Disseminated Microsporidiosis in an Immunosuppressed Patient

Eric G. Meissner

, John E. Bennett, Yvonne Qvarnstrom, Alexandre da Silva, Emily Y. Chu, Maria Tsokos, and Juan Gea-Banacloche

Author affiliations: National Institutes of Health, Bethesda, Maryland, USA (E.G. Meissner, J.E. Bennett, E.Y. Chu, M. Tsokos, J. Gea-Banacloche); and Centers for Disease Control and Prevention, Atlanta, Georgia, USA (Y. Qvarnstrom, A. da Silva)

Abstract

We report a case of disseminated microsporidiosis in a patient with multiple myeloma who had received an allogeneic stem cell transplant requiring substantial immunosuppression. The causative organism was identified as Tubulinosema acridophagus, confirming this genus of microsporidia as a novel human pathogen.

Microsporidia fungi are human pathogens known for causing diarrheal illness in persons infected with HIV; however, there is growing awareness of their involvement in other cases of host immunosuppression. A case of Tubulinosema sp. microsporidian myositis was recently reported in a patient with chronic lymphocytic leukemia (1). We describe a second case of disseminated microsporidiosis caused by a Tubulinosema sp. in an immunosuppressed patient who received an allogeneic stem cell transplant for multiple myeloma.

Case Report

The patient was a 33-year-old woman with multiple myeloma. After receiving an autologous stem cell transplant (SCT), she experienced a relapse of disease and was enrolled in an experimental protocol of immunoablative chemotherapy, followed by hematopoietic SCT at the National Institutes of Health Clinical Center in Bethesda, Maryland (www.ClinicalTrials.gov

identifier NCT00520130). Patients in this study are given a conditioning regimen of chemotherapy drugs (including fludarabine and cyclophosphamide), followed by prophylaxis against graft-versus-host disease (alemtuzumab and cyclosporine).
The patient received a 7/8 HLA-matched allogeneic peripheral blood SCT (with a single mismatch at the DRB1 locus) from an unrelated donor. Her clinical course was complicated by vancomycin-resistant Enterococcus faecium bacteremia, meningitis, and concomitant noncommunicating hydrocephalus and retinal hemorrhages. The bone marrow did not reconstitute, and 35 days after the initial transplant, the patient received a second SCT from the same donor after a conditioning regimen with antithymocyte globulin. Engraftment took place on day 49, 14 days after the second transplant. Progressive respiratory failure and pulmonary infiltrates had developed over the preceding week despite administration of broad-spectrum antimicrobial drugs. Results of a bronchoscopy on day 49 showed diffuse alveolar hemorrhage and did not identify a pathogen. Treatment with activated factor 7 and corticosteroids was given with some clinical improvement as well as improvement shown on chest radiograph.
A second bronchoalveolar lavage (BAL), performed on day 64, again showed diffuse alveolar hemorrhage and absence of pathogens. The patient received a second course of corticosteroids and activated factor 7. On day 77, an ophthalmologic examination was performed during a routine follow-up, and new retinal lesions suggestive of candida chorioretinitis were seen. Liposomal amphotericin B was substituted for prophylactic anidulafungin, and an intravitreal injection of amphotericin B was given for a subfoveal lesion.