ulcers with thin, colorless, scanty exudates are usual. Glandular tularemia is characterized by fever and tender lymphadenopathy without a skin ulcer. Infection of the conjunctiva results in oculoglandular tularemia; this form is characterized by painful, unilateral, purulent conjunctivitis with preauricular or cervical lymphadenopathy. In some cases, there may be chemosis, periorbital edema and multiple small nodules or ulcerations on the conjunctiva. When the ulceroglandular disease occurs only in the throat, it is called oropharyngeal tularemia. In this form, there is an acute exudative or membranous pharyngotonsillitis with cervical lymphadenopathy.
Pneumonic tularemia can occur after inhalation or by secondary hematogenous spread. Victims develop severe, sometimes fulminant, atypical pneumonia. There may be signs of lung consolidation and, in come cases, delirium. Sometimes, the only symptoms may be a dry, unproductive cough, with decreased breath sounds and substernal discomfort. The pneumonic form can occur with any other form and has a high mortality rate. It develops in 10 to 15% of all cases of ulceroglandular tularemia and about 50% of cases of typhoidal tularemia.
Communicability
Person to person transmission has not been seen; however, infectious organisms can be found in the blood and other tissues.
Diagnostic Tests
Tularemia is often diagnosed by immunofluorescent staining of F. tularensis antigens in tissue samples or blood, and by serology. Commonly used serologic tests include tube agglutination, microagglutination and enzyme-linked immunosorbent assays (ELISA). A rising titer is diagnostic. Significant titers begin to appear during the second week of infection, although some specific antibodies are seen within the first 7 days. Cross-reactions occur with Brucella species, Proteus OX19, and Yersinia.
Tularemia can also be diagnosed by isolating F. tularensis from blood, sputum, pharyngeal or conjunctival exudates, ulcers, lymph nodes and gastric washings. F. tularensis does not grow well on standard media but may be isolated on media containing cysteine or sulfhydryl compounds. On McCoy medium, colonies are small, prominent, round and transparent. Confluent, milky, mucoid colonies develop on Francis medium and modified Thayer/Martin agar. Growth is slow and may take up to 3 weeks. Identification is by the absence of growth on ordinary media, morphology, immunofluorescence and slide agglutination. Organisms are non-motile, Gram negative small coccobacilli, with bipolar staining in young cultures. Bacteria from older cultures may be pleomorphic. F. tularensis tularensis can be distinguished from F. tularensis palaearctica by glycerol fermentation, ribosomal RNA probes and polymerase chain reaction (PCR) tests. Organisms in culture are highly infectious to humans and special precautions must be taken during isolation.
Treatment and Vaccination
F. tularensis is susceptible to a variety of antibiotics. Relapses are not common but can occur if treatment is stopped before all bacteria are eliminated. Live attenuated vaccines may be recommended for people at a high risk of infection, such as laboratory workers.
Morbidity and Mortality
Tularemia can affect all ages. Infections occur most often in hunters, butchers, farmers, fur handlers and laboratory workers. In natural infections, ulceroglandular tularemia is the most common form; it occurs in 75 to 85% of cases. The typhoidal form is seen in 5 to 15%, the glandular form in 5-10% and the oculoglandular form in 1 to 2%. Typhoidal tularemia would be expected to be the predominant form after an attack by aerosolized F. tularensis in a biological weapon.
The mortality rate is approximately 30 to 35% for untreated F. tularensis tularensis infections and 5 to 15% for F. tularensis holarctica infections. Typhoidal tularemia is the most dangerous form; if untreated, the case fatality rate is approximately 35%. In contrast, the case fatality rate for the untreated ulceroglandular form is 5%. Naturally acquired cases are rarely fatal if treated; case fatality rates up to 1-3% are cited by some authorities. Higher fatality rates would be expected after a biological attack. Permanent immunity usually develops after a single episode of tularemia.
Species Affected
More than a hundred species of animals can be infected with F. tularensis. The natural hosts include cottontail and jack rabbits, hares, voles, vole rats, squirrels, muskrat, beaver and lemmings. Among domestic animals, sheep seem to be particularly susceptible to clinical disease. Tularemia has also been seen in dogs, cats, pigs and horses; cattle seem to be resistant. Infections in birds, reptiles and fish have been reported.
Incubation Period
The incubation period is 1 to 10 days.
Clinical Signs
The full spectrum of clinical signs is not known in animals. Many cases may be asymptomatic. Signs of septicemia can be seen in sheep and other mammals; symptoms may include fever, lethargy, anorexia, stiffness, increased pulse and respiration, coughing, diarrhea and pollakiuria. Rabbits and rodents may be depressed, anorectic and ataxic, with a roughened coat and tendency to huddle. Anorexia, weight loss and vomiting have been reported in cats. Skin lesions are rarely seen in animals. Symptoms usually last 2 to 10 days in susceptible animals and may end in prostration and death. Susceptible species may be found dead without other symptoms.
Communicability
Yes. Infectious organisms can be found in the blood, tissues and feces. Humans and other animals can be infected through the skin or mucous membranes; routes of transmission include aerosols and ingestion. Infected cats may be able to transmit the organism in bites.
Diagnostic Tests
Impression smears of liver, spleen, bone marrow, kidney, lung or blood may be helpful for a presumptive diagnosis; small Gram negative coccobacilli can sometimes be found inside cells and scattered among tissue debris. F. tularensis is very small (0.2-0.7 µm) and easy to miss. Definitive diagnosis is by immunofluorescent detection of organisms in impression smears from these tissues, agglutination with specific antiserum, culture and occasionally serology. Animal inoculation can be used but it is dangerous and not recommended for routine identification.
F. tularensis can be isolated from enlarged lymph nodes, blood and tissues including liver, spleen and bone marrow; overgrowth of other bacteria may prevent recovery from animals found dead. This organism does not grow well on standard media but can be isolated on media containing cysteine or sulfhydryl compounds. On McCoy medium, colonies are small, prominent, round and transparent. Confluent, milky, mucoid colonies develop on Francis medium and modified Thayer/Martin agar. Growth is slow and may take up to 3 weeks. Identification is by the absence of growth on ordinary media, morphology, immunofluorescence and slide agglutination. The organisms are non-motile, Gram negative, small coccobacilli, with bipolar staining in young cultures. Bacteria from older cultures may be pleomorphic. F. tularensis tularensis can be distinguished from F. tularensis holarctica by glycerol fermentation, ribosomal RNA probes and polymerase chain reaction (PCR) tests. Organisms in culture are highly infectious to humans and special precautions must be taken during isolation.
Serology is occasionally useful. Species sensitive to tularemia typically die before specific antibodies develop; however, significant titers can be found in more resistant species such as sheep, cattle, pigs, moose, dogs and birds. Available tests include tube agglutination and enzyme-linked immunosorbent assay (ELISA).
Treatment and Vaccination
Tularemia can be treated with various antibiotics but long-term treatment may be necessary; early treatment is expected to reduce mortality. Vaccines are not marketed specifically for animals.
Morbidity and Mortality
Tularemia is relatively common and often fatal in wild animals; disease is particularly common among rabbits, rodents, pheasants and quail. This disease is rare among domestic rabbits and rodents, but may be seen in animals kept outside. Outbreaks of F. tularensis tularensis infections, characterized by high mortality, have been seen in sheep. Mortality rates up to 15% are seen in untreated lambs.
Post-Mortem Lesions
Most animals with acute tularemia are in good body condition. The most consistent lesions are miliary, grayish-white necrotic foci in the liver and sometimes the spleen, bone marrow and lymph nodes. Some of these necrotic foci may be barely visible. Enlargement of the liver, spleen and lymph nodes is also common. In rabbits, the white necrotic foci on a dark, congested liver and spleen have been compared to the Milky Way. Congestion and edema is frequent in the lungs; consolidation and fibrinous pneumonia or pleuritis may also be found. The abdominal cavity sometimes contains fibrin. In some species, the lesions can resemble tuberculosis and chronic granulomas may be found in the liver, spleen, kidneys and lungs.
“Bacterial infections caused by Gram-negative bacilli. Enterobacteriaceae.” In The Merck Manual, 17th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 8 Nov 2002
<http://www.merck.com/pubs/mmanual/section13/chapter157/157d.htm>.
Biberstein, E.L. and J. Holzworth. “Bacterial Diseases. Tularemia.” In Diseases of the Cat. Edited by J. Holzworth. Philadelphia, PA: W.B. Saunders, 1987, p. 296.
Collins, F.M. “Pasteurella, Yersinia, and Francisella.” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 20 November 2002
< http://www.gsbs.utmb.edu/microbook/ch029.htm>.
“Control of Communicable Diseases.” Edited by J. Chin. American Public Health Association, 2000, pp.532-535.
“Material Safety Data Sheet –Francisella tularensis.” Canadian Laboratory Centre for Disease Control, May 2001. 20 November 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds68e.html>.
Pearson, A. In Zoonoses. Edited by S.R. Palmer, E.J.L. Soulsby and D.I.H Simpson. New York: Oxford University Press, 1998, pp. 267-279.
“Tularemia.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000, pp. 756-761.
“Tularemia.” In Medical Management of Biological Casualties Handbook, 4th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 19 Nov 2002
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“Tularemia.” In The Biology and Medicine of Rabbits and Rodents, 2nd ed. Edited by J.E. Harkness and J.E. Wagner. Philadelphia: Lea and Febiger, 1977, pp. 179-80.
“Tularemia.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 494-5; 1394.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: Epidemic typhus, Louse-borne typhus fever, Typhus exanthematicus, Classical typhus fever, European typhus, Brill-Zinsser disease, Jail fever
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Epidemic typhus results from infection by Rickettsia prowazekii, a Gram negative, obligate intracellular bacterium. At least two strains can be distinguished by genetic analysis. One strain is found only in humans; the other also occurs in flying squirrels in the United States.
Geographic Distribution
R. prowazekii has been found worldwide. Foci of disease currently exist in many countries in Asia, central and east Africa, and the mountainous regions of Mexico, Central and South America. War and famine can result in explosive outbreaks of disease.
In the United States, R. prowazekii is endemic in flying squirrels. This form is zoonotic; sporadic human cases have been seen in Georgia, Virginia, West Virginia, North Carolina, Tennessee, Indiana, Illinois, Ohio, Pennsylvania, Maryland, Massachusetts, New Jersey, New York and California.
