Human/animal diseases

Ce texte relativement daté a largement été diffusé sur les premiers forums et newsgroups consacrés à la zoophilie. Il a accompagné la constitution de notre communauté.

Texte original

Human/animal diseases

(essay by Pony)

A little while ago I asked Pony to put together a few words for me addressing health concerns. I got this in the mail a couple of weeks later. Almost everything you could ever need on the subject. Hats off to Pony for excellent work. --- midnitecrow

ZOONOTIC DISEASES

If you are, or think you are sick, DO NOT rely on this information to self diagnose, or treat yourself!!! As far as I know, there is NOTHING which you may get after sharing an intimate moment with an animal, that you could not get innocently elsewhere, or from a human, so DO NOT be embarrassed, seek help, and go see your doctor.. Oh, and get your animal for periodic checkups…(although if you have recently been intimate with your animal, it may be wise to not schedule any general health check too soon after) J

Each year, we choose to share our lives, (and occasionally our beds) with animals. But how safe a relationship is that? Okay, so we know that our dog is able to bite us, and can imagine what damage may occur to us if that were to happen, but can those animals we love actually pose a significant hazard to our health? Could the family rabbit possibly put you in hospital? Or if we became intimate with a horse, is that likely to present a risk of, at the worst, more than a kick? The simple answer to this is…yes; it is possible for anyone to contract a disease from virtually any animal. In addition to this, it does not have to come via intimate or sexual contact in many cases. There have been cases reported (and quite frequently) of people who have suffered badly from pathogens (germs, spores etc.) which they have been exposed to just by kissing, or petting an animal. The risks to your health increase dramatically as the level of intimacy increases. This is not meant to be a scare story! Whilst this text does not claim to be complete in any way, what I wanted as far as possible to do, is to break down each and every zoonotic (contagious between animals and humans) disease that I knew something about. So that there is and can be, far less concern about such diseases or the possibility of contracting them.

Firstly, we live in a disease prevalent world, we are surrounded daily by the agents responsible for the most serious and deadly diseases that have ever ravaged the earth. Influenza, salmonella, legionnaire's disease, the common cold, there would not be enough space to even think about the number of contaminants that we encounter during the average day. So why are we not already sick or dead? The body has it's own immune system that usually keeps us safe from most things. This coupled with a clean and healthy lifestyle should keep us safe from harm. Occasionally, the body may encounter something which is stronger than our own defenses, or we ourselves are already unfit, or run down. This is when we get sick, and sometimes fatally so. But, as mentioned before, if we keep fit and healthy, there is little risk of harm. Okay, so this long list of animal to human diseases will look scary, but in reality, the risks to your health are no greater than crossing a road. I have extensively searched both the Internet, and my own personal textbooks on this subject, and am greatly indebted to all those who have researched this subject, and publicized their findings. Without such research, the human race would doubtless be in a much poorer state than it already is. My thanks also goes to the many educational and university sites, which have greatly assisted me with this piece. As far as I can ascertain, this (as a compilation of scientific data and general information) is not copywritten. I have done my best to acknowledge all contributors and authors. If you feel that you need greater credit for the information contained within, then please contact me. I have broken the information down, so that it is simple to understand, and clear about the risks to you and your health. I apologize for the many long technical terms used within this page, but these are the REAL terms, and any attempt by me to alter or to simplify these, will result in some or all of the actual definition being lost. There are, however, a few things that you should generally bear in mind, when considering ANY relationship with animals, and these should keep you much safer…and hopefully a little more comfortable with the situation.

Animals that are sick, or have been badly kept, are run down, previously straying, or even living wild have a MUCH greater chance of infecting you with a disease. Also, if you are sick, or recovering from any illness, the chance of contracting a disease is greater. Be especially wary of an animal that shows any sign of illness Eg. Parasites, sores, abbrasions etc.

As long as you and the animal are in reasonable health, there are FAR FEWER diseases that you can catch from an animal, than you can contract from a fellow human. So, if you tell Fido to leave the bed…you also have to tell your (should you have one) human partner too!!

Anyone with any other input for this, please contact me at [email protected]

…and best wishes to you….and those you love.

BRUCELLOSIS

(In humans: Mediterranean fever, undulant fever, Malta fever. In animals: contagious abortion, epizootic abortion, and Bang's disease)

• AGENT:

Brucella abortus: cattle, sheep Brucella canis: dogs Brucella melitensis: sheep, goats Brucella suis: swine

• RESERVOIR AND INCIDENCE

Of the above species, Brucella canis is most likely zoonotic agent of the above list, which the zoophile may encounter, due to the popularity of dogs in zoophilic relationships. Prevalence: 1 to 10% in dogs, throughout the U.S. B. canis is well adapted to dogs, and is not the subject of a large scale eradication program in the general dog population, as Brucella has been in other animals. Human brucellosis due to B. canis is uncommon but can be acquired from dogs; most cases resulted from contact with aborting bitches. In 1988, the CDC noted 96 cases of brucellosis reported in the U.S.: 22 from Texas and 20 from Calif.

• TRANSMISSION:

Ingestion of unpasteurized milk Poorly defined transmission cycle in zoonotic diseases: contact with infected animals especially aborted fetuses, fluids or membranes, or urine. Possibly airborne.

• DISEASE IN ANIMALS:

Abortions are followed by immunity, though carrier state persists especially with secretions from the udder. Infertility, testicular abnormalities, poor semen quality in dogs, inapparent infection may be common, as indicated by seropositivity.

• DISEASE IN MAN:

Lymphadenopathy, splenomegaly, fever, headache, chills, orchitis, weakness, nausea, weight loss. The chronic form may assume an undulant nature, with periods of normal temperature between acute attacks; symptoms may persist for years, either continuously or intermittently. Antibiotics can effect a cure within one year in about 80% of cases. Case fatality if untreated is less than 2%.

• DIAGNOSIS:

Rapid slide agglutination test is available. Blood culture and additional serologic tests used to confirm slide test results.

• TREATMENT:

Single-drug regimens are not recommended because the relapse rate may be as high as 50%. Combination regimens of two or three drugs are more effective. (1) Doxycycline plus rifampin or streptomycin (or both) (2) trimethoprim-sulfamethoxazole plus rifampin or streptomycin (or both) are effective in doses for 21 days. Longer courses of therapy may be required to cure relapses, osteomyelitis, or meningitis.

• PREVENTION\CONTROL:

Be EXTREMELY careful if you have a bitch which aborts a pregnancy, this is an indication that something is not right. Protect yourself and the animal. Use disposable gloves, chlorine based bleach, or iodine to disinfect any contaminated surfaces. Then contact your vet to arrange for a brucellosis test, and general health checkup for your bitch.

SALMONELLOSIS

(Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food poisoning worldwide. Over 1800 food-poisoning serotypes of salmonella (bacterium) exist. The prevalence of individual serotypes constantly changes. In the U.S., 5 million cases are diagnosed annually. S. typhi, the cause of Typhoid Fever, rarely occurs in the U.S. and is not discussed here.

• RESERVOIR AND MODE OF TRANSMISSION:

Salmonellas are common commensals of all animals and birds and are excreted in feces. Host-adapted strains may cause serious illness (e.g., S. dublin in cattle, S. pullorum in chickens), but most human food-poisoning salmonellas do not cause clinical signs in animals. The main reservoirs for human infection are poultry, cattle, sheep and pigs. Infection in animals is maintained by recycling slaughterhouse waste as animal feed, fecal oral spread and fecal contamination of hatching eggs. Transmission occurs when organisms, introduced into the kitchen in poultry carcasses, meat or unpasteurized milk, multiply in food owing to inadequate cooking, cross-contamination of cooked foods and inadequate storage. Person-to-person spread is common in institutions such as hospitals. The organism inhabits the intestinal tract of many animals including birds, cattle, sheep, pigs, and rats, mice, hamsters, guinea pigs, nonhuman primates and humans. Salmonella occurs worldwide. *The house mouse may also be a reservoir of the infection and may play a role in human and animal salmonellosis. Humans, rarely, and animals may be carriers and asymptomatic shedders of the organism. *Salmonella prevalence in the U.S. canine population may be 10% or more. *Prevalence data from 8 studies conducted worldwide indicated that a wide range (0.6-27%) of cats were culture-positive for Salmonella. *Salmonella carriers in newly imported Rhesus and Cynomolgus monkeys exceeded 20% in some shipments. *Birds, reptiles, and turtles are especially dangerous sources of Salmonellosis. 94% of all reptiles harbor Salmonella. Turtles alone in 1970 may have caused 280,000 human cases of Salmonellosis. *In 1975 the FDA ruled it illegal to sell a. Viable Turtle eggs b. Live turtles with a carapace length < 10.2cm (4 inches) c. Exceptions - Educational & scientific institutions and marine turtles. d. Marine turtles have not been shown to be a reservoir of Salmonella

• TRANSMISSION:

Indirect transmission via contaminated food and water are the most common sources but transmission may also be by direct contact. It is a common contaminant of sewage. Found in many environmental water sources. Environmental contamination continues to be a potential source of infection for lab animals and secondarily for personnel handling those animals. *Animal feed containing animal by products continues to be a source of Salmonella contamination, especially if the diets consist of raw meal and have not undergone the pelleting process.

• INCUBATION PERIOD:

Humans. 12-72 hours. Animals. 1-5 days.

• CLINICAL FEATURES:

Humans. The presence and severity of symptoms depends on the infecting dose. Typically there is watery diarrhea for about ten days, possibly leading to dehydration, with abdominal pain and low-grade fever. Septicemia and abscess formations are rare. Animals. Subclinical infection is common and many animals may be intermittent or persistent carriers. However, cows may suffer with fever, diarrhea and abortion. Calves undergo epizootic outbreaks of diarrhea with high mortality. In pigs, fever and diarrhea are less common than in cattle. Infected sheep, goats and poultry usually show no signs of infection.

• PATHOLOGY:

Humans. Enteritis is a feature. Extraintestinal infection may cause abscesses. Animals. Penetration of the infection into the mucosa is followed by inflammation, especially ileitis, progressing to inflamed mesenteric lymph nodes in the mesentery, possibly progressing to septicemia and pneumonia especially in calves. Dehydration and rapid loss of weight are due to stimulation of chloride excretion and inhibition of sodium absorption. Abortion in cattle is caused by massive proliferation of salmonella in the placenta leading to placental necrosis.

• DIAGNOSIS:

Humans. Isolate salmonella from feces and suspected foods using selective media followed by serotyping and, if appropriate, phage typing. Animals. Culture feces, postmortem tissues and foods of animal origin. Serological tests are of limited value as many noninfected animals have titers from past infections. Humans. Usually only a self-limiting illness occurs. Deaths from dehydration or septicemia are rare and occur usually in infants, or debilitated or elderly patients. Animals. There is abortion in cattle and endometritis with temporary infertility. In calves, dehydration and septicemia may lead to death.

• PREVENTION:

Humans. Educate food handlers in good kitchen hygiene. Ensure thorough cooking of meat, refrigerate cooked foods and prevent cross-contamination. Pasteurize all milk. Ensure personal hygiene. Reduce contamination of poultry carcasses at abattoirs. Irradiation of meat and other foods before purchase will reduce contamination. Animals. This is difficult and often impractical because there are many sources of infection. Principles of control include the following: maintain closed herds and flocks; keep animals in small groups; purchase replacements direct from the farm of origin; avoid mixing animals from different sources; sterilize ingredients of animal feed; provide mains drinking water for grazing livestock; prevent access of wild birds and rodents to animal houses; completely de-stock animals and thoroughly cleanse and disinfect housing between batches; monitor poultry breeding stock and remove excreters; disinfect hatching eggs and fumigate incubators.

• TREATMENT:

Humans. Treatment of uncomplicated enterocolitis is symptomatic only. Young, malnourished, or immuno-compromised infants, severely ill patients, those with sickle cell disease, and those with suspected bacteremia should be treated for 3-5 days with trimethoprim-sulfamethoxazole (one double-strength tablet twice a day), ampicillin (100 mg/kg IV or orally), or ciprofloxacin 9750 mg twice daily). Animals. Treatment with antibiotics and sulfonamides immediately diarrhea and fever occur reduces mortality but is contraindicated in healthy carriers in which treatment may prolong the carrier state.

• VACCINATION:

Humans. None. Animals. Vaccines are available against S. dublin and S. typhimurium in calves. A live vaccine prepared from a rough strain of S. dublin gives good protection in calves against both S. dublin and S. typhimurium.

• LEGISLATION:

Humans. The disease is notifiable specifically in the USA, Australia, New Zealand and several European countries, or as food poisoning as in the UK. Animals. Notification of infection in food animals is obligatory in some countries, including the UK, with statutory sampling of animal protein for animal feed. Heat treatment of waste food applies in the UK. A slaughter policy is claimed in Luxembourg, Germany and Czechoslovakia.

SHIGELLOSIS

SYNONYM: Bacillary dysentery.

• ETIOLOGY:

The type species is Shigella dysenteriae, other agents are S. flexneri, S. boydii, and S. sonnei. The first three species are subdivided into serotypes.

• GEOGRAPHIC DISTRIBUTION:

Worldwide.

• THE DISEASE IN MAN:

It is seen most often in preschool-age children. A new serotype introduced into tropical areas where the population is undernourished provokes disease in all age groups, particularly children, the elderly, and debilitated individuals. Generally, the incubation period is less than 4 days. The disease begins with fever and abdominal pains, followed by diarrhea and dehydration for 1 to 3 days. A second phase of the symptomatology can last for several weeks. The main symptom is tenesmus; in serious cases, stools contain blood, mucus, and pus. The symptomatology is usually variable. In many countries, strains of Shigella resistant to sulfonamides and to several antibiotics have been observed.

• THE DISEASE IN ANIMALS:

A clinical picture similar to that in man occurs in monkeys.

• SOURCE OF INFECTION AND MODE OF TRANSMISSION:

The principal reservoir of the infection for man is other humans that are sick or carriers. The sources of the infection are feces and contaminated objects. The most common mode of transmission is the fecal-oral route. Outbreaks comprising numerous cases have had their origin in a common source of infection, such as foods contaminated by hands or feces of carrier individuals. Insects, particularly flies, can also play a role as mechanical vectors. Bacillary dysentery is a serious disease with high mortality in nonhuman primates in captivity, but there is doubt that monkeys can harbor the etiologic agent in their natural habitat. Monkeys probably contract the infection by contact with infected humans. The infection spreads rapidly in nonhuman primate colonies because the monkeys defecate on the cage floor and also often throw their food there.

• ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:

Of little significance. Cases of human bacillary dysentery contracted from nonhuman primates are known. The victims are mainly children. In highly endemic areas, dogs may shed Shigella temporarily. The etiologic agent has also been isolated from horses, bats, and rattlesnakes. Nevertheless, animals other than nonhuman primates play an insignificant role.

• DIAGNOSIS:

Definitive diagnosis depends on isolation of the etiologic agent by culture of fecal material on selective media. Serologic identification and typing are important from the epidemiologic viewpoint.

• TREATMENT:

In humans, treatment of dehydration and hypotension is lifesaving in severe cases. The current antimicrobial treatment of choice is trimethoprim-sulfamethoxazole (one double-strength tablet twice a day), or ciprofloxacin (750 mg twice a day; contraindicated in children and pregnant women). Parental hydration and correction of acidosis and electrolyte disturbances are of primary importance. Antispasmodics (e.g., tincture of belladonna) are helpful when cramps are severe. Drugs that inhibit intestinal peristalsis (paregoric, diphenoxylate with atropine) may ameliorate symptoms but prolong fever, diarrhea, and excretion of Shigella in feces. Appropriate precautions should be taken both in the hospital and in the home to limit spread of infection.

• CONTROL:

In man, control methods include a) environmental hygiene, especially disposal of human waste and provision for potable water; b) personal hygiene; c) education of the public and of food handlers about the sources of infection and methods of transmission; d) sanitary supervision of the production, preparation, and preservation of foods: e) control of flies; f) reporting and isolation of cases and sanitary disposal of feces; and g) search for contacts and the source of infection. A live, streptomycin-dependent vaccine, administered orally in three or four doses has given good protection against the clinical disease for 6 to 12 months. Its use is indicated in institutions where shigellosis is endemic. Indiscriminate use of antibiotics must be avoided in order to prevent the emergence of multi-resistant strains and to ensure that these medications remain available for use in severe cases. In animals, control consists of a) isolation and treatment of sick or carrier monkeys: b) careful cleaning and sterilization of cages; c) prevention of crowding in cages: and d) prompt disposal of wastes and control of insects.

YERSINIA

Animals are susceptible to three Yersinia species that are potentially zoonotic: AGENT: Gram negative, non spore forming rods

1. YERSINIA PSEUDOTUBERCULOSIS AND ENTEROCOLITICA (Pseudotuberculosis)

• RESERVOIR AND INCIDENCE

Ubiquitous in nature, isolated from dust, soil, water, and milk. Natural infections occur in man, birds, rodents, rabbits , guinea pigs, mice, cats, nonhuman primates, sheep, swine, goats.

• TRANSMISSION:

direct contact, or fecal contaminated food or water cause most transmission from animals to man. Human cases of have been reported in association with disease in household pets, particularly sick puppies and kittens. The most important source of Y. enterocolitica infection may be pork, as the pharynx of pigs may be heavily colonized.

• DISEASE IN ANIMALS:

guinea pigs, rabbits, and hamsters exhibit poor condition and enlarged lymph nodes. Subacute clinical signs are common, with diarrhea and weight loss, possibly death within 2 weeks to 3 months. Chinchillas are very susceptible to infection with Y. enterocolitica. In sheep, abortions, epididymitis and orchitis occur with high mortality. In cattle, abortion and pneumonia occur. Nonhuman primates exhibit an ulcerative colitis. Histopathological lesions include acute inflammation of the terminal ileum with mesenteric lymphadenitis occurs. Sometimes abscesses develop in the liver, spleen, and lungs. Usually self-limiting, but there is a fatality rate of 5-7%.

• DISEASE IN MAN:

acute watery diarrhea, mesenteric lymphadenitis which can be confused with appendicitis, fever, headache, pharyngitis, anorexia, vomiting erythema nodosum (in about 10% of adults), post-infectious arthritis, iritis, cutaneous ulceration, hepatosplenic abscesses, osteomyelitis and septicemia.

• DIAGNOSIS:

fecal culture using cold enrichment technique. Serologic diagnosis can be made by an agglutination test or by ELISA.

• TREATMENT:

usually resistant to penicillin and its derivatives. Agents of choice are the aminoglycosides and cotrimoxazole. Both are usually sensitive to the tetracyclines.

• PREVENTION/CONTROL:

Control rodents and prevent contamination of food and water by rodents and birds. Pasteurize milk. Cook pork thoroughly. Personal hygiene is important.

2. YERSINIA PESTIS

(Plague, Pest, black death, pestilential fever) The second pandemic of plague, known then as the "Black Death," originated in Mesopotamia about the middle of the 11th century, attained its height in the 14th century and did not disappear until the close of the 17th century. It is thought that the Crusaders, returning from the Holy Land in the 12th and 13th centuries, were instrumental in hastening the spread of the disease. Again the land along trade routes was primarily involved and from them the infections spread east, west, and north. During the course of the disease, 25,000,000 people perished, a fourth of the population of the world.

• AGENT:

a gram negative coccobacillus

• RESERVOIR AND INCIDENCE

Endemic in wild rodents in Southwestern U.S., as well as in Africa and Asia. Most important reservoirs worldwide are the domestic rat, Rattus rattus, and the urban rat, Rattus norvegicus. Human infections have increased since 1965 and usually result from contact with infected fleas or rodents. The disease is also associated with cats, goats, camels, rabbits, dogs and coyotes. Dogs and cats may serve as passive transporters of infected rodent fleas into the home.

• TRANSMISSION:

Contact with infected rodent fleas or rodents. Fleas may remain infected for months. Note: a protein secreted by the Yersinia is a coagulase that causes blood ingested by the flea to clot in the proventriculus. The bacillus proliferates in the proventriculus, and thousands of organisms are regurgitated by obstructed fleas and inoculated intradermally into the skin. This coagulase is inactive at high temperatures and is thought to explain the cessation of plague transmission during very hot weather. Pulmonary form spread by airborne or droplet infection. Human infections from non-rodent species usually result from direct contact with infected tissues, by scratch or bite injuries, and handling of infected animals. Several recent reports have detailed human plague associated with exposure to domestic cats. Exposure can be from inhalation of respiratory secretions of cats with pneumonic plague or by contaminating mucous membranes or skin wounds with secretins or exudates.

• DISEASE IN ANIMALS:

dogs usually have a brief self-limiting illness cats usually exhibit severe and often fatal infection, with fever, lymphadenopathy, hemorrhagic pneumonia, and encephalitis. rodents may carry the disease asymptomatically or develop fatal disease. infected rats and squirrels frequently die unless they are from an enzootic area and have acquired immunity.

• DISEASE IN MAN:

Incubation period 2 to 6 days. In humans the disease is called Bubonic, Septicemic, or Pneumonic plague depending on the pattern of distribution of the infection. Bubonic is the most common form causing fever and swollen, tender lymph nodes (called Buboes). Pneumonic plague is systemic plague with lung involvement. Mortality may exceed 50%. Plague is also called the "black death" because disseminated intravascular coagulation takes place and areas of skin undergo necrosis.

