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Primate Bacterial Diseases

Like man, the nonhuman primate is susceptible to the wide variety of bacterial agents. There is little difference in susceptibility between most primate species; however, the macaques are more susceptible to tuberculosis and enteric bacteria, whereas the New World primates are more susceptible to the water-borne agents (Pseudomonas or Klebsiella). The bacteria that deserve the most concern are Mycobacteriaciae, Shigella/Salmonella, Campylobacter, and Klebsiella.

Mycobacteriaciae - Mycobacteria are responsible for tuberculosis, the scourge of the primate owner and veterinarian. Tuberculosis has been recognized as a common disease of captive primates for many years. Early outbreaks were devastating, causing the loss of hundreds of primates of many species. Species most susceptible are the macaques and apes; the New World species seemingly are more resistant. Almost all species can be experimentally infected. Historically, the three major species of mycobacteria--avium, bovis, and tuberculosis--have been incriminated as causing tuberculosis in the nonhuman primate. Recently, many atypical mycobacteria have also been reported in the nonhuman primate, including M. kansasii and M. scrofulaceum, all of which are potential hazards to man. The extreme susceptibility of monkeys to tuberculosis is often discussed; the disease is usually miliary, and arrest and calcification are unusual. The danger to owners and others who come in contact with infected monkeys is obvious. Control requires an effective quarantine for newly arrived primates, isolation from infected persons, and a rigorous testing program. It is generally agreed that the route of initial infection is usually respiratory (60 per cent) or intestinal (40 per cent). Because of their fulminating nature, terminal infections often present difficulty in establishing the portal of entry because so many organs are involved in the generalized infection.

The clinical signs of tuberculosis are not striking until the disease is in an advanced stage. The first sign may be a slight behavioral alteration. The animal may be slower than normal or stay along the floor of the enclosure rather than climb the enclosure or cage wall. Soon the infected animal will exhibit a dull appearance, crouch in the corner, and refuse to eat. The latter may be all the owner notices; coughing or other respiratory signs are conspicuously absent. Less common signs that may or may not be present with tuberculosis include diarrhea, skin ulceration, suppuration of Iymph nodes, and visible enlargement of the spleen and liver. Often there are no clinical signs, and the owner reports that the animal died suddenly without explanation. Radiographs of the lungs, ect., are usually nondiagnostic because of lack of calcification. The usual presence of mite (Pheumonysis spp.) lesions in normal rhesus monkeys complicates the radiographic diagnosis.

The lesions seen at necropsy are fairly typical yellowish-white to grey nodules that range from pinpoint size to several millimeters in diameter and appear just under the surface of the affected organs. As the disease progresses, the nodules fill with caseous material and may rupture and produce cavitation. Caseous, enlarged mediastinal lymph nodes in the rhesus monkeys are almost pathognomonic for tuberculosis. In baboons and apes, the disease is much more like that seen in man, with caseation and eventual calcification. Cutaneous tuberculosis in primates usually migrates to the regional Iymph nodes, and any draining lymph node should be suspected as a tubercular lesion until proven otherwise. Tuberculosis of the spine, or Pott's disease, also occurs in monkeys and should be considered whenever there is unexplained paralysis of the hind limbs.

Tuberculin skin testing must be part of any physical examination of a nonhuman primate. Newly imported primates should be tested biweekly and isolated until five negative tests have been certified. Approximately 15,000 tuberculin units (0.1 ml) of full-strength mammalian tuberculin is given intradermally in alternating eyelids. The test is read at 24, 48, and 72 hours. A positive reaction is any erythema and/or edema that persists for 48 hours or longer. Suspicious tests may be repeated at 7 days in the opposite eyelid or abdomen. Stabilized Old World primates should be tested quarterly, and New World monkeys semi-annually. Because of the public health danger and the potential resistance to treatment, positive animals should be euthanatized; treatment is NOT recommended. Atypical tuberculosis, other serologic methods, and so on, are beyond the scope of this article.

Shigella and Salmonella - Although shigellosis and salmonellosis are caused by two separate organisms, the symptons, signs, and treatment are similar, so they will be discussed together. Shigella and salmonella are frequently present in the alimentary tract of nonhuman primates. Isolation of the organism from the carrier animal is difficult, requiring numerous samples and enrichment techniques. A single negative culture means nothing. Fortunately, the most serious human pathogens of these two groups, Shigella dysenterriae type 1 and Salmonella typhi, have only rarely been isolated from nonhuman primates; however, several others (Shigella flexneri, S. sonnei, and Salmonella typhimirium, for example), which are also infectious to man, have been recovered.

The literature contains many reports of infection in primates and few reports of transmission to human beings. One of the earlier transmissions reported was a case of shigellosis in a child who licked an ice cream cone that had been touched by a monkey in a pet shop. This illustrates the potential danger for infants and children in contact with the species. Fortunately, the published reports of primate-to-man infections are rare. The primate carrying the organism can have a fulminating fatal infection at any time, with excretion of large numbers of organisms during the course of the disease. This acute infection is usually precipitated by some stress, such as environmental change of corticosteroids.

Clinical signs of shigellosis and salmonellosis are weakness, prostration edema of the face and neck, emaciation, and diarrhea with mucas and/or blood. As a rule, a bloody dysentery eventually occurs in shigellosis. Prolapse of the rectum is commonly seen, with death in a few days to 2 weeks after the onset of signs. At necropsy, the large intestine and diphtheritic colitis occurs with a varying degree of exudation and necrosis of the mucous membrane and ulceration that may penetrate the serosal surface.

Diagnosis is based on signs, necropsy, and culture results. Culture must be fresh, byt, even so, the isolation rate is low. Treatment for both entities is as follows: (1) take offor reduce feed; (2) provide fluids--lactated Ringers, 1/2 strength with 2.5 per cent dextrose given at a rate of 20 ml per kg or higher, depending on the state of dehydration; (3) administer antibiotics--trimethoprim and sulfadiazine (Tribrissen) will eliminate the carrier state if given conscientiously; and (4) administer kaolin plus pectin (Pectolin).

The family medical practitioner should be made aware of any pet monkey with symptoms of these diseases, particularly if children are or will be contact with the primate.

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