Transmission
Transmission of epidemic typhus occurs by arthropod vectors. The primary vector in person-to-person transmission is the human body louse (Pediculus humanus corporis). Lice become infected when they feed on the blood of infected patients; the lice defecate when they feed on a new host, excreting R. prowazekii in the feces. Transmission occurs when organisms in the louse feces or crushed lice are rubbed into the bite wound or other breaks in the skin. The rickettsia are also infectious by inhalation or contact with the mucous membranes of the mouth and eyes. In most parts of the world, humans are the only reservoir host for R. prowazekii. Infections can become latent and later recrudesce; humans with recrudescent typhus are capable of infecting lice and spreading the disease.
In the United States, flying squirrels also serve as a reservoir host. Infections are spread between squirrels by squirrel lice (Neohaematopinus scuiropteri), particularly during the winter when populations are concentrated in nests. N. scuiropteri does not feed on humans but squirrel fleas (Orchopeas howardi) and other mammalian fleas are susceptible and may be important in spreading the disease to humans. Inhalation of organisms in infected louse feces or contact with squirrels may also be routes of transmission.
Lice infected with R. prowazekii excrete organisms in the feces after 2 to 6 days and die prematurely, within 2 weeks. Bacteria can survive in the feces and the dead lice for weeks.
Disinfection
R. prowazekii is susceptible to 1% sodium hypochlorite, 70% ethanol, glutaraldehyde and formaldehyde. It can also be inactivated by moist heat (121° C for a minimum of 15 min) and dry heat (160-170° C for a minimum of an hour).
Incubation Period
The incubation period is 1 to 2 weeks; most infections become evident after 12 days.
Clinical Signs
The onset of epidemic typhus is often sudden. The initial symptoms may include headache, chills, fever, prostration and myalgia. In approximately 50% of cases, a rash develops after 4 to 6 days. Small pink macules usually appear first on the upper trunk or axillae then spread to the entire body with the exception of the face, palms and soles. As the disease progresses, the rash usually becomes dark and maculopapular or, in severe cases, petechial and hemorrhagic. Splenomegaly, hypotension, nausea, vomiting and confusion may also be seen. The fever lasts approximately 2 weeks. In seriously ill patients, vascular collapse, renal insufficiency, ecchymosis with gangrene, and symptoms of encephalitis or pneumonia may occur. Children and people with partial immunity can have a mild infection with no rash.
R. prowazekii sometimes remains latent and recrudesces years later; this form is called Brill-Zinsser disease. Recrudescent typhus is usually mild, with lower mortality rates.
The symptoms of the zoonotic form resemble classic typhus but are almost always mild. The fever usually lasts for 7 to 10 days and the rash is often barely visible or absent. Deaths are not seen with this form.
Communicability
R. prowazekii is not transmitted from person to person. Patients can infect lice while the fever is present and may continue to be infectious for another 2 to 3 days. Patients with Brill-Zinsser disease are also infectious for lice.
Diagnostic Tests
Epidemic typhus is usually diagnosed by serology; a fourfold rise in titer is diagnostic. Titers usually become detectable during the second week. Serologic tests include the indirect fluorescence antibody test, latex agglutination, complement fixation, enzyme immunoassay (EIA) and the toxin-neutralization test. R. prowazekii may cross-react with R. typhi (the agent of murine typhus) in some tests.
Organisms can also be identified in tissue samples, including skin biopsies, by immunohistochemical staining. Polymerase chain reaction (PCR) assays may be available in some laboratories. Isolation and identification of R. prowazekii is not widely available or used for diagnosis, as rickettsia are both fastidious and dangerous to laboratory personnel.
Treatment and Vaccination
Early treatment with antibiotics is effective and relapses are uncommon. Treatment is sometimes begun before laboratory confirmation, particularly when the symptoms are severe. Antibiotics can also speed recovery in patients with zoonotic form. No commercial vaccines have been licensed, but experimental vaccines are produced by military sources in the United States and may be available for high-risk situations.
Residual insecticide treatment of the clothing and hair is recommended for people who may have been exposed to infected lice.
Morbidity and Mortality
Epidemics of typhus usually occur where louse populations are high. Infections are typically seen in populations living in unsanitary, crowded conditions; outbreaks are often associated with wars, famines, floods and other disasters. Most epidemics occur during the colder months. Sporadic cases of zoonotic typhus are seen in the United States.
The overall case fatality rate for untreated infections is 10 to 40%; the mortality rate increases with age. Infections are rarely fatal in children less than 10 years old; in people over 50 years old, the mortality rate can be as high as 60% without treatment. Deaths have not been seen in the zoonotic form, regardless of treatment.
In the United States, R. prowazekii is endemic in flying squirrels (Glaucomys volans). Infections can be transmitted to humans from this species but little has been published about the disease in squirrels. Dogs have been experimentally infected but seroconverted with no clinical signs; no organisms were recovered from the blood.
Azad A.F. and C.B. Beard. “Rickettsial pathogens and their arthropod vectors.” Emerging Infectious Diseases 4, no. 2 (Apr-Jun 1998). 4 Dec 2002 <http://www.cfsresearch.org/rickettsia/other/9nf.htm>.
Breitschwerdt E.B., B.C. Hegarty, M. G. Davidson and N.S.A. Szabados. “Evaluation of the pathogenic potential of Rickettsia canada and Rickettsia prowazekii organisms in dogs.” J. Am. Vet. Med. Assoc. 207, no. 1 (Jul 1995):58-63.
“Epidemic typhus.” In The Merck Manual, 17 th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 4 Dec 2002 <http://www.merck.com/pubs/mmanual/section13/chapter159/159b.htm>.
“Epidemic typhus associated with flying squirrels -- United States.” Morbidity and Mortality Weekly Report 31, no. 41 (Oct 22, 1982): 555-6;561. 4 Dec 2002 <http://www.cdc.gov/mmwr/preview/mmwrhtml/00001177.htm>.
Huffman J. and V. Nettles. “Typhus and flying squirrels.” Southeastern Cooperative Wildlife Disease Study (SCWDS) Briefs, October 1999, 15.3. 3 December 2002 <http://www.uga.edu/scwds/topic_index/1999/TyphusandFlyingSquirrels.pdf>.
“Material Safety Data Sheet – Rickettsia prowazekii.” January 2001 Canadian Laboratory Centre for Disease Control. 4 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds128e.html>.
“Surveillance and reporting guidelines for typhus.” Washington State Department of Health, Oct 2002. 4 December 2002 <http://www.doh.wa.gov/notify/guidelines/typhus.htm>.
“Typhus Fevers.” Centers for Disease Control and Prevention, Feb 2002. 4 December 2002 <http://www.cdc.gov/travel/diseases/typhus.htm>.
Walker, D.H. “Rickettsiae.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 4 Dec 2002 <http://www.gsbs.utmb.edu/microbook/ch038.htm>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Synonyms: African Hemorrhagic Fever
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Ebola and Marburg are caused by Ebola virus and Marburg virus, the only members of the family Filoviridae. These two viruses are closed related and are considered to be serotypes or genotypes within a single genus. Ebola virus is subdivided into three subtypes: Zaire, Sudan, and Reston. An isolate from a 1994 Ivory Coast outbreak is probably a fourth subtype.
Geographic Distribution
Ebola-Zaire, Ebola-Sudan, and Ebola-Ivory Coast outbreaks have been seen in Sudan, Zaire, the Ivory Coast and the Democratic Republic of the Congo. Ebola-Reston outbreaks have occurred in non-human primates in the Italy and United States; these outbreaks were traced to monkeys imported from the Philippines. Wild non-human primates in the Philippines may have antibodies to Ebola-Reston.
Marburg has been seen in Uganda, Kenya, Zimbabwe and South Africa. Outbreaks also occurred in Germany and Yugoslavia, in humans exposed to African green monkeys from East Africa.
Transmission
Human filovirus outbreaks seem to have a zoonotic source, but the reservoir host has not been identified. Transmission among humans and other primates is by direct contact with infected blood, secretions, organs or semen, and on fomites. Virus has also been found in urine. Marburg and Ebola can be transmitted by aerosols and small droplets among monkeys; however, aerosol transmission does not appear to be a major route of spread between humans infected with Ebola. Filoviruses can survive for several weeks in blood and corpses.
Disinfection
Hypochlorite or phenolic disinfectants are generally recommended for disinfection. Ebola virus is susceptible to 2% sodium hypochlorite, 2% glutaraldehyde, 5% peracetic acid and 1% formalin. This virus is also inactivated by ultraviolet light, gamma irradiation, 0.3% betapropiolactone for 30 minutes at 37° C, or heating to 60° C for 1hr. Marburg virus is susceptible to 1% sodium hypochlorite, 2% glutaraldehyde or formaldehyde, ultraviolet light or heat.
Incubation Period
The incubation period is 2 to 21 days for Ebola and 3 to 10 days for Marburg.
Clinical Signs
Ebola usually begins with the abrupt onset of headache, sore throat, fever, myalgia, joint pain and weakness, followed by diarrhea, vomiting and stomach pain. A maculopapular rash on the truck, red eyes and hiccups are also seen. Hemorrhages are common and may include petechiae, ecchymoses, bloody diarrhea, bleeding from puncture sites and mucous membranes, and other internal and external bleeding. Early symptoms may be nonspecific and resemble other illnesses. Ebola-Reston can infect humans but hemorrhagic illnesses have not been seen.
The symptoms of Marburg are very similar to Ebola. This disease also begins with the acute onset of fever, chills, headache and myalgia. Approximately five days later, a maculopapular rash may appear on the trunk, followed by a sore throat, nausea, vomiting, chest pain, abdominal pain or diarrhea. Other symptoms may include severe weight loss, jaundice, delirium, shock, pancreatitis, liver failure, massive hemorrhaging and multi-organ dysfunction.
Communicability
Yes. Filoviruses can be spread between humans by contact with blood, secretions, organs, or semen. Ebola virus has been found in large quantities in the skin. Aerosol transmission is at least theoretically possible.
Diagnostic Tests
Early in the course of infection, Ebola can be diagnosed by an antigen-capture enzyme-linked immunosorbent assay (ELISA), virus isolation, detection of viral RNA by polymerase chain reaction (PCR) or the detection of virus-specific IgM by ELISA. Serology for IgG antibodies is useful later in the disease. At necropsy, immunohistochemistry, virus isolation or PCR can be employed.
Early Marburg infections can de diagnosed by antigen-capture ELISA, virus isolation, polymerase chain reaction (PCR) or an ELISA to detect Ebola-specific IgM. An IgG specific ELISA is useful later in the disease or after recovery. Diagnosis at necropsy is by immunohistochemistry on blood or tissue, virus isolation or PCR.
Treatment and Vaccination
No specific treatment is available for Ebola or Marburg; supportive therapy is given, with appropriate barrier precautions against infection of medical personnel. Transfusions of fresh-frozen plasma and other replacements for clotting proteins have been tried. Heparin has also been used, although its use is controversial.