• DIAGNOSIS:

Impression smears of aspirates or blood stained with gram or Giemsa. Organisms have a typical "safety pin" appearance culture of the organisms can be performed, by reference lab FA of smear is confirmatory. Serology via Complement fixation, passive hemagglutination, and immunofluorescence (IFA)

• TREATMENT:

streptomycin with tetracycline or chloramphenicol.

• PREVENTION\CONTROL:

Wild rodents should be controlled and fleas should be eliminated. It is important to control rodents and fleas for outdoor housed animals. Sentinel animal programs used in endemic areas. Endemic areas of the U.S. include California, Nevada, Arizona, and New Mexico. Masks gowns, and gloves should be worn when handling cats suspected to be infected and all contaminated surfaces disinfected. Notify Health Department of suspected cases Vaccines available for high-risk personnel.

TUBERCULOSIS

(Consumption)

• AGENT, RESERVOIR AND INCIDENCE

TB is caused by the gram positive, acid fast, aerobic, bacillus of the Mycobacterium genera. The most common species of mycobacteria are: 1. M. bovis (cattle, dogs, swine) 2. M. avium (birds, swine, sheep) 3. M. tuberculosis (man, nonhuman primates, cattle, dogs, swine, psitticines). 4. M. marinum, fortuitum, platypolcitis (fish) Note: Atypical mycobacterium, M. scrofulaceum, M. kansasii, and M. intracellulare have been reported in NHP's and are also present in soil and water. They can cause pulmonary disease refractory to treatment in man, and are most often seen in immunocompromised people. Specific reagents can be used to skin test for these bacteria. TB continues to be a major cause of morbidity and mortality throughout the world. One billion people are infected with the tubercle bacillus, and there are 8 million new cases and 3 million deaths annually. Cases of active tuberculosis are increasing in the United States after years of decline. The end of 1990 reported a provisional total of 23,720 cases. Case rates increased 4.4 percent between 1988 and 1989, and perhaps another 1 percent in 1990. Overall rate was 9.5 per 100,000 in 1989, with the Middle Atlantic and Pacific regions reporting the highest rates, 36 percent and 34 percent, respectively, above the U.S. total. The lowest rates were in the West, North, Central, and Mountain regions. Rates continue to be higher among urbanites, minorities, the poor, and the homeless, substance abusers and persons infected with HIV. All three types are capable of causing disease in man although M. tuberculosis (variety hominis) is by far the most common. Nonhuman primates can carry all three types but most infections are caused by M. tuberculosis variety hominis. While most nonhuman primates are capable of contracting TB, Old World species appear to be more susceptible to the disease than New World species and great apes. Most cases of TB in monkeys are thought to arise from human contact. Animals may be imported from areas of the world where the incidence of the disease is high and where contact between humans and simians is frequent. In close confinement the disease can spread rapidly.

• TRANSMISSION:

Mycobacterium bacilli are transmitted from infected animals or infected tissue primarily via the aerosol route. May also be contracted via ingestion or cutaneous inoculation of the bacilli. Personnel caring for infected animals as well as those performing necropsies on infected animals are at risk for contracting the disease. Exposure to dusty bedding of infected animals, coughing of infected animals, and aerosolization of the organism during sanitation procedures may also be sources of the disease in the lab environment. Once within the body the organism may spread throughout the lungs, lymphatics, blood vascular system, and many visceral organs.

• DISEASE IN NONHUMAN PRIMATES:

The signs of TB may be insidious with only slight behavioral changes noticed, followed by anorexia and lethargy. Often animals die suddenly while appearing to be in good condition. Other signs that might be seen include diarrhea, suppuration of lymph nodes, ulceration of the skin, and palpable splenomegaly and hepatomegaly. The organ of predilection is the lung but lesions may also be seen in the pleura, intestines, lymph nodes, liver, kidney, spleen, and peritoneum. Under the surface of these tissues are yellowish-white to gray nodules filled with caseous material which may rupture and produce cavitation. Although skeletal involvement in primates is rare, tuberculosis of the spine may cause paralysis of the hindlimbs (Pott's disease).

• DISEASE IN FISH:

In infected fish, granulomatous lesions are usually observed.

• DISEASE IN MAN:

In humans the clinical signs depend on the organ system involved. The most familiar signs related to pulmonary TB are cough, sputum production, and hemoptysis. The patient may be asymptomatic for years. General signs may include anorexia, weight loss, lassitude, fatigue, fever, chills and cachexia. Skin lesions are characterized by ulcers or by papular lesions progressing to dark suppurative lesions. TB may affect virtually every other organ system with signs or symptoms relating to the individual system. Miliary TB is most often seen in the very young and old people.

• DIAGNOSIS:

The diagnosis of TB is often difficult. Four tests are commonly used for presumptive diagnosis: 1. Intradermal TB test - Mammalian tuberculin 2. Radiography 3. Acid fast stained sputum smear 4. ELISA Confirmation by culture, histopath, or animal inoculation.

• TREATMENT:

Regimens currently accepted in the USA include isoniazid combined with rifampin, with or without pyrazinamide.

• PREVENTION\CONTROL:

Multifaceted and includes: personnel education wearing of protective clothing when handling nonhuman primates a regular health surveillance program for humans and nonhuman primates isolation and quarantine of suspect animals rapid euthanasia and careful disposal of infected animals Vaccine - A vaccine, BCG, is available (Bacille Calmette-Guerin, strain of M. Bovis) a. Used in humans quite often in G. Britain b. Used in high risk groups c. Effective, but it causes the patient to have a positive TB test. Personnel working with NHP's who convert to a positive skin test should be referred for appropriate medical treatment and follow up and should not work with animals until shown to be noninfectious.

LEPROSY

SYNONYM: Hansen's disease.

• ETIOLOGY:

Mycobacterium leprae, a polymorphic acid-alcohol-fast bacillus. M. leprae is hard to distinguish from other unculturable mycobacteria naturally infecting animals. The failure of attempts to culture M. leprae in vitro constitutes a great barrier to better determining its biochemical characteristics for identification purposes as well as for therapeutic and immunologic studies. In part, this difficulty has been overcome, first, by in vivo culture on mouse foot pads and, lately, by the discovery that the leprosy organism can infect the nine-banded armadillo (Dasypus novemcinctus). At present, the latter serves as a model for lepromatous leprosy and provides a large number of bacilli for research.

• OCCURRENCE IN MAN:

An estimated 12 million people are affected by leprosy. The highest prevalence is in tropical and subtropical regions of Asia, Africa, Latin America, and Oceania. Leprosy is very prevalent in India, Southeast Asia, the Philippines, Korea, southern China, Papua New Guinea, and some pacific islands. Ninety percent of the cases reported in the Americas come from five countries: Argentina, Brazil, Colombia, Mexico, and Venezuela. Chile is the only South American country free of the infection. In the United States 2,500 cases are known, most of them in immigrants. Autochthonous cases arise in Hawaii, Puerto Rico, Texas, and Louisiana. The infection's prevalence is related to the socioeconomic level of the population. The fact that the disease has practically disappeared in Europe is attributed to the improved standard of living there. The proportion of total leprosy cases represented by lepromatous leprosy (see The Disease in Man) varies with the region. In Asia and the Americas this form makes up between 25 and 65% of all cases, while in Africa it accounts for only 6 to 20%.

• THE DISEASE IN MAN:

The incubation period is usually 3 to 5 years, but it can vary from 6 months to 10 years or more. Clinical forms of leprosy cover a wide spectrum, ranging from mild self-healing lesions to a progressive and destructive chronic disease. The polar form at one end of the spectrum is tuberculoid leprosy, and at the other, lepromatous leprosy. Intermediate forms are also found. Tuberculoid leprosy is characterized by localized lesions of the skin and nerves, often asymptomatic. Basically, the lesions consist of a granulomatous, paucibacillary, inflammatory process. The bacilli are difficult to detect, and can be observed most frequently in the nerve endings of the skin. This form results from active destruction of the bacilli by the cellular immunity of the patient. On the other hand, serum antibody titers are generally low. Nerve destruction causes lowered conduction; heat sensibility is the most affected, tactile sensibility less so. Trophic and autonomic changes are common, especially ulcers on the sole and mutilation of body members. Lepromatous leprosy is characterized by numerous symmetrical skin lesions consisting of macules and diffuse infiltrations, plaques, and nodules of varying sizes (lepromas). There is involvement of the mucosa of the upper respiratory tract, of lymph nodes, liver, spleen, and testicles. Infiltrates are basically histiocytes with a few lymphocytes. Cellular immunity is absent (negative reaction to lepromin) and antibody titers are high. In this form of the disease, as in the borderline, erythema nodosum leprosum (ENL) often appears. The indeterminate form of leprosy has still not been adequately characterized from the clinical point of view; it is considered to be the initial stage of the disease. The first cutaneous lesions are flat, hypopigmented, and have ill-defined borders. If this form is not treated, it may develop into tuberculoid, borderline, or lepromatous leprosy. Bacilli are few, and it is difficult to confirm their presence. Finally, the borderline form occupies a position intermediate between the two polar forms (tuberculoid and lepromatous), and shares properties of both; it is unstable and may progress in either direction. Destruction of nerve trunks may be extensive. Bacilli are observed in scrapings taken from skin lesions. An estimated one-third of clinical cases become incapacitated. half of them completely. Nevertheless, these proportions are now changing, due to both prevention/control programs and early implementation of effective treatments. There is evidence that inapparent infection may occur with a certain frequency among persons, especially family members, in contact with patients.

• THE DISEASE IN ANIMALS:

The disease in armadillos (Dasypus novemcinctus) is similar to the lepromatous form in man. Infection in these animals is characterized by macrophage infiltrates containing a large number of bacilli. Skin lesions vary from mild to severe. The small dermal nerves are invaded by the etiologic agent. Many bacilli are seen in the macrophages of the lymph tissue, in the pulp of the spleen, and in Kupffer's cells in the liver. M. leprae is known to prefer the cooler parts of the human or mouse body. For this reason, armadillos were used as experimental animals even before natural inaction was confirmed in them, since their body temperature is from 30 to 35oC. Experimental inoculation of armadillos with human leproma material reproduces the disease, characterized by broad dissemination of the agent, and involvement of lymph glands, liver, spleen, lungs, bone marrow, meninges, and other issues, in a more intense form than is usually observed in man. The disease in the chimpanzee appeared as a progressive chronic dermatitis with nodular thickening of the skin of the ears, eyebrow nose, and lips. Lesions of the nose, skin, and dermal nerves contained copious quantities of acid-fast bacteria. The case was histologically classified as borderline 12 months after the clinical symptoms were first observed, and as lepromatous after a later biopsy. In the case of the Cercocebus monkey, the initial lesion consisted of nodules on the face. Four months later, a massive infiltration and ulceration were seen on the face and nodules appeared on the ear and the forearms. Sixteen months after cutaneous lesions were first observed. The animal began to suffer deformities and paralysis of the extremities. Histopathologic findings indicated the subpolar or intermediate lepromatous form. The disease was progressive, with neuropathic deformation of feet and hands. It seemed to regress when specific treatment was administered. The animal apparently contracted the disease from a patient with active leprosy. Experimental infections carried out to date have indicated that these animals may experience a spectrum of different forms similar to those in man.

• SOURCE OF INFECTION AND MODE OF TRANSMISSION:

Man is the principal reservoir of M. leprae. The method of transmission is still not well known due to the extended incubation period. Nevertheless, the principal source of infection is believed to be lepromatous patients, in whom the infection is multibacillary, skin lesions are often ulcerous, and a great number of bacilli are shed through the nose similarly. Bacilli are found in the mouth and pharynx. Consequently, transmission might be effected by contact with infected skin, especially through wounds or abrasions, and by aerosols, as is the case in tuberculosis. Lately, more importance has been attributed to aerosol transmission. Oral transmission and transmission by hematophagous arthropods are not discounted, but they are assigned less epidemiologic importance. Until recently, leprosy was believed to be an exclusively human disease. But research in recent years has demonstrated that the infection and the disease also occur naturally in wild animals. Even though some researchers have expressed doubt that the animal infection is identical to the human, at present an accumulation of evidence indicates that the etiologic agent is the same. The origin of infection in animals is unknown. It is believed that armadillos contracted the infection from a human source, perhaps from multibacillary patients before the era of sulfones. In this regard, it should be pointed out that leprosy bacilli may remain viable for a week in dried nasal secretions and that armadillos are in close contact with the soil. The high disease prevalence in some localities would indicate armadillos can transmit the infection to one another, either by inhalation or direct contact. Another possible transmission vehicle is maternal milk, in which the agent has been detected. It is difficult to demonstrate that armadillos are a source infection for man because of the long incubation period in humans and the impossibility of excluding a human source in an endemic area. In Texas, a case of human leprosy was attributed to a patient's practice of capturing armadillos and eating their meat. Subsequently, another five cases with hand lesions were detected in natives of the same state who habitually hunted and cleaned armadillos but had no known contact with human cases. The prevalence of leprosy in armadillos in Louisiana and Texas suggests that these animals could serve as a reservoir of M. leprae; however, nothing is known about the frequency of infection in nonhuman primates and the role they may play in transmission of the disease. The sources of the cases of leprosy in these animals were probably people with lepromatous leprosy.

• DIAGNOSIS:

Laboratory confirmation of leprosy requires the demonstration of acid-fast bacilli in scrapings from slit skin smears or the nasal septum. Biopsy of skin or of a thickened involved nerve also gives a typical histologic picture. M. leprae does not grow in artificial media.

• CONTROL:

Control is based on early detection and chemotherapy. In the face of multiple confirmed cases of resistance to dapsone, combination of this medication with rifampicin is presently recommended for paucibacillary leprosy, and the same two medications in combination with clofazimine for multibacillary leprosy. Rifampicin has a rapid bactericidal effect and eliminates contagion in patients in 1 to 2 weeks. The isolation of patients in leprosariums is no longer necessary, since the chemotherapy effectively eliminates infectiousness and thereby interrupts transmission of the disease.

VIBRIOSIS

Vibrios other than Vibrio cholerae that cause human disease are Vibrio parahaemolyticus, Vibrio vulnificus and Vibrio alginolyticus. All are halophilic marine organisms. Infection is acquired by exposure to organisms in contaminated, undercooked, or raw crustaceans or shellfish and warm ( 20o C) ocean waters and estuaries. Infections are more common during the summer months from regions along the Atlantic coast and the Gulf of Mexico in the United States and from tropical waters around the world. Oysters are implicated in up to 90% of food-related cases. V. parahaemolyticus causes an acute watery diarrhea with crampy abdominal pain and fever, typically occurring within 24 hours after ingestion of contaminated shellfish. The disease is self-limited, and antimicrobial therapy is usually not necessary. V. parahaemolyticus may also cause cellulitis and sepsis, though these findings are more characteristic of V. vulnificus infection. V. vulnificus and V. alginolyticus-neither of which is associated with diarrheal illness-are important causes of cellulitis and primary bacteremia, which may follow ingestion of contaminated shellfish or exposure to sea water. Cellulitis with or without sepsis may be accompanied by bulla formation and necrosis with extensive soft tissue destruction, at times requiring debridement and amputation. The infection can be rapidly progressive and is particularly severe in immunocompromised individuals-especially those with cirrhosis-with death rates as high as 50%. Patients with chronic liver disease and those who are immunocompromised should be cautioned to avoid eating raw oysters. Tetracycline at a dose of 500 mg four times a day is the drug of choice for treatment of suspected or documented primary bacteremia or cellulitis caused by Vibrio species. V. vulnificus is susceptible in vitro to penicillin, ampicillin, cephalosporins, chloramphenicol, aminoglycosides, and fluoroquinolones, and these agents may also be effective. V. parahaemolyticus and V. alginolyticus produce betalactamase and therefore are resistant to penicillin and ampicillin, but susceptibilities otherwise are similar to those listed for V. vulnificus.

LISTERIOSIS

(Circling disease)

• AGENT

- Listeria monocytogenes, gram positive, pleomorphic rod

• RESERVOIR AND INCIDENCE

Isolated from fish, birds, swine, horses, ruminants, guinea pigs, ferrets, gerbils, rabbits, and chinchillas. The principle reservoir of the organism is in forage, water, mud, and silage. The seasonal use of silage as fodder is frequently followed by an increased incidence of listeriosis in animals.

• TRANSMISSION:

outbreaks have been reported associated with ingestion of unpasteurized milk and cheese and contaminated vegetables; some sporadic cases may also be due to foodborne transmission. Refrigeration of foods may provide selective growth of Listeria. Papular lesions on hands and arms may occur from direct contact with infectious material or soil contaminated with infected animal feces. In neonatal infections, the organism may have been transmitted from mother to fetus in utero or during passage through the infected birth canal. Person-to-person transmission through venereal contact is possible, as is infection from inhalation of the organism.

• DISEASE IN ANIMALS:

Two forms exist, the meningoencephalitic and visceral. The former involves neurological signs with dullness and somnolence. Drooling and lack of interest in food and mastication soon follow. There is lateral deviation of the head with a tendency to circle. Paralysis then sets in with recumbency and death from respiratory failure. The visceral from involves abortion, with retained placenta. Microabscesses occur throughout the brain. Visceral lesions involve multiple foci of necrosis in the liver, spleen and heart. Placental lesions are characteristic with yellow necrotic foci and multiple granulomas in the fetal liver. Abscess formation in the eye can lead to blindness. Fatality is very high, approaching 3-30% in outbreaks.

• DISEASE IN MAN:

Symptomless fecal carriage is common. Fever, headache, nausea, vomiting, endocarditis, granulomatous lesions in multiple organs, cutaneous involvement, coryza, conjunctivitis, metritis with abortion, sepsis, & meningitis. Granulomatous lesions and abscesses occur in the liver and other organs and beneath the skin. Focal necrosis in the placenta with mononuclear infiltration is seen. Fatality rates may exceed 20%.

• DIAGNOSIS:

culture and isolation (special media required). Serologic tests are unreliable because of cross reactions with other bacterial species.

• TREATMENT:

ampicillin plus an aminoglycoside or Trimethoprim-sulfamethoxazole.

• PREVENTION\CONTROL:

caution and protective clothing when handling infected tissues. Pregnant women and immunocompromised individuals should avoid contact with potentially infective materials such as aborted animal fetuses and known infected persons; they should eat only properly cooked meats and pasteurized dairy products.

LEPTOSPIROSIS

[Weil's disease, Hemorrhagic jaundice (Leptospira icterohaemorrhagiae), canicola fever (L. canicola), dairy worker fever (L. hardjo)]

• AGENT

Spirochete, Leptospira. Pathogenic leptospires belong to the species Leptospira interrogans, which is subdivided into more than 200 serovars. The main natural reservoirs for human infection vary with serovar: L. canicola in dogs, L. hardjo in cattle, L. pomona in swine, and L. icterohaemorrhagiae in rats.

• RESERVOIR AND INCIDENCE

Rats, mice, field moles, guinea pigs, gerbils, squirrels, rabbits, hamsters, reptiles, nonhuman primates, livestock, and dogs. In one study, 40 % of stray dogs were seropositive. Rats and mice are common animal hosts for L. ballum. Infection in mice is inapparent and can persist for the animal's lifetime. *Rodents are the only major animal species that can shed leptospires throughout their life-span without clinical manifestations. Active shedding by lab animals can go unrecognized until personnel handling the animals become clinically ill.

• TRANSMISSION:

Handling affected animals, contaminating hands, or abrasions with urine, or aerosol exposure during cage cleaning are most common. The organism is often transmitted to humans by the urine of the reservoir host. The organism may also enter through minor skin lesions and probably via the conjunctiva. Many infections have followed bathing or swimming in infected waters.

• DISEASE IN ANIMALS:

In cattle, fever and anorexia occur with rapid decline in milk yield and atypical mastitis. Pregnant cows abort with retention of the placenta. Also, mild jaundice and severe anemia occurs with enlarged and friable liver and swollen kidneys. In pigs subclinical infection is common, though it can cause abortion and birth of weak piglets. In dogs and cats, gastroenteritis, jaundice, and nephritis may occur.

• DISEASE IN MAN:

Ranges from inapparent infection to severe infection and death. Biphasic Illness a. Weakness, headache, myalgia, malaise, chills, & fever. b. Leukocytosis, painful orchitis (testes not usually enlarged), conjunctival effusion, and rash. Icteric leptospirosis (Weil's syndrome-usually caused by L. icterohaemorrhagiae) is the most severe form of the disease, characterized by impaired renal and hepatic function, abnormal mental status, hypotension, and a 5-10% mortality rate. Signs and symptoms are continuous and not biphasic.

• DIAGNOSIS:

Early in the disease, the organism may be identified by darkfield examination of the patient's blood or by culture on a semisolid medium. Culture is difficult and requires several weeks. A rapid diagnosis is made with the DOT-ELISA test. *Leptospires can be recovered only from mature mice even though antibodies can be detected from infected mice of all ages.

• TREATMENT:

Penicillins or tetracyclines. Can eliminate L. ballum from a colony (mice) with 1000 gm chlortetracycline HCL/Ton of feed for ten days.

• PREVENTION\CONTROL:

Vaccination in cattle, swine, and dogs Avoid swimming in or drinking from potentially contaminated water. Protect workers by providing boots and gloves. Rodent control. Drain wet ground. Doxycycline chemoprophylaxis for persons at high exposure.

