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Principles and practice of Clinical parasitology - Gillespie S.

Gillespie S. Principles and practice of Clinical parasitology - Wiley publishing , 2001. - 675 p.
ISBN 0-471-97729-2
Download (direct link): principlesandpracticeofclin2001.pdf
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PATHOGENESIS AND IMMUNOLOGY
Neither the pathogenesis nor the immunology of human isosporiasis has received any experimental
attention, although studies of individual patients have afforded some insight into the impact of this infection on the intestinal epithelium (Brandborg et al., 1970; Soave and Johnson, 1988; Trier et al., 1974). Intestinal biopsies, often performed in protracted or refractory infections, have revealed a flattened mucosa with shortened villi and hypertrophic crypts. The parasite developmental stages are found predominantly within the epithelial cells and rarely in the lamina propria or submucosa. The reported inflammatory response in the lamina propria may be mixed, consisting of mononuclear cells (lymphocytes, plasma cells), polymorphonuclear leukocytes and often eosinophils. Consistent with these observations, malabsorption of fat, protein, sugar and vitamin B12 have been reported.
EPIDEMIOLOGY
Humans are the only recognized source of I. belli infection and, thus, unlike cryptosporidiosis, iso-sporiasis is not a zoonotic infection (Kirkpatrick,
1988). Given the usual need for sporulation of the oocysts of I. belli outside the human host, I. belli is believed to be transmitted primarily by contaminated food or water. Person-to-person spread through oral-anal contact in individuals with AIDS has been suggested (DeHovitz et al., 1986; Forthal and Guest, 1984; Ma and Soave, 1983).
I. belli is reported more commonly from tropical and subtropical areas of the world, but its true prevalence is unknown (Faust et al., 1961; Hunter et al., 1992; Soave and Johnson, 1988). In recent years, more attention has been drawn to this parasitic infection because of the recognition that it was a relatively common and treatable cause of persistent or chronic diarrhea in patients with AIDS living outside the USA (DeHovitz et al., 1986; Pape et al., 1989). In the USA, <0.2% of patients with AIDS have been recognized to have I. belli infection, whereas this infection is identified in approximately 15-20% of patients with chronic diarrhea and AIDS from, for example, Haiti, Zambia, Uganda and the Democratic Republic of Congo (formerly Zaire [1971-1997]) (Colebunders et al., 1988; Conlon
CRYPTOSPORiDiOSiS
157
et al., 1990; Henry et al., 1986; Hunter et al., 1992; Sewankambo et al., 1987; Soave and Johnson, 1988). I. belli infection is recognized as a cause of acute, persistent (>14-30 days) or chronic (>30 days) diarrhea in travelers (God-iwala and Yaeger, 1987; Shaffer and Moore,
1989). Occasional institution-based epidemics of I. belli infection have been reported suggesting that nosocomial spread or spread within daycare centers is feasible (Henderson et al., 1963).
CLINICAL FEATURES
In both immunocompetent and immunocompromised hosts, a non-specific watery diarrheal illness accompanied by abdominal cramps, nausea, malaise, anorexia and weight loss is the most common presentation of I. belli infection. Most infections in immunocompetent individuals are expected to be short-lived, whereas individuals with defects in cell-mediated immunity, such as AIDS, are predominantly reported to experience chronic diarrheal illnesses (DeHovitz et al., 1986; Forthal and Guest, 1984; Whiteside et al., 1984). However, the illness may be severe, resulting in dehydration. Up to 6 liters of stool output has been reported in an apparent immunocompetent host (Brandborg et al., 1970). This general pattern of illness makes this infection clinically indistinguishable from C. parvum infection. One of the notable features of I. belli infection is the ability of the parasite to cause strikingly protracted illnesses in immunocompetent hosts (Brandborg et al., 1970; Shaffer and Moore, 1989; Trier et al., 1974). Intermittent diarrheal illnesses of several months to possibly years in duration have been reported in immunocompetent individuals, including travelers. Dysentery or high fevers are not features of I. belli infection but, as indicated above, malabsorption is likely. Extraintestinal dissemination of infection has been reported in an AIDS patient (Restrepo et al., 1987).
intermittent, stool concentration and examination of multiple stools are advised to improve diagnostic sensitivity. The optimum number of stools necessary to establish a diagnosis is unknown, but examination of two unconcentrated stools had a diagnostic sensitivity of approximately 80% in AIDS patients (Pape et al., 1989). Similar to C. parvum, I. belli oocysts are acid-fast and will be detected using the rhodamine-auramine stain (Ma and Soave, 1983; Ng et al., 1984). The distinct morphology of I. belli oocysts permits them to be readily distinguished from either C. parvum or Cyclo-spora cayetanensis oocysts (Figure 6.4). Typically, the excreted unsporulated I. belli oocysts contain two sporoblasts. I. belli oocysts do not stain with hematoxylin, trichrome or iodine. In the absence of effective antibiotic treatment, oocyst excretion post-infection can be very protracted, often lasting 1-2 months with as long as 4 months reported (Henderson et al., 1963). The developmental stages of the parasite can be demonstrated in the epithelium of small bowel biopsies but this should only rarely be necessary for diagnosis (Brandborg et al., 1970; Trier et al., 1974). Neither fecal leukocytes nor blood are clearly reported in stools of patients infected with I. belli, although sensitive (but nonspecific) assays for intestinal inflammation, such as the fecal lactoferrin test, have not been evaluated (DeHovitz et al., 1986; Matsubayashi and Nozawa, 1948; Soave and Johnson, 1988). A notable feature of I. belli infection is its propensity to stimulate an eosinophilic response in the lamina propria, with concomitant Charcot-Leyden crystals detectable in stool samples. In addition, mild to moderate systemic eosinophilia in the absence of leukocytosis is commonly reported, although not always clearly attributable to I. belli infection (Brandborg et al., 1970; Matsubayashi and Nozawa, 1948; Trier et al., 1974).
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