ZOONOTIC DISEASES

ZOON | NOSES = ANIMALS | DISEASES

(Text Modified from Document Created by Michael S. Rand, DVM, ACLAM)

INTRODUCTION

The World Health Organization defines Zoonoses (Zoonosis, sing.) as "Those diseases and infections which are naturally transmitted between vertebrate animals and man".

I. Impact of zoonotic disease

Illness
Delay or terminate
Monetary loss
Adverse effect on morale of personnel
Unfavorable publicity
Medicolegal implications
Man-hours lost

II. Epidemiologic Concepts

Incidental host - not required for the perpetuation of the organism.
Link host - bridges the gap between the maintenance host and man.
Amplifier host - increases the number of the infective agents (viruses and bacteria) to which man may be exposed.
A laboratory animal can be both a link host and an amplifier host.

III. Mode of transmission

Feces
Urine
Saliva
Blood
Milk
via aerosol, oral, contact with bedding or animals, etc.

IV. The probability of disease transmission from animals to man is influenced by several factors:

  1. Length of time the animal is infective.
  2. Length of the incubation period in animals (this is important in some diseases with long incubation periods, because the animals may be studied and euthanatized before they become infective for humans).
  3. The stability of the agent. Most important in direct transmission, where the agent is exposed to environmental changes.
  4. Population density of the animals in the colony.
  5. Husbandry practices.
  6. Maintenance procedures and control of wild rodents and insects.
  7. Virulence of the agent.
  8. Route of transmission.

V. Classification of zoonoses

A classification system based on the type of life cycle of the infective organism seems the most useful in planning a preventive medicine program. The following categories are recommended by the World Health Organization Expert Committee on Zoonoses:

VI. Direction of transmission

Anthropozoonoses - Infections transmitted to man from lower vertebrates.
Zooanthropozoonoses - Infections transmitted from man to animals.
Amphixenoses - Infections maintained in both man and lower vertebrates, and may be naturally transmitted in either direction.

VII. "Emerging zoonoses"

are defined as zoonotic diseases caused either by apparently new agents, or by previously known microorganisms, appearing in places or in species in which the disease was previously unknown. New animal diseases with an unknown host spectrum are also included in this definition. Natural animal reservoirs represent a more frequent source of new agents of human disease than the sudden appearance of a completely new agent. Factors explaining the emergence of a zoonotic or potentially zoonotic disease are usually complex, involving mechanisms at the molecular level, such as genetic drift and shift, and modification of the immunological status of individuals and populations. Social and ecological conditions influencing population growth and movement, food habits, the environment and many other factors may play a more important role than changes at the molecular level.

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BACTERIAL DISEASES SYSTEMIC INFECTIONS

BRUCELLOSIS

(In humans: Mediterranean fever, undulant fever, Malta fever. In animals: contagious abortion, epizootic abortion, 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 in the lab animal facility due to the extensive use of random source and lab bred dogs, in contrast to use of large domestic animals. 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 Lab accidents 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. Either (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:
Quarantine and test Disposable gloves Chlorine, organic iodine, quaternary ammonium compounds are rapid bactericidal agents.

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, 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
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 diarrhoea for about ten days, possibly leading to dehydration, with abdominal pain and low-grade fever. Septicemia and abscess formation are rare. Animals. Subclinical infection is common and many animals may be intermittent or persistent carriers. However, cows may suffer with fever, diarrhoea and abortion. Calves undergo epizootic outbreaks of diarrhoea with high mortality. In pigs, fever and diarrhoea 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 destock 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 immunocompromised 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 diarrhoea 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 tn order to prevent the emergence of multiresistant 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

Laboratory 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, 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 or laboratory.
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. A provisional total of 23,720 cases was reported by the end of 1990. 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, 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 which 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 coolish 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 car 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, diarrhoea, 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
name="b17">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 laboratory environment. (Natural disease or zoonotic transmission from lab 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. Natural infection in laboratory animals and zoonotic transmission from them has NOT been reported.
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. Laboratory accidents have occurred.
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 diarrhoea. 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 laboratory 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 laboratory 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. Laboratory 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 laboratory 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 laboratory 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