Search

Despite numerous advances in the diagnosis and control of infectious diseases of nonhuman primates in the laboratory setting, a number of infectious agents continue to plague colonies. Some, such as measles virus and Mycobacterium tuberculosis, cause sporadic outbreaks despite well-established biosecurity protocols, whereas others, such as retroperitoneal fibromatosis-associated herpesvirus, have only recently been discovered, often as a result of immunosuppressive experimental manipulation. Owing to the unique social housing requirements of nonhuman primates, importation of foreign-bred animals, and lack of antemortem diagnostic assays for many new diseases, elimination of these agents is often difficult or impractical. Recognition of these diseases is therefore essential because of their confounding effects on experimental data, impact on colony health, and potential for zoonotic transmission. This review summarizes the relevant pathology and pathogenesis of emerging and reemerging infectious diseases of laboratory nonhuman primates.

An outbreak of natural measles virus infection occurred in a group of Japanese macaques (Macaca fuscata). Over a period of 4 months, 12 of 53 Japanese macaques died following a 2-23-day history of anorexia, diarrhea, and dermatitis. The monkeys were kept in outdoor exhibits but had been moved temporarily into indoor caging and then transferred to new outdoor exhibits. Ten monkeys died while they were in temporary caging, and two monkeys died after they were moved to new outdoor exhibits. The diagnoses were made based on the results of histopathology, immunohistochemistry (IHC), in situ hybridization (ISH), and electron microscopy. Measles virus antigens were detected in the lung, stomach, skin, salivary gland, spleen, and lymph nodes. Tangled, tubular nucleocapsids compatible with paramyxovirus were noted in the lung tissue. As a result of immunosuppression following measles virus infection, various secondary infections including disseminated cytomegalovirus infection, adenoviral and bacterial pneumonia, and Candida albicans-associated gingivitis and esophagitis were noted. The primary infective source or the mode of infection could not be determined in this outbreak, but measles virus may have been transmitted to the monkeys from human visitors while the monkeys were on exhibit.

Two female rhesus macaques (Macaca mulatta) and one female pigtailed macaque (M. nemestrina) developed acute neurological signs including ataxia, muscular incoordination, and seizures. Light microscopy showed Cowdry Type A intranuclear inclusion bodies in astrocytes and neurons of the cerebral cortex and Purkinje's cells of the cerebellum. Many cells also had intracytoplasmic inclusion bodies. Electron microscopy identified paramyxoviral nucleocapsids in the intranuclear and intracytoplasmic inclusions in two monkeys. We believe these monkeys had measles encephalitis because measles virus is the only paramyxovirus known to cause inclusion bodies in macaques and because the lesions in these monkeys resembled measles encephalitis in man.