Morbidity and Mortality
The case fatality rate is 50 to 90% for Ebola and 23 to 25% for Marburg. Bleeding is a poor prognostic sign. Ebola-Reston can infect humans but hemorrhagic illnesses have not been seen.
Species Affected
Ebola-Zaire, Ebola-Sudan and Ebola-Ivory Coast affect humans and non-human primates; Ebola-Reston causes hemorrhagic fever in monkeys but does not seem to be pathogenic for humans. Naturally-occurring Ebola antibodies have been found in rhesus monkeys, African green monkeys, cynomolgus monkeys and baboons. Chimpanzees, gorillas, rhesus monkeys, vervet monkeys, cynomolgus monkeys, newborn mice and guinea pigs can develop clinical illness. Experimentally infected rabbits, pigeons and various species of mice, bats, frogs, geckos, snakes, tortoises and arthropods did not develop clinical signs; however, virus replication was seen in bats and possibly snakes, mice and spiders. The natural reservoir of this virus is unknown.
Marburg virus can infect humans and non-human primates, including African green monkeys. Antibodies have been found in captive vervet monkeys and baboons in Kenya. The natural host is unknown.
Incubation Period
The incubation period for Marburg or Ebola-Zaire infections in rhesus monkeys and African green monkeys is 4 to 16 days. In guinea pigs, the incubation period is 4 to 10 days.
Clinical Signs
Filovirus infections result in severe, often fatal, hemorrhagic fevers in non-human primates. Clinical signs may include fever, anorexia, vomiting, splenomegaly, weight loss and a skin rash. Hemorrhages can occur in any organ and may include petechiae, bleeding into the gastrointestinal tract, or bleeding from puncture wounds and mucous membranes. Guinea pigs infected with unpassaged virus from primates usually develop a fever and weight loss but recover; animals infected with serially passaged virus may develop fatal liver disease.
Communicability
Yes. Blood, secretions, organs, semen and urine may contain infectious virus; virus can probably be found almost anywhere in the body. Aerosol transmission of both Ebola and Marburg viruses has been seen in primates.
Diagnostic Tests
Filovirus infections can be diagnosed by virus isolation; Vero cells or MA-104 cells are commonly used for Ebola virus. In humans, Ebola virus is most reliably isolated from acute-phase serum but can also be found in throat washes, urine, semen, anterior eye fluid and other fluids. In necropsied monkeys, filoviruses have been found in particularly high concentrations in the liver, spleen, lungs and lymph nodes. Electron microscopy can also detect virus particles in tissues: filoviruses are pleomorphic, long and filamentous and may be branched. Some may be U-shaped, b-shaped or circular. Viral antigens can be detected with an enzyme-linked immunosorbent assay (ELISA) or by immunofluorescence. Skin biopsies collected into formalin may be helpful for diagnosis; large amounts of Ebola antigen have been found in skin. A reverse transcriptase-polymerase chain reaction (RT-PCR) assay can identify Marburg or Ebola RNA.
Serologic tests include indirect immunofluorescence assays (IFA), immunoblotting and ELISAs. Neutralization tests are unreliable for filoviruses. Paired serum samples should be tested; low IFA titers in single samples cannot be interpreted. The significance of antibody titers in asymptomatic primates is controversial.
Treatment and Vaccination
No specific therapy or vaccine is available.
Morbidity and Mortality
Marburg and Ebola infections have a very high mortality rate in non-human primates and experimentally infected suckling mice. Guinea pigs infected with Ebola virus from primates usually recover; animals infected with serially passaged virus may develop fatal liver disease.
Post-Mortem Lesions
At necropsy, there may be widespread petechiae and hemorrhages. Hemorrhages can occur in any organ but are particularly common in the gastrointestinal tract, kidneys, and pleural, pericardial and peritoneal spaces. The liver and spleen may be swollen and friable. Animals may have a maculopapular rash. There can also be signs of interstitial pneumonia, nephritis, and necrosis of the liver, lymphoid tissue, adrenal cortex or pulmonary epithelium.
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Bowen E.T., G.S. Platt, D.I. Simpson, L.B. McArdell and R.T. Raymond. “Ebola haemorrhagic fever: experimental infection of monkeys.” Trans. R. Soc. Trop. Med. Hyg. 72, no. 2 (1978): 188-91.
Chepurnov, A.A., A.A. Dadaeva and S.I. Kolesnikov. “Study of the pathogenesis of Ebola fever in laboratory animals with different sensitivity to the virus.” Bulletin of Experimental Biology and Medicine 132, no. 6 (December 2001): 1182-6.
Dalgard, D.W.R.J. Hardy, S.L. Pearson, G.J. Pucak, R.V. Quander, P.M. Zack, C.J. Peters and P.B. Jahrling. “Combined simian hemorrhagic fever and Ebola virus infection in cynomolgus monkeys.” American Association for Laboratory Animal Science 42, no. 2 (Apr 1992): 152-157.
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Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
WASHINGTON, D.C., December 15, 2018—The United States Department of Agriculture’s (USDA) Animal and Plant Health Inspection Service (APHIS) confirmed the presence of virulent Newcastle disease in a commercial chicken flock in Riverside County, California. This finding is part of an outbreak in southern California that began in May 2018 in backyard birds. This is the first case in commercial poultry since 2003. Read more here.
Virulent Newcastle Disease (vND), formerly known as Exotic Newcastle Disease is a contagious and fatal viral disease affecting the respiratory, nervous and digestive systems of birds and poultry. The disease is so virulent that many birds and poultry die without showing any clinical signs. vND is not a food safety concern. No human cases of Newcastle disease have ever occurred from eating poultry products. Properly cooked poultry products are safe to eat. In very rare instances people working directly with sick birds can become infected with mild symptoms.
vND has not been found in commercial poultry in the U.S. since 2003.
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On May 17, 2018, the United States Department of Agriculture’s Animal and Plant Health Inspection Service confirmed the presence of virulent Newcastle disease in a small flock of backyard exhibition chickens in Los Angeles County, California. To track the spread of the disease, click here: https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-disease-information/avian-influenza-disease/vnd To Report Sick or Dead Poultry New Jersey Department of Agriculture, Division of Animal Health 609-671-6400 or state.veterinarian@ag.state.nj.us -OR- USDA APHIS Veterinary Services NJ Area Office 609-259-5260 or toll-free at 1-866-536-7593 To Report Sick/Dead Wild Birds, Wild Waterfowl, Pators, Shorebirds or Gulls: USDA APHIS Wildlife Services 908-735-5654 ext.2 -OR- NJDEP Hotline, toll-free 877-WARN-DEP (877-927-6337) |
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
West Nile fever results from infection by the West Nile virus, a mosquito-borne arbovirus in the genus Flavivirus, family Flaviviridae. Two genetic lineages exist; viruses in lineage 1 but not lineage 2 have been definitely linked to human disease. The strain found in the United States may have originated in the Middle East. It appears to be related to a lineage 1 virus found in Israel from 1997 to 2000.
Geographic Distribution
West Nile fever has been seen in Africa, Eastern Europe, the Mediterranean region, the Rhone River delta of France, Russia, west and central Asia and the Middle East. Since 1999, the West Nile virus has also been found in the United States. The first infections were seen in New York; the virus has now spread along the East Coast and into the Midwest and South
Transmission
The West Nile virus is transmitted by mosquitoes. At least 29 species of North American mosquitoes are susceptible to infection. Culex pipiens, Culex restuans, and Culex salinarius appear to be the most important maintenance vectors in the United States. Infections have also been documented in ticks in Asia and Russia, but their role in transmission is uncertain.
Birds are the primary reservoir hosts. In endemic regions, West Nile virus is maintained in an enzootic cycle between culicine mosquitoes and birds. When environmental conditions favor high viral amplification, significant numbers of "bridge vector" mosquitoes (mosquitoes that feed on both birds and mammals) become infected in the late summer and can spread the virus to humans, horses and other incidental hosts. Migratory birds may carry West Nile virus into new areas. Direct transmission between animals has not been seen in experimentally infected chickens or turkeys, but has been documented in geese. Infected humans and horses do not seem to spread the virus to other mammals.
Disinfection
Little or no information has been published on the susceptibility of West Nile virus to disinfectants; however, related flaviviruses (St. Louis encephalitis, yellow fever and dengue viruses) are destroyed by many disinfectants including 1% sodium hypochlorite, 2% glutaraldehyde and 70% ethanol.
Incubation Period
The incubation period is currently estimated to be 3 to 14 days.
Clinical Signs
Most cases of West Nile fever are mild and flu-like, with fever, headache and body aches. Weakness, malaise, anorexia, lymphadenopathy, nausea and vomiting may also be seen. An erythematous macular, papular, or morbilliform skin rash occasionally develops on the neck, trunk, arms or legs. Most uncomplicated infections resolve in 3 to 6 days.
Communicability
Yes. C. jejuni is found in the feces and can be shed for as long as 2 to 7 weeks in untreated infections; however, humans rarely become chronic carriers. C. fetus subsp. fetus is communicable for several days to several weeks.
In more severe cases, there may be signs of encephalitis, meningoencephalitis or meningitis; the symptoms may include a high fever, headache, neck stiffness, stupor, disorientation, tremors, convulsions, severe muscle weakness, flaccid paralysis and coma. Ataxia, cranial nerve abnormalities, myelitis, eye pain, polyradiculitis, and seizures have also been seen. In some outbreaks, myocarditis, pancreatitis, and fulminant hepatitis occur.
Diagnostic Tests
In humans, West Nile fever can be diagnosed by a rising titer or by finding IgM in serum or cerebrospinal fluid, using an IgM antibody-capture ELISA. A plaque reduction neutralization test, indirect immunofluorescence and hemagglutination inhibition tests are also available. Cross-reactions may be seen with other flaviviruses, including yellow fever, Japanese encephalitis, St. Louis encephalitis or dengue. False positive reactions may be clarified with the plaque reduction neutralization test but the results may still be ambiguous.
The West Nile virus, viral antigens or nucleic acids may also be detected in cerebrospinal fluid, tissue, blood and other body fluids. Virus isolation from cerebrospinal fluid and brain tissue is often negative. Polymerase chain reaction assays may also be available.
Treatment and Vaccination
No specific treatment, other than supportive care, is available. Intensive care and mechanical ventilation may be required in some cases. Ribavirin and interferon are effective in vitro. Human vaccines are not yet available but are in development.
