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Chapter 140 : Microsporidia

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Abstract:

Recent genome-wide sequence and synteny analyses indicate that the parasites of the phylum Microsporidia belong to the kingdom of the Fungi. Direct zoonotic transmission of microsporidia infecting humans has not been verified but appears likely because many microsporidial species can infect both humans and animals. Microsporidiosis has been associated with abnormalities in structures and functions of infected organs, but the mechanisms of pathogenicity of the different microsporidial species are not sufficiently understood. The most robust technique for the diagnosis of microsporidial infection is light microscopic detection of the parasites themselves. Evaluation of patients with suspected intestinal microsporidiosis should begin with light microscopic examination of stool specimens, and microsporidia which cause systemic infection are best detected in urine sediments or other body fluids. Microsporidial species causing disseminated infection have been found in almost every organ system. Only highly experienced pathologists have reliably and consistently identified microsporidia in tissue sections by using routine techniques such as hematoxylin and eosin staining. The isolation of microsporidia has no relevance for diagnostic purposes but is an important research tool. Microsporidial ultrastructure is unique and pathognomonic for the phylum, and ultrastructural features can distinguish all microsporidial genera. Observational studies showed that an improvement of immune functions by potent antiretroviral combination therapy results in complete clinical response and normalization of intestinal architecture, which parallels the clearance of intestinal microsporidia. Furthermore, various microsporidial species may cause self-limited diarrhea or keratoconjunctivitis in immunocompetent and otherwise healthy persons.

Citation: Weber R, Deplazes P, Mathis A. 2011. Microsporidia , p 2190-2199. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch140

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Image of FIGURE 1
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 parasite 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.

Citation: Weber R, Deplazes P, Mathis A. 2011. Microsporidia , p 2190-2199. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch140
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Image of FIGURE 2
FIGURE 2

Transmission electron micrograph showing the duodenal epithelium of an 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.)

Citation: Weber R, Deplazes P, Mathis A. 2011. Microsporidia , p 2190-2199. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch140
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Image of FIGURE 3
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).

Citation: Weber R, Deplazes P, Mathis A. 2011. Microsporidia , p 2190-2199. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch140
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Image of FIGURE 4
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).

Citation: Weber R, Deplazes P, Mathis A. 2011. Microsporidia , p 2190-2199. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch140
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Tables

Generic image for table
TABLE 1

Microsporidial species pathogenic in humans, and clinical manifestations

has been detected using PCR among persons with traveler's diarrhea and coinfection with sp. ( ); thus, the pathogenic role of remains unknown. Microscopic detection of spores in stool has not been reported so far.

is a collective generic name for microsporidia that cannot be classified because available information is not sufficient.

Citation: Weber R, Deplazes P, Mathis A. 2011. Microsporidia , p 2190-2199. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch140

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