• BORRELIOSIS

(Relapsing fever, tick-borne relapsing fever, spirochetal fever, vagabond fever, famine fever) A widely distributed bacterial infection spread from wild rodents by ticks or lice, with high fatality Tick-borne relapsing fever occurs in Africa, the Americas, Asia and possibly parts of Europe. The causative agents are Borrelia recurrentis and several other borrelia strains (bacterium). There is no vaccine.

• RESERVOIR AND MODE OF TRANSMISSION:

Epidemic louse-borne infection is not considered zoonotic. Endemic tick-borne relapsing fever is transmitted from the natural wild rodent reservoir by tick bites to humans and dogs. Transovarial transmission in ticks occurs. Blood-borne person-to-person and intrauterine transmission have been reported.

• INCUBATION PERIOD:

Humans: 1-15 days. Animals.Unknown.

• CLINICAL FEATURES:

Humans. Sudden onset of fever lasting for 3-5 days ends with a crisis. Then a febrile period of 2-4 days is followed by one to ten or more recurrences of fever accompanied by severe headaches, nausea, vomiting, diarrhea, jaundice and sometimes a macular rash with bleeding due to thrombocytopenia. Meningitis and cranial nerve involvement are possible. Animals. Arthritis and fever predominate in infected dogs. The arthritis recurs and may progress to chronic deformity.

• PATHOLOGY:

Humans. Many lesions occur, including enlarged, soft, infarcted spleen, hepatomegaly, hemorrhages in bone marrow and skin, myocarditis, bronchopneumonia, and meningitis. Animals. Arthritis, especially of the phalangeal joints, occurs with the possibility of progression to fibrosis of the joint capsule and ankylosis.

• DIAGNOSIS:

Humans. Identify borrelia in thick blood smears. Otherwise isolate the pathogen by inoculation of blood into susceptible animals if possible. Animals. Inoculate blood or tissues into rats or mice.

• PROGNOSIS:

Humans. The fatality rate is up to 40 per cent. Animals. Although fatality is uncommon, the lesions tend to be progressive.

• PREVENTION:

Humans and animals. Control tick vectors and prevent tick bites.

• TREATMENT:

Humans. A single dose of tetracycline or erythromycin, 0.5 g orally, or a single dose of procaine penicillin G, 600,000 units intramuscularly, probably constitutes adequate treatment for louse-borne relapsing fevers. Because of higher relapse rates, tick-borne disease is treated with 0.5 g of tetracycline or erythromycin given 4 times daily for 5-10 days. Jarisch-Herxheimer reactions may occur and respond to aspirin given every 4 hours. Pretreatment with steroids is not effective in preventing this reaction. Animals. Tetracycline, penicillin, erythromycin, and ceftriaxone at standard dosages for 21-28 days.

• LEGISLATION:

Humans.Louse-borne relapsing fever is notifiable to the World Health organization. Tick-borne infection may be notifiable in some countries (e.g. the UK). Animals.None.

LYME DISEASE

(Lyme arthritis, Bannworth's syndrome, tick-borne meningopolyneuritis, erythema chronicum migrans [ECM], Steere's disease)

• AGENT:

spirochete, Borrelia burgdorferi

• RESERVOIR AND INCIDENCE

First implicated in 1982 as agent in a 1975 epidemic of juvenile inflammatory arthropathy in Old Lyme Connecticut. Cases have been reported from 46 states and the annual number of Lyme disease cases has increased 18 fold from 497 to 8803. It is now the most common tick transmitted disease in the USA. Also seen in Europe, England, Soviet Union, China, Japan, Southeast Asia, South Africa, Australia, and Canada.

• TRANSMISSION:

Transmitted mostly by Ixodes dammini and other ixodid ticks (three host tick with a two to three year life cycle). Ixodes dammini has a broad range of hosts; adults prefer white tailed deer but will also parasitize dogs, horses, and humans. Larvae feed primarily on rodents, especially mice. Nymphs feed on all hosts and appears to be primarily responsible for transmission of the disease to people. Birds are an important reservoir and means of dispersal. Also found in Dermacentor, Rhipicephalus and Amblyomma and other ticks and biting insects, including mosquitoes, fleas, and biting flies. Because of lack of any proof to the contrary it is generally believed at this time that any potential increased risk to human beings from infected animals is attributable to animals bringing ticks into areas of human habitation rather than any pet transmission. Dogs appear to be at greater risk than humans.

• DISEASE IN ANIMALS:

Serologic evidence has been reported in the dog, cat, horse, and ruminants. However, correlation with disease is lacking except in the dog. The dog exhibits the same symptoms as noted below for humans. Expanding skin lesions have been noted in mice and rabbits.

• DISEASE IN MAN:

Multisystemic disease which may have chronic sequelae; an annular rash known as erythema chronicum migrans (ECM) develops in 60-80% of patients in the area of the tick bite and is considered pathognomonic. Also flu like symptoms, which resolve in about three weeks. 8-10% of people develop cardiac involvement several weeks later. Manifestations include atrioventricular block, cardiomyopathy, heart failure, myocarditis, and pancarditis. 15% develop neurologic disorders such as facial nerve palsies which usually resolve. Other manifestations include meningitis, cranial neuritis, radiculoneuritis, neuropathy, and encephalopathy. 60% develop the most common sequelae, arthritis. Disease may remain latent with symptoms developing 4 years after seroconversion.

• DIAGNOSIS:

Most common test is detecting antibody titers by IFA or ELISA (on blood, CSF or synovial fluid). Culture is definitive but is difficult and requires special media such as Barbour-Stoener-Kelly media. Histologically with Dieterle Silver Stain or immunoperoxidase stains, but is often unrewarding.

• TREATMENT:

A positive serology is no grounds for treatment when no clinical signs are present. Borrelia burgdorferi is sensitive to tetracycline and moderately sensitive to penicillin. amoxicillin, ceftriaxone, and imipenem are also highly active.

• PREVENTION\CONTROL:

Tick control care when removing ticks or when handling potentially infective materials a vaccine against Lyme Disease tested in hamsters has been found effective. More research is needed but in the future vaccination may be beneficial for those at constant risk of exposure.

ENTERIC INFECTIONS

CAMPYLOBACTERIOSIS

(Vibriosis, vibrionic abortion)

• AGENT:

Campylobacter (Vibrio) fetus ss. jejuni, a gram negative, microaerophilic, curved, motile rod that is worldwide in distribution.

• RESERVOIR AND INCIDENCE

isolated from laboratory animals including dog, cat, hamsters, ferrets (>60 % in one study), nonhuman primates, rabbits, swine, sheep, cattle, and birds Although most cases of human campylobacteriosis are of unknown origin, infection after contact with sick animals has been well documented. *In most reports of pet to human transmission of C. jejuni, diarrheic puppies or kittens from pounds have been the source of infection. Pet birds, chickens, and kittens are implicated in other reports. A lab animal technician developed Campylobacter enteritis after feeding and cleaning up after a recently imported nonhuman primate. The organism was first isolated from nonhuman primates from Macaca fascicularis in 1979 and has since been reported in baboons, rhesus, patas, and marmosets. Can be shed for long periods of time in stool by asymptomatic carriers. Younger animals seem more likely to acquire the infection and hence may more commonly shed the organism.

• TRANSMISSION:

Transmission is thought to occur by the fecal-oral route, through contamination of food or water, or by direct contact with infected fecal material. The organism has also been isolated from houseflies. At 40 C the organism is viable for three weeks in feces and milk, four weeks in water, and five weeks in urine. Campylobacter is shed in the feces for at least six weeks after infection. Infected children may transmit infection to puppies or kittens, which may then expose other children. Poultry and cattle are the main reservoirs for human infection, which is acquired by ingesting contaminated raw milk, undercooked chicken or other food contaminated in the kitchen.

• DISEASE IN NONHUMAN PRIMATES:

Variable. the majority are asymptomatic carriers. Mild to severe enteritis may be seen accompanied by fever, vomiting, and mucus and blood in the feces. Bacteremia may occur complicated by meningitis or abortion. Most signs appear 1 to 7 days after exposure and affect primarily the jejunum, ileum, and colon.

• DISEASE IN FERRETS:

Asymptomatic to proliferative colitis. Shed organisms for long period of time (> 16 weeks).

• DISEASE IN OTHER ANIMALS:

Has also been shown to cause hepatitis in poultry, proliferative ileitis in hamsters, and abortion in ruminants. In all animals, it may be associated with diarrhea, especially when acting secondarily to virus infection.

• DISEASE IN MAN:

Acute gastrointestinal illness, diarrhea with or without blood, abdominal pain, and fever. It may cause pseudoappendicitis and, rarely, septicemia and arthritis. Usually a brief, self-limiting disease. In humans the asymptomatic carrier state is rare. Reinfection is possible in both animals and man.

• DIAGNOSIS:

1. Rapid diagnosis is done with dark field or phase contrast microscopy of fecal material. 2. This is confirmed by stool culture which requires a special selective growth media(CAMPY-BAP) and incubation at 43oC with 10% CO2, 5% O2 and 85% Nitrogen. 3. Warthin Starry stain and histo 4. Various techniques are being used to detect seroconversion to the antigens of Campylobacter.

• TREATMENT:

Animals can be treated based on culture and sensitivity. Currently erythromycin is the drug of choice, but does not eliminate the carrier state. Tetracycline or ciprofloxacin are alternatives.

• PREVENTION\CONTROL:

Vaccines provide partial protection of short duration and routine use is not recommended. Control is aimed at isolation of affected individuals and personal hygiene. An increased awareness of the potential of infection due to Campylobacter is of primary importance. Thoroughly cook all foodstuffs derived from animal sources, particularly poultry. Recognize, prevent, and control Campylobacter infections among domestic animals and pets. Wash hands after handling poultry and animal feces.

COLIBACILLOSIS

(Colibacteriosis, colitoxemia, white scours, gut edema of swine)

• AGENT:

Escherichia coli are gram-negative, aerobic, and facultatively anaerobic medium-sized rods.

• RESERVOIR AND INCIDENCE

Worldwide; some endemic areas exist in developing countries.

• TRANSMISSION:

Some serotypes are species-specific, others are not. Milk, milk products, and meat products can contain pathogenic serotypes. Foods of animal origin and contact with dogs and cats have been indicated as sources of infection for children.

• DISEASE IN ANIMALS:

Calf diarrhea (white scours) is an acute disease causing mortality in calves less than 10 days old. It manifests itself as serious diarrhea, with whitish feces and rapid dehydration. Mastitis caused by E. coli appears especially in older cows with dilated milk ducts. A long-term study of horse fetuses and newborn colts found that close to 1% of abortions and 5% of deaths of newborns were due to E. coli. Neonatal enteritis caused by E. coli in suckling pigs begins 12 hours after birth with a profuse watery diarrhea, and may end with fatal dehydration. Edema in suckling pigs (gut edema) is an acute disease that generally attacks between 6 and 14 weeks of age. It is characterized by sudden onset, incoordination, and edema of the eyelids, the cardiac region of the stomach, and sometimes other parts of the body. During septicemic diseases of fowl, such as cases of salpingitis and pericarditis, pathogenic serotypes of E. coli have been isolated. A colibacillary etiology has also been attributed to Hjarre's disease (coligranuloma), which is a condition in adult fowl characterized by granulomatous lesions in the liver, cecum, spleen, bone marrow, and lungs.

• DISEASE IN HUMANS:

The enterotoxigenic stains (ETEC) cause profuse and watery diarrhea, abdominal colic, vomiting, acidosis, and dehydration. Enteroinvasive strains cause a dysenteric syndrome with mucoid diarrhea, at times tinged with blood. E. coli is also an important agent of urogenital infections.

• DIAGNOSIS:

Stool culture or immunoassays for enterotoxins.

• TREATMENT:

Ciprofloxacin or trimethoprim-sulfa.

• PREVENTION/CONTROL:

With respect to man, control measures include: a) personal cleanliness and hygienic practices, sanitary waste removal and b) protection of food products. Vaccines for swine and bovine have been developed.

SALMONELLOSIS

(Enteric paratyphosis)

• AGENT:

Gram negative bacteria. Out of 1600 recognized serotypes of Salmonella, S. typhimurium & S. enteritidis have been associated most commonly with lab animal colony infections. In the U.S., 5 million cases are diagnosed annually. S. typhi, the cause of Typhoid Fever, rarely occurs in the U.S. and is not discussed here.

• RESERVOIR AND INCIDENCE

The organism inhabits the intestinal tract of many animals including birds, cattle, sheep, pigs, lab. animals (rats, mice, hamsters, guinea pigs, nonhuman primates) and humans. Salmonella occurs worldwide. *The house mouse may also be a reservoir of the infection and may play a role in human and animal salmonellosis. Humans, rarely, and animals may be carriers and asymptomatic shedders of the organism. *Salmonella prevalence in the U.S. canine population may be 10% or more. *Prevalence data from 8 studies conducted worldwide indicated that a wide range (0.6-27%) of cats were culture-positive for Salmonella. *Salmonella carriers in newly imported Rhesus and Cynomolgus monkeys exceeded 20% in some shipments. *Birds, reptiles, and turtles are especially dangerous sources of Salmonellosis. 94% of all reptiles harbor Salmonella. Turtles alone in 1970 may have caused 280,000 human cases of Salmonellosis. *In 1975 the FDA ruled it illegal to sell a. Viable Turtle eggs b. Live turtles with a carapace length < 10.2cm (4 inches) c. Exceptions - Educational & scientific institutions and marine turtles. d. Marine turtles have not been shown to be a reservoir of Salmonella THERE WAS A 77% DECREASE IN TURTLE ASSOCIATED SALMONELLOSIS AFTER ENACTMENT OF THIS LAW.

• TRANSMISSION:

Indirect transmission via contaminated food and water are the most common sources but transmission may also be by direct contact. It is a common contaminant of sewage. Found in many environmental water sources. Environmental contamination continues to be a potential source of infection for lab animals and secondarily for personnel handling those animals. *Animal feed containing animal by products continues to be a source of Salmonella contamination, especially if the diets consist of raw meal and have not undergone the pelleting process.

• DISEASE IN ANIMALS:

Can be asymptomatic with clinical signs precipitated by stress; penetration of the infection into the mucosa is followed by inflammation, especially ileitis, progressing to inflamed mesenteric lymph nodes in the mesentery, possibly progressing to septicemia and pneumonia especially in calves. Calves undergo epizootic outbreaks of diarrhea with high mortality. Abortion in cattle is caused by massive proliferation of salmonella in the placenta leading to placental necrosis. High percentage of survivors become carriers. Infected sheep, goats, and poultry usually show no signs of infection.

• DISEASE IN MAN:

Acute gastroenteritis with sudden onset of abdominal pain, diarrhea, nausea, and fever. May lead to septicemia. May be an inapparent infection.

• DIAGNOSIS:

Fecal Culture with selective media. Can get false negatives, though because organism is shed intermittently. In the carrier state bacterium resides in the gall bladder (NHP).

• TREATMENT:

Symptomatic. Severely ill patients are treated with trimethoprim-sulfamethoxazole, ampicillin, or ciprofloxacin.

• PREVENTION\CONTROL:

Rapid detection and treatment (acute and chronic) in lab animals. Treatment based on culture and sensitivity. Cull carrier animals. Watch during quarantine period. Sanitation and hygiene, protective clothing, gloves Rodent, bird & wild animal control is important. Examine feed and bedding and pasteurize or autoclave, if necessary. Consider screening animal care personnel for inapparent Salmonella infection to prevent the introduction of Salmonella into the colony from infected workers. Thoroughly cook all foodstuffs derived from animal sources. Exclude animal care personnel with diarrhea.

=STAPHYLOCOCCAL FOOD POISONING

(Staphylococcal Alimentary Toxicosis, Staphylococcal Gastroenteritis)

• AGENT:

Coagulase-positive strains of Staphylococcus aureus, a gram-positive cocci.

• RESERVOIR AND INCIDENCE

Worldwide. The principle reservoir is the human carrier. Infected cows, fowls, and dogs may give rise to and be a source of staphylococcal poisoning in man.

• TRANSMISSION:

A high proportion of healthy humans (30-35%) have staphylococci in the nasopharynx and on the skin. Sneezing, coughing, expectorating can contaminate food. Similarly, he may contaminate foods handled if he has a skin lesion. Milk from cow udders infected can contaminate numerous milk products. Contaminated egg contents can also be a source of infection.

• DISEASE IN ANIMALS:

Mastitis in cattle. Pyoderma, impetigo, folliculitis, and furunculosis in dogs. In fowl, staphylococcal infection can cause diseases ranging from pyoderma to septicemia with different locations (salpingitis, arthritis, and other disorders).

• DISEASE IN HUMANS:

The major symptoms are nausea, vomiting, abdominal pains, and diarrhea. It is the cause of toxic shock syndrome in women.

• DIAGNOSIS:

Culture of vomitus, feces, or a suspected food item.

• TREATMENT:

Electrolyte and fluid replacement. Ciprofloxacin.

• PREVENTION/CONTROL:

Reduce food handling time. Exclude persons with boils, abscesses, and other purulent lesions from handling food. Educate food handlers in strict food hygiene.

ANTHRAX

(Malignant pustule, woolsorter's disease, charbon, malignant edema, splenic fever)

• AGENT:

Bacillus anthracis, a gram-positive spore-forming aerobic rod.

• RESERVOIR AND INCIDENCE

Occurrence is worldwide. Most mammals susceptible; most commonly seen in cattle, sheep, horses, swine, goats (guinea pigs, rabbits, mice, experimentally)

• TRANSMISSION:

Herbivorous animals infected by ingestion of spores which are viable in soil for years. Man is infected by handling contaminated carcasses, wool, hide, or hair. Also can be infected by ingestion or inhalation of spores or bacilli. Recent outbreaks have been related to prospective military use of the organism.

• DISEASE IN ANIMALS:

Sudden, acute illness, with high fever, localized swellings, bleeding from body orifices, death in 1 to 3 days. Blood is non-clotting.

• DISEASE IN MAN:

Cutaneous form ("malignant pustule"): most common, incubation 1 to 7 days, then an erythematous papule appears on an exposed area of skin and becomes vesicular, with a purple to black center. The center of the lesion finally forms a necrotic eschar and sloughs. Regional adenopathy, fever, malaise, headache, and nausea and vomiting may be present. After the eschar sloughs, hematogenous spread and sepsis may occur, resulting in shock, cyanosis, sweating, and collapse. Hemorrhagic meningitis may also occur. 20% fatality if not treated. Pulmonary form ("woolsorter's disease"): following the inhalation of spores from hides, bristles, or wool, incubation 1 to 5 days, fever, cough, dyspnea, respiratory failure and death in 24 hours. 100% fatality. Intestinal form: incubation 12 hours to 5 days, anorexia, vomiting, diarrhea, 50% fatality if untreated.

• DIAGNOSIS:

o Gram or Giemsa stain of sputum, blood or tissue o culture

• TREATMENT:

Penicillin G. For mild cases, tetracycline.

• PREVENTION\CONTROL:

o Vaccine for livestock and high risk personnel. o avoid necropsy of suspect animals, o disinfect wool or hair from animals in endemic areas with 10% formalin, 5%lye

STAPHYLOCOCCAL FOOD POISONING

• SYNONYMS:

Staphylococcal alimentary toxicosis, staphylococcal gastroenteritis.

• ETIOLOGY:

Coagulase-positive strains of Staphylococcus aureus that produce enterotoxins. Very few coagulase-negative stains are enterotoxigenic. The toxin is preformed in the food involved. To date, six types of enterotoxins are known: A, B, C, D, E, and F; of these A is the most prevalent in outbreaks. Enterotoxin F is implicated in toxic shock syndrome (TSS). Some strains can produce two or even three different enterotoxins. The toxins are heat-resistant and can withstand a temperature of 100oC for 30 minutes.

• GEOGRAPHIC DISTRIBUTION:

Worldwide.

• THE DISEASE IN MAN:

The incubation period is short, generally 3 hours after ingestion of the food involved. The interval between consumption of the enterotoxin and the first symptoms can vary from 30 minutes to 8 hours, depending on the quantity of toxin ingested and the susceptibility of the individual. The major symptoms are nausea, vomiting, abdominal pains, and diarrhea. Some patients may show low pyrexia (up to 38oC). More serious cases manifest prostration, cephalalgia, abnormal temperature, and lowered blood pressure, as well as blood and mucus in the stool and vomit. The course of the disease is usually benign and the patient recovers without medication in 24 to 72 hours. Recently, a toxic shock syndrome has been described. Symptoms consist of vomiting, diarrhea, high fever, erythroderma, edema, renal insufficiency, and toxic shock. Most patients are women who become ill during their menstrual period. The above-described symptoms also are observed in association with abscesses and osteomyelitis caused by S. aureus. A staphylococcal enterotoxin designated F was isolated from 94% of these patients strains of S. aureus from nine patients with toxic shock were examined, and production of enterotoxin F was confirmed in eight of them; only 42% of 50 strains isolated from other hospitalized patients produced this toxin. Toxin F production was not found in 48 strains originating from animal clinical specimens. Of 24 strains from healthy human carriers, 25% produced the toxin.

