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Before 1985, few human microsporidial infections had been reported. Since then, the number of cases has increased dramatically because of recognition of this pathogen in patients infected with HIV. Although most reported infections have occurred in HIV-infected people, the organism is recognized increasingly as pathogenic in other immunocompromised populations (e.g., organ transplant recipients), as well as in immunocompetent hosts.
Pathogen
Microsporidia are obligate, intracellular, spore-forming parasites that have been reclassified from protozoa to fungi ( Fig. 268.1 ). They are ubiquitous and infect most animal groups, including humans ( Table 268.1 ). At least 15 species of microsporidia have been reported to be pathogenic in humans. , Microsporidia are characterized by spore size, nuclear configuration, and relationship between the organism and its host cell. Replication occurs within the cytoplasm of the host cell by both binary fission (merogony) and multiple fission (schizogony), and it culminates in spore production (sporogony). Maturing spores accumulate within a vacuole that eventually ruptures and releases the spores. All microsporidial spores contain a complex tubular extrusion mechanism that injects the infectious substance (sporoplasm) from an infected cell into an uninfected host cell.
TABLE 268.1
Clinical Diseases Associated With Microsporidia
| Organism | Disease |
|---|---|
| Anncaliia algerae | Myositis, disseminated disease, keratopathy, skin infection |
| Anncaliia connori | Disseminated disease, keratopathy |
| Anncaliia vesicularum | Myositis |
| Encephalitozoon cuniculi | Encephalitis, hepatitis, peritonitis, keratopathy, sinusitis, osteomyelitis, pulmonary disease, disseminated disease |
| Encephalitozoon hellem | Keratopathy, disseminated disease, sinusitis, pneumonitis, nephritis, urethritis, cystitis |
| Encephalitozoon intestinalis | Diarrhea, cholangitis, disseminated disease, nodular skin lesions, keratopathy |
| Enterocytozoon bieneusi | Diarrhea, cholangitis, pulmonary disease |
| Microsporidium africanum | Keratopathy |
| Microsporidium ceylonensis | Keratopathy |
| Nosema ocularum | Keratopathy |
| Pleistophora ronneafiei | Myositis, disseminated disease, sinusitis |
| Trachipleistophora hominis | Myositis, disseminated disease |
| Trachipleistophora anthropophthera | Disseminated disease, encephalitis |
| Tubulinosema acridophagus | Disseminated disease |
| Vittaforma corneae | Keratopathy, urinary tract infection, diarrhea |
Epidemiology
The epidemiology of microsporidial disease is not defined clearly. Antibodies against Encephalitozoon cuniculi are relatively common in selected human populations, a finding suggesting that latent human infection may occur.
Transmission is thought to occur from person to person and through ingestion of contaminated water and food. Following ingestion, infectious spores travel to the intestine, where their contents are injected into cytoplasm of host cells. Intracellular division produces new spores that can spread to nearby cells, disseminate to other host tissues, or be passed into the environment through feces. Spores also have been detected in urine and respiratory tract epithelium, thus suggesting that related body fluids also can be infectious and that transmission also can be airborne. , Once in the environment, microsporidial spores remain infectious for ≤4 months. Zoonotic transmission has been proposed, as has vector-borne transmission. , The potential for vertical transmission of infection from an infected mother has not been documented in humans, but it occurs in other mammals.
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