Morbidity and Mortality
Most human infections appear to be asymptomatic. In 1999, a survey found that 20% of seropositive individuals in New York reported symptoms consistent with West Nile fever; approximately half had visited a physician at the time of the illness. Neurologic disease is more likely to develop in those over 50 years old and to be more serious in this group. An estimated one in 140 to one in 320 infections are thought to result in meningitis or encephalitis.
The case fatality rate in outbreaks ranges from 4 to 14%. The mortality rate is higher among older patients. Case fatality rates of 15 to 29% have been seen in those over 70 years old. There is some evidence that concurrent disease such as diabetes or immunosuppression increases the risk of death. There is also evidence that seriously ill patients may suffer substantial long-term morbidity after recovery. In New York, 67% of hospitalized patients had continued fatigue one year after discharge; memory loss was seen in 50%, difficulty walking in 49%, muscle weakness in 44% and depression in 38%.
Species Affected
Wild birds are the main reservoir hosts. Many birds carry the virus without clinical signs, but symptomatic infections can be seen in crows, ravens, jays, pigeons, domestic geese and some other avian species. Among mammals, neurologic disease has been seen mainly in horses and humans. Infections have also been documented in gray squirrels, chipmunks, skunks, domestic rabbits, cats, dogs, a wolf, sheep, goats, bats, an alpaca, a fox squirrel and a mountain goat. Mice, hamsters and rhesus monkeys can be infected experimentally.
Incubation Period
The incubation period in horses appears to be 5 to 15 days. The incubation period for other species is unknown.
Clinical Signs
Infections in Birds
Infections in many birds appear to be asymptomatic, but high mortality can be seen in crows, ravens and jays. Affected wild birds are usually found dead and the clinical signs in these species have not been well described. In some cases, myocarditis and encephalitis are found post-mortem. Naturally or experimentally infected chickens and turkeys are asymptomatic. Domestic geese can show clinical signs; in natural and experimental infections, the symptoms may include weight loss, decreased activity, depression, myocarditis and neurologic signs including torticollis, opisthonos and rhythmic side-to-side head movements. Infections in geese can be fatal.
Infections in Mammals
In horses, West Nile virus causes neurologic disease. The clinical signs may include anorexia, depression, ataxia, muscle twitches, partial paralysis, impaired vision, head pressing, teeth grinding, aimless wandering, convulsions, circling and an inability to swallow. Attitudinal changes including depression, somnolence, listlessness, apprehension or periods of hyperexcitability may be seen. Weakness, usually in the hind limbs, is sometimes followed by paralysis. Coma and death may occur. Fever has been seen in some but not all cases. Fatal hepatitis developed in one donkey with neurologic signs in France.
There is limited evidence of pathogenicity in other species. Recently, deaths were reported in an infected 3-month old wolf and an 8-year old dog in the United States. The dog was suffering from an immune-mediated disease. There are few reports of experimental infections; however, in one study, two of three experimentally infected dogs developed a mild recurrent myopathy. West Nile virus has also been recovered from the brain of a cat with neurologic signs, two other fatally ill cats and dead squirrels. Fatal encephalitis is seen in experimentally infected mice, hamsters and rhesus monkeys.
Communicability
Horses, chickens and turkeys do not seem to infect other animals by direct contact. Experimentally infected geese may be able to spread the virus without a mosquito vector.
Diagnostic Tests
West Nile fever can be diagnosed by virus isolation. Virus can be recovered from the brain, spinal cord, blood and other tissues of infected horses, and the brain, heart, kidney and intestines of geese. Vero cells are often used for isolation. A reverse transcription- polymerase chain reaction (RT-PCR) test and immunohistochemical staining can detect viral RNA and antigens, respectively.
Serology may also be helpful. Assays include a plaque-reduction neutralization test (PRNT) and an IgM-capture enzyme-linked immunosorbent assay (ELISA). A fourfold increase in titer should be seen in the PRNT test. There is some evidence that IgM may be low or undetectable in some recently infected horses. The efficacy of serologic tests has not been determined in cats; this species does not develop antibodies in response to some flaviviruses.
Treatment and Vaccination
No specific treatment is available but animals may recover on their own if they are given supportive care. Mild cases have, in some cases, recovered without treatment. A vaccine has been conditionally approved for horses and is available from Fort Dodge Laboratories.
Morbidity and Mortality
Birds are the main reservoir host and can infected asymptomatically. In endemic areas, the prevalence of infection in wild birds ranges from 10 to 53%. Mammals can also be infected without disease. Antibodies have been found in normal dogs, horses, donkeys and mules in endemic regions, including the United States. In some cases, the prevalence of infection may be high. In 1959, 54% of the horses, donkeys and mules in Egypt were seropositive. More recently, West Nile antibodies were found in 37% of dogs in the highveld region of South Africa.
Estimates of the morbidity rates in horses vary. During outbreaks, 20 to 43% of infected horses appear to develop acute neurologic signs. Experimental studies have been equivocal. In one recent study, only one of 12 horses experimentally infected by mosquito vectors developed encephalitis. The other 11 horses seroconverted but remained asymptomatic. Higher rates of encephalitis and fever have been seen when foals and horses were infected subcutaneously and intravenously; 4 of 9 animals in two studies became ill.
The case fatality rate in horses has varied from 25 to 45% in different outbreaks. In the current epidemic in the United States, the case fatality rate is approximately 35 to 45%. Deaths have also been seen in squirrels in endemic areas, although West Nile virus has not been proven to be the cause.
Post-Mortem Lesions
Severe myocarditis and encephalitis have been found post-mortem in some but not all wild birds. Geese may be dehydrated and in poor condition, with subcutaneous hemorrhages around the joints, pale lungs, a pale beak, and petechial hemorrhages in the splenic capsule. An enlarged gall bladder, severe thymic and cloacal bursa atrophy and excess cerebrospinal fluid have also been seen in this species.
In horses, a moderate to severe meningoencephalitis, associated with hemorrhages, may be seen in the central nervous system. The lesions are most often found in the brainstem and ventral horns of the lumbo-sacral spinal cord. Few abnormalities are seen in the brain and cerebellum.
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Centers for Disease Control and Prevention (CDC) |
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Articles on West Nile Virus Emerging Infectious Diseases Vol. 7, No. 4 (Jul–Aug 2001) |
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West Nile Virus USDA Animal and Plant Health Inspection Service (APHIS) |
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West Nile Virus Guidelines for Horse Owners Nebraska Cooperative Extension |
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West Nile Virus: A Primer for the Clinician Annals of Internal Medicine |
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What you should know about West Nile virus. American Veterinary Medical Association |
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USDA APHIS West Nile Index |
Anderson, K. “West Nile virus guidelines for horse owners.” Nebraska Cooperative Extension, Aug 2002. 5 Dec 2002 <http://www.ianr.unl.edu/pubs/animaldisease/nf542.htm>.
“Arthropod-Borne Viral Fevers.” In Control of Communicable Diseases Manual, 17th ed., edited by James Chin. Washington, D.C.: American Public Health Association, 2000, pp. 48-50.
Barlow, J. “UI lab confirms first cases of West Nile in canines, squirrels.” University of Illinois, Champaign Urbana, Sept 2002. 5 Dec 2002 <http://www.news.uiuc.edu/scitips/02/0917westnile.html>.
Blackburn N.K., F. Reyers, W.L. Berry and A.J. Shepherd. “Susceptibility of dogs to West Nile virus: a survey and pathogenicity trial.” J. Comp. Pathol. 100, no. 1 (Jan 1989): 59-66.
Bunning M.L., R.A. Bowen, C.B. Cropp, K.G. Sullivan, B.S. Davis, N. Komar, M.S. Godsey, D. Baker, D.L. Hettler, D.A. Holmes, B.J. Biggerstaff, C.J. Mitchell. “Experimental infection of horses with West Nile virus.” Emerg. Infect. Dis. 8, no. 4 (2002): 380-6. 8 Dec 2002 <http://www.medscape.com/viewarticle/432142_print>.
“Human, animal cases of West Nile continue to climb. Virus identified in small number of new animal species.” American Veterinary Medical Association, Nov 2002. 5 Dec 2002 <http://www.avma.org/onlnews/javma/nov02/021101g.asp>.
Langevin S.A., M. Bunning, B. Davis and N. Komar. “Experimental infection of chickens as candidate sentinels for West Nile virus.” Emerg. Infect. Dis. 7, no. 4 (Jul–Aug 2001):726-9. 5 Dec 2002 <http://www.cdc.gov/ncidod/eid/vol7no4/langevin.htm>.
Leake, C.J. “Mosquito-Borne Arboviruses.” In Zoonoses. Edited by S.R. Palmer, E.J.L. Soulsby and D.I.H Simpson. New York: Oxford University Press, 1998, pp. 401-413.
Komar N., N.A. Panella and E. Boyce. “Exposure of domestic mammals to West Nile virus during an outbreak of human encephalitis, New York City, 1999.” Emerg. Infect. Dis. 7, no. 4 (Jul–Aug 2001):736-8. 5 Dec 2002 <http://www.cdc.gov/ncidod/eid/vol7no4/komar1.htm>.
“Material Safety Data Sheet – Dengue fever virus.” Canadian Laboratory Centre for Disease Control, March 2001. 9 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds50e.html>.
“Material Safety Data Sheet –St. Louis encephalitis.” Canadian Laboratory Centre for Disease Control, April 2001 9 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds174e.html>.
“Material Safety Data Sheet – Yellow fever virus” Canadian Laboratory Centre for Disease Control, March 2001 9 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds167e.html>.
Murgue B., S. Murri, S. Zientara, B. Durand, J.-P. Durand and H. Zeller. “West Nile outbreak in horses in southern France, 2000: The return after 35 years.” Emerg. Infect. Dis. 7, no. 4 (Jul–Aug 2001):692-6. 5 Dec 2002 <http://www.cdc.gov/ncidod/eid/vol7no4/murgue.htm>.
Ostlund E.N., R.L. Crom, D.D. Pedersen, D.J. Johnson, W.O. Williams and B.J. Schmit. “Equine West Nile encephalitis, United States.” Emerg. Infect. Dis. 7, no. 4 (Jul–Aug 2001):665-9. 5 Dec 2002 <http://www.cdc.gov/ncidod/eid/vol7no4/ostlund.htm>.
Peiris, J.S. Malik and F.P. Amerasinghe. “West Nile Fever.” In Handbook of Zoonoses, 2nd ed. Edited by G.W. Beran. Boca Raton, Florida: CRC Press, 1994, pp. 139-148.
Perl S., L. Fiette, D. Lahav, N. Sheichat, C.Banet, U. Orgad, Y. Stram and M. Malkinson. “West Nile encephalitis in horses in Israel.” Israeli Veterinary Medical Association 57, no. 2 (2002). 8 Dec 2002 <http://www.isrvma.org/article/57_2_2.htm>.