• SOURCE OF INFECTION AND MODE OF TRANSMISSION:

The principal reservoir of is S. aureus is the human carrier. A high proportion (from 30 to 35%) of healthy humans have staphylococci in the nasopharynx and on the skin. A carrier with a respiratory disease can contaminate foods by sneezing coughing, or expectorating. Similarly, he may contaminate foods he handles if he has a staphylococcal skin lesion. However. even if not sick himself, the carrier may spread the agent by handling food ingredients. utensils, and equipment. or the finished food product. According to different authors, the proportion of enterotoxin-producing S. aureus strains of human origin varies between 18 and 75%. The proportion of toxigenic strains isolated from various sources (human, animal, and food) is very high. Strains of human origin predominate in epidemics, but animals are also reservoirs of the infection. Milk from cow udders infected with staphylococci can contaminate numerous milk products. Many outbreaks have been produced by consumption of inadequately refrigerated raw milk or cheeses from cows whose udders harbored staphylococci. The largest outbreak affected at least 500 students in California between 1977 and 1981 and was traced to chocolate milk. In developing countries, where refrigeration after milking is often inadequate, milk and milk products may be an important source of staphylococcal intoxication. According to recent investigations, a high proportion of strains isolated from staphylococcal mastitis produce enterotoxin A, which causes many outbreaks in humans. In several investigations it was possible to isolate from skin lesions and cow's milk the S. aureus phage type 80/81, which is related to epidemic infections in man. One of the studies proved that phage type 80/81 produced interstitial mastitis in cows. The same phage type was found among animal caretakers, which indicates that the bacterium is intertransmissible between man and animals and that the latter may reinfect man. Infected fowl and dogs may also give rise to and be a source of staphylococcal poisoning in man. One subject that deserves special attention is the appearance of antibiotic-resistant strains in animals whose food includes antibiotics. Concern exists over the possible transmission of these strains to man. On several occasions, resistant stains have been found both in animals (cows, swine, and fowl) and in their caretakers, with the same antibiotic resistance. Moreover, "human" strains (phage typed) have on occasion been isolated from the nostrils and lesions of other species of domestic animals. A variety of foods and dishes may be vehicles of the toxin. If environmental conditions are favorable, S. aureus multiplies in the food and produces enterotoxins. Once made, the toxin is not destroyed even if the food is subjected to boiling while being cooked. Consequently, the toxin may be found in the food whereas staphylococci are not. An important causal factor in food-borne intoxications is holding food at room temperature, which permits multiplication of staphylococci. Lack of hygiene in food handling is another notable factor. Frequently, outbreaks of food poisoning may be traced to a single dish.

• THE ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:

Most outbreaks are caused by human strains, and to a lesser degree by strains from cattle and other domestic animals. Animal products -- such as meat, ham, milk, cheese, cream, and ice cream -usually constitute a good substrate for staphylococcal multiplication. Milk pasteurization offers no guarantee of safety if toxins were produced before heat treatment, as the toxins are heat-resistant. Outbreaks have been caused by reconstituted powdered milk, even when the dried product contained few or no staphylococci.

• DIAGNOSIS:

The short incubation period between ingestion of contaminated food and appearance of symptoms is the most important clinical criterion. Laboratory confirmation, when possible, is based above all on demonstration of the presence of enterotoxin in the food. Biological methods (inoculation of cats with cultures of the suspect food, or of rhesus monkeys with the foodstuffs or cultures) are expensive and not always reliable. As substitutes, serologic methods such as immunodiffusion, immunofluorescence, hemagglutination inhibition, and, recently, ELISA are increasingly used. In febrile patients, blood cultures are indicated. Isolation of enterotoxigenic staphylococcal strains from foods and typing by phage or, more recently, by immunofluorescence have epidemiologic value. Quantitative examination of staphylococci in processed or cooked foods serves as an indicator of hygienic conditions in the processing plant and of personnel supervision.

• TREATMENT:

In humans, treatment usually consists of replacement of fluids and electrolytes and, very rarely, management of hypovolemic shock and respiratory embarrassment. If botulism is suspected, polyvalent antitoxin must be administered. Historically, antimicrobial drugs have not been recommended unless a specific microbial agent producing progressive systemic involvement can be identified. Preliminary data now suggest that ciprofloxacin, 500 mg every 12 hours for 5 days, may shorten the duration of diarrhea and lead to a more rapid resolution of symptoms. Antimotility drugs may relieve cramping and decrease diarrhea in mild cases. Their use should be limited to patients without fever and without dysentery (bloody stools), and they should be used in low doses.

• CONTROL:

It includes the following measures: a) education of persons who prepare food at home or commercially in proper personal hygiene; b) exclusion from handling food of individuals with abscesses or other skin lesions; and c) refrigeration of all foods to prevent bacterial multiplication and formation of toxins. Foods should be kept at room temperature as little time as possible. The veterinary milk inspection service should supervise dairy installations, ensuring that refrigeration units function correctly and are used immediately after milking, and that milk is refrigerated during transport to pasteurization plants. The veterinary meat inspection service should be responsible for enforcing hygienic regulations before and after slaughter as well as during handling and production of meat products. Control of hygienic conditions in meat retail establishments ts also important.

LEPROSY

(Hansen's disease)

• AGENT:

Mycobacterium leprae, a polymorphic acid-fast bacillus.

• RESERVOIR & INCIDENCE:

The world prevalence is estimated to be between 10 and 12 million. Newly recognized cases in the USA are diagnosed principally in California, Hawaii, Texas, Florida, Louisiana, and New York City, and in Puerto Rico. Most of these cases are in immigrants and refugees whose disease was acquired in their native country; however, the disease remains endemic in Hawaii, Texas, California, Louisiana and Puerto Rico. Man is the only significant reservoir. Armadillos, mangabey monkeys, and chimpanzees can acquire the disease from humans. Epidemiologic data on leprosy in the U.S. reveal very high ratios of native to foreign-born leprosy patients in Texas and Louisiana in comparison to all other states. These are the 2 states known to have the highest prevalences of leprosy in wild armadillos.

• TRANSMISSION:

Respiratory and involves prolonged exposure in childhood. Only rarely have adults become infected.

• DISEASE IN ANIMALS:

The disease in armadillos (Dasypus novemcinctus) is similar to the lepromatous form in man. Infection in these animals is characterized by macrophage infiltrates containing a large number of bacilli. M. leprae is known to prefer the coldest parts of the human body. For this reason, armadillos are used as experimental animals since their body temperature is 30-35oC. In chimpanzees, the disease appears as a progressive chronic dermatitis with nodular thickening of the skin of the ears, eyebrows, nose, and lips. Sooty mangabey monkeys develop lepromatous leprosy with neuropathic deformities of the extremities, including clawing of the digits.

• DISEASE IN HUMANS:

In lepromatous leprosy, nodules, papules, macules and diffuse infiltrations are bilaterally symmetrical and usually numerous and extensive; involvement of the nasal mucosa may lead to crusting, obstructed breathing and epistaxis; ocular involvement leads to iritis and keratitis. In tuberculoid leprosy, skin lesions are single or few, sharply demarcated, anesthetic or hyperesthetic, and bilaterally asymmetrical; peripheral nerve involvement tends to be severe.

• DIAGNOSIS:

Demonstration of acid-fast bacilli from skin or nasal septum scrapings.

• TREATMENT:

Combination therapy is recommended since single-drug treatment is accompanied by emergence of resistance. Lepromatous leprosy is treated with dapsone, clofazimine, and rifampin. Tuberculoid leprosy is treated with dapsone and rifampin.

• PREVENTION/CONTROL:

early detection and treatment. Contact isolation for lepromatous leprosy but not necessary for tuberculoid leprosy.

DERMATOPHILOSIS

(Streptotrichosis, Mycotic Dermatitis of Sheep)

• AGENT:

Dermatophilus congolensis. An aerobic actinomycete with gram positive long branching filaments and coccoid bodies.

• RESERVOIR AND INCIDENCE

Occurs in temperate regions worldwide. Natural disease described in horses, cattle, sheep, goats, cottontail rabbits, owl monkeys, lizards & humans.

• TRANSMISSION:

The etiologic agent is an obligate parasite that has been isolated only from lesions in animals. Human cases have arisen from direct contact with infected animals. The most common means of transmission between animals is mechanical thru arthropod vectors. The infection may also be transmitted by means of objects, such as plant thorns or shears.

• DISEASE IN ANIMALS:

Circumscribed areas of alopecia, elevated crusty papillomatous lesions, and exudative dermatitis. **Owl monkeys may have relapsing Dermatophilosis after apparently appropriate antibiotic regimens. Therefore organism may persist on pelage of animals after resolution of lesions. In cats, the lesions differ from those of other domestic animals by affecting deeper tissues. In cats, granulomatous lesions have been found on the tongue, bladder, and popliteal lymph nodes.

• DISEASE IN MAN:

pustular desquamative dermatitis

• DIAGNOSIS:

Microscopic exam of stained material from lesions and culture.

• PREVENTION\CONTROL:

1. Treatment with antibiotics 2. Isolate affected animals 3. Protective clothing, gloves, personal hygiene 4. Tick control

ERYSIPELOID

(Rosenbach's erysipeloid, erythema migrans, erysipelotrichosis, rose disease in swine, diamond skin disease in swine, fish-handler's disease or fish rose in man)

• AGENT:

Erysipelothrix rhusiopathiae (insidiosa). 22 different serotypes are recognized. *Discovered by ROBERT KOCH==He called it the Bacillus of Mouse Septicemia

• RESERVOIR AND INCIDENCE

Saprophyte in soil, water, and decaying organic matter. Pathogen in swine, lambs, calves, poultry, fish, & wild and lab mice. *Pigs probably represent the most likely source of exposure in the zoophile community. (Natural disease or zoonotic transmission from rodents has NOT been reported.)

• TRANSMISSION:

contamination of wounds while handling infected tissues

• DISEASE IN ANIMALS:

Diamond skin disease in pigs. Arthritis in sheep and swine. Cyanosis and hemorrhages in turkeys. Can be septicemic disease in many species.

• DISEASE IN MAN:

Disease in humans is called Erysipeloid, and is primarily occupation related. Inflammatory lesions of the skin, with elevated erythematous edge; spreads circumferentially. Septicemia is an infrequent complication.

• DIAGNOSIS:

Culture from lesion or blood

• PREVENTION\CONTROL:

Treatment with Penicillin Gloves when handling animals Vaccine for swine and turkeys

MELIOIDOSIS

(Pseudoglanders, Whitmore's disease)

• AGENT:

Pseudomonas pseudomallei (Malleomyces pseudomallei, Actinobacillus pseudomallei ) --MOTILE, Gram negative rod

• RESERVOIR AND INCIDENCE

Normal inhabitant of surface soil and water in Southeast Asia, and tropical areas. Recent studies have shown that the water of tanks in which exotic aquarium fishes were imported was contaminated. Occurs in wild rodents, goats, pigs, sheep. Also identified in Chimps, orangutans, and macaques. There is no evidence that animals are important reservoirs, except in the transfer of the agent to new foci. Rare in the U.S. except in drug users.

• TRANSMISSION:

by inhalation from moist soil-water reservoir, by contact with contaminated soil or water thru overt or inapparent skin wounds, or by ingestion of contaminated feeds. Can be venereal in man.

• DISEASE IN ANIMALS:

Signs include loss of weight, swelling of joints, fever, cough, and chest pain. Skin lesions with fistulous tracks can develop. Emaciation and multiple abscesses in lung, bone, viscera. A chronic draining purulent skin lesion in a primate is suspect. Incubation period can be 6 months to three years. Sheep seem especially susceptible- over 25% mortality can occur in outbreaks.

• DISEASE IN MAN:

Clinical disease is not common in man but subclinical disease in endemic areas based on serology is common. It may simulate typhoid fever or TB including pulmonary cavitation, empyema, chronic abscesses and osteomyelitis. High case fatality rate (80%) in people who do develop clinical signs.

• DIAGNOSIS:

Culture and isolation from lesions, a rising serological titer is confirmatory.

• TREATMENT:

ceftazidime. Alternates: Chloramphenicol or Trimethoprim-sulfamethoxazole.

• CONTROL:

Safe disposal of sputum and wound discharges.

GLANDERS

(Farcy)

• AGENT:

Pseudomonas mallei (Actinobacillus mallei) NONMOTILE, gram negative rod

• RESERVOIR AND INCIDENCE

disease of equidae and rarely man. Occasionally reported in dogs, cats, sheep, and goats. Mostly seen in Asia and Mediterranean areas, rare in North America.

• TRANSMISSION:

spread by contamination by infectious discharges of wounds and mucus membranes and by ingestion.

• DISEASE IN ANIMALS AND MAN:

pulmonary form: cough, nasal discharge. cutaneous form: multiple, purulent, cutaneous eruptions, often following lymphatics. Usually affects hind legs of horses. May have long periods of remission. The fatality rate in humans is 95% if left untreated. Horses usually suffer chronic and sometimes fatal illness. Asses and mules usually suffer acute disease which is often fatal.

• DIAGNOSIS:

Cannot be differentiated from P. pseudomallei serologically. Specific diagnosis can be made only by characterization of the isolated organism.

• TREATMENT:

Streptomycin + tetracycline or chloramphenicol + streptomycin

• PREVENTION/CONTROL:

1. Treatment with antibiotics 2. Elimination of carrier animals 3. Gloves, protective clothing when handling infected animals.

TULAREMIA

(Francis' disease, deer-fly fever, rabbit fever, O'Hara disease)

• AGENT

- Francisella tularensis, a small pleomorphic, gram-negative, nonmotile rod or coccobacillus that can survive several weeks in the external environment.

• RESERVOIR AND INCIDENCE

Common often fatal septicemic disease of rabbits, squirrels, muskrats, deer, bull snakes, sheep, wild rodents, cats and dogs. Major reservoirs are RABBITS, TICKS, MUSKRATS. Has been reported in NHP's at an urban zoo.

• TRANSMISSION:

handling tissue of infected animals (direct contact with UNBROKEN skin is sufficient). Reported human infections due to a cat bite and scratch and a NHP bite also reported. transmitted by biting insects inhalation, ingestion

• DISEASE IN ANIMALS:

Clinical signs usually occur alongside heavy infestation with ticks, and include sudden high fever, anorexia and stiffness, eventually leading to prostration and death. In sheep, pregnant ewes may abort. Affected dogs have soft nodular swellings under the skin. Miliary foci of necrosis occur in the liver, spleen and lymph nodes. Severe lesions in the lung involve widespread consolidation with edema and pleurisy.

• DISEASE IN MAN:

Fever, headache, and nausea begin suddenly, and a local lesion-a papule-develops and soon ulcerates. Regional lymph nodes may become enlarged and tender and may suppurate. The local lesion may be on the skin of an extremity (ulceroglandular disease) or in the eye. Pleuropulmonary disease may develop from hematogenous spread or may be primary after inhalation. Following ingestion of infected meat or water, an enteric (typhoidal) form may be manifested by enteritis, stupor, and delirium. In any type of involvement, the spleen may be enlarged and tender and there may be nonspecific rashes, myalgias, and prostration. A case fatality rate of 5-10% mainly from the typhoidal or pulmonary form exists.

• DIAGNOSIS:

Culture (requires specialized laboratory and dangerous, therefore, not recommended) A positive agglutination test (>1:80) develops in the second week after infection and may persist for several years.

• TREATMENT IN MAN:

streptomycin + tetracycline. Chloramphenicol may be substituted for tetracycline.

• PREVENTION\CONTROL:

wear impervious gloves while handling animals or tissues cook the meat of wild rabbits and rodents thoroughly vaccine available for high risk personnel avoid bites of flies, mosquitos, and ticks and avoid drinking, bathing, swimming in untreated water in endemic areas.

STREPTOCOCCOSIS

• AGENT:

The causative agents are various streptococci species, including Streptococcus suis and S. zooepidemicus.

• RESERVOIR AND INCIDENCE

Pigs are the reservoir of S. suis.

• TRANSMISSION:

Humans are infected with S. suis by handling infected meat. S. zooepidemicus has occurred in persons in direct contact with domestic animals and from drinking raw milk.

• DISEASE IN ANIMALS:

S. suis epizootics may occur in pigs with high mortality, heralded by signs of meningitis including depression, fever, incoordination and paralysis. Suppurative arthritis may occur. More usually the disease is subclinical. S. zooepidemicus may cause mastitis in cattle.

• DISEASE IN MAN:

S. suis causes fever and occasionally meningitis. S. zooepidemicus may cause upper respiratory tract symptoms, cervical adenitis, pneumonia, endocarditis and nephritis. A fatality rate of 8% has been reported for S. suis, with residual deafness in a high proportion of survivors.

• DIAGNOSIS:

isolation and culture

• TREATMENT:

Benzathine Penicillin G. For persons allergic to penicillin, erythromycin is an effective alternative. However, increasing reports of resistance from Europe threatens its clinical utility.

• PREVENTION/CONTROL:

Exercise caution in handling pig meat. Dress all wounds to avoid contamination. Pasteurize milk.

RAT BITE FEVER

(Streptobacillary fever, Haverhill fever, epidemic arthritic erythema, sodoku)

• AGENT:

Gram negative, pleomorphic bacillus. Two different agents can cause disease: 1. Streptobacillus moniliformis (Haverhill Fever) *Named after a 1926 outbreak in Haverhill, Mass. attributed to contaminated milk. 2. Spirillum minus (Sodoku)

• RESERVOIR AND INCIDENCE

Present in the oral and respiratory passages of a large number of asymptomatic rodents, including Rats and Mice. Incidence of disease appears to be low. Historically, wild rat bites and subsequent illness (usually small children) relate to poor sanitation and overcrowding.

• TRANSMISSION:

Man infected by bite of infected rodent or via contaminated milk or food

• DISEASE IN ANIMALS:

Rats: inapparent infection Mice: acute, systemic, fatal disease in immunologically inexperienced mice. Surviving mice (or if endemic disease), exhibit suppurative polyarthritis, swelling and loss of digits or limbs.

• DISEASE IN MAN:

Acute febrile disease following bite from a rodent. Can see inflammation, lymphadenopathy, and nonspecific signs. May exhibit rash on extremities, often soles and palms. May see arthritis with S. moniliformis. Incubation period variable: S. moniliformis: hours to 1 to 3 days S. minus: 1 to 6 weeks Symptoms usually resolve spontaneously. Complications, if not treated promptly, lead to pneumonia, hepatitis, enteritis, endocarditis with a 10% fatality rate.

• DIAGNOSIS:

Culture: S. moniliformis requires 10 to 20% horse or rabbit serum and reduced oxygen tension. S. minus- won't grow in vitro. Must inoculate culture specimens into lab animals and use dark field microscopy.

• TREATMENT:

Treat with procaine penicillin G or tetracycline HCl. Give supportive and symptomatic measures as indicated.

• PREVENTION/CONTROL:

Bacteriologic monitoring Proper treatment of rodent bites

PASTEURELLOSIS

(Shipping or transport fever, hemorrhagic septicemia)

• AGENT:

Pasteurella multocida, small, nonmotile, polymorphic, gram-positive bacilli

• RESERVOIR AND INCIDENCE

inhabits the oral cavity and upper respiratory tract of many animals (Rabbits, rodents, dogs, cats, mice, birds, swine). Dogs and cats are frequently healthy carriers.

• TRANSMISSION:

All animals and birds may be colonized by pasteurellas, and human infection occurs by wound infection from bites or scratches. Animal-to-animal transmission may occur by ingestion and inhalation. 1986 case report of meningitis in a woman who kissed her dog (cultured positive for organism) and also had dental caries which was considered to be the route of infection.

• DISEASE IN ANIMALS:

can cause acute pneumonia or septicemic disease in many species. May cause chronic infection of upper respiratory and middle ear especially in the rabbit.

• DISEASE IN MAN:

Local inflammation occurs around the bite or scratch, possibly leading to abscess formation with systemic symptoms.

• TREATMENT:

Penicillin, tetracycline, or cephalosporin

• PREVENTION/CONTROL:

Proper treatment of bite Protective clothing (mask,gloves) Euthanize aggressive dogs and cats. Vaccinate cattle and sheep.

ANTHRAX

(Malignant pustule, wool-sorters' disease, charbon, malignant edema, splenic fever) An acute bacterial infection of humans and animals which may be rapidly fatal. The disease occurs worldwide and is enzootic in certain African and Asian countries. It is an occupational hazard of persons such as wool-sorters, fellmongers, knackermen, farm workers and veterinarians in contact with infected animals or their products (e.g., blood, wool, hides and bones). The causative agent is Bacillus anthracis (bacterium).

• RESERVOIR AND MODE OF TRANSMISSION:

All domestic, zoo and wild animals are potentially at risk of infection. Anthrax bacilli are released from infected carcasses and form resistant spores on exposure to air. These spores contaminate soil for many years. Humans are usually infected by inoculation from direct contact with infected animals, carcasses or animal products and contaminated soil. Inhalation or ingestion of spores may occur. Animals are infected from contaminated feed, forage, water or carcasses.

• INCUBATION PERIOD:

Humans. Cutaneous 3-10 days inhalation 1-5 days gastrointestinal 2-5 days. Animals. 1-5 days.

• CLINICAL FEATURES:

Humans. Various forms include: 1. Cutaneous anthrax; localized ulceration and scab with fever and headache which may be followed within a few days by septicemia and meningitis. 2. Inhalation anthrax; fulminating pneumonia. 3. Intestinal anthrax; acute gastroenteritis with bloody diarrhea. Animals. Peracute cases are found dead or moribund. Acute cases show fever, excitation followed by depression, incoordination, convulsion and death. Chronic cases show edema of throat, pharynx and brisket, especially in pigs.

