Human/animal diseases

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

Texte original

Human/animal diseases

(essay by Pony)

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

ZOONOTIC DISEASES

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

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

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

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

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

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

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

BRUCELLOSIS

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

• AGENT:

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

• RESERVOIR AND INCIDENCE

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

• TRANSMISSION:

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

• DISEASE IN ANIMALS:

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

• DISEASE IN MAN:

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

• DIAGNOSIS:

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

• TREATMENT:

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

• PREVENTION\CONTROL:

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

SALMONELLOSIS

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

• RESERVOIR AND MODE OF TRANSMISSION:

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

• TRANSMISSION:

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

• INCUBATION PERIOD:

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

• CLINICAL FEATURES:

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

• PATHOLOGY:

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

• DIAGNOSIS:

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

• PREVENTION:

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

• TREATMENT:

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

• VACCINATION:

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

• LEGISLATION:

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

SHIGELLOSIS

SYNONYM: Bacillary dysentery.

• ETIOLOGY:

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

• GEOGRAPHIC DISTRIBUTION:

Worldwide.

• THE DISEASE IN MAN:

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

• THE DISEASE IN ANIMALS:

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

• SOURCE OF INFECTION AND MODE OF TRANSMISSION:

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

• ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:

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

• DIAGNOSIS:

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

• TREATMENT:

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

• CONTROL:

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

YERSINIA

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

1. YERSINIA PSEUDOTUBERCULOSIS AND ENTEROCOLITICA (Pseudotuberculosis)

• RESERVOIR AND INCIDENCE

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

• TRANSMISSION:

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

• DISEASE IN ANIMALS:

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

• DISEASE IN MAN:

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

• DIAGNOSIS:

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

• TREATMENT:

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

• PREVENTION/CONTROL:

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

2. YERSINIA PESTIS

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

• AGENT:

a gram negative coccobacillus

• RESERVOIR AND INCIDENCE

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

• TRANSMISSION:

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

• DISEASE IN ANIMALS:

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

• DISEASE IN MAN:

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

• DIAGNOSIS:

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

• TREATMENT:

streptomycin with tetracycline or chloramphenicol.

• PREVENTION\CONTROL:

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

TUBERCULOSIS

(Consumption)

• AGENT, RESERVOIR AND INCIDENCE

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

• TRANSMISSION:

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

• DISEASE IN NONHUMAN PRIMATES:

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

• DISEASE IN FISH:

In infected fish, granulomatous lesions are usually observed.

• DISEASE IN MAN:

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

• DIAGNOSIS:

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

• TREATMENT:

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

• PREVENTION\CONTROL:

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

LEPROSY

SYNONYM: Hansen's disease.

• ETIOLOGY:

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

• OCCURRENCE IN MAN:

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

• THE DISEASE IN MAN:

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

• THE DISEASE IN ANIMALS:

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

• SOURCE OF INFECTION AND MODE OF TRANSMISSION:

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

• DIAGNOSIS:

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

• CONTROL:

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

VIBRIOSIS

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

LISTERIOSIS

(Circling disease)

• AGENT

- Listeria monocytogenes, gram positive, pleomorphic rod

• RESERVOIR AND INCIDENCE

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

• TRANSMISSION:

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

• DISEASE IN ANIMALS:

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

• DISEASE IN MAN:

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

• DIAGNOSIS:

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

• TREATMENT:

ampicillin plus an aminoglycoside or Trimethoprim-sulfamethoxazole.

• PREVENTION\CONTROL:

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

LEPTOSPIROSIS

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

• AGENT

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

• RESERVOIR AND INCIDENCE

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

• TRANSMISSION:

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

• DISEASE IN ANIMALS:

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

• DISEASE IN MAN:

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

• DIAGNOSIS:

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

• TREATMENT:

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

• PREVENTION\CONTROL:

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

• BORRELIOSIS

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

• RESERVOIR AND MODE OF TRANSMISSION:

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

• INCUBATION PERIOD:

Humans: 1-15 days. Animals.Unknown.

• CLINICAL FEATURES:

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

• PATHOLOGY:

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

• DIAGNOSIS:

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

• PROGNOSIS:

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

• PREVENTION:

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

• TREATMENT:

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

• LEGISLATION:

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

LYME DISEASE

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

• AGENT:

spirochete, Borrelia burgdorferi

• RESERVOIR AND INCIDENCE

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

• TRANSMISSION:

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

• DISEASE IN ANIMALS:

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

• DISEASE IN MAN:

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

• DIAGNOSIS:

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

• TREATMENT:

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

• PREVENTION\CONTROL:

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

Source

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