Petersen L.R. and A.A. Marfin. “West Nile virus: a primer for the clinician.” Ann. Intern. Med. 137, no. 3 (Aug 2002:173-9. <http://www.annals.org/issues/v134n3/full/200208060-000009.html>.
Swayne D.E., J.R. Beck, C.S. Smith, W.-J. Shieh and S.R. Zaki. “Fatal encephalitis and myocarditis in young domestic geese (Anser anser domesticus) caused by West Nile virus.” Emerg. Infect. Dis. 7, no. 4 (Jul–Aug 2001):751-3. 5 Dec 2002 <http://www.cdc.gov/ncidod/eid/vol7no4/swayne.htm>.
Trock S.C. B.J. Meade, A.L. Glaser, E.N. Ostlund, R.S. Lanciotti, B.C. Cropp, V. Kulasekera, L.D. Kramer and N. Komar. “West Nile virus outbreak among horses in New York State, 1999 and 2000.” Emerg. Infect. Dis. 7, no. 4 (Jul–Aug 2001):745-7. 5 Dec 2002
<http://www.cdc.gov/ncidod/eid/vol7no4/trock.htm>.
“West Nile virus.” USDA Animal and Plant Health Inspection Service (APHIS), January 2002. 5 Dec 2002 <http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahwnv.html>
“What you should know about West Nile virus.” American Veterinary Medical Association, November 5, 2002. 5 Dec 2002 <http://www.avma.org/communications/brochures/wnv/wnv_faq.asp>.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
Contagious Equine Metritis
CEM Facility Call for Applications (Application Period Closed)
New Jersey CEM Quarantine Facility Application
SAMPLE New Jersey CEM Quarantine Facility License Agreement
Learn More: USDA APHIS Contagious Equine Metritis
Equine Encephalomyelitis
Synonyms: : “Sleeping Sickness”
Eastern Equine Encephalomyelitis – EEE, Eastern equine encephalitis, Eastern encephalitis
Western Equine Encephalomyelitis – WEE,
Western equine encephalitis
Venezuelan Equine Encephalomyelitis – VEE, VE, Peste loca, Venezuelan equine encephalitis, Venezuelan encephalitis, Venezuelan equine fever
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Eastern, Western and Venezuelan equine encephalomyelitis result from infection by the respectively named viruses in the genus Alphavirus (family Togaviridae). In the human literature, the disease is usually called Eastern, Western or Venezuelan equine encephalitis.
Eastern Equine Encephalomyelitis Virus
There are two variants of the Eastern equine encephalomyelitis (EEE) virus. The virus found in North America is more pathogenic than the variant that occurs in South and Central America. The Eastern equine encephalitis virus can cause disease in humans, horses and some species of birds.
Western Equine Encephalomyelitis Viruses
The Western equine encephalomyelitis (WEE) virus group includes the Western equine encephalitis (WEE), Sindbis, Ft. Morgan, Aura and Y 61-33 viruses. The Western equine encephalitis virus can cause disease in humans, horses and some species of birds. A related virus, the Highlands J virus, is sometimes isolated in the eastern United States. The Highlands J virus can cause disease in turkeys. It has also been linked to a single case of encephalitis in a horse.
Venezuelan Equine Encephalomyelitis Viruses
The Venezuelan equine encephalomyelitis (VEE) complex contains at least 8 viral subtypes; these viruses are divided into epizootic and enzootic groups. The epizootic subtypes are responsible for most epidemics. They are highly pathogenic for horses and also cause illness in humans. Enzootic (sylvatic) subtypes are generally found in limited geographic areas, where they occur in natural cycles between rodents and mosquitoes. The enzootic subtypes can cause human disease. They are usually nonpathogenic for horses; however, in 1993 an enzootic variant was responsible for an outbreak of VEE among horses in Mexico.
Geographic Distribution
The Western, Eastern and Venezuelan encephalomyelitis viruses are found in North, Central and South America. The WEE viruses occur in western Canada, Mexico, parts of South America, and west of the Mississippi in the United States. The EEE virus is found in eastern Canada, all states east of the Mississippi, Arkansas, Minnesota, South Dakota and Texas. It also occurs in the Caribbean and regions of Central and South America, particularly along the Gulf coast. VEE viruses are endemic in South and Central America and Trinidad. Enzootic subtypes of VEE are also found in Florida, the Rocky Mountains and northern plains of the United States. Most epidemics of VEE occur in northern and western South America, but some may spread into adjacent countries, including the United States.
Transmission
Eastern and Western Equine Encephalomyelitis
The Eastern and Western encephalomyelitis viruses are transmitted mainly by mosquitoes. Normally, these two viruses cycle between birds and mosquitoes. Humans and horses are incidental, dead end hosts.
The EEE virus can be isolated from 27 species of mosquitoes in the United States. Culiseta melanura, a mosquito that primarily feeds on birds, is the most important vector in the enzootic cycle. During some years, the virus is spread to mammalian hosts by bridge vectors (mosquitoes that feed on both birds and mammals) such as Coquilletidia perturbans, Aedes canadensis, Aedes sollicitans, Aedes vexans and Culex nigripalpus. WEE cycles between passerine birds and culicine mosquitoes. Culex tarsalis appears to be the most important vector; other significant vectors include Aedes melanimon, Aedes dorsalis and Aedes campestris. The EEE and WEE viruses may be transmitted vertically in mosquitoes.
In birds, EEE and WEE are occasionally spread by non-arthropod-borne routes. During outbreaks of disease in game birds, infections are introduced by mosquitoes but spread in the flock mainly by feather picking and cannibalism. EEE and WEE viruses do not survive outside the host.
Venezuelan Equine Encephalomyelitis
The Venezuelan equine encephalomyelitis viruses are also spread mainly by mosquitoes. The enzootic subtypes of VEE cycle between rodents and mosquitoes, mainly Culex species. Birds may also be involved in some cycles. Humans and horses are incidental hosts.
The natural host for the epizootic subtypes, between epidemics, is unknown. Horses infected with the epizootic subtypes can infect mosquitoes and are the main amplifiers for VEE during epidemics. Other mammals, including cattle, pigs and dogs, can be infected but do not usually become ill or spread the virus. Many different species of mosquitoes and other hematogenous insects can transmit epizootic VEE. Efficient vectors include arthropods in the genera Aedes, Anopheles, Culex, Deinocerites, Mansonia, Haemogogus, Sabethes and Psorophora.
In some cases, humans have also developed VEE after being exposed to debris from the cages of infected laboratory rodents. Person-to-person transmission has not been reported; however, the VEE virus can be found in pharyngeal secretions in humans and is stable when aerosolized. The virus can also occur in dried blood and exudates.
Disinfection
EEE and WEE viruses do not persist in the environment but the VEE virus may be found in dried blood and exudates. VEE, EEE and WEE are susceptible to many disinfectants including 1% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde and formaldehyde. They can also be destroyed by moist or dry heat, as well as drying.
Incubation Period
In humans, the incubation period is usually 1 to 6 days for VEE and 4 to 15 days for WEE and EEE.
Clinical Signs
Eastern and Western Equine Encephalitis
Eastern equine encephalitis usually begins abruptly, with fever, myalgia and headache and sometimes nausea and vomiting. This prodrome is often followed by neurologic signs; the symptoms may include confusion, focal neurologic deficits, somnolence, neck stiffness, stupor, disorientation, coma, tremors, seizures and paralysis. Abdominal pain, diarrhea and a sore throat can also occur. The mortality rate for EEE is high.
Western equine encephalitis resembles EEE but is usually asymptomatic or mild in adults, with nonspecific signs of illness and few deaths. The symptoms usually appear abruptly and may include fever, headache, nausea, vomiting, anorexia and malaise. Many adults do not develop other symptoms. In more severe cases, neurologic symptoms, similar to those seen in EEE, can develop. WEE can be severe in children, particularly infants under a year of age.
Venezuelan Equine Encephalitis
In humans, VEE is usually an acute, often mild, systemic illness. The clinical signs may include fever, generalized malaise, severe headache, photophobia and myalgia, particularly in the legs and lumbosacral region. These symptoms usually last for 24 to 72 hours and may be followed by a cough, sore throat, nausea, vomiting and diarrhea. The disease usually lasts 1 to 2 weeks. In pregnant women, VEE can affect the fetus; fetal encephalitis, placental damage, abortion or severe congenital neurologic anomalies may be seen.
Encephalitis usually develops in 4% of children and less than 1% of adults. In mild cases, the symptoms may include lethargy, somnolence, or mild confusion. Severe infections are characterized by seizures, ataxia, paralysis or coma. An increased incidence of encephalitis would be expected after a biological attack with aerosolized viruses.
Communicability
WEE and EEE viruses are not found in the blood or cerebrospinal fluid after the symptoms appear, and only low titers develop during the viremic phase. These viruses do not seem to be spread directly from person to person. Humans do not transmit EEE or WEE viruses to mosquitoes.
Person-to-person transmission is theoretically possible for VEE, but has not been reported in natural cases. Humans with VEE can infect mosquitoes for approximately 72 hours.
Diagnostic Tests
Eastern, Western and Venezuelan equine encephalitis can be diagnosed by virus isolation, serology or other tests. In humans, VEE virus can be isolated from blood, cerebrospinal fluid or throat swabs. Serology is also useful; a rise in titer or the presence of specific IgM is diagnostic. A variety of serologic tests may be available, including virus neutralization, ELISA, hemagglutination inhibition and complement fixation. Indirect immunofluorescence assays have been developed for VEE. Polymerase chain reaction (PCR) or immunohistochemistry may be available at some laboratories.
During the febrile stage of the illness, antigen-capture ELISAs can often detect VEE antigens in the blood. This test is generally not useful during the encephalitic stage. PCR assays may also be available.
Treatment and Vaccination
Treatment consists of supportive care. Investigational VEE, EEE and WEE vaccines may be available for humans at high risk of infection. The VEE vaccine may not be effective for all of the VEE complex viruses.
Morbidity and Mortality
Eastern Equine Encephalitis
In the United States, approximately 12 to 17 cases of EEE are reported to the Centers for Disease Control and Prevention (CDC) each year. The infection rate is approximately 33% and the morbidity rate 90%. Most cases are seen in people over 55 and children younger than 15. Eastern equine encephalitis is often severe in humans. Estimates of the case fatality rate vary from 33 to 70% and permanent neurologic deficits can occur in survivors.