• PATHOLOGY:

Humans. Features include black scab (eschar) with edema, enlargement of regional lymph nodes and possibly septicemia; pneumonia and generalized hemorrhages. Animals. Carcasses should not be opened, hence necropsy is rarely carried out. Main features include failure of the blood to clot and hemorrhages throughout the body. The spleen is enlarged and softened. The subcutaneous swelling, mainly about the neck and throat of affected pigs and horses, contains gelatinous fluid. The blood contains very large numbers of B. anthracis.

• DIAGNOSIS:

Humans. Identify B. anthracis in stained blood smears or by inoculation of animals. Culture swabs from wounds. Animals. As for humans. Specific antigen for anthrax may be found in animal products (e.g. hides) using a precipitin (Ascoli) test.

• PROGNOSIS:

Humans. Untreated cutaneous anthrax has a fatality rate of 5-20 Per cent and gastrointestinal anthrax of 25-75 per cent. Pulmonary anthrax is usually fatal. Animals. The condition is usually fatal in cattle unless treated early. Pigs and horses are more resistant.

• PREVENTION:

Humans. Prohibit contact with infected animals and their products. Establish environmental and personal hygiene (e.g., ventilation and protective clothing) where a special risk exists. Treat wounds promptly and disinfect imports of hairs and wool. Vaccination may protect those occupationally exposed to risk. Apply strict safety measures. Isolate infected patients, with concurrent disinfection. Animals. Sterilize, or avoid using, meat and bone meal from high-risk countries for animal feed. Vaccinate livestock grazing in enzootic area. Dispose of infected carcasses safely and fence off areas contaminated by inadequately buried carcasses.

• TREATMENT:

Humans. The mortality rate is high despite proper therapy, especially in pulmonary disease. Penicillin G, 2 million units IV every 4 hours, is the therapy of choice. tetracycline, 500 mg orally every 6 hours, may be used for mild, localized cutaneous infection. Animals. Penicillin injection of all animals showing fever after the first case is confirmed. This involves checking temperatures twice daily.

• VACCINATION:

Humans. Offered to workers at risk. Animals. Non-encapsulated Stern strain vaccine can be used in all species of domestic animal. Annual vaccination of grazing animals using spore or alum precipitated antigen vaccine in areas of high risk is recommended.

• LEGISLATION:

Humans. The disease is notifiable in most countries. It is a recognized occupational disease in some countries, including the UK. Animals. Notifiable in many countries with mandatory disposal of infected carcasses by burning or deep burial under lime. Opening of moving suspect carcasses is prohibited.

CLOSTRIDIAL INFECTIONS

(Clostridial myositis: black leg, malignant edema, gas gangrene. Enterotoxemia: pulpy kidney, struck, lamb dysentery, braxy. Tetanus: lockjaw)

• AGENT:

Clostridium tetani (horses)--tetanus Clostridium perfringens (cattle, sheep)--gas gangrene Clostridium septicum (cattle) malignant edema

• RESERVOIR AND INCIDENCE

Clostridia are normal intestinal flora and also survive by spores in the soil.

• TRANSMISSION:

Infection may be by contamination of deep, penetrating wounds to cause tetanus, by ingestion of preformed toxin or spores which vegetate in the digestive tract to cause enterotoxemia, or by ingestion of spores which are carried by the blood to muscles where they remain dormant until activated by trauma to produce necrotizing myositis. C. perfringens food poisoning is due to spore contamination of foods which survive heating to vegetate in unrefrigerated conditions. Neonatal tetanus in humans is frequently caused by contamination of the umbilicus.

• DISEASE IN ANIMALS:

Tetanus: as in humans. In myositis (black leg) cases a limb is still and painful with crepitus on palpation. Signs of toxemia. Rapidly fatal. C. chauvoei, novyi, and septicum toxins produce massive muscle necrosis, often with edema and SC gas formation. C. perfringens causes a variety of profound toxemias with cloudy swelling of parenchymatous organs and excess fluids, often bloodstained in serous cavities.

• DISEASE IN MAN:

Tetanus: painful toxic contractions of muscles and trismus. The case fatality rate for tetanus is 30-90% even when treated. Gas gangrene: fever, toxemia, painful edema spreading from the edges of wounds, interstitial emphysema, neck stiffness. Food poisoning: vomiting and diarrhea of a few days' duration.

• TREATMENT:

Myositis: penicillin, adequate surgical debridement and exposure of infected areas. Tetanus: immune globulin, penicillin, mechanical ventilation. Spasms are controlled with chlorpromazine or diazepam combined with a sedative.

• PREVENTION/CONTROL:

immunization with toxoids (good for 10 years), proper treatment of wounds. Good food hygiene is essential. In animals, prevent wound contamination during lambing, shearing, castration and docking.

CAPNOCYTOPHAGA

• AGENT:

Capnocytophaga canimorsus (formerly Dysgonic fermenter-2), a recently described aerobic, gram negative bacillus with unusual fermentation pattern.

• RESERVOIR AND INCIDENCE

Found as part of oral flora of normal dogs and cats. C. canimorsus has been isolated from the mouths of 24% and 17% of normal dogs and cats respectively. Serious infections in man are most commonly reported in splenectomized or immunocompromised people, alcoholics, or persons who have chronic respiratory disease. More than 40 cases reported, many fatal, since first reported in 1976.

• TRANSMISSION:

Contact, bite or scratch from dog or cat

• DISEASE IN MAN:

can lead to cellulitis and overwhelming bacteremia, meningitis, endocarditis, septic arthritis, and DIC. The organism appears to have an affinity for the eye, causing angular blepharitis and severe keratitis. Accidental corneal inoculation occurred during a tooth extraction in a Poodle causing severe refractory keratitis in a veterinarian. The predisposition of the cornea to infection may be due to its avascularity and to the low concentrations of immunoglobulins and complement components in the tissue. Most serious disease and fatalities have occurred in splenectomized people. Case fatality rates of 4-27% have been reported.

• DIAGNOSIS:

History, clinical signs, and culture. ORGANISM IS SLOW GROWING. May require 8 days of incubation. Micro exam of blood smear or buffy coat with gram stain to detect organisms.

• PREVENTION/CONTROL:

Awareness, especially of high risk individuals Treatment of bite wounds, Penicillin G. (Treatment of high risk people even without sign of infection recommended.)

PSITTACOSIS

(Ornithosis, Parrot Fever, Chlamydiosis)

• AGENT:

Obligate,intracellular organism with a unique development cycle and worldwide distribution Genus Chlamydia has only four species, many strains 1. Chlamydia trachomatis- humans, mice (Zoonotic potential not known) 2. Chlamydia psittaci- BIRDS, Mice, g. pig, rabbits, cats, frogs, ruminants 3. Chlamydia pneumoniae- humans 4. Chlamydia pecorum- ruminants

• RESERVOIR AND INCIDENCE

The mammalian strains appear to be a zoonotic problem only rarely. 2 cases of human conjunctivitis reported from close association with cats with chlamydial pneumonitis and conjunctivitis. Birds are the main reservoir of human infection, however, 25% of human cases have no history of avian contact. Ovine strains may infect pregnant women.

• TRANSMISSION:

Inhalation; dry feces produce highly infective aerosols Direct contact with feces or respiratory secretions May survive in dust for several months.

• DISEASE IN ANIMALS:

There are many strains of C. psittaci which produce a diverse disease spectrum in animals, e.g., conjunctivitis, air sacculitis, pericarditis, hepatitis, meningoencephalitis, enteritis, urethritis, arthritis, and endometritis with abortion. G.I. infection results in enteric shedding of the organism. Latency - Well recognized feature of Chlamydia infection, i.e., the organism can cause inapparent infection or fulminant infection in the same host. In clinically healthy birds, stress can precipitate clinical signs and shedding of the organism.

• DISEASE IN MAN:

Asymptomatic or clinical disease after 1-2 week incubation period. Fever, chills, myalgia, anorexia, headache, nonproductive cough. Pneumonitis or atypical pneumonia may be present. May see a toxic or septic form with hepatosplenomegaly, hepatitis, meningoencephalitis and cardiac involvement with endocarditis. Ovine chlamydial infection in pregnant women is life-threatening, causing late abortion and neonatal death and disseminated intravascular coagulation in the mother.

• DIAGNOSIS:

fecal culture (rarely successful) serology (CF, IFA) [Note: African Grey Parrot, cockatiel, and budgie may remain serologically negative despite active infection.] ELISA-based tests for antigen in feces has proven reliable.

• TREATMENT:

Tetracycline or Erythromycin.

• PREVENTION/CONTROL:

Treatment with tetracycline Introduce birds into colony from psittacosis-free flocks or use chlortetracycline chemoprophylaxis. Protective clothing (masks, gowns, gloves). Wild caught birds should be placed on chlortetracycline during quarantine. In sheep, keep flocks closed or vaccinate annually. Isolate aborting ewes until discharges cease.

BLASTOMYCOSIS

SYNONYMS: North American blastomycosis, Chicago disease, Gilchrist's disease.

• ETIOLOGY:

Blastomyces dermatitidis, a dimorphic fungus existing in mycelial form in cultures and as a budding yeast in the tissues of infected mammals.

• GEOGRAPHIC DISTRIBUTION:

The disease has been observed in the United States, eastern Canada, Zaire, Tanzania, South Africa, and Tunisia. Autochthonous cases may have occurred in some Latin American countries.

• THE DISEASE IN MAN:

The incubation period is not well known; it possibly extends to several weeks or months. Blastomycosis is a chronic disease that principally affects the lungs. The respiratory symptomatology initially resembles influenzas purulent or bloody expectoration, weight loss, and cachexia, in addition to fever and cough, may develop later. If the infection remains localized, it can become asymptomatic. When it disseminates, it can cause subcutaneous abscesses as well as localized infections in several organs. Death frequently results in cases of untreated disseminated infection. The cutaneous form is commonly secondary to the pulmo-nary and is characterized by an irregular-shaped, scabby ulcer that has raised borders and contains minute abscesses. Lesions develop on exposed parts of the body.

• THE DISEASE IN ANIMALS:

The highest incidence is observed in dogs around 2 years of age. The symptoms consist of weight loss, chronic cough, dyspnea, cutaneous abscesses, fever, anorexia, and sometimes blindness. The lesions localize in the lungs, lymph nodes, eyes, skin, and joints and bones. Of 47 clinical cases recently described, 72% occurred in large males. There were lesions of the respiratory tract in 85% of the cases.

• SOURCE OF INFECTION AND MODE OF TRANSMISSION:

The reservoir is environmental, probably the soil, but the ecologic biotope has not been determined. Transmission to man and to animals is effected by aerosols; the fungal conidia are the infecting element. Persons at highest risk are those having the most contact with the soil. Dogs most frequently infected are sporting and hunting breeds.

• ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:

None. It is a disease common to man and animals. Cases of transmission from individual to individual (man or animal) are not known.

• DIAGNOSIS:

Diagnosis is based on direct microscopic examination of sputum and material from lesions, on isolation of the agent in culture media, and on examination of histologic preparations. B. dermatitidis grows well in Sabouraud's culture medium or other adequate median it is most distinctive in its sprouting yeast form, and therefore the inoculated medium should be incubated at 37oC, since at ambient temperature the mycelial form of the fungus is obtained. B. dermatitidis in its yeast form (in tissues or cultures at 37oC) is characterized by a single bud attached to the parent cell by a wide base, from which it detaches when it has reached a size similar to the parent cell. In contrast, Paracoccidioides brasiliensis, the agent of paracoccidioidomycosis ("South American blastomycosis"), has multiple buds in the yeast phase. Serologic tests in use are complement fixation and gel immunodiffusion; the latter gives better results. It should be borne in mind that cross-reactions with Histoplasma and Coccidioides may occur. At present, the intradermal test is considered to have no diagnostic value.

• TREATMENT:

Humans. Itraconazole, 100-200 mg/d orally, is now the therapy of choice for nonmeningeal disease, with a response rate of over 70%. Amphotericin B is given for treatment failures or cases with central nervous system involvement. Follow-up for relapse should be regularly made for several years so that therapy may be resumed or another drug instituted. Animals. Rare primary cutaneous disease may persist for months; these lesions should be removed surgically since blastomycosis responds poorly to therapy. Amphotericin B is considered the drug of choice, but treatment is of little avail once the disease is disseminated. The combination of amphotericin B and ketoconazole has been suggested to reduce the rate of relapse.

• CONTROL:

As long as the ecologic biotope remains poorly defined, practical prevention methods cannot be established.

CAT SCRATCH DISEASE

(Cat Scratch Fever, Benign Lymphoreticulosis, Benign nonbacterial Lymphadenitis, Bacillary Angiomatosis, Bacillary Peliosis Hepatis)

• AGENT:

Controversial, it is not currently possible to definitively name the causative agent responsible for CSD. Felt to be either Afipia felis, a gram-negative rod or Rochalimaea henselae and Rochalimaea quintana. Both are members of class Proteobacteria and both are intracellular parasitic bacteria.

• RESERVOIR AND INCIDENCE

Associated with domestic cats throughout the USA, and worldwide. Over 6000 cases annually. Seen more often in men than in women . Have seen clusters of infection within families within a 2 to 3 week period, suggesting that shedding by cats may occur periodically. Other sources of infection have included scratches from other species including dogs, squirrels, and goats and from wounds induced by crab claws, barbed wire, and plant material.

• TRANSMISSION:

90% of patients have been exposed to a cat. 75% of these have been bitten, scratched, or licked. Most affected individuals are <20 years of age. 75-80% of the cases of CSD are diagnosed between September and February with a peak incidence in December. 4 to 6% of the general population and 20% of veterinarians have positive skin test reactions to CSD antigen.

• DISEASE IN ANIMALS:

Subclinical

• DISEASE IN MAN:

Different distinct syndromes exist:

Typical CSD A primary lesion, most common on neck or extremities, will develop in 50% of the cases and appear approximately 10 days after a bite or scratch. A pustule persists for 1-2 weeks. 10-14 days after the lesion appears, lymphadenopathy develops and usually regresses within 6 weeks. 30-50% of the enlarged nodes become suppurative. Of the approximately 65% who develop systemic illness, fever and malaise are the symptoms most often noted. The disease is usually benign and most patients recover spontaneously without sequelae within 2-4 months. Many unrecognized cases probably occur. Disease appears to confer lifelong immunity.

Atypical CSD The atypical forms of CSD, which constitute 11% of all cases, are extremely varied. The most common, representing 6% of all cases, is Parinaud's oculoglandular syndrome (POGS), or granulomatous conjunctivitis with preauricular adenopathy. Other, atypical presentations include tonsillitis, encephalitis, cerebral arteritis, transverse myelitis, radiculitis, granulomatous hepatitis and/or splenitis, osteolysis, atypical pneumonia, hilar adenopathy, pleural effusion, erythema nodosum, erythema annulare, maculopapular rash, thrombocytopenic purpura, and breast tumor. Bacillary Angiomatosis Dermal BA presents in several ways. The commonest form is an enlarging red papule with some resemblance to a cranberry, often with a collarette of scale and sometimes with a suggestion of surrounding erythema. This type of lesion may be mistaken for pyogenic granuloma, unless fairly deep biopsy specimens are examined. These lesions begin as small papules and enlarge, occasionally becoming several centimeters in diameter and rarely ulcerating. They may be single or quite numerous. Another form of dermal BA is a deeper, subcutaneous nodule that appears flesh-colored and may be either fixed to subcutaneous tissues or freely mobile. Rarely BA may present as a dermal plaque. BA has been reported to occur in every organ system, including the brain, and is often difficult to differentiate from mycobacterial and fungal infections or malignancy without the use of biopsy. It is unclear if the personality changes, ranging from frank psychosis to depression, that have been described in association with BA represent CNS involvement or a neurotoxic product of this infection. Bacillary Peliosis Hepatis BPH, a vasoproliferative condition involving the liver of HIV-infected patients, is characterized by a proliferation of cystic blood-filled spaces surrounded by fibromyxoid stroma in which one can see bacteria similar to those seen in BA. Clinically these patients may or may not have visible bacillary angiomas. Their symptoms usually include fever, weight loss, and abdominal pain or fullness. Physical exam may reveal organomegaly. Studies usually demonstrate elevation of alkaline phosphatase and ç-glutamyltransferase levels out of proportion to those of aminotransferase and bilirubin.

• DIAGNOSIS:

The sedimentation rate is elevated, the white blood cell count normal, and the pus from the nodes is sterile. ID skin testing with antigen prepared from the pus is positive. Excisional biopsy, usually performed to exclude lymphoma, confirms the diagnosis.

• TREATMENT:

For CSD: Rifampin, ciprofloxacin, gentamycin, and trimethoprim-sulfa. Aspiration of suppurating nodes is recommended for relief of pain. Symptoms resolve without treatment in 2-4 months. BA and BPH respond to erythromycin, rifampin, or doxycycline. Therapy must be continue for 4-6 weeks to avoid relapse.

• PREVENTION/CONTROL:

Education. Wash hands after handling cat. Wash cuts and scratches promptly and don't allow cat to lick open wound.

RICKETTSIAL DISEASES

Q-FEVER

(Query fever, Balkan influenza, Balkan grippe, pneumorickettsiosis, abattoir fever)

• AGENT:

Coxiella burnetii Multiplies only in living cells. Stains red with Gimenez & Macchiavello stains and purple with Giemsa. Infections in lab workers have been recognized for many years. Serious hazard in research facilities where infected "asymptomatic" ewes are used for projects.

• RESERVOIR AND INCIDENCE

Found worldwide in wild and domestic animals in two self perpetuating cycles: 1. Wild animals, with numerous tick hosts 2. Domestic animals - sheep, goats, cattle. Widespread in sheep in the U.S. Dogs, cats, and chickens can also be infected. Enzootic infection among domestic animals is the main reservoir of infection for humans.

• TRANSMISSION:

Organism shed in urine, feces, milk, and especially birth products of domestic ungulates that generally do not show clinical disease (usually sheep and goats). Organism is resistant to drying and can persist for months while providing extensive environmental contamination. Aerosol is a major means of transmission. Contact with infected tissues: placenta of the infected ewe contains 109 organisms per gram of tissue. Amniotic and fetal tissues are highly infective. Soiled linen may infect personnel in the laundry. One organism is considered to be enough to cause infection in humans. Ingestion.

• DISEASE IN MAN:

Two weeks to one month incubation. Febrile illness or subacute endocarditis. No skin eruption or rash, which distinguishes it from other Rickettsial species infections. Severe frontal headache with retro-orbital pain, profuse sweating, myalgia, and nausea. Pulmonary involvement in half the cases. Asymptomatic in many cases. Most cases resolve in two weeks but may be protracted or relapsing in the elderly. Chronic endocarditis, particularly in persons with preexisting valvular disease, is difficult to treat and the case fatality rate may be as high as 60%.

• DIAGNOSIS:

Leukopenia with a diagnostic rise in specific CF antibodies to Coxiella phase 2. The Weil-Felix test (a test specific for typhus and other rickettsial diseases) is negative. Liver function tests are often abnormal. In Q fever endocarditis, there is a titer of 1:200 or more by CF or IFA with phase 1 antigen. Isolation of the organism from blood or sputum is rarely attempted due to zoonotic concerns.

• TREATMENT:

Treatment with tetracyclines can suppress symptoms and shorten the clinical course but does not always eradicate the infection. Even in untreated patients, the mortality rate is usually low, except with endocarditis. Treatment of endocarditis consists of protracted (often for years) of antibiotic therapy; valves often need replacement.

• PREVENTION/CONTROL:

Use male or nonpregnant female sheep for research, when possible. Q-Fever free sheep - limited practicality because requires intense surveillance program and frequent testing. Also, serologic status is not a useful indicator of whether the animal is shedding virus. Personnel education and control. Physical separation of infected animals from humans are current methods ofcontrol. Restrictions on movement of animals within thefacility (with considerations of air handling). Label all potentially infected material and sterilize or disinfect it. Protective clothing, masks, gloves, & shoe covers. Intensive medical surveillance and health education program. Treatment of acute disease in humans with tetracycline. Experimental vaccine for sheep has shown promise. Delayed hypersensitivity skin test is available for high risk personnel.

• SUITABLE DISINFECTANTS FOR Q-FEVER:

1:100 dilution of chlorine bleach containing 5-25% hypochlorite. 5% hydrogen peroxide. 1:100 Lysol.

EHRLICHIOSIS

(Tick-borne fever)

• AGENT:

an intraleukocytic rickettsia, E. canis (many species of Ehrlichia exist. Previously only E. sennetsu was known to infect man). Occurs intracytoplasmically, singly or in compact clusters (morulae) in circulating leukocytes.

• RESERVOIR AND INCIDENCE

First recognized in dogs in 1935. Epizootic occurred in military working dogs in Vietnam 1968-1970. Now known to have worldwide distribution. 11 to 58% of dogs in U.S. are serologically positive. First reported case of E. canis in man in 1987. Several cases since then.

• TRANSMISSION:

tick vector, Rhipicephalus sanguineus, Brown Dog Tick. It is presumably transmitted to humans by tick bite.

• DISEASE IN DOGS:

Incubation period 10 to 14 days. Fever, lymphadenopathy, edema of legs and scrotum, epistaxis. Acute disease followed by a subclinical carrier stage.

