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symptoms lasting only days to weeks, but AIDS patients have a chronic intermittent diarrhea
lasting for months. After ingestion, infective oocysts release sporozoites that invade intestinal
epithelium where they develop into trophozoites, then schizonts. The schizonts may then release
merozoites, which invade other epithelial cells and become either schizonts or gametocytes,
which form zygotes and transform into infective oocysts passed with feces. By light
microscopy, the small intestinal mucosa (less frequently the colon in severe infections) shows
shortening and flattening of the villi with acute and chronic inflammation. Isospora organisms
develop within vacuoles 3-15 microns in size on histologic section in the intestinal epithelial
cells, and sometimes merozoites are visible. The infective oocysts of Isospora average 20-30
microns and can be seen easily in concentrated stool specimens with acid-fast staining.[401,486]
Microsporidiosis is produced by spore-forming intracellular protozoan parasites
identified in two genuses: Enterocytozoon and Encephalitozoon (Septata). In the genus
Enterocytozoon several species have been identified in persons with AIDS: E bieneusi, E
cuniculi, and E hellum. Encephalitozoon (Septata) intestinalis has also been
identified.[487,490,491] When diagnostic techniques are available, microsporidia may be even
more frequent than cryptosporidia as a cause for chronic diarrhea in AIDS patients. The clinical
features of GI infection with microsporidiosis mimic cryptosporidiosis. Microsporidia may also
be found outside of the intestine in biliary tract, urinary tract, and eye, while more uncommon
locations for involvement include nasal sinuses, respiratory tract, and central nervous
system.[487]
Microsporidial infection in man occurs when ingested spores invade intestinal epithelial
cells. The spores proliferate by fission to produce meronts. From meronts, sporonts develop and
divide into sporoblasts which then undergo metamorphosis to spores that are passed into
feces.[401,486] Diagnosis is made by small intestinal biopsy with characteristic transmission
electron microscopic appearance in villous epithelial cells of clusters of supranuclear
intracytoplasmic 4 to 5 micron sized meronts and sporonts or 1 to 2 micron acid fast spores.[492]
Microsporidiosis can also be diagnosed by light microscopy in tissue sections with Giemsa stain,
modified trichrome, or fluorescence staining of direct smears of unconcentrated stool or
duodenal aspirate specimens fixed with formalin.[486,487]
A modified trichrome stain can be useful for diagnosis of microsporidia in direct smears
of stool and duodenal aspirates that are unconcentrated and have been formalin-fixed.[491] In
addition, fluorescence methods can be utilized for detection of microsporidia (Enterocytozoon
and Septata species). The Fungifluor, Calcofluor white, and Fungiqual A fluorochrome stains
can be applied to stool specimens, enteric fluids, and tissue biopsies. Spores of these organisms
are best detected either in unfixed or in formalin-fixed specimens. These methods can be applied
to paraffin-embedded tissues.[493] Use of the polymerase chain reaction can also aid in
identification of microsporidial organisms.[487]
Another organism that can cause a diarrhea lasting for weeks to months leading to fatigue
and weight loss similar clinically to cryptosporidial diarrhea is Cyclospora cayetanensis.
Cyclosporiasis is a cause for traveler's diarrhea in both immunocompetent as well as
immunocompromised persons. Diarrhea may not be more severe in persons with HIV infection,
but has a high recurrence rate.[494] The causative agent is a small coccidian protozoa, originally
described as a blue-green algae or cyanobacterium, that can be detected in stool by acid fast
staining. The acid fast stained organisms demonstrate orange autofluorescence with blue (450 to
490 nm) fluorescent light microscopy. The organisms resemble a large cryptosporidium; they
are 8 to 10 microns in size, with a double cyst wall and a central morula. Small intestinal biopsy