Western Equine Encephalitis
The annual incidence of WEE is highly variable; during an epidemic in 1941, over 3000 human cases occurred in the United States and Canada. The case-infection ratio is approximately 1:1000 in adults, 1:58 in children from 1 to 4 years old and 1:1 in infants up to a year of age. The overall mortality rate is 3 to 4%. Most infections in adults are asymptomatic or mild, without neurologic disease. Infections in children, particularly infants under one year old, can be severe. Approximately 5 to 30% of young patients have permanent neurologic damage.
Venezuelan Equine Encephalomyelitis
In natural epidemics of VEE, human cases are usually preceded by an epidemic in horses. After an attack by a biological weapon, cases would be expected simultaneously in both species or first in humans. Caution should be used in interpreting such patterns of infection, as VEE may be missed in wild or free-ranging equines.
Humans are highly susceptible to VEE; approximately 90 to 100% of exposed individuals become infected and nearly 100% of these infections are symptomatic. However, most infections are mild. Less than 1% of adults develop encephalitis and approximately 10% of these cases are fatal. The overall case fatality is less than 1%. Very young or elderly patients are more likely to develop severe infections. Encephalitis occurs in approximately 4% of children less than 15 years old; the case fatality rate in children with neurologic disease is 35%. A higher incidence of neurologic disease could be seen in adults as well as children after a biological attack with aerosolized virus; mortality rates would be expected to be correspondingly higher.
Species Affected
The equine encephalomyelitis viruses usually cause illness only in equine species and humans. These viruses can also infect a variety of other animals, often asymptomatically.
Eastern and Western Equine Encephalomyelitis
Eastern equine encephalitis virus infects horses, pigs, birds, bats, reptiles, amphibians, forest-dwelling marsupials and rodents. WEE virus can infect birds, horses and a variety of mammals. Most WEE and EEE infections in birds are asymptomatic; however, disease can be seen in chukar partridges, pheasants, psittacine birds, ratites and whooping cranes.
Venezuelan Equine Encephalomyelitis
Rodents seem to be the natural hosts for the enzootic subtypes of VEE but, in some cases, birds may also be involved. VEE virus can cause serious disease in horses, mules, burros and donkeys. Cattle, pigs and dogs can be infected asymptomatically. VEE can also infect a wide variety of laboratory animals.
Incubation Period
The incubation period for WEE or EEE is 5 to 14 days. The clinical signs of VEE are usually seen 1 to 5 days after infection.
Clinical Signs
Eastern and Western Equine Encephalomyelitis in Horses
Eastern and Western equine encephalomyelitis are very similar in horses. The initial clinical signs are usually fever, anorexia and depression. In severe cases, this prodromal stage is followed by neurologic signs; the symptoms may include involuntary muscle movements, impaired vision, aimless wandering, head pressing, circling, an inability to swallow, ataxia, paresis, paralysis and convulsions. Periods of excitement or intense pruritus can also be seen. Laterally recumbent animals may develop a characteristic “paddling” motion. Both EEE and WEE can also cause asymptomatic infections or mild disease without neurologic signs. Occasional cases of encephalitis have been seen in pigs.
Venezuelan Equine Encephalomyelitis in Horses
The enzootic subtypes usually infect horses subclinically. The epizootic subtypes can cause asymptomatic infections or two clinical syndromes. One syndrome resembles EEE and WEE; in this form, a febrile prodrome is followed by neurologic signs and sometimes diarrhea and colic. Death can occur within hours after the onset of neurologic signs or after protracted disease. Animals that recover may have permanent neurologic signs. The second form of VEE is a generalized acute febrile disease without neurologic signs. The symptoms may include fever, weakness, depression, anorexia, colic and diarrhea.
Western and Eastern Equine Encephalitis Viruses in Birds
Western and Eastern equine encephalomyelitis virus infections are asymptomatic in most species of birds, but fatal infections can occur in some species. Most reported outbreaks have been caused by EEE. Chukar infected with the EEE virus are usually dull and listless, with ruffled feathers. The birds are typically found sitting on their hocks with the beak on the ground. In pheasants, the symptoms may include incoordination, weakness and progressive paralysis. In the late stages of the disease, the birds cannot stand but can still move their wings. Whooping cranes may develop lethargy, ataxia and paresis of the legs and neck. The EEE virus has also been isolated from psittacine birds with viral serositis.
Both EEE and WEE viruses can cause fatal hemorrhagic enteritis in ratites; the characteristic clinical signs include depression, hemorrhagic diarrhea, and vomiting of bloodstained material. Highlands J and EEE infections can also cause depression, somnolence, decreased egg production and increased mortality in turkeys.
Communicability
Birds can amplify the Western and Eastern equine encephalomyelitis viruses and are infectious for mosquitoes. Horses are dead-end hosts for these viruses. Direct transmission has been seen only between birds.
Both horses and birds infected with the VEE virus are infectious for mosquitoes. In horses, the virus can be found in bodily fluids. Some authorities suggest that transmission may be possible by direct contact or aerosols but natural transmission between horses or from horses to humans has not been seen. Humans can be infected by laboratory rodents.
Diagnostic Tests
Eastern and Western Equine Encephalomyelitis
In horses, Eastern and Western equine encephalomyelitis can be diagnosed by serology. Tests include plaque reduction neutralization (PRN), hemagglutination inhibition, antibody-capture enzyme linked immunosorbent assay (ELISA) and complement fixation. Cross-reactions may occur between EEE and WEE antibodies in the complement fixation and hemagglutination inhibition tests.
Clinical infections in birds are usually diagnosed by virus isolation. In horses, virus isolation is useful in cases of EEE; it is rarely successful in WEE. The EEE virus can usually be recovered from the brain of infected horses; other tissues such as the liver or spleen may also be positive. EEE and WEE viruses can be isolated in newborn mice, embryonating chicken eggs, newly hatched chicks or cell cultures including primary chicken or duck embryo fibroblasts, African green monkey kidney (Vero), rabbit kidney (RK-13), and baby hamster kidney (BHK-21) cells. Virus identity can be confirmed by complement fixation, immunofluorescence or plaque reduction neutralization (PRN) tests. EEE viruses can also be detected in the brain with immunohistochemistry or an antigen-capture ELISA.
Venezuelan Equine Encephalomyelitis
VEE can be diagnosed by virus isolation or serology. VEE virus can often be recovered from the blood during the febrile stage and is sometimes isolated from the brain of animals with encephalitis. Virus is also found occasionally in the pancreas or other tissues. Animals with neurologic signs are not usually viremic. VEE virus can be isolated in guinea pigs, hamsters, mice, embryonated chicken eggs or cell lines including Vero, RK-13, BHK-21 and duck or chicken embryo fibroblasts. The virus can be identified by complement fixation, hemagglutination inhibition, plaque reduction neutralization (PRN) or immunofluorescence assays. Subtypes can be characterized by immunofluorescence, differential PRN tests or nucleic acid sequencing.
VEE can also be diagnosed by serology. Serologic tests include the PRN test, complement fixation, hemagglutination inhibition and ELISAs. Cross-reactions can occur between VEE, EEE and WEE viruses in the hemagglutination inhibition test. Animals may have pre-existing antibodies to enzootic variants of VEE.
Treatment and Vaccination
Treatment consists of supportive care. Equine vaccines are available for EEE, WEE and VEE. EEE vaccines are also available for susceptible birds, but do not always prevent disease.
Morbidity and Mortality
Eastern and Western Equine Encephalomyelitis
WEE often occurs as sporadic cases of encephalitis in horses, scattered over a wide area. Clinical cases of EEE are usually more clustered. EEE is often fatal in horses; the mortality rate is 50 to 90%. WEE is more likely to be asymptomatic or mild, with mortality rates of approximately 20 to 30%. Significant morbidity and mortality can also occur in poultry, game birds and ratites. In pheasants and other susceptible species of birds, both the morbidity and mortality rates may be up to 90%. The morbidity and mortality rates for emus with hemorrhagic enteritis can be greater than 85%.
Venezuelan Equine Encephalomyelitis
Most enzootic VEE subtypes do not result in serious disease or deaths in horses. Epizootic subtypes can cause significant morbidity and mortality; the morbidity rate can be as high as 90% and the mortality rate varies from 30 to 90%.
Post-Mortem Lesions
The gross lesions are usually nonspecific. In horses with VEE, the lesions in the central nervous system vary from no lesions to extensive necrosis with hemorrhages. Necrotic foci are sometimes seen in the pancreas, liver and heart of horses with VEE. Congestion of the brain and meninges is found in some cases of EEE and WEE. Antemortem trauma can result in ecchymotic hemorrhages.
Microscopic analysis of the brain tissue is often diagnostic. The typical lesion is severe inflammation of the gray matter; neuronal degeneration, infiltration by inflammatory cells, gliosis, perivascular cuffing and hemorrhages may be seen. WEE, EEE and VEE can sometimes be differentiated by the location and pattern of the lesions in the brain.
“Arthropod-Borne Viral Diseases.” In Control of Communicable Diseases Manual, 17th ed. Edited by James Chin. Washington, D.C.: American Public Health Association, 2000, pp. 28-47.
“Eastern Encephalitis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 1970-1.
“Eastern Encephalomyelitis.” In The Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 931-4.
“Equine Encephalomyelitis (Eastern and Western).” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000. 16 Dec 2002
<http://www.oie.int/eng/normes/mmanual/A_00071.htm>.
“Equine Viral Encephalomyelitis.” In Manual for the Recognition of Exotic Diseases of Livestock: A Reference Guide for Animal Health Staff. Food and Agriculture Organization of the United Nations, 1998. 16 Dec 2002 <http://panis.spc.int/RefStuff/Manual/Equine/EQUINE%20VIRAL%20ENCEPH.HTML>.
“Information on Arboviral Encephalitides.” Centers for Disease Control and Prevention (CDC), 2001. 16 Dec 2002
<http://www.cdc.gov/ncidod/dvbid/arbor/arbdet.htm>.
Leake, Colin J. “Mosquito-Borne Arboviruses.” In Zoonoses. Edited by S.R. Palmer, E.J.L. Soulsby and D.I.H Simpson. New York: Oxford University Press, 1998, pp. 401-413.
“Material Safety Data Sheet –Eastern equine encephalitis virus, Western equine encephalitis virus.” March 2001 Canadian Laboratory Centre for Disease Control. 4 October 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds52e.html>.
“Material Safety Data Sheet –Venezuelan equine encephalitis virus.” Canadian Laboratory Centre for Disease Control, September 2001. 10 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds162e.html>.
Nandalur M. and A.W. Urban. “Eastern Equine Encephalitis.” eMedicine, Sept 2002. 16 Dec 2002
<http://www.emedicine.com/med/topic3155.htm>.
