Most Escherichia coli strains live harmlessly in the intestines and rarely cause disease in healthy individuals. Nonetheless, a number of pathogenic strains can cause diarrhea or extraintestinal diseases both in healthy and immunocompromised individuals. Diarrheal illnesses are a severe public health problem and a major cause of morbidity and mortality in infants and young children, especially in developing countries. E. coli strains that cause diarrhea have evolved by acquiring, through horizontal gene transfer, a