Objective: To demonstrate the ultrastructural features of normal and atypical (teratoid) developmental stages of Enterocytozoon bieneusi in naturally infected rhesus monkeys (Macacca mulatta).
Design and methods: Two rhesus monkeys with chronic simian immunodeficiency virus infection developed naturally acquired microsporidian infections. The gallbladder had a high parasite burden and was evaluated by transmission electron microscopy. The microsporidian agent was confirmed as E bieneusi by polymerase chain reaction.
Results: In addition to normal sporogonial plasmodia and spores of E bieneusi, abnormal teratoid structures were noted. These structures were greatly enlarged (up to 10 microm) and were surrounded by an electron-dense exospore and electron-lucent endospore typical of mature spores. Unlike mature spores, the abnormal structures contained multiple nuclei and polar tubes in varying proportions, which were reminiscent of sporogonial plasmodia.
Conclusions: These teratoid structures represent aberrant sporogonial stages, a result of defective maturation in which abnormal cytokinetic replication of organelles occurs, and normal development into uninucleate sporoblasts and spores is inhibited. This leads to the development of teratoid stages having mature spore walls, but containing multiple sets of nuclei and polar tubes, unusual polyribosomal arrays and vacuoles, or persistent cleavage. The biological significance of these atypical spores is unknown, but it is evident that they develop in the absence of antimicrosporidian drugs in extraintestinal tissues from nonhuman primates. Teratoid spores of E bieneusi should not be misinterpreted as another microsporidian species or confused with other pathogenic protozoa, nor should their presence be misconstrued as evidence of antimicrosporidian drug efficacy or toxicity.