Intestinal microsporidiosis was documented by detecting abundant slightly curved spores (2.9 x 1.2 pm) in the faeces of five of twelve skinks Mabuya perrotetii Duméril et Bibron, 1839 that originated from Ghana. Clinically, the microsporidiosis was characterized by decreased appetite, diarrhea, and weight loss. Histopathological changes consisted of villous atrophy, blunting of mucosa and flattening of individual epithelial cells in the large intestine. The ultrastructure of microsporidian spores was consistent with an Encephalitozoon species. The PCR-RFLP assay and the heleroduplex mobility shift analyses were used to verify that the skink microsporidian is a species of the genus Encephalitozoon Levaditi, Nicolau et Schoen, 1923 and indicate that this microsporidian is not E. hellem, E. intestinalis or a strain of E. cuniculi. The microsporidia in African skink represent an Encephalitozoon species morphologically identical to Encephalitozoon lacerine Canning, 1981.
Relatively few effective compounds are available for treating microsporidiosis in humans. In this study, several compounds were assayed for activity against Encephalitozoon intestinalis (Cali, Kotier et Orenstein, 1993) and Vittaforina corneae Shadduck, Meccoli, Davis ct Font, 1990 in vitro. Of the benzimidazoles tested, albendazole was most effective and the MIC50 values were 8.0 ng/ml and 55.0 ng/ml for E. intestinalis and V. corneae, respectively. Fumagillin and its analogue, TNP-470 were nearly equally effective against both E. intestinalis and V. comeae. The MIC50 values of fumagillin were 0.52 ng/ml and 0.81 ng/ml, and the MIC5() values of TNP-470 were 0.35 ng/ml and 0.38 ng/ml for E. intestinalis and V. comeae, respectively. In addition, 12 of 44 purines and pteridines with putative tubulin binding activity that were synthesized at Southern Research Institute (SRI), inhibited microsporidia) replication by more than 50% at concentrations that were not toxic to the host cells. Several chitin synthesis/assembly inhibitors inhibited growth of the microsporidia in vitro but were toxic for the host cells making it difficult to interpret the results. One exception was Iufcnuron, which caused no significant toxicity to the host cells and expressed approximate MICS0 values of 2.95 pg/ml and 6.3 pg/ml against E. intestinalis and V. comeae, respectively. These results warrant further studies on albendazole, fumagillin, TNP-470, lufenuron, and the selected SRI purines and pteridines for developing therapeutic strategies for microsporidiosis.