1980
DOI: 10.1093/infdis/142.3.318
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Enterotoxigenic Escherichia coli and Other Gram-Negative Bacteria of Infantile Diarrhea: Surface Antigens, Hemagglutinins, Colonization Factor Antigen, and Loss of Enterotoxigenicity

Abstract: Heat-labile enterotoxin (LT)-producing Escherichia coli and other enteric bacteria isolated from diarrheal Ethiopian children were studied for O and K antigen, production of heat-stable enterotoxin (ST), stability of LT production, properties of mannose-resistant hemagglutination (MRHA) (indicative of adhesive properties), and colonization factor antigen (CFA). Of the E. coli strains, 33% possessed O6, O8, or O78; 93% of these were stable producers of LT, and 86% produced both Lt and ST. O78 strains possessed … Show more

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Cited by 63 publications
(36 citation statements)
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“…It has been reported that toxins produced by other enterobacteria may be less stable than that produced by E. coli (19). This appears not to be an absolute finding, based on our results.…”
Section: Fig 1 T I M E Course O F Enterotoxic Activities O F E Colcontrasting
confidence: 68%
“…It has been reported that toxins produced by other enterobacteria may be less stable than that produced by E. coli (19). This appears not to be an absolute finding, based on our results.…”
Section: Fig 1 T I M E Course O F Enterotoxic Activities O F E Colcontrasting
confidence: 68%
“…Heat-stable enterotoxin is produced by other bacteria considered autochthonous, such as Klebsiella pneumoniae (127), Enterobacter cloacae (128), and Proteus spp. (10). Thus, certain plasmidborne virulence genes may readily be exchanged by several bacterial genera; some may be transferred along with antibiotic resistance on resistance transfer factors (204).…”
Section: Microbial Ecology Of the Human Gastrointestinal Tractmentioning
confidence: 99%
“…Acute diarrhea is a significant worldwide health problem, especially for residents of, and travellers to, less developed nations. ETEC is a major cause of diarrheal disease in developing countries [1][2][3][4]. There is general agreement that maximal immunoprotection against ETEC is elicited by natural clinical infection, in which there is a high degree of intimate contact between bacterial anti-0920-8534/88/$03.50 ~ 1988 Federation of European Microbiological Societies gens, including virulence factors, and the intestinal immune system [5][6][7][8].…”
Section: Introductionmentioning
confidence: 99%