Chapter 128 : Microsporidia

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Microsporidia, Page 1 of 2

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Microsporidia are obligate intracellular, unicellular, spore-forming eukaryotes that belong to the kingdom of the Fungi. Their host range is extensive, including most invertebrates and all classes of vertebrates. More than 160 microsporidial genera and 1,300 species have been identified. Nine genera (, , , , , , , , and ) and unclassified microsporidia have been implicated in human infections. Microsporidiosis appears to occur most frequently in HIV-infected patients, but it is emerging in otherwise immunocompromised and also in immunocompetent persons. The sources of microsporidia infecting humans and their modes of transmission are uncertain but ingestion of the environmentally resistant spores is probably the most important mode of transmission; transmission by dust or aerosol may also occur. Waterborne, foodborne, and zoonotic infections have been reported. In the immunocompromised host, microsporidial infections were found in organ-transplant recipients, in patients with hematologic malignancies receiving monoclonal antibody therapy, in patients with rheumatic disease undergoing anti-tumor necrosis factor therapy, in the elderly, and in malnourished children. The clinical manifestations are diverse, including intestinal, pulmonary, ocular, muscular, cerebral, renal disease, and disseminated infection. In immunocompetent persons, microsporidia are associated with keratoconjunctivitis, self-limiting diarrhea, and rarely cerebral infection. Microsporidia are also detected in asymptomatic persons. Diagnosis is made by morphological or molecular detection of the organisms. Immunofluorescence technique, electron microscopy, or genetic analyses allow species identification. Treatment options are limited; some microsporidial species respond to albendazole. The most frequent HIV-associated opportunistic species, , causing diarrhea, is not susceptible to albendazole but may be treated with the experimental drug fumagillin.

Citation: Weber R, Deplazes P, Mathis A. 2015. Microsporidia, p 2209-2219. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch128
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Image of FIGURE 1

Generalized life cycle of microsporidia and identifying characteristics of the genera known to infect humans. Light stippling indicates merogonic stages; heavy stippling indicates sporogonic stages; no stippling indicates spores and sporoplasm. (A) Basic life cycle, illustrated by Development may occur in direct contact with host-cell cytoplasm (, , and ) or in isolation by host cell membranes ( and ) or a cyst-like sporophorous vesicle of pathogen origin ( and ). 1, Sporoplasm: the infective stage emergent from the spore. It may have unpaired nuclei (monokaryotic) or two nuclei in close apposition (diplokaryotic), depending on the genus. 2, Merogony: proliferative stage. It may have a simple plasma membrane, but a surface coat is present in , , and . Division can be by binary or multiple fission into two or more individuals. 3, Sporont: the first stage of sporogony. If not already present, a surface coat is added (this step is delayed in ). 4, Sporogony: divisions culminating in spore production. Binary or multiple fissions give rise to sporoblasts. 5, Sporoblasts: end products of sporogony, which mature into spores. 6, Spores: resistant stages for transmission. Spores are characterized by an extrusion apparatus (polar tube), which serves to conduct the sporoplasm into a host cell. The polar tube may be of uniform diameter (isofilar) or show a sharp decrease in diameter in the most posterior coils (anisofilar). (B to G) Identifying characteristics of genera. (B) . Members of this genus are diplokaryotic and disporoblastic; the life cycle is like that of , but meronts are of bizarre shapes and possess a surface coat with vesiculotubular structures (vt) embedded in it and extended from it. (C) . Members of this genus are diplokaryotic and polysporoblastic; all stages, including spores, are isolated in a close-fitting, ribosome-studded cisterna of host endoplasmic reticulum (er). (D) . Members of this genus are monokaryotic and polysporoblastic; meronts and sporonts are multinucleate stages called plasmodia; a thick surface coat is already present on meronts and sporonts ( ); this coat separates from the sporogonial plasmodium to form a cyst-like vesicle, the sporophorous vesicle; the plasmodium divides within it to produce numerous spores ( ). (E) . Members of this genus are monokaryotic and polysporoblastic. The meront surface coat has branched extensions ( ); these are withdrawn when the coat separates to form the sporophorous vesicle around a uninucleate sporont; the sporont undergoes a series of binary fissions ( and ) and finally encloses numerous spores ( ). (F) . Members of this genus are monokaryotic and di- or tetrasporoblastic; all stages of the life cycle, developing from the sporoplasm, occur concurrently within a host cell vacuole (parasitophorous vacuole); merogonic stages are appressed against the vacuole wall; sporogonic stages are free; the vacuole is finally packed with spores, so that it superficially resembles a sporophorous vesicle. (G) . Members of this genus are monokaryotic and polysporoblastic; meronts ( ) have irregular nuclei and lucent clefts; sporonts ( ) are multinucleate with rounded nuclei and have highly characteristic electron-dense disks, which are polar tube precursors; all spore organelles are formed prematurely, so that constriction around the sets of organelles and a nucleus ( ) gives rise directly to almost mature spores. The surface coat is deposited only during constriction. doi:10.1128/9781555817381.ch128.f1

Citation: Weber R, Deplazes P, Mathis A. 2015. Microsporidia, p 2209-2219. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch128
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Image of FIGURE 2

Transmission electron micrograph showing the duodenal epithelium of a HIV-infected patient infected with . The different developmental stages between the enterocyte nuclei and the microvillus border include a proliferative plasmodium ( ), late sporogonial plasmodia ( ), and mature spores (arrow). Magnification, ×5,370. (Courtesy of M. A. Spycher, University Hospital, Zurich, Switzerland.) doi:10.1128/9781555817381.ch128.f2

Citation: Weber R, Deplazes P, Mathis A. 2015. Microsporidia, p 2209-2219. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch128
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Image of FIGURE 3

Smear of a stool specimen from a patient with AIDS and chronic diarrhea, showing pinkish red-stained spores of that measure 0.7 to 1.0 by 1.1 to 1.6 μm. Chromotrope staining was used. Magnification, ×1,000 (oil immersion). doi:10.1128/9781555817381.ch128.f3

Citation: Weber R, Deplazes P, Mathis A. 2015. Microsporidia, p 2209-2219. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch128
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Image of FIGURE 4

(Left) Terminal ileal tissue obtained by ileocolonoscopy from a patient with AIDS and chronic diarrhea due to infection. Gram-labile microsporidial spores, measuring 0.7 to 1.0 by 1.1 to 1.6 μm, are found at a supranuclear location within small intestinal enterocytes. Brown-Brenn stain was used. Magnification ×1,000. (Middle) Cytospin preparation of bronchoalveolar-lavage fluid from a patient with AIDS and intestinal infection, showing intracellular microsporidia. Giemsa stain was used. Magnification ×1,000 (oil immersion). (Right) Urine sediment from a patient with AIDS and disseminated infection, showing pinkish red-stained microsporidial spores measuring 1.0 to 1.5 by 2.0 to 3.0 μm. Chromotrope stain was used. Magnification, ×1,000 (oil immersion). doi:10.1128/9781555817381.ch128.f4

Citation: Weber R, Deplazes P, Mathis A. 2015. Microsporidia, p 2209-2219. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch128
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Microsporidial species pathogenic in humans, and clinical manifestations

Citation: Weber R, Deplazes P, Mathis A. 2015. Microsporidia, p 2209-2219. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch128

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