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A captive, adult male Goeldi's monkey (Callimico goeldii) (GM) presented in acute respiratory distress 4 yr after importation into the United States from Europe. Radiographs and echocardiogram were consistent with heart failure. The monkey died within 24 hr of presentation. Necropsy findings included multicentric arteritis and aortitis with aneurysm associated with microsporidian organisms morphologically consistent with Encephalitozoon species. Polymerase chain reaction confirmed organisms were Encephalitozoon cuniculi. Sequence analysis of amplicons generated by using primers specific for the polar tube protein of E. cuniculi determined the organism to be genotype II. An E. cuniculi serosurvey of potentially exposed conspecifics that represented approximately 40% of the captive GM population in the United States was conducted. Multiple individuals that had been imported from Europe with the individual of this report were seropositive via an immunofluorescent antibody assay for E. cuniculi. Multiple samples were available from 3 individuals that demonstrated a decrease in titer or reversion to seronegative status within 3 yr of initial positive status. All other GM were negative on serology. This case is unique in that the genotype identified (genotype II) was different than the genotype (genotype III) reported in other New World primate (NWP) species, the patterns of arteritis were different from the typical pattern of microsporidial vasculitis described in other species, and clinical disease was observed in an adult. Most reported cases of clinical disease secondary to E. cuniculi in NWP have been in neonates and juveniles.

The phylum Microspora contains a diverse group of single-celled, obligate intracellular protozoa sharing a unique organelle, the polar filament, and parasitizing a wide variety of invertebrate and vertebrate animals, including insects, fish, birds, and mammals. Encephalitozoon cuniculi is the classic microsporidial parasite of mammals, and encephalitozoonosis in rabbits and rodents has been and continues to be recognized as a confounding variable in animal-based biomedical research. Although contemporary research colonies are screened for infection with this parasite, E. cuniculi remains a cause of morbidity and mortality in pet and conventionally raised rabbits. In addition, E. cuniculi is a potential pathogen of immature domestic dogs and farm-raised foxes. The recent discovery and identification of Encephalitozoon intestinalis, Encephalitozoon hellem, and Enterocytozoon bieneusi, in addition to E. cuniculi, as opportunistic pathogens of humans have renewed interest in the Microspora. Veterinary pathologists, trained in the comparative anatomy of multiple animal species and infectious disease processes, are in a unique position to contribute to the diagnosis and knowledge of the pathogenesis of these parasitic diseases. This review article covers the life cycle, ultrastructure, and biology of mammalian microsporaidia and the clinical disease and lesions seen in laboratory and domestic animals, particularly as they relate to Encephalitozoon species. Human microsporidial disease and animal models of human infection are also addressed. Often thought of as rabbit pathogens of historical importance, E. cuniculi and the related mammalian microsporidia are emerging as significant opportunistic pathogens of immunocompromised individuals.

Background and Purpose: The gastrointestinal tract is a common portal of entry for Encephalitozoon cuniculi, one of several microsporidial organisms emerging as opportunistic pathogens in immunocompromised humans. Although most human microsporidial pathogens can be propagated in vitro and in a variety of laboratory animals, an experimental animal system to specifically study intestinal uptake and systemic spread of these organisms does not exist., Methods: Paired segments of near-term fetal rabbit small intestine were implanted subcutaneously into 25 athymic nude or 10 severe combined immune deficient mice. Five weeks after surgery, 65 xenografts were inoculated intraluminally with E. cuniculi (n = 14), E. intestinalis (n = 27), E. hellem (n = 20), or RK-13 cells (n = 2), or were left uninoculated (n = 2)., Results: Intestinal xenograft infection with E. cuniculi (n = 11), E. intestinalis (n = 17), and E. hellem (n = 18) was determined by light microscopy; control xenografts remained uninfected. Extraintestinal infection with E. cuniculi developed in host mouse brain, respiratory tract, spleen, salivary glands, and gastrointestinal tract (3 of 3 mice), and infection with E. intestinalis developed in the liver (8 of 15 mice)., Conclusion: Intestinal xenografts provide a unique, sterile, and biologically relevant animal model system for studying host enterocyte/parasite interactions, mechanisms of microsporidial pathogenicity, antimicrosporidial chemotherapeutic agents, and immune effector mechanisms. This model provides evidence for persistent graft infection with three Encephalitozoon spp., and for intestinal spread of E. cuniculi and E. intestinalis from infected enterocytes in immunoincompetent mice.