Nandalur M. and A.W. Urban. “Western Equine Encephalitis.” eMedicine, June 2002. 16 Dec 2002
<http://www.emedicine.com/MED/topic3156.htm>.
Schmaljohn A.L. and D. McClain. “Alphaviruses (Togaviridae) and Flaviviruses (Flaviviridae).” In Medical Microbiology. 4th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 16 Dec 2002 <http://www.gsbs.utmb.edu/microbook/ch054.htm>.
“Venezuelan Equine Encephalitis.” In Medical Management of Biological Casualties Handbook, 4th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 10 Dec 2002
<http://www.vnh.org/BIOCASU/14.html>.
“Venezuelan Equine Encephalomyelitis.” USDA Animal and Plant Health Inspection Service (APHIS), Sept 2002. 16 Dec 2000 <http://www.aphis.usda.gov:80/oa/pubs/fsvee.html>.
“Venezuelan Equine Encephalomyelitis.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000. 16 Dec 2002 <http://www.oie.int/eng/normes/mmanual/A_00078.htm>.
Walton, T.E. “Venezuelan Equine Encephalomyelitis.” In Foreign Animal Diseases. Richmond, VA: United States Animal Health Association, 1998, pp 406-414.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
"Poultry" includes livestock such as chickens, turkeys, waterfoul, and game birds rasied in captivity, excluding doves and pigeions.
All poultry owners, whether commercial producers or backyard enthusiasts, need to report sick or unexplained bird deaths to State/Federal officials immediately. For small flocks, this can include deaths of one bird per day for two days in a row.
For more information or to report sick or dead poultry contact:
New Jersey Department of Agriculture, Division of Animal Health
609-671-6400 or state.veterinarian@ag.nj.gov
-OR-
USDA APHIS Veterinary Services NJ Area Office
609-259-5260 or toll-free at 1-866-536-7593
Dead Wild Bird – What to do next
Call:
- USDA Wildlife Services 908-735-5654
- NJDA 609-671-6400
- USDA Veterinary Services 609-259-5260
Click here for handling instructions for a dead wild bird.
WHERE DOES AVIAN INFLUENZA COME FROM?
Avian influenza is a viral disease of poultry that can be of low pathogenicity (LPAI), causing mild disease with or without clinical signs, or of high pathogenicity (HPAI), causing severe disease and significant death loss. Wild birds, especially migratory waterfowl (ducks and geese) are passive carriers of the flu virus, meaning they can pass the disease along without becoming seriously ill. Avian Influenza viruses can enter the body by inhalation, ingestion or through other mucous membranes such as the conjunctiva. Feces, saliva and respiratory secretions from infected birds contain large amounts of the virus. Once introduced into a flock, the virus can spread within hours.
The New Jersey Department of Agriculture and USDA APHIS Veterinary Services conduct surveillance on commercial operations, on backyard and hobby flocks, in poultry auctions and in the live bird marketing system.
The New Jersey Department of Agriculture has an emergency response plan in place for the rapid control and elimination of the virus during outbreaks of both LPAI and HPAI. The plan includes provisions for limiting the spread of the disease through increased biosecurity including limiting the traffic to and from the infected premises, increased surveillance in designated quarantine areas, rapid turn-around time for submitted samples and depopulation and disposal for infected birds.
CLINICAL SIGNS OF AVIAN INFLUENZA
LPAI in chickens and turkeys resembles any other mild respiratory disease. With HPAI, birds may die suddenly without any signs of disease. Signs of HPAI may include:
Sudden increase in bird deaths
- Sneezing, gasping for air, coughing and nasal discharge (runny nose)
- Watery and/or green diarrhea
- Lack of energy and poor appetite
- Drop in egg production or soft- or thin-shelled misshapen eggs
- Swelling around the eyes, neck and head
- Purple discoloration of the wattles, combs and legs
HPAI Online Permitting
The NJDA now has an online process for HPAI permits.
Click here for the Online HPAI Permitting Instructions
Click here for the HPAI Permit Request Form
Click here to see a list of 2022-24 confirmations of Highly Pathogenic Avian Influenza in commercial and backyard flocks in the U.S.
Click here for a map of Avian Influenza cases in domestic poultry and wild birds that have been confirmed in North America.
Highly Pathogenic Avian Influenza Letter for Veterinarians
Highly Pathogenic Avian Influenza Letter to Poultry Owners
Highly Pathogenic Avian Influenza Letter to Live Bird Markets
Highly Pathogenic Avian Influenza Letter to Poultry Distributors
Highly Pathogenic Avian Influenza Disease Alert Informational Flyer
POULTRY GROWERS - PROTECT YOUR FLOCK WITH GOOD BIOSECURITY
The USDA is hosting a Defend the Flock Webinar on April 17 on how to "Safeguard Your Poultry on a Multi-Species Farm." Register here and read more here.
Avian influenza spreads from bird to bird, from manure, contaminated vehicles, equipment, egg flats and poultry transport crates. The virus can be transported through bird droppings on clothes or boots into poultry houses and bird pens. Help protect your birds by following these practices:
- Minimize your flock's exposure to wild waterfowl
- Keep poultry away from water which wild waterfowl use
- Don’t use surface water (such as pond water) as a drinking source for your poultry
- Always use dedicated foot wear or use disinfectant footbaths prior to entering bird pens
- Clean up outside feed spills
- Only allow essential workers and vehicles to enter your farm; clean and disinfect vehicle wheels before letting them drive onto and off your farm
- Don’t lend or borrow equipment from other farms
- Avoid visiting other poultry farms and auctions. If you do, change clothes and footwear before working with your own birds
Improving Biosecurity With Wildlife Management Practices
Preventing Access to Barns and Other Facilities
For more information click here
Click here for Livestock and Poultry Import Requirements.
For States with HPAI, click here for Permitting Procedures.
Click here for the Pennsylvania HPAI address search map.
ADDITIONAL RESOURCES
Considerations for Hauling Manure From States That Have A Confirmed Case of Highly Pathogenic Avian Influenza
Avian Influenza
USDA Response Plan - The Red Book
VIDEO LINKS
All these, and more, can be found at the Defend the Flock Resource Center
Biosecurity Practices to Protect Your Poultry
Clean and Disinfect Equipment and Vehicles
Proper Cleaning Procedures Before and After Handling Birds
Establish Perimeters and Boundaries
Don’t Borrow Disease from Your Neighbor
BOVINE INFLUENZAS A INFORMATIONAL RESOURCES
2024 HPAI Letter to Dairy Owners
Avian Influenza in Dairy Cattle FAQs
USDA Influenza A Detections in Livestock
USDA VS Recommendations for Influenza A Virus in Livestock
National Milk Producers Federation Influenza A updates
Dairy Biosecurity Recommendations for HPAI
Infections in Humans
Infections in Animals
Internet Resources
References
Etiology
Botulism is caused by botulinum toxin, a potent neurotoxin produced by Clostridium botulinum and a few strains of C. baratii and C. butyricum. Clostridium botulinum is an anaerobic, Gram-positive, spore-forming rod.
Botulism can result from the ingestion of preformed toxin or the growth of C. botulinum in anaerobic tissues. Seven types of botulinum toxin, designated A through G, have been identified. Types A, B, E and F cause illness in humans. Type C is the most common cause of botulism in animals. Type D is sometimes seen in cattle and dogs, and type B can occur in horses. Types A and E are found occasionally in mink and birds. Type G rarely causes disease, although a few cases have been seen in humans. All types of botulinum toxin produce the same disease; however, the toxin type is important if antiserum is used for treatment.
Geographic Distribution
C. botulinum is found worldwide and cases of botulism can be seen anywhere. In ruminants, botulism mainly occurs in areas where phosphorus or protein deficiencies are found. Botulism is seen regularly in cattle in South Africa and sheep in Australia. This disease is rare in ruminants in the United States, although a few cases have been reported in Texas and Montana.
Transmission
C. botulinum and its spores are widely distributed in soils, sediments in fresh and coastal waters, the intestinal tracts of fish and mammals, and the gills and viscera of shellfish. The bacteria can only grow under anaerobic conditions. Botulism occurs when animals ingest preformed toxins in food or C. botulinum spores germinate in anaerobic tissues and produce toxins as they grow.
Botulism in Humans
In humans, botulism is classified into three forms: foodborne, wound, and infant or intestinal botulism. Foodborne botulism is the most common form and occurs when humans ingest toxins in various foods. The foods associated with botulism are usually low acid (pH greater than 4.6) and may include home-canned foods, sausages, meat products, canned vegetables and seafood products. Commercial foods are occasionally implicated. Wound botulism occurs when an anaerobic wound is contaminated with C. botulinum, usually from the soil. Infant botulism is seen only in children less than a year of age. In this form, C. botulinum spores germinate in the intestinal tract and produce toxin. Honey has been associated with some cases of infant botulism but spores can also be found in many other sources. Adults with altered intestinal flora, secondary to gastrointestinal surgery or antibiotic therapy, may also be able to develop this form.
Botulism in Animals
Preformed toxins in a variety of sources, including decaying vegetable matter (grass, hay, grain, spoiled silage) and carcasses can cause botulism in animals. Carnivores, including mink and commercially raised foxes, usually ingest the toxins in contaminated meat such as chopped raw meat or fish. Cattle in phosphorus-deficient areas may chew bones and scraps of attached meat; a gram of dried flesh may have enough botulinum toxin to kill a cow. Similar cases occur in Australia, where protein-deficient sheep sometimes eat the carcasses of rabbits and other small animals. Ruminants may also be fed hay or silage contaminated by toxin-containing carcasses of birds or mammals. Horses usually ingest the toxin in contaminated forage. Birds can ingest the toxins in maggots that have fed on contaminated carcasses or in dead invertebrates from water with decaying vegetation. Cannibalism and contaminated feed can also result in cases in poultry.
The toxicoinfectious form of botulism corresponds to the wound and intestinal forms in humans. C. botulinum may grow in necrotic areas in the liver and GI tract, abscesses in the navel and lungs, or anaerobic wounds in the skin and muscles. This form of botulism appears to be responsible for shaker foal syndrome in horses. Toxicoinfectious botulism is also seen in chickens, when broilers are intensively reared on litter; the cause of this phenomenon is unknown.
Botulinum and Bioterrorism
In a bioterrorist attack, botulinum toxin could be delivered by aerosols, as well as food or water. After aerosol transmission, the clinical disease is expected to be similar to foodborne botulism.