• DISEASE IN MAN:

similar to Rocky mountain spotted fever, but no rash. 12 to 14 day incubation period and prodrome consisting of malaise, back pain and nausea, the patient develops sudden fever, bradycardia, and headache. Leukopenia and absolute lymphopenia as well as thrombocytopenia occur frequently.

• DIAGNOSIS:

Not easy to identify in peripheral blood smears but can attempt to identify organisms in leukocytes. An IFA assay that may be used to diagnose infection is available thru CDC and requires acute and convalescent sera.

• TREATMENT:

Tetracycline

• PREVENTION/CONTROL:

Control ticks

ROCKY MOUNTAIN SPOTTED FEVER

(American Tick Typhus, Tick-borne Typhus Fever)

• AGENT:

Rickettsia rickettsii.

• RESERVOIR AND INCIDENCE

Dogs, wild rodents and rabbits. Reported from most of continental U.S., highest incidence in S. Atlantic and South Central States. 2/3 of human cases are reported in children.

• TRANSMISSION:

Ixodid ticks (especially Dermacentor) or their host species. Most rickettsias are obligate intracellular parasites of the gut cells of invertebrates and can only survive briefly outside living cells. Crushed ticks or mites and their feces may infect through broken skin. Transmission from tick bite occurs only after several hours of attachment.

• DISEASE IN ANIMALS:

Subclinical only.

• DISEASE IN MAN:

Fever has a sudden onset, with chills, headache, severe muscle pains, photophobia and meningism for four weeks. A red, morbilliform rash develops within 3-5 days of onset of fever and with hemorrhages spreading on limbs. Enlarged liver and spleen, myocarditis, renal tubular necrosis and bronchopneumonia occur. Damage to endothelial cells of blood vessels by invasion of rickettsias causes thrombi and hemorrhages. Focal liver necrosis, hemorrhages in genitalis and gangrene of the scrotum may occur. The case fatality rate in untreated cases is 15-20%, but with prompt treatment is about 5%.

• DIAGNOSIS:

Rickettsiae can sometimes be isolated in special laboratories from blood obtained in the first few days of illness. A rise in antibody titer during the second week of illness can be detected by specific CF, IFA, and microhemagglutination tests or by the Weil-Felix test. Antibody response may be suppressed if antimicrobial drugs are given very early.

• TREATMENT/PREVENTION/CONTROL:

Treatment of human disease with tetracycline or chloramphenicol. Control ticks on newly arrived animals.

RICKETTSIALPOX

(Vesicular Rickettsiosis, Kew Gardens Spotted Fever)

• AGENT:

R. akari

• RESERVOIR AND INCIDENCE

House mouse is reservoir host; most commonly seen in rodent infested urban dwellings ie New York City and other Eastern U.S. cities. Rats and moles can also harbor the organism. Not identified as a natural disease in domestic rodents.

• TRANSMISSION:

Mite, Allodermanyssus sanguineus, transmits to mice or to man. Lab infections in humans via respiratory route have occurred but lab infections due to mite bite have not been reported.

• DISEASE IN ANIMALS:

Not known in wild animals. In experimental mice death follows pneumonia.

• DISEASE IN MAN:

Illness lasting about a week is associated with an eschar which develops at the site of the mite bite, regional lymphadenopathy and fever. A vesicular rash over the body and limbs develops within 1-4 days.

• DIAGNOSIS:

Leukopenia and a rise in antibody titer with rickettsial antigen in CF tests. However, the Weil-Felix test is negative.

• TREATMENT:

Tetracycline

• PREVENTION/CONTROL:

Eliminate wild mice from animal facilities Control mites.

MURINE TYPHUS

(Flea-borne Typhus Fever, Endemic Typhus Fever, Urban Typhus)

• AGENT:

Rickettsia typhi

• RESERVOIR AND INCIDENCE

natural pathogen of rats and mice. Other mammals including cats, and their ectoparasites have been found infected. Outbreaks continue to occur in U.S., especially Texas. Natural lab infections have not been reported but lab acquired infections in people handling experimentally infected mice have been documented.

• TRANSMISSION:

transmitted by flea or lice (Xenopsylla cheopis, Nosopsyllus fasciatus) to rodents or man. Humans are infected by contamination of flea bites, broken skin or conjunctiva by flea feces. Domestic animals may transport the flea vector to humans. Inhalation of contaminated dust may be a route of infection.

• DISEASE IN ANIMALS:

The agent localizes in the brain and various organs but with no known lesions.

• DISEASE IN MAN:

There is a gradual onset of fever with severe headache, rigors, generalized pains and dry cough (sometimes developing to bronchopneumonia) of about 2 weeks. A macular rash appears by about 5 days, first appearing on the trunk and lasting about six days. CNS manifestations are possible. Damage is caused to vascular endothelia by invasion of rickettsia, possibly leading to thrombosis and hemorrhage. In untreated case, the case fatality rate is 1-2%.

• DIAGNOSIS:

CF or IFA.

• TREATMENT:

Tetracycline or chloramphenicol.

• PREVENTION/CONTROL:

control wild rodents. In endemic areas control fleas while exterminating rats.

FUNGAL INFECTIONS

DERMATOMYCOSES

(Ringworm, Dermatophytosis, Tinea, Trichophytosis, Microsporosis, Jock Itch, Athlete's Foot)

• AGENT:

Organisms are subclassified into: 1. Geophilic - inhabit soil 2. Zoophilic - parasitic on animals 3. Anthropophilic - Primarily infects humans All can produce disease in humans. Grouped in three genera 1. Microsporum 2. Trichophyton 3. Epidermophyton

• RESERVOIR AND INCIDENCE

Fungal spores remain viable for long periods on carrier animals and fomites. Exposure to reservoir hosts harboring different dermatophytes determines the type and incidence of infection in humans. Microsporum canis can be carried by up to 89% of nonsymptomatic cats. Up to 50% of people exposed to infected cats, both symptomatic and asymptomatic, have acquired infection. Pets may also acquire disease from humans. **T. mentagrophytes is most commonly transmitted to man from rodents, M. canis from dogs and cats, and T. verrucosum from cattle and horses.

• TRANSMISSION:

Direct or indirect contact with asymptomatic animals or with skin lesions of infected animals Contaminated bedding Equipment Fungi in air, dust, or on surfaces of room (spores persist on contaminated surfaces)

• DISEASE IN ANIMALS:

In rodents is often asymptomatic and not recognized until people are affected. In cats is often asymptomatic. Dogs often show classic skin lesions. Varying severity of dermatitis occurs with local loss of hair. Deeper invasion produces a mild inflammatory reaction which increases in severity with the development of hypersensitivity.

• DISEASE IN MAN:

Often mild, self limiting; scaling, redness, and occasionally vesicles or fissures. Thickening & discoloring of nails. May show circular lesions which clear in the center forming a ring. Fungal infections in man are categorized as to the location on the body: 1. Tinea capitis - Scalp & hair 2. Tinea corporis - Body (extremities, arm and hand, are most often affected in infections acquired from lab animals.) 3. Tinea pedis - foot 4. Tinea unguium - Nails

• DIAGNOSIS:

KOH mount of skin scrapings, Fungal culture

• TREATMENT:

Macerated (moist softening and fissuring) stage- aluminum subacetate ("Domeboro") solution soaks with potassium permanganate for secondary infections. Athlete's feet may respond better to 30% aqueous aluminum chloride or the carbol-fuchsin paint than to antifungal agents. Broad spectrum antifungal creams and solutions containing imidazoles or ciclopirox) instead of tolnaftate and haloprogin help to combat diphtheroids and other gram-positive organisms present at this stage and alone may be adequate therapy. Dry and scaly stage- several topical creams, liquids, or lotions are recommended (miconazole, clotrimazole, ketoconazole, econazole, sulconazole, oxiconazole, ciclopirox or naftifine. Betamethasone dipropionate with clotrimazole is recommended for acutely inflamed tinea lesions. For severe cutaneous infections, griseofulvin or ketoconazole is recommended.

• PREVENTION/CONTROL:

Screen newly received animals. Routine sanitization of contaminated environment, equipment, and caging. Gloves, protective clothing, wash hands after exposure.

---

SPOROTRICHOSIS

• AGENT:

Sporothrix schenckii, dimorphic fungus

• RESERVOIR AND INCIDENCE

distributed worldwide with sporadic outbreaks. Saprophyte that grows on soil or vegetation. Has been reported in horses, dogs, cats and many other species. 19 cases of Sporotrichosis have been reported in man following contact with feline abscesses or ulcers (12 of these were veterinarians).

• TRANSMISSION:

Penetrating injury, or contact with plant or soil. Transmission from feline to man by direct contact with lesions (penetrating injury NOT required). Inhalation can lead to pulmonic disease.

• DISEASE IN ANIMALS:

Lesions can be anywhere but are usually located on distal extremities, head, or base of tail. Appear as draining puncture wounds, cellulitis. Can ulcerate and become nodular with seropurulent exudate. May cavitate and expose muscle and bone. May lead to disseminated disease which is usually fatal

• DISEASE IN MAN:

The most common clinical form is cutaneolymphatic; it begins with a nodule or pustule at the point where broken skin allowed inoculation. The infection may remain confined or may eventually spread and produce SC nodules along the enlarged lymph ducts. These nodules may ulcerate, and a gray or yellowish pus appears. Disseminated forms, which are rare, may give rise to localizations in different organs, especially the bones and joints, as well as in the mouth, nose, kidneys, or the SC tissue. Pulmonary sporotrichosis can be confused with TB.

• DIAGNOSIS::

Biopsy and histo fungal culture cytology of impression smear of exudate. Organisms are numerous in cats but are difficult to detect in man, horses, and dogs. Organism can also be found in feces of infected cat. Antigen tests are used to diagnose disseminated disease.

• TREATMENT:

Potassium iodide, Amphotericin B, or itraconazole.

• PREVENTION/CONTROL:

Gloves when handling infected animals. Wash with iodine or chlorhexidine.

---

CRYPTOCOCCOSIS AND HISTOPLASMOSIS

Cryptococcosis and histoplasmosis are systemic fungal infections caused by the organisms Cryptococcus neoformans and Histoplasma capsulatum. Cases of infection are worldwide and sporadic. These organisms are found in soil, pigeons, and starlings and are spread in bird feces. These systemic fungi have a predilection for the lung and central nervous system. There is an increased susceptibility in humans on steroid therapy and with disorders of the reticuloendothelial system.

VIRAL DISEASES

Pox Viruses -Many poxvirus infections of lab animals are also pathogenic for humans. Humans usually exhibit proliferative cutaneous or subcutaneous self-limiting lesions. Occasionally see systemic disease, particularly when diseases of NHP's involved.

---

CONTAGIOUS ECTHYMA

(Orf, Contagious pustular dermatitis, Contagious Pustular Stomatitis, Ecthyma Contagiosum)

• AGENT:

Genus Parapoxvirus of Family Poxviridae.

• RESERVOIR AND INCIDENCE

- Sheep and goats worldwide.

• TRANSMISSION:

- crusted areas on muzzle, eyelids, oral cavity, feet, or external genitalia are laden with virus. Transmitted easily from animals to man by contact. The virus is highly resistant to adverse environments and persists for many years.

• DISEASE IN ANIMALS:

necrosis in the skin and mucous membranes of the gastrointestinal and urogenital tracts. Intense pain can interfere with eating.

• DISEASE IN MAN:

Large painful nodules usually distributed on the hands. Weeping red surfaces. These resolve with minimum scarring 1-2 months later.

• DIAGNOSIS:

Diagnosis is made by a history of contact with sheep, goats, or wild ungulates; by EM demonstration of the poxvirus in the lesion; cell culture; or serologically.

• PREVENTION/CONTROL:

Wear rubber gloves when handling infected sheep and when working in an environment near infected sheep.

---

MONKEY POX

• AGENT:

Orthopoxvirus Disease in humans is indistinguishable from smallpox, (Variola) i.e., serologic & clinical syndrome.

• RESERVOIR AND INCIDENCE

Animals: Nine reported outbreaks in captive NHP's, primarily rhesus and cynomolgus. Has also been reported in languors, baboons, chimpanzees, orangutans, marmosets, gorillas, gibbons, and squirrel monkeys. The virus has been isolated from a wild squirrel. Man: The first human case of Monkey Pox was reported in 1970. Between 1970 and 1986, over 400 cases had been reported from tropical rain forested areas of West and Central Africa.

• TRANSMISSION:

Transmission can be via direct contact, aerosol, ingestion, or parenteral administration. Person to person transmission can occur.

• DISEASE IN NONHUMAN PRIMATES:

Usually exhibit a high morbidity and low mortality. Clinical signs may be inapparent or an animal may exhibit fever, lymphadenopathy, and cutaneous eruptions of the extremities, trunk, lips, or face. Cynos seem to be most severely affected. Death is uncommon except in infant monkeys.

• DISEASE IN MAN:

Signs in man include fever, sore throat, headache, and a vesiculopustular rash of peripheral distribution which clears up in 5 to 25 days. Severe complications include bronchopneumonia, vomiting, and diarrhea. Case fatality rate 10-15%. Although the disease is not common in man it is important from the standpoint of differentiating it from smallpox.

• DIAGNOSIS:

based on progression of lesions, histopathology and virus isolation. On histological examination epidermal cells contain eosinophilic cytoplasmic and intranuclear inclusions. ELISA

• TREATMENT:

Symptomatic.

• PREVENTION/CONTROL:

Sanitation, isolation. Vaccination with vaccinia virus is protective in both man and nonhuman primates.

---

YABAPOX

• AGENT:

Poxvirus

• RESERVOIR AND INCIDENCE

Affects mangabeys, rhesus, cynos, vervets, stumptails, and patas monkeys. Latent infection in African species that can infect Asian primates and U.S. born African primates.

• TRANSMISSION:

Need further clarification of the epidemiology of this disease. Role of insect vectors has not been determined. Aerosol transmission has been proven experimentally. *Transmission to humans from monkeys has not been recorded. The virus can affect man usually after accidental skin puncture.

• DISEASE IN NONHUMAN PRIMATES:

Subcutaneous benign tumors (Histiocytomas) that may reach several cm. in diameter. They usually regress spontaneously in 3 to 6 weeks.

• DISEASE IN MAN:

Lesions similar to those seen in monkeys

• PREVENTION/CONTROL:

Usual care should be exercised by animal handlers, including wearing of protective clothing.

---

TANAPOX

(Benign Epidermal Monkeypox, BEMP)

• AGENT:

Tanapox virus.

• RESERVOIR AND INCIDENCE

Monkeys. In 1966 23 human cases were reported in the U.S. among personnel who worked with monkeys affected at 3 primate centers. A serologic study carried out on 263 monkeys of Asian origin (Macaca) revealed a 15% rate; in 55 African Green Monkeys, the rate was 76%.

• TRANSMISSION:

Aerosols or vectors. Human cases have resulted from contamination of abrasions or scratches.

• DISEASE IN NONHUMAN PRIMATES:

Lesions occur primarily on the face, consisting of raised areas with a central scab. Papules ulcerate, scab and heal.

• DISEASE IN HUMANS:

There is a fever for a few days, with headache and prostration and a single skin vesicle. Cytoplasmic inclusions are seen in skin lesions. Within 3 weeks of onset, the lesion spontaneously regresses.

• DIAGNOSIS:

EM of skin scrapings or viral isolation.

• TREATMENT:

Symptomatic.

• PREVENTION/CONTROL:

Mosquito control. Asian and African monkeys should be housed separately. Wear protective clothes.

---

HERPESVIRUSES

There are more than 35 Herpesviruses of NHPs most of which are NOT zoonotic.

---

HERPES B

(Herpesvirus simiae, Simian B Disease)

• AGENT:

Double-stranded DNA Virus. Direct zoonosis. For each Herpesvirus there exists a host for which the virus is almost uniformly fatal and reservoir hosts in which the virus exists in subclinical or latent infection. a. H. suis latent in swine, fatal in cattle. b. H. simplex I latent in man, fatal in Aotus, Gibbon, Marmoset (especially). c. H. saimiri I latent in Saimiri sciureus, fatal in Marmosets, Aotus (also known as Herpes T, Herpes M, Herpes Tamarinus). d. H. saimiri II latent in Saimiri sciureus, fatal in Marmosets, Aotus (this is an oncogenic virus, causing Malignant Melanoma of Reticulum Cell Type). e. H. simiae latent in rhesus and other macaques, fatal in man (also known as Herpes B Virus). f. Liverpool Vervet Monkey Virus: reservoir host ???, fatal in Cercopithecus aethiops. The Herpesviruses are serologically distinct but do share some antigenic properties. Herpes B Virus has been shown to have some antigenic relationship to Herpesvirus simplex by serum neutralization tests. However, antibody from Herpesvirus simplex does not confer immunity to Herpes B Virus.

• RESERVOIR AND INCIDENCE

Incidence of infection of the reservoir host is normally high but you rarely see clinical disease. Clinical disease is usually confined to the very young or to the immunologically compromised. On occasion lethal infection occurs in the reservoir host: in humans, generalized Herpes simplex is often fatal in infants; in swine, Herpes suis is fatal in piglets. Natural infection does not result in elimination of the virus or in immunity but produces a latent infection or carrier, which always makes vaccination of reservoirs impractical. Herpesvirus B was first described in 1934 by Sabin/Wright. The virus was recovered from a laboratory worker who had been bitten 18 days previously by an apparently healthy rhesus. Since 1934, there have been 24 reported cases, all fatal, except four. Of the four, only one is reasonably free of severe neurological deficits. (Patients have remained in coma for as long as 40 months prior to succumbing to the disease.) Incubation is considered to be 10-20 days from exposure to the virus; however, in the Pensacola cases, clinical disease occurred within 4-5 days of exposure. Contact with macaques does not constitute exposure. The susceptibility of man to clinical B infection is low although mortality is high.

• TRANSMISSION:

direct contact, including sexual transmission, aerosols, and fomites.

• THE DISEASE IN NHP:

The reservoir hosts for Herpesvirus simiae are monkeys of the genus Macaca. Monkeys incriminated include M. mulatta (rhesus), M. fascicularis (cyno), M. fuscata (Japanese macaque), and M. arctoides (Stump-tail macaque). B virus may produce mild cold-sore type lesions, primarily at mucocutaneous junctions, mucous membranes, and tongue. But, it has been demonstrated that infection is not confined to the mouth but can also be found in the genitalia. These lesions are similar to those caused by Herpesvirus simplex I in man. Two factors have been associated with antibody increases with age; 80-100% of imported adult rhesus may have antibody compared to 20% imported juveniles. The second factor was type of caging. Animals housed together had significantly higher titers than individually-caged animals. Clinical disease may develop at the time of primary infection but it is not known if lesions invariably follow infection. However, periodic shedding of the virus may occur without the presence of visible lesions. Once a monkey is infected with B Virus, it should be considered infective for life.

• THE DISEASE IN MAN:

Human infection is characterized by encephalitis with diplopia; nystagmus, patch paresthesia of head, neck and upper extremities. Acute abdominal pain, fever and diarrhea have also been observed prior to neurologic symptoms. Patients may also have a vesicular rash and/or keratoconjunctivitis. The histopathological changes resemble those of fatal, systemic Herpesvirus simplex in infants: encephalitis, myelitis and foci of necrosis in liver, spleen, lymph nodes and adrenals. The case fatality rate is 70%.

• DIAGNOSIS:

ELISA and viral isolation.

• TREATMENT:

acyclovir.

• PREVENTION/CONTROL:

Control includes personal hygiene, protective clothing and common sense in handling monkeys. The virus is susceptible to oxidizing agents, soap, and water. Guidelines for prevention and treatment have been developed. The reader is referred to the reference by Holmes, GP, et al for further details. Emphasis can not be too strong concerning the use of protective clothing when entering a room with macaques. A perfectly healthy monkey may be lethal to you.

---

Arthropod borne ARBOVIRUSES:

GENERAL: In most man is an accidental host infected when arthropods feed on him. Therefore quarantine of wild caught animals and elimination of ectoparasites should prevent: Examples: TICK BORNE viruses: 1. Russian-Spring-Summer Encephalitis 2. Louping Ill MOSQUITO BORNE viruses, ie 1. DENGUE (Breakbone Fever, Dengue Hemorrhagic Fever)

• AGENT:

Flavivirus, Flavidviridae RESERVOIR: nonhuman primates, occurs in Asia, Africa, Australia, the Caribbean including Puerto Rico, the Pacific Islands, S. Europe, S. America

• TRANSMISSION:

mosquito vector (Aedes)

• DISEASE IN NONHUMAN PRIMATES:

subclinical DISEASE IN HUMANS: The first phase of illness is usually mild fever, headache, myalgia, lymphadenitis, pharyngitis, rhinitis and cough lasting 1-5 days and is followed by 1-2 days of remission. The second peak of fever is accompanied by a morbilliform maculopapular rash. Severe hemorrhagic manifestations occur during the second phase especially in children.

• DIAGNOSIS:

> HI, CF, ELISA, or virus isolation. TREATMENT: Treat shock by expanding circulating blood volume. Acetaminophen given for discomfort. Prolonged convalescence.

