This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Three species of microsporidia were identified as causes of morbidity and mortality in fruit bats, salamanders, and tamarins that were reported in three sets of case reports. Their relevance was that these microsporidia species also infect humans so these infected animals may serve as reservoirs of infection.Disseminated microsporidiosis was diagnosed in an adult female Egyptian fruit bat (Rousettus aegyptiacus) that died unexpectedly in a zoo. Gross findings included poor body condition, bilateral renomegaly, and mottling of the liver. Histopathological lesions consisted of inflammation associated with intracytoplasmic microsporidian spores in the urogenital tract and liver. PCR established the microsporidian as Encephalitozoon hellem. This is the first documented case of E. hellem in a non-human mammalian species.Captive refugia for four species of plethodontid salamanders were established. Following this successful maintenance, two of the species presented with kyphosis. In one of these species (San Marcos salamander, Eurycea nana), microsporidial organisms within the epaxial musculature were identified in post-mortem histopathology and confirmed by polymerase chain reaction rDNA sequence as most closely similar to Encephalitozoon hellem. However, ultrastructural analysis and further rDNA sequencing suggested a new species of Pleistophora. In these affected individuals, the microsporidial infection produced kyphosis resulting from inflammation and fibrosis of the expaxial musculature to the parasite.Disseminated encephalitozoonosis was diagnosed in 2 sibling, juvenile cotton-top tamarins (Saguinus oedipus) and 3 sibling, neonatal, emperor tamarins (S. imperator) that were captive born in zoos in North America. Histologic examination, histochemical analysis, electron microscopy, and PCR were used to identify the cause as Encephalitozoon cuniculi genotype III. The dam, but not sire, of the emperor tamarins was seropositive for E. cuniculi by ELISA and Western blot immunodetection. The death of two less than one-day-old emperor tamarins from a seropositive dam supports the likelihood of vertical transmission in the tamarins.

National Institute of Health (NIH)
National Center for Research Resources (NCRR)
Primate Research Center Grants (P51)
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Special Emphasis Panel (ZRR1-CM-9 (01))
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Tulane University
Schools of Medicine
New Orleans
United States
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