Disinfection/ Inactivation
Botulinum toxins are large, easily denatured proteins. Toxins exposed to sunlight are inactivated within 1 to 3 hours. Botulinum can also be inactivated by 0.1% sodium hypochlorite, 0.1N NaOH, heating to 80°C for 30 minutes or 100°C for 10 minutes. Chlorine and other disinfectants can destroy the toxins in water.
The vegetative cells of Clostridium botulinum are susceptible to many disinfectants, including 1% sodium hypochlorite and 70% ethanol. The spores are resistant to environmental conditions but can be destroyed by moist heat (120°C for at least 15 min).
Incubation Period
The incubation period for foodborne infections is a few hours to 10 days; most cases become symptomatic after 18 to 36 hours. Wound infections may become evident within a few days to 2 weeks. The incubation period for intestinal or infant botulism is unknown. Inhalation botulism usually develops 12 to 36 hours after exposure, but in some cases the incubation period may be up to several days.
Clinical Signs
Foodborne Infections
In foodborne infections, gastrointestinal disturbances – including nausea, vomiting and abdominal pain - are often the first sign. Either diarrhea or constipation may occur. As the disease progresses, a symmetric, descending flaccid paralysis develops in the motor and autonomic nerves. The clinical signs may include blurred or double vision, photophobia, drooping eyelids, slurred speech, dysphagia, urine retention, a dry mouth and muscle weakness. In untreated progressive infections, descending paralysis of the respiratory muscles, arms and legs is seen. Fatal respiratory paralysis may occur within 24 hours in severe cases. Fever is not usually seen.
Wound Botulism
Wound botulism is very similar to foodborne infections; however, gastrointestinal signs are not usually present and patients may have a wound exudate or develop a fever.
Infant Botulism
Most cases of infant botulism occur in 2-week to 6-month-old babies. The first symptom is usually constipation. Other signs may include lethargy, weakness, excessively long sleep periods, diminished suck and gag reflexes and dysphagia with drooling. Some babies develop a weak or altered cry. In progressive cases, the infant may develop flaccid paralysis; a “floppy head” is typical. In severe cases, there may be respiratory arrest and death. The symptoms and severity of this disease vary considerably in different babies.
Intestinal botulism in adults
The initial symptoms of intestinal botulism in adults may include lassitude, weakness and vertigo. As the disease progresses, patients may experience double vision and have progressive difficulty speaking and swallowing. Other symptoms may include dyspnea, general muscle weakness, abdominal distention and constipation.
Communicability
No person-to-person transmission has been seen.
Diagnostic Tests
Botulism can tentatively diagnosed by the clinical signs and the exclusion of other neurologic diseases. The definitive diagnosis relies on identifying the toxin in feces, blood, vomitus, gastric aspirates, respiratory secretions or food samples. Feces are usually the most reliable clinical sample in foodborne or infant botulism; the toxin may be found for days or weeks in foodborne cases. Botulinum toxin is rarely found in the blood in adults but is occasionally detected in infants. The toxin can be identified by mouse inoculation studies (the mouse neutralization test), ELISAs or electrochemiluminescent (ECL) tests. Botulinum toxins can be typed with neutralization tests in mice. Serology is not useful for diagnosis, as small amounts of toxin are involved and survivors rarely develop antibodies.
C. botulinum can often be cultured from the feces in infant botulism or the wound in wound botulism. In foodborne cases, the food is usually cultured as well as tested for the toxin. C. botulinum is an anaerobic, Gram positive, spore-forming rod. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony. The iridescent zone around the colony is usually larger for C, D and E toxins.
Treatment and Vaccination
Supportive treatment, with respiratory support if necessary, is the cornerstone of treatment. Botulinum antitoxin, given early, may prevent the disease from progressing and decrease the duration of symptoms. In foodborne illness, the amount of toxin in the gastrointestinal tract can be reduced with stomach lavage and enemas. Antibiotics and debridement are used in cases of wound botulism. Antibiotics are also used occasionally in foodborne cases, but are not generally recommended in infant botulism as they may change the intestinal flora. Investigational vaccines may be available for humans who have a high risk of exposure.
Morbidity and Mortality
Outbreaks of botulism can occur worldwide. Approximately 10 to 30 outbreaks are seen annually in the United States. In 1999, 107 cases of infant botulism, 26 cases of foodborne botulism and 41 cases of wound botulism were reported in the United States.
The death rate is high in untreated cases, but has been decreasing with improvements in supportive care. Before 1950, the mortality rate was 60%; currently, it is less than 5%. Recovery may be slow and can take several months or longer. In some cases, survivors report fatigue and shortness of breath for years.
Botulinum toxins are known to have been weaponized by several countries and terrorist groups.
Species Affected
Many species of mammals and birds, as well as some fish, can be affected by botulism. Clinical disease is seen most often in wildfowl, poultry, mink, cattle, sheep, horses and some species of fish. Dogs, cats and pigs are resistant; botulism is seen occasionally in dogs and pigs but has not been reported from cats.
Incubation Period
The incubation period can be 2 hours to 2 weeks; in most cases, the symptoms appear after 12 to 24 hours. Mink are often found dead within 24 hours of ingesting the toxin.
Clinical Signs
Botulism is characterized by progressive motor paralysis. Typical clinical signs may include muscle paralysis, difficulty chewing and swallowing, visual disturbances and generalized weakness. Death usually results from paralysis of the respiratory or cardiac muscles.
Ruminants
In cattle, the symptoms may include drooling, restlessness, incoordination, urine retention, dysphagia and sternal recumbency. Lateral recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur.
Horses
The clinical signs in horses are similar to cattle. The symptoms may include restlessness, knuckling, incoordination, paralysis of the tongue, drooling and sternal recumbency. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, head and neck.
The shaker foal syndrome is usually seen in animals less than 4 weeks old. The most characteristic signs are a stilted gait, muscle tremors and the inability to stand for more than 4 to 5 minutes. Other symptoms may include dysphagia, constipation, mydriasis and frequent urination. In the later stages, foals usually develop tachycardia and dyspnea. Death generally occurs 24 to 72 hours after the initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.
Pigs
Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation and muscle paralysis.
Foxes and Mink
During outbreaks of botulism, many animals are typically found dead, while others have various degrees of paralysis and dyspnea. The clinical picture is similar in commercially raised foxes.
Birds
In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck and eyelids. Wildfowl with paralyzed necks may drown. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess urates.
Communicability
Botulism is not communicable by casual contact but, in some cases, tissues from dead animals can be toxic if ingested by other animals.
Diagnostic Tests
Botulism can be difficult to diagnose, as the toxin is not always found in clinical samples or the feed. Diagnosis is often a matter of excluding other diseases. A definitive diagnosis can be made if botulinum toxin is identified in the feed, stomach or intestinal contents, vomitus or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice.
In toxicoinfectious botulism, the organism can be cultured from tissues. C. botulinum is an anaerobic, Gram positive, spore-forming rod. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony. The iridescent zone around the colony is usually larger for C, D and E toxins.
Treatment and Vaccination
The treatment is usually supportive and may include gastric lavage to remove some of the toxin. Botulinum antitoxin is sometimes used in animals; the success rate may depend on the type of toxin causing the disease and the species of animal. Type C antitoxins have been effective in some outbreaks in birds and mink. There are also some reports of success with guanidine hydrochloride. Antibiotics are used in the toxicoinfectious form, but are not always successful in birds.
In endemic areas, vaccines can be used in horses, cattle, sheep, goats, mink and pheasants. In chickens, they may not be cost-effective.
Morbidity and Mortality
Botulism is common in wild waterfowl; an estimated 10 to 50 thousand wild birds are killed annually. In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. Botulism also affects commercially raised poultry. In chickens, the mortality rate varies from a few birds to 40% of the flock. Some affected birds may recover without treatment.
Botulism seems to be relatively uncommon in most domestic mammals; however, in some parts of the world, epidemics with up to 65% morbidity are seen in cattle. The prognosis is poor in large animals that are recumbent. In cattle, death generally occurs within 6 to 72 hours after sternal recumbency. Most dogs with botulism recover within 2 weeks.
Post-Mortem Lesions
There are no pathognomonic lesions; the lesions are usually the result of general muscle paralysis. Respiratory paralysis may cause nonspecific signs in the lungs. In shaker foal syndrome, the most consist lesions are excess pericardial fluid with strands of fibrin, pulmonary edema and congestion. Foreign material in the fore-stomachs or stomach may suggest botulism.
“Botulinum.” In Medical Management of Biological Casualties Handbook, 4 th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 10 Dec 2002 <http://www.vnh.org/BIOCASU/17.html>.
“Botulism.” Centers for Disease Control and Prevention (CDC), June 2002. 10 Dec 2002 <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/botulism_t.htm>.
“Botulism.” In Control of Communicable Diseases Manual, 17 th ed. Edited by J. Chin. Washington, D.C.: American Public Health Association, 2000, pp. 70-75.
“Botulism.” In The Merck Veterinary Manual, 8 th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 442-444; 916 1315; 1362; 1969-70.
“Clostridium botulinum.” In Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. U.S. Food & Drug Administration, Center for Food Safety & Applied Nutrition, Feb 2002. 12 Dec 2002
<http://www.cfsan.fda.gov/~mow/chap2.html>
Herenda, D., P.G. Chambers, A. Ettriqui, P. Seneviratna, and T.J.P. da Silva. “Botulism.” In Manual on meat inspection for developing countries. FAO Animal Production and Health Paper 119. 1994 Publishing and Multimedia Service, Information Division, FAO, 12 Dec 2002
<http://www.fao.org/docrep/003/t0756e/T0756E03.htm#ch3.3.2>.
“Material Safety Data Sheet –Clostridium botulinum.” January 2001 Canadian Laboratory Centre for Disease Control. 10 Dec 2002
<http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds35e.html>.
Solomon H.M. and T. Lilly, Jr. “Clostridium botulinum.” In Bacteriological Analytical Manual Online, 8 th ed. U.S. Food and Drug Administration, January 2001. 12 Dec 2002
<http://vm.cfsan.fda.gov/~ebam/bam-17.html>.
Wells C.L. and T.D. Wilkins. “Clostridia: sporeforming anaerobic bacilli.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 10 Dec 2002
<http://www.gsbs.utmb.edu/microbook/ch018.htm>.
Weber, J.T., C.L. Hatheway and M.E. St. Louis. “Botulism” In Infectious Diseases, 5 th ed. Edited by P.D. Hoeprich, M.C. Jordan, and A.R. Ronald. Philadelphia: J. B. Lippincott Company, 1994, pp. 1185-1194.
Copyright 2003, ISU
Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
Phone: 515 294 7189
Fax: 515 294 8259
Email: cfsph@iastate.edu
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