• PREVENTION/CONTROL:

Mosquito control by screening and insect repellents. Examples:

1. EQUINE ENCEPHALITIDES (EASTERN, WESTERN, AND VENEZUELAN). These are diseases of horses, mules, birds, humans, and other animals caused by the neurotropic viruses, Alphavirus and Flavivirus. Wild birds serve as a reservoir, and the virus requires an arthropod vector to transfer from reservoir host to other susceptible species. Mosquitoes, chicken mites and lice, ticks, and any other bloodsucking insects can serve as vectors. This group of encephalitis viruses is unique to the New World. Prevention is accomplished by adequate vector control and vaccination of horses. Pigeons, chickens, pheasants, prairie chickens, ducks, and geese are susceptible and, if infected when suitable vectors are present, may pose a potential source of disease for humans. There is a high mortality in humans infected with these viruses.
2. CRIMEAN CONGO HEMORRHAGIC FEVER. Nairovirus, Bunyaviridae family. Causes epidemics in Bulgaria, USSR, and sporadic cases in Iraq, Pakistan and East Africa. Associated with tick bites, primarily Hyalomma genus. Also nosocomial outbreaks among hospital personnel.
3. OMSK HEMORRHAGIC FEVER (rodents)
4. KYASANUR FOREST DISEASE (monkeys) Togaviridae occurs in bonnet macaques, languors, and rodents in India spread by ticks lab workers in the US affected while working with infected primates (no vector) NHP exhibit fever, vomiting, diarrhea, epistaxis, and death. In humans, there is a sudden onset of fever which may be biphasic, with headache, generalized pains, prostration, conjunctivitis, diarrhea, and vomiting. Vesicles occur on the soft palate. Hemorrhagic manifestations may follow. Case fatality rate is 2-50%. Diagnosed thru serology or viral isolation. Treatment is supportive. Convalescent plasma with a high neutralizing antibody titer has been reported to be useful. Prevention is thru tick control.
5. CHIKUNGUNYA: Maintained by vervets and baboons in Southern Africa. Transmitted by biting flies and mosquitoes
6. RIFT VALLEY FEVER (Enzootic Hepatitis)

• AGENT:

Phlebovirus, Bunyaviridae

• RESERVOIR AND INCIDENCE

endemic in Africa and Egypt. Affects nonhuman primates, and man. Cattle, bats, and sheep may be reservoir hosts.

• TRANSMISSION:

mosquito vector highly contagious among laboratory workers where transmission does not require vector.

• DISEASE IN ANIMALS:

Rapid death after fever occurs in lambs. In cattle abortion and diarrhea occur. Liver lesions predominate histologically, with areas of necrosis. Widespread hemorrhages occur.

• DISEASE IN MAN:

Fever (which may be biphasic) has a sudden onset, with severe headache, muscle and joint pains and photophobia. In a small proportion of cases there are hemorrhages, liver necrosis, encephalitis and retinitis.

• DIAGNOSIS:

Serology and virus isolation.

• PREVENTION/CONTROL:

Control mosquitos. Precaution in handling necropsy specimens. Arbovirus where the natural cycle of transmission DOES involve man:

---

ST. LOUIS ENCEPHALITIS

SYNONYMS: Type C lethargic encephalitis.

• ETIOLOGY:

RNA virus belonging to the genus Flavivirus (formerly group B of the arboviruses) of the family Togaviridae; forms part of the virus complex including Murray Valley, West Nile, and Japanese B encephalitides. There are indications that strains of the virus isolated in different zones differ in their capacity to produce viremia in birds, virulence in 3-week-old mice, and neurovirulence in rhesus monkeys. By the technique of nucleotide mapping, considerable genetic variation among the strains of the virus was demonstrated, and it was proposed to name these geographic variants as topotypes.

• GEOGRAPHIC DISTRIBUTION

The agent is distributed from Argentina to Canada. The disease is unknown outside the Americas.

• THE DISEASE IN MAN:

The clinical infection presents a wide spectrum, from an undifferentiated febrile disease similar to influenza to severe encephalitis. Three syndromes can be distinguished: febrile disease, aseptic meningitis, and encephalitis. The febrile syndrome usually has a benign course, with fever and intense cephalalgia lasting several days, followed by complete recovery. The aseptic meningitis has a sudden onset, with fever, stiffness of the neck, and positive Kemig and Brudzinski signs, but without neurologic dysfunction. Pleocytosis is common. The disease characterized by encephalitis also begins suddenly, with fever and one or more signs of brain inflammation, such as personality changes, confusion. delirium, lethargy, paresis, convulsions, and others. The encephalitis syndrome is more frequent in elderly persons; its frequency increases from 56% in patients up to 20 years old to 87% in those over 60. Convalescence in these cases lasts several weeks. The incubation period is estimated at 4 to 21 days. In the United States, the case fatality rate in 2,261 confirmed clinical cases between 1955 and 1968 was 5 to 10%. The majority of deaths were in persons over 50 years old, among whom the fatality rate can be as high as 30% or more. During the 1962 epidemic in Tampa Bay, Florida, the highest fatality rate (36.3%) was recorded in patients 65 years of age and older in Pinellas County, where a large number of retired persons live. In that county the general mortality rate was 22.2%, while the rate was 9.8% in the remaining three counties in that area. In Central and South America, most of the small number of recorded patients did not exhibit impairment of the central nervous system.

• THE DISEASE IN ANIMALS:

The infection is subclinical in animals. Experimental peripheral inoculation of the virus produces viremia without clinical symptoms in domestic and wild fowl and in various species of insectivorous bats. When the disease occurs in man, antibodies for SLE are generally found in horses and in some other mammals. In contrast to western, eastern, and Venezuelan equine encephalitides, St. Louis encephalitis does not cause clinical illness in equines. Some equines inoculated experimentally develop viremia.

• SOURCE OF INFECTION AND MODE OF TRANSMISSION:

The basic cycle of the infection involves wild birds and omithophilic mosquitoes. Culex salinarius, from which the SLE virus has been isolated, could be the vector in the wild enzootic cycle. In the United States, two different epidemiologic situations are known, depending on the habits of the primary vector and other ecologic conditions. West of the Rocky Mountains the disease is rural and sporadic because the vector, C. tarsalis, is sparse and the widely scattered human population has a high rate of subclinical infection, protecting it against reinfection. Though the vector and birds reach high concentrations in areas flooded by irrigation water, human cases are not numerous for the reasons given. In the south-central and north-central states of the country, by contrast, the disease is urban-suburban in character, primarily because the vectors are the peridomestic and domestic mosquitoes C. quinquefasciatus and C. pipiens. These vectors proliferate where water contaminated with organic wastes collects, that is, in poorer urban and suburban areas deficient in environmental sanitation. The same conditions favor the proliferation of sparrows, pigeons, and other birds that feed among household wastes. Peridomestic birds and domestic fowl serve as amplifiers of the virus: that fact, together with the increased density of the human population, creates the conditions necessary for epidemics. During the 1964 epidemic in Houston, the virus was isolated from geese, domestic pigeons, and various other species of birds. In addition, antibodies were found in 20% of the birds, especially house sparrows (Passer domesticus), and in almost all poultry examined. How the virus gets into urban areas is not yet established, but it is suspected that migratory wild birds may introduce it. As is true for many other arboviruses, the mechanism that allows the virus to overwinter in temperate climates is not fully known. The virus has been isolated from hibernating adult female C. pipiens, which indicates that the virus can persist in the vector during the winter in temperate climates. It also has been proven experimentally that low-level transovarial transmission occurs in C. pipiens.

• ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:

Man is an accidental host of the virus and does not play any role in the natural maintenance cycle. The basic reservoir is wild birds and perhaps the vector mosquitoes; poultry and peridomestic and domestic birds act as amplifiers of the virus, which circulates from one host to another by means of mosquitoes. Wild and domestic mammals are not thought to play a role in the virus cycle because their viremia is low-level and transitory and virus strains isolated from them possess low virulence. In Panama, sloths inoculated with the SLE virus developed prolonged high-titer viremia, but the role of these animals under natural conditions has not been determined. Likewise, bats may be involved in the virus's overwintering within enzootic foci in temperate climates, as well as in its dissemination to epizootic foci, a subject that requires further study.

• DIAGNOSIS:

SLE may be confused clinically with other febrile diseases or with encephalitides and aseptic meningitis caused by different agents. Laboratory confirmation is essential. Laboratory diagnosis is based primarily on serology. only on a few occasions has it been possible to isolate the etiologic agent from the blood of viremic patients. Most successful isolations have been made from the brain of patients who died a short time after contracting the disease.

• DIAGNOSIS:

is based on demonstrating serologic conversion in the patient by comparing titers of serum samples taken during the acute phase with those taken during convalescence. The most widely used tests are complement fixation, neutralization (which is the most specific), and hemagglutination inhibition. Antibodies can be detected during the first week of the disease by the hemagglutination inhibition and neutralization tests, while the complement fixation antibodies appear during the second or third week. In Latin American and Caribbean countries, where infections due to several flaviviruses occur, tests must include all of the other viruses of the group known to be present in the area.

• TREATMENT:

Vigorous supportive therapy. Such measures include reduction of intracranial pressure (mannitol), monitoring of intraventricular pressure, the control of convulsions, maintenance of the airway, administration of oxygen, and attention to adequate nutrition during periods of prolonged coma. No antiviral agent is effective for arboviral encephalitis.

• CONTROL:

The only preventive measure available is control of the vector. Programs of epidemiologic surveillance and vector control have given satisfactory results in California against C. tarsalis, in Florida against C. nigripalpus, and in Texas against C. quinquefasciatus. An effective vaccine is not yet available.

---

YELLOW FEVER

(Black Vomit)

• AGENT:

RNA virus, Family Togaviridae, (Group B Arbovirus)

• RESERVOIR AND INCIDENCE

all primates susceptible; major Public Health problem in Central and S. America and Africa.

• TRANSMISSION:

o mosquito vector: Aedes and Hemagogues

• DISEASE IN NONHUMAN PRIMATES:

There is high fever and vomiting, with jaundice, oliguria, and generalized hemorrhages. Microglobular fatty degeneration of liver cells occurs with disruption of the hepatic lobule and necrosis of midzonal liver cells, producing so called "Councilman" bodies. Degeneration and necrosis of the kidney tubules occurs. There are hemorrhages in tissues.

• DISEASE IN MAN:

Most cases have fever, severe headache and backache, jaundice and albuminuria, followed by full recovery with a week, but in severe cases there is a second episode of fever, prostration, jaundice, renal failure and generalized hemorrhages. Microglobular fatty degeneration of liver cells occurs with disruption of the hepatic lobule and necrosis of midzonal liver cells, producing so called "Councilman" bodies. Degeneration and necrosis of the kidney tubules occurs. There are hemorrhages in tissues. The case fatality rate among indigenous populations of endemic regions is <5%, but may exceed 50% among nonindigenous groups and in epidemics.

• DIAGNOSIS:

Virus isolation or serology.

• TREATMENT:

Consists of limiting food to high-carbohydrate, high-protein liquids, IV glucose and saline, analgesics and sedatives, and saline enemas.

• PREVENTION/CONTROL:

Monkeys should originate from a yellow fever free area, or be maintained in a double-screened mosquito-proof enclosure, or have been immunized against yellow fever. For humans, mosquito control, vaccination, and adherence to PHS quarantine standards.

---

HANTAVIRUS PULMONARY SYNDROME

INTRODUCTION: On May 14, 1993, the New Mexico Department of Health was notified of 2 persons who had died within 5 days of each other. Their illnesses were characterized by abrupt onset of fever, myalgia, headache, and cough, followed by the rapid development of respiratory failure. Tests for Yersinia pestis and other bacterial and viral pathogens were negative. After additional persons who had recently died following a similar clinical course were reported by the Indian Health Service, the health services of Arizona, Colorado and Utah were contacted to seek other possible cases. Blood and tissue specimens were sent to the Centers for Disease Control and Prevention (CDC). The results were negative except for signals for the Puumala hantavirus. Relying on molecular and immunological research performed by the Army, the National Institutes of Health, and the CDC itself, by June 9th, the CDC was able to prove that a new hantavirus was the culprit (1). As of November 5th, laboratory evidence of acute hantavirus infection had been confirmed in 42 persons. Twenty-six (62%) of these persons have died. Most cases were in the Southwest but some have been reported as far afield as North Dakota and California (1). This paper presents a brief overview of hantavirus infections with primary focus on Hantavirus Pulmonary Syndrome (HPS) and recommended precautions to reduce the risk of accidental exposure. Other detailed reviews are available elsewhere (2-7).

• AGENT:

Isolation of the first recognized hantavirus (Hantaan virus) was reported from the Republic of Korea in 1978. The genus Hantavirus is a member of the family Bunyaviridae. Hantaviruses are further divided into genotypes. Representative viruses in each genotype are the Hantaan virus, the Seoul virus, the Puumala virus, and the Prospect Hill virus. Additional groups exist. Hantaan, Puumala, and Seoul viruses are known human pathogens; Prospect Hill has not been associated with disease. The causative agent of HPS represents a previously unidentified genotype. Since the 1930s, epidemic and sporadic hantavirus-associated disease has been described throughout Eurasia, especially in Scandinavia and Northeastern Asia. In the 1950s, thousands of United Nations military personnel were infected with hantavirus during the Korean conflict; more recently, transmission has been documented among United States military personnel training in the Republic of Korea. Hantaviruses have been isolated from rodents in the United States, and serological studies have documented human infections with hantaviruses. However, acute disease associated with infection by pathogenic hantaviruses has not previously been reported in the Western Hemisphere (8). Previously called the Four Corners Virus and Muerto Canyon Virus, the causative genotype for HPS is now called Sin Nombre Virus.

• DISEASE IN HUMANS:

The clinical manifestations previously associated with hantavirus infections have been characterized by hemorrhagic features and by renal involvement. In HPS, however, onset of illness has been characterized by a prodrome consisting of fever, myalgia, and variable respiratory symptoms followed by the abrupt onset of acute respiratory distress. Other symptoms reported during the early phase of illness have included headache and gastrointestinal complaints. Hemoconcentration and thrombocytopenia have developed in a majority of the cases. The hospital course has been characterized by bilateral pulmonary infiltration, fever, hypoxia, and hypotension; recovery in survivors has been without sequelae. It is important to note that no defined set of symptoms and signs reliably distinguishes HPS from other forms of noncardiogenic pulmonary edema or adult respiratory distress syndrome (9). Postmortem examination has routinely revealed serous pleural effusions and heavy edematous lungs. Microscopic findings have included interstitial infiltrates of mononuclear cells in the alveolar septa, congestion, septal and alveolar edema with or without mononuclear cell exudate, focal hyaline membranes, and occasional alveolar hemorrhage. Large mononuclear cells with the appearance of immunoblasts have been found in red and periarteriolar white pulp of the spleen, hepatic portal triads, and other sites. Hantavirus antigens, localized primarily in endothelial cells, have been detected in most organs, with marked accumulations in the lungs (9). The incubation period for the known pathogenic hantaviruses, although highly variable, generally range from 2 to 4 weeks (8). Based on reported cases, the incubation period for HPS appears to be one to three weeks (10).

• RESERVOIRS:

Rodents are the primary reservoir hosts with each hantavirus appearing to have a preferential rodent host. The epidemiological characteristics of outbreaks of human disease and the severity for the infection are determined mainly by the rodent host. Available data strongly supports the deer mouse (Peromyscus maniculatus) as the primary reservoir of the newly recognized hantavirus (11). Serologic evidence of infection has also been found in pi¤on mice (P. truei) and the brush mice (P. boylii). Other rodent species that have tested positive so far include the house mouse (Mus musculus), the harvest mouse (Reithrodontomys sp.), the rock squirrel (Spermophalus variegatus), the white-throated wood rat (Neotoma albigula), and the western chipmunk (Tamias spp.). P. maniculatus is highly adaptable and is found in different habitats, including human residences in rural and semirural areas, but generally not in urban centers (12). The wood mouse or striped field mouse (Apodemus sp.) associated hantaviruses also cause severe human disease with mortality rates between 3 and 7%. Rattus associated disease is less severe and asymptomatic infections may be more common. The most benign form of hantaviral disease (HVD), also called Nephropathia epidemica and first described in Scandinavia, is caused by a hantavirus that infects voles (Clethrionomys species). Infected voles and human disease occur throughout western Europe (13). The hantaviruses have been identified in other animals. At the International Symposium on Hemorrhagic Fever with Renal Syndrome (HFRS), Leningrad, 5-10 May 1991, the presence of hantaviral antigen was reported in 13 species of birds in eastern parts of the former U.S.S.R. (13). The CDC is also investigating whether other animals, particularly those that prey on rodents, may carry the virus. The impetus for this research is a 1987 study suggesting that cats, which tested positive for two other hantaviruses-the Hantaan and Seoul types-may help transmit the virus to humans in China. As for the HPS virus, so far CDC scientists have identified one infected nonrodent species (aside from humans): the desert cottontail (Sylvilagus auduboni). But virologists think most nonrodents are "dead-end" hosts that shed little virus and are unlikely to infect people (14) Rats, which were a reservoir of hantavirus, have been responsible for several outbreaks of HVD among animal caretakers and laboratory workers at research institutions in Korea, China, the former Soviet Union, Japan, Scandinavia, the U.K., France, the Netherlands and Belgium (13). Transmission of Hantavirus from laboratory reared mice and rats has not been documented in the United States.

• TRANSMISSION:

Susceptibility of rodents may vary depending on the combination of rodent species and virus strains; however, Hantaviruses do not cause apparent illness in their reservoir hosts (15). In rodents, the virus is detected primarily in the lung and kidney, where it persists despite the presence of serum antibodies. Infected rodents shed large quantities of virus in saliva, urine, and feces for many weeks, but the duration and period of maximum infectivity are unknown. Although the main route of transmission is aerosolization, the demonstrated presence of infectious virus in saliva of infected rodents and the marked sensitivity of these animals to hantaviruses following inoculation suggests that biting may also be an important mode of transmission among rodents (12). Arthropod vectors are not known to have a role in the transmission of hantaviruses. Domestic animals may bring infected rodents into contact with humans (12). Human infection may occur when infective saliva or excreta are inhaled as aerosols produced directly from the animal. Transmission may also occur when dried materials contaminated by rodent excreta are disturbed, directly introduced into broken skin, introduced onto the conjunctivae, or, possibly, ingested in contaminated food or water. Persons have also become infected after being bitten by rodents (12). Person-to-person transmission has not been associated with any of the previously identified hantaviruses nor with the recent outbreak in the Southwest (16). In the current epidemic, known hantavirus infections of humans have occurred primarily in adults and are associated with domestic, occupational, or leisure activities that bring humans into contact with infected rodents, usually in a rural setting. Cases have been epidemiologically associated with the following situations: Planting or harvesting field crops Occupying previously vacant cabins or other dwellings Cleaning barns and other outbuildings Disturbing rodent-infested areas while hiking or camping Inhabiting dwellings with indoor rodent populations Residing in or visiting areas in which the rodent population has shown an increase in density (12). In Europe, isolation of hantaviruses from immunocytomas and ascites tumors has highlighted additional risks from working with persistently infected rodents. Tumors, passaged over the years in hantavirus-infected laboratory rats, transfer the virus when implanted in hantavirus-free rats. Since, in rodents, hantaviruses are not transmitted vertically but horizontally, the use of caesarian section and foster mother techniques have been recommended for laboratories breeding rodent colonies. Before implantation, tumors should be checked for the presence of the hantaviruses (this precaution should be followed by laboratory workers in the U.S. importing tumors, organs, or live rodents from hantavirus endemic areas) (12).

• DIAGNOSIS:

The CDC in consultation with the Council of State and Territorial Epidemiologists has developed screening criteria for HPS (9). Cases meeting the screening criteria should be reported to the CDC through state health departments. These criteria are: Potential case-patients must have one of the following: a febrile illness (temperature ò101 oF [ò38.3 oC]) occurring in a previously healthy person characterized by unexplained adult respiratory distress syndrome, or bilateral interstitial pulmonary infiltrates developing within 1 week of hospitalization with respiratory compromise requiring supplemental oxygen, OR an unexplained respiratory illness resulting in death in conjunction with an autopsy examination demonstrating noncardiogenic pulmonary edema without an identifiable specific cause of death. Potential case-patients are to be excluded if they have any of the following: a predisposing underlying medical condition (e.g., severe underlying pulmonary disease, solid tumors or hematologic malignancies, congenital or acquired immunodeficiency disorders, or medical conditions [e.g., rheumatoid arthritis or organ transplant recipients] requiring immunosuppressive drug therapy [e.g., steroids or cytotoxic chemotherapy]). an acute illness that provides a likely explanation for the respiratory illness (e.g., recent major trauma, burn, or surgery; recent seizures or history of aspiration; bacterial sepsis; another respiratory disorder such as respiratory syncytial virus in young children; influenza; or legionella pneumonia). Confirmed case-patients must have the following: at least one specimen (i.e., serum and/or tissue) available for laboratory testing for evidence of hantavirus infection. AND in a patient with a compatible clinical illness, diagnosis is confirmed when any of the following criteria are met: IgM antibodies to hantavirus antigens, fourfold or greater increase in immunoglobulin G titers to hantavirus antigens in paired serum specimens, a positive immunohistochemical stain for hantavirus antigen in tissues, or positive polymerase chain reaction (PCR) for hantavirus ribonucleic acid. Currently, diagnosis of the HPS strain of Hantavirus in animals is in its infancy. IFA based tests offered by national research laboratories may be used for screening; however, false negatives can occur depending on the antigen used. PCR remains the method of choice for strain identification. Presently, one laboratory (Rockefeller University Laboratory Animal Research Center, [212]327-8522) offers this service with more, hopefully, coming on line in the future (17).

