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Microsporidiosis After Solid Organ Transplantation: A Multi-Species Case Series
Jack McHugh1, Zahra N Sohani1, Raymund R Razonable1,2
1Division of Public Health, Infectious Diseases, and Occupational Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Background:
Microsporidiosis is an uncommon opportunistic infection in solid organ transplant (SOT) recipients. Case-level data on multi-species disease and management remain limited.
Methods:
We retrospectively reviewed SOT recipients with microsporidiosis at Mayo Clinic from January 2000 through February 2026. Cases were identified by text search and institutional polymerase chain reaction (PCR) records. Clinical, microbiologic, treatment, immunosuppression, and outcome data were abstracted.
Results:
Ten recipients were identified: six kidney, two kidney-pancreas, and two heart recipients. Eight had enteritis and two had disseminated disease. Enterocytozoon bieneusi caused seven infections; the remaining cases were Encephalitozoon sp. enteritis, disseminated E. cuniculi, and disseminated Anncaliia algerae. All enteritis cases experienced diarrhea; seven experienced weight loss, five developed acute kidney injury, and five required hospitalization. The most common treatment administered was nitazoxanide (n = 6). Among these three achieved clinical remission, one improved without documented remission, and two had transient or partial improvement followed by recurrent diarrhea. Among four patients whose antimetabolite was held, reduced, or replaced at or before treatment, all improved clinically. In the two initially treated without antimetabolite modification, responses were transient or incomplete. Both Encephalitozoon infections achieved clinical remission with albendazole. Disseminated A. algerae was fatal.
Conclusions:
Microsporidiosis after SOT demonstrated a species-associated clinical spectrum: E. bieneusi was confined to enteritis, whereas non-E. bieneusi species caused both enteric and disseminated disease. In E. bieneusi enteritis, nitazoxanide improved symptoms, but responses were incomplete when antimetabolite therapy was continued. Encephalitozoon infections responded to albendazole, whereas disseminated A. algerae was refractory and fatal.
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