Entamoeba histolytica-associated diarrheal illness is negatively associated with the growth of preschool children: evidence from a prospective study.
ABSTRACT The enteric protozoa, Cryptosporidium, Giardia and Entamoeba histolytica, cause diarrhea in children. We investigated the association of enteric protozoan-associated diarrheal illness with the nutritional status and growth of preschool children in Dhaka, Bangladesh. The subjects were 221 children aged 2-5 years who were followed prospectively for diarrheal illness for 3 years. The weight and height of the children were measured at entry and at 4-month intervals. Cryptosporidium and E. histolytica were diagnosed with commercially available stool antigen detection kits. Giardia was diagnosed by conventional microscopy. Cryptosporidium- and Giardia-associated diarrheal illness was not associated with the growth of the children. Children with E. histolytica-associated diarrheal illness had lower weight for age Z-score changes (-0.103+/-0.120 vs. 0.176+/-0.052, P=0.038). Similarly, the change in height for age Z-score was lower in children with E. histolytica-associated diarrheal illness (-0.348+/-0.186 vs. 0.142+/-0.08, P=0.018). Children with E. histolytica-associated diarrheal illness were 2.93 times (95% CI 1.01-8.52, P=0.047) more likely to be malnourished and 4.69 times (95% CI 1.55-14.18, P=0.006) more prone to be stunted. Entamoeba histolytica-associated diarrheal illness was negatively associated with the growth of preschool children.
Article: Tissue invasion by Entamoeba histolytica: evidence of genetic selection and/or DNA reorganization events in organ tropism.[show abstract] [hide abstract]
ABSTRACT: Entamoeba histolytica infection may have various clinical manifestations. Nine out of ten E. histolytica infections remain asymptomatic, while the remainder become invasive and cause disease. The most common form of invasive infection is amebic diarrhea and colitis, whereas the most common extra-intestinal disease is amebic liver abscess. The underlying reasons for the different outcomes are unclear, but a recent study has shown that the parasite genotype is a contributor. To investigate this link further we have examined the genotypes of E. histolytica in stool- and liver abscess-derived samples from the same patients. Analysis of all 18 paired samples (16 from Bangladesh, one from the United States of America, and one from Italy) revealed that the intestinal and liver abscess amebae are genetically distinct. The results suggest either that E. histolytica subpopulations in the same infection show varying organ tropism, or that a DNA reorganization event takes place prior to or during metastasis from intestine to liver.PLoS Neglected Tropical Diseases 02/2008; 2(4):e219. · 4.69 Impact Factor
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ABSTRACT: Amoebiasis (a human intestinal infection affecting 50 million people every year) is caused by the protozoan parasite Entamoeba histolytica. To study the molecular mechanisms underlying human colon invasion by E. histolytica, we have set up an ex vivo human colon model to study the early steps in amoebiasis. Using scanning electron microscopy and histological analyses, we have established that E. histolytica caused the removal of the protective mucus coat during the first two hours of incubation, detached the enterocytes, and then penetrated into the lamina propria by following the crypts of Lieberkühn. Significant cell lysis (determined by the release of lactodehydrogenase) and inflammation (marked by the secretion of pro-inflammatory molecules such as interleukin 1 beta, interferon gamma, interleukin 6, interleukin 8 and tumour necrosis factor) were detected after four hours of incubation. Entamoeba dispar (a closely related non-pathogenic amoeba that also colonizes the human colon) was unable to invade colonic mucosa, lyse cells or induce an inflammatory response. We also examined the behaviour of trophozoites in which genes coding for known virulent factors (such as amoebapores, the Gal/GalNAc lectin and the cysteine protease 5 (CP-A5), which have major roles in cell death, adhesion (to target cells or mucus) and mucus degradation, respectively) were silenced, together with the corresponding tissue responses. Our data revealed that the signalling via the heavy chain Hgl2 or via the light chain Lgl1 of the Gal/GalNAc lectin is not essential to penetrate the human colonic mucosa. In addition, our study demonstrates that E. histolytica silenced for CP-A5 does not penetrate the colonic lamina propria and does not induce the host's pro-inflammatory cytokine secretion.PLoS Neglected Tropical Diseases 01/2009; 3(11):e551. · 4.69 Impact Factor