• TREATMENT:

Supportive care and meticulous monitoring of vital signs and fluid balance are the basis for therapy. Severe hypoxia and overhydration should be avoided or prevented. Pressors or cardiotonic drugs should be employed to maintain perfusion without excessive fluid administration (9). In one controlled study involving HFRS, intravenous administration of the antiviral drug ribavirin was effective in treating severe cases of hantavirus infection when administered early in the course of illness (8). The effectiveness of using ribavirin to treat HPS has not been established, yet.

• PREVENTION AND CONTROL:

Hantaviruses have lipid envelopes that are susceptible to most disinfectants (e.g., dilute hypochlorite solutions, detergents, ethyl alcohol (70%), or most general-purpose household disinfectants). How long these viruses survive after being shed in the environment is uncertain (12). The reservoir hosts of the hantavirus in the southwestern United States also act as hosts for the bacterium Yersinia pestis, the etiology agent of plague. Although fleas and other ectoparasites are not known to play a role in hantavirus epidemiology, rodent fleas transmit plague. Control of rodents without concurrent control of fleas may increase the risk of human plague as the rodent fleas seek an alternative food source. Thus, eradicating the reservoir hosts of hantaviruses is neither feasible nor desirable. Once the virus has been cultured, it might be possible to develop a vaccine against the HPS strain. However, currently, the best available approach for disease control and prevention is risk reduction through environmental hygiene practices that deter rodents from colonizing the home and work environment (12). No restriction of travel to areas affected by this outbreak is considered necessary; however, activities that may disrupt rodent burrows or result in contact with rodents or aerosolization or rodent excreta should be avoided. People practicing universal precautions while processing routine clinical materials (such as blood, urine, and respiratory specimens) are not considered to be at increased risk for hantavirus infection. However, human-acquired infections have occurred among persons who handled infected wild or domesticated rodents. Therefore, exposure that may result in propagation of hantaviruses should be conducted in a special facility (biosafety level 3) (8). Recommendations for animal facilities housing wild-caught rodents include: Access to rooms should be restricted to only those individuals who have a legitimate need to be in the room. Colony should be serologically screened for the agent. Animals should be housed and handled under standard microisolation techniques. Biological safety cabinets should be used and not laminar flow workbenches. Until the status of the colony can be ascertained, individuals working with the rodent should: a. Obtain a baseline serum sample. The serum should be stored at -20oC. b. Insure that all persons involved are informed of the symptoms of the disease and given detailed guidance on prevention measures. c. Seek immediate medical attention if a febrile or respiratory illness develops within 45 days of the last potential exposure. The attending physician should be informed of the potential occupational risk of hantavirus infection. d. Wear an half-face air-purifying (or negative-pressure) respirator or powered air-purifying respirator with HEPA filter when handling rodents or their cages. Respirators are not considered protective if facial hair interferes with the face seal. Respirators should be fitted by trained personnel in accordance with OSHA standards. e. Wear rubber or plastic gloves when handling rodents or cages. Gloves should be washed and disinfected before removing them. f. Wear dedicated outer garments (disposable, if possible), rubber boots or disposable shoe covers and protective goggles. Personal protective gear should be decontaminated upon removal. If not disposable, they should be laundered on site using hot water and detergent. Machine-dry using a high setting. If no laundry facilities are available, non-disposable items should be immersed in liquid disinfectant until they can be washed. All potentially infective waste material (including respirator filters, bedding, caging, disposable protective garments, and used disposables such as syringes, gauze, etc.) should be placed in autoclavable plastic bags and sterilized. Needles, scalpels, pipettes, and other sharp materials should be placed in puncture proof containers and sterilized. Spread from feral rodents was postulated as the cause of one source of contamination (18). Therefore, facilities and individual rooms should be vermin-proof to prevent accidental egress and ingress of rodents. All openings greater than ¬ inch should be screened or sealed. Carcasses should be placed in a plastic bag and disposed as biohazard waste or incinerated. Since feral rodents may transmit the disease, it is recommended that Hantavirus testing be included in animal health monitoring programs. Why the Current Epidemic? Because of the rodent connection with this disease, medical investigators and public health officials sought ecological information on the deer mouse and other native rodent species. Anecdotal information from residents in the afflicted areas suggested that rodents were exceptionally abundant last winter, and scientists speculated that, if true, the increased potential for rodent-human contact and disease transmission might account for the sudden epidemic. Biologists with the Sevilleta, New Mexico Long-Term Ecological Research (LTER) site have long-term data on rodent communities in the region. At the request of the CDC and the New Mexico Health Department, LTER researchers provided detailed demographic analyses from 1989-1993 for the 22 rodent species inhabiting the area. The LTER data showed tenfold population increases in various Peromyscus species and wood rats (Neotoma spp.) during the spring of 1993. Population increases occurred simultaneously in grasslands, desert-shrublands, and woodlands. Comparisons of the rodent data to the region's climatological data indicated that rodent population dynamics is associated with above-average precipitation during the winter of 1992-93, in turn leading to abundant food sources (19).

References Marshall, E. 1993. Hantavirus outbreak yields to PCR. Science. 262:832-836. LeDuc, J. W., J. E. Childs, and G. E. Glass. 1992. The Hantaviruses, etiologic agents of hemorrhagic fever with renal syndrome. Annu Rev Public Health. 13:79-98. Niklasson, B. S. 1992. Hemorrhagic fever with renal syndrome, virological and epidemiological aspects. Pediatr Nephrol. 6(2):201-204. Cosgriff, T. M. and R. M. Lewis. 1991. Mechanisms of disease in hemorrhagic fever with renal syndrome. Kidney Int Suppl. 35:S72-79. Tkachenko E. A. and H. W. Lee. 1991. Etiology and epidemiology of hemorrhagic fever with renal syndrome. Kidney Int Suppl. 35:S54-61. Beaty, B. J. and C. H. Calisher. 1991. Bunyaviridae--natural history. Curr Top Microbiol Immunol. 169:27-78. Gonzalez-Scarano, F., M. J. Endres, and N. Nathanson. 1991. Bunyaviridae: Pathogenesis. Curr Top Microbiol Immunol. 169:217-249. 1993. Emerging infectious diseases. Outbreak of acute illness. Wkly Epidemiol Rec. 68(25):186-8. 1993. Emerging infectious diseases. Update: Hantavirus Disease. MMWR. 42(29, 31, and 42). Sands, L. 1993. Guidelines for

• DIAGNOSIS:

and treatment of unexplained adult respiratory distress syndrome. Arizona Department of Health Services.

Nichol, S. T., C. F. Spiropoulou, S. Morzunov, et al. 1993. Genetic identification of a Hantavirus associated with an outbreak of acute respiratory illness. Science. 262:914-917. 1993. Hantavirus infection-Southwestern United States: interim recommendations for risk reduction. MMWR. 42(RR-11). McKenna, P., G. VanDerGroen, G. Hoofd, et al. 1992. Eradication of hantavirus infection among laboratory rats by application of caesarian section and a foster mother techniques. J Infect. 25:181-190. Stone, R. 1993. The mouse-pion nut connection. Science. 262:833. Kawamura, K., X. K. Zhang, J. Arikawa, et al. 1991. Susceptibility of laboratory and wild rodents to Rattus or Apodemus-type hantaviruses. Acta Virol. 35:54-63. Hughes, J. M., C. J. Peters, M. L. Cohen, et al. 1993. Hantavirus pulmonary syndrome: an emerging infectious disease. Science. 262:850-851. Morse, S. 1994. Personal communication. Wong, T. W., Y. C. Chan, E. H. Yap, et al. 1988. Serological evidence of Hantavirus infection in laboratory rats and personnel. Int J Epidemiol. 17(4):887-890. Dybas, C. 1993. NSF-funded researchers find rodent population explosion may be behind hantavirus epidemic in southwest. NSF Bulletin #93-59.

---

HEMORRHAGIC FEVER WITH RENAL SYNDROME [HFRS]

(Korean Hemorrhagic Fever, Nephropathia Epidemica, Epidemic Hemorrhagic Fever, Hemorrhagic Nephrosonephritis)

• AGENT:

Bunyaviridae family, Hantaan virus genus

• RESERVOIR AND INCIDENCE

Recognized originally in troops serving in the Korean war. Named Hantaan after river in endemic area of Korea. Isolated in 1978 in Apodemus agrarius, then adapted to tissue culture and laboratory rats. Serologic mapping indicates that Hantaviruses have infected large numbers of people in the region from Japan across central and north Asia to the Scandinavian Peninsula, and southward in Europe to the Balkans. Other Hantaviruses have been identified in urban rats captured in major Asian and Western cities, including the USA and Brazil. Hosts of hantavirus are wild Rodents Several antigenic subtypes exist, each associated with a single rodent species: Apodemus species - Striped field mouse - A. agrarius (Korea) associated with KHF. Domestic Rattus norvegicus and Rattus rattus in Korea and Domestic Rattus norvegicus in the U.S. had virus similar to prototype Hantaan virus yet distinct from it. Microtus pennsylvanicus: the meadow vole. Reservoir for Prospect Hill virus, most recently isolated Hantavirus. Isolated at NIH and named for Prospect Hill in Frederick, MD where the vole was captured that yielded the first isolate. No human disease associated with this so far but antibody has been identified among mammalogists in the U.S.(1982). Cletheronomys glareolus: the bank vole. Reservoir for Puumala virus, cause of Nephropathia epidemica (NE), a mild form of HFRS found in Scandinavia, Western Soviet Union and much of Europe.

• TRANSMISSION:

Aerosol transmission from rodent excreta is presumed. Virus is present in urine, feces and saliva of persistently infected asymptomatic rodents; highest virus concentration is found in the lungs. Human to human transmission does not occur.

• DISEASE IN RODENTS:

Chronic, ASYMPTOMATIC infection. Following infection, rodent is viremic for about 1 week when virus is disseminated throughout the body. After viremia antigen is usually abundant in the lungs, spleen and kidneys. Antibody is produced and persists but does not diminish the abundance of antigen expressed in organs.

• DISEASE IN MAN:

Symptoms begin with the sudden onset of fever which lasts 1-2 weeks, accompanied by prostration, anorexia, generalized pains, conjunctivitis, proteinuria and hypotension, possibly followed by hemorrhages and hematuria with renal failure. Case fatality rate is 7%.

• DIAGNOSIS:

Serology using indirect immunofluorescence or ELISA.

• TREATMENT:

IV ribavirin

• PREVENTION/CONTROL:

Although most US commercial animal breeders have eliminated these viruses through barrier breeding and caesarean derivation, small suppliers and producers of select inbred strains may be at risk of infection. Be aware of potentially infected animals when receiving shipments from Japan, Belgium or other countries which may have the agent present in lab. animals (where virus-free certification cannot be provided). Animals should be serologically tested in advance of shipment. Test all rodent tissues, tumors, cell lines received from source that cannot provide virus free certification. Education and awareness of potential problem. Exclude rodents from housing and other buildings in endemic areas.

---

OTHER HEMORRHAGIC FEVERS

(Arenaviruses) All have natural persistent infection in rodents with humans being accidental hosts. Route of transmission to humans is generally thought to occur thru contamination of food, water, or air by rodent feces or urine or by inoculation of skin abrasions. Humans are infected primarily through infected rodents invading human habitats. Contact with infected rodent feces has produced disease in laboratory personnel.

• DIAGNOSIS:

is by serology or virus isolation. Control is to reduce opportunity for exposure to infected rodents. 1. JUNIN VIRUS: produces Argentinian hemorrhagic fever There is an illness of 1-2 weeks with insidious onset of fever, malaise, rigors, fatigue, headache, vomiting, constipation or diarrhea, conjunctival congestion, retro-orbital pain, epistaxis, petechial hemorrhages beneath skin, palate and gums. Edema of the upper body is possible. In severe cases hematemesis and melena, encephalopathy, bradycardia and hypertension occur. Case fatality rate 5-30%. Several hundred cases reported each year in Argentina. Associated with at least 3 different cricetine rodent species in Argentina 2. MACHUPO VIRUS: produces Bolivian Hemorrhagic fever Signs and case fatality rate like Junin virus. Case #s have been decreasing rapidly since initiation of rodent control programs in 1975. Associated with Calomys callosus (Bolivia). 3. LASSA FEVER: Serologically related to Lymphocytic Choriomeningitis, Machupo, and Junin virus. Fever has insidious onset over 2-3 days and may persist for up to 4 weeks, with malaise, headache and generalized aching and sore throat. Vomiting and diarrhea, possibly edema of face and neck, lymphadenopathy with hemorrhages and renal failure occurs in the second week. The prostration is out of proportion to fever. Often there is a maculopapular rash. Occurs in large areas in West Africa. Documented man to man transmission. Found in common rodent Mastomys natalensis, multimammate rat (West Africa).

---

LYMPHOCYTIC CHORIOMENINGITIS - LCM

• AGENT:

Arenavirus Of many latent viruses present in mice, only LCM naturally infects humans. LCM can easily be transmitted from animals to humans. Isolated by Armstrong and Lillie during investigation of a St. Louis Encephalitis outbreak in 1933.

• RESERVOIR AND INCIDENCE

Worldwide in wild mice (M. musculus). This disease is principally confined to the eastern seaboard and northeastern states in the U.S. Wild mice infect the lab mouse. Mouse and hamster are the only species in which long term, asymptomatic infection is known to exist. *LCM virus is present in experimental mouse tumors which is a second source of infection for humans. This was first recognized in a transplantable leukemia of C58 mice. The disease can also be transmitted to laboratory animals via inoculation of infected tissue culture cells. The infection also occurs in guinea pigs, rabbits, rats, canines, swine, and primates.

• TRANSMISSION:

Infection in mice is maintained by congenital infection followed by lifelong carriage and excretion of virus in saliva, urine, and feces. Human infections are probably from contaminated food and dust, the handling of dead mice, and mouse bites. Bloodsucking arthropod vectors such as ticks, lice, and mosquitos may transmit the disease. Person to person transmission does not occur.

• DISEASE IN ANIMALS:

The clinical signs of LCM depend on the host's resistance and age when infected, although the various categories of the disease are not always clearly delineated. Animals infected in utero or during the first 48 hours postpartum may develop a transient viremia but recover completely within a few weeks. Other animals similarly infected may develop a persistent tolerant infection (PTI) that continues asymptomatically for 6 or more months. Animals infected after the first few days, when the virus will be recognized as foreign, often overcome the infection completely, but an acute, usually fatal syndrome can develop. Signs of acute infection in mice continue for 1-2 weeks and include decreased growth, rough hair coat, hunched posture, blepharitis, weakness, photophobia, tremors, and convulsions. The terminal stage of the PTI, which occurs over several weeks to 5 to 12 month old mice, is characterized by weight loss, blepharitis, and impaired reproductive performance and runted litters. The important necropsy signs are microscopic. Visceral organs, including the liver, kidneys, lungs, pancreas, blood vessels, and meninges, are infiltrated by lymphocytes. A glomerulonephritis of probable immune complex origin is a characteristic feature of terminal PTI.

• DISEASE IN MAN:

The features may include influenza-like illness for up to 2 weeks, possibly with orchitis. Sometimes meningitis, paralysis and coma follow. Joint pains occur during convalescence.

• DIAGNOSIS:

CF or virus isolation.

• PREVENTION/CONTROL:

serologic monitoring Infection can be eradicated by cesarean derivation prevent wild mice from entering facilities control ectoparasites and roaches Restrict flow of traffic into and out of LCM infected colonies Protective clothing and proper care when handling infected animals or tissues. Basic hygienic practices Screen tissue culture cell lines and murine tumor lines and animals periodic serologic testing of high risk personnel

---

CALIFORNIA ENCEPHALITIS/LA CROSSE ENCEPHALITIS

(USA) (Tahyna virus [Europe]) A mild, febrile, viral disease which occasionally causes severe encephalitis. It is transmitted by mosquitoes from small wild mammals, mainly in summer, to persons frequenting woodland areas of the USA and Canada, and certain European countries such as Yugoslavia and the USSR. The causative agents are the California encephalitis group of viruses (Bunyaviridae). There is no vaccine.

• RESERVOIR AND MODE OF TRANSMISSION:

The virus cycles amongst small wild animals (e. chipmunks, squirrels, rabbits and hares) and a variety of mosquito species. The infection can be maintained independently over several years by transovarial transmission in the mosquito. Humans are accidental hosts infected by mosquito bite during occupational or recreational activities in wooded areas. Accidental infections from laboratory accidents have occurred.

• INCUBATION PERIOD:

Humans. 5-15 days. Animals. Unknown.

• CLINICAL FEATURES:

Humans. Symptoms lasting about 5-10 days range from fever and headache with nausea and vomiting to fits and signs of aseptic meningitis, encephalitis and neurological sequelae. Animals. Unknown but assumed subclinical.

• PATHOLOGY:

Humans. Encephalitis. Animals. Unknown.

• DIAGNOSIS:

Humans. The virus may sometimes be isolated from blood or rarely, from cerebrospinal fluid. Serologic tests of blood or cerebrospinal fluid may be diagnostic in specific types of encephalitis (by demonstrating virus-specific IgM or a fourfold change in complement-fixing or neutralizing antibodies). Animals. Impracticable.

• PROGNOSIS:

Humans. In humans, fatality is rare but neurological defects may persist. Animals. Thought to be subclinical.

• PREVENTION:

Humans. Prevent mosquito bites. Control the mosquito vector. Apply laboratory safety procedures. Animals. Impracticable.

• TREATMENT:

Humans. Vigorous symptomatic therapy. Such measures include reduction of intracranial pressure (Mannitol), monitoring of intraventricular pressure, the control of convulsions, maintenance of the airway, administration of oxygen, and attention to adequate nutrition during periods of prolonged coma. Animals. Not applicable.

• LEGISLATION:

Humans. Acute encephalitis is notifiable in many countries, including the USA and the UK. Animals.None.

---

MARBURG VIRUS

(African Hemorrhagic Fever, Green or Vervet Monkey Disease)

• AGENT:

Agent is classified as a Filovirus. It is an RNA virus, superficially resembling rhabdoviruses but has bizarre branching and filamentous or tubular forms shared with no other known virus group on EM.

• RESERVOIR AND INCIDENCE

An acute highly fatal disease first described in Marburg, Germany in 1967. Brought to Marburg in a shipment of infected African Green Monkeys from Uganda. 31 people were affected and 7 died in 1967. Exposure to tissue and blood from African Green monkeys (Cercopithecus aethiops) or secondary contact with infected humans led to the disease. No disease occurred in people who handled only intact animals or those who wore gloves and protective clothing when handling tissues. A second outbreak was reported in Africa in 1975 involving three people with no verified contact with monkeys. Third and fourth outbreaks in Kenya 1980 and 1987. Natural reservoir is unknown. Monkeys thought to be accidental hosts along with man. Antibodies have been found in African Green monkeys, baboons, and chimpanzees. 100% fatal in experimentally infected African Green Monkeys, Rhesus, squirrel monkeys, guinea pigs, and hamsters.

• TRANSMISSION:

Direct contact with infected blood or tissues or close contact with infected patients. Virus has also been found in semen, saliva, and urine.

• DISEASE IN NONHUMAN PRIMATES:

No clinical signs occur in green monkeys, but the disease is usually fatal after experimental infection of other primate species. Leukopenia and petechial hemorrhages throughout the body of experimentally infected monkeys, sometimes with GI hemorrhages.

• DISEASE IN MAN:

5-7 day incubation period. Headache, fever, muscle pain, vomiting, diarrhea, hemorrhagic diathesis, Conjunctivitis, photophobia, skin rash, and jaundice. Leukopenia, thrombocytopenia, proteinuria. Shock and death in 25% of cases. Hemorrhages throughout the body on post mortem examination.

• DIAGNOSIS:

IFA, ELISA, Western blot, EM, or virus isolation.

• TREATMENT:

Supportive Possibly immune serum

• PREVENTION/CONTROL:

Strict quarantine on newly imported, wild-caught primates. Naturally infected monkeys should become ill or die within several weeks. Hygiene, sanitation, and protective clothing Isolation of human patients with prevention of sexual intercourse until semen is free of virus.

---

EBOLA

(African Hemorrhagic Fever)

• AGENT:

similar to Marburg morphologically similar but antigenically distinct. Both are RNA Filoviruses and have bizarre branching and filamentous or tubular forms shared with no other known virus group.

• RESERVOIR AND INCIDENCE

Reservoirs unknown. Monkeys are probably accidental hosts, along with humans. First recognized in 1976 in Northern Zaire and Southern Sudan, 500 cases with 350 deaths reported.

• TRANSMISSION:

Person-to-person transmission occurs by direct contact with infected blood, secretions, organs or semen. Nosocomial infections have been frequent; all Zaire cases acquired from contaminated syringes and needles died.

• DISEASE IN MAN:

Fever, headache, malaise, followed by chest discomfort, diarrhea, and vomiting. Case fatality rate is 50-90%.

• DIAGNOSIS:

IFA, ELISA, Western blot, EM, or virus isolation.

• TREATMENT:

Supportive Possibly immune serum

• PREVENTION/CONTROL:

Strict quarantine on newly imported, wild-caught primates. Naturally infected monkeys should become ill or die within several weeks. Hygiene ,sanitation, and protective clothing Isolation of human patients with prevention of sexual intercourse until semen is free of virus.

Source

http://packman.ianszoolinks.com/ponyzoohealth.htm