Chapter 16 : Emerging Enteric Protozoa: , , and Microsporidia

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The sometimes desperate search for an etiology of severe, life-threatening, and persistent diarrhea in patients with AIDS has led attention to three "new" or emerging protozoan enteric pathogens: , , and microsporidia. All three of these emerging enteric protozoa disrupt the intestinal epithelium and tend to cause persistent diarrhea. A recent longitudinal review in a community hospital suggests that elderly patients may also be predisposed to cryptosporidiosis, as 36% of infected patients in the study were 63 years of age or older. The prognosis is clearly better in individuals whose CD4 counts return toward normal, and preliminary results from two studies evaluating the efficacy of highly active antiretroviral therapy document improvement in either diarrhea or parasite shedding in patients with cryptosporidiosis or microsporidiosis. Since glutamine-coupled sodium absorption remains largely intact (and may be superior to glucose), oral rehydration and nutrition therapy (ORNT) holds promise both in rehydration and in speeding repair of disrupted bowel function in patients with cryptosporidial and other persistent diarrheas. Cyclosporiasis appears to have a striking summer rainy-season seasonality like cryptosporidiosis and has been associated with drinking contaminated water despite apparently adequate chlorination. , , and microsporidia clearly pose increasingly recognized threats to both immunocompetent and immunocompromised individuals through food and water supplies. Improved detection and animal models are needed in order to better understand the pathogenesis and epidemiology of infections, and little is known about the reservoir and potential vehicles and means of transmission of microsporidia.

Citation: Guerran R, Thielman N. 1998. Emerging Enteric Protozoa: , , and Microsporidia, p 233-245. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch16
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Image of Figure 1.
Figure 1.

History and presentation of , , and microsporidia.

Citation: Guerran R, Thielman N. 1998. Emerging Enteric Protozoa: , , and Microsporidia, p 233-245. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch16
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Image of Figure 2.
Figure 2.

Taxonomic relationship of , , and microsporidia. (Adapted from reference ).

Citation: Guerran R, Thielman N. 1998. Emerging Enteric Protozoa: , , and Microsporidia, p 233-245. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch16
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Figure 3.

Alterations in normal intestinal absorptive physiology by cryptosporidiosis. Studies by Argenzio et al. ( ) in a piglet model of cryptosporidiosis show (i) loss of nearly two-thirds of the vacuolated villus tip epithelium and surface area, accompanied by (ii) nearly 50% loss of glucose-coupled sodium cotransport and (iii) a predominance of transitional, junctional epithelium in which increased glutamine metabolism drives a sodium-hydrogen exchange coupled to chloride absorption. Studies further showed increased macrophage and tumor necrosis factor production in the lamina propria in Cryptosporidium-infected piglets and an indomethacin (or bumetanide)-inhibitable secretory effect in epithelial cells in Ussing chambers only when fibroblasts were also added ( ). 1bese results suggest a prostaglandin-dependent secretion via the bumetanide-sensitive chloride channels in the crypts and via inhibition of the amiloride-sensitive Na:H exchanger in the transitional epithelium. as shown.

Citation: Guerran R, Thielman N. 1998. Emerging Enteric Protozoa: , , and Microsporidia, p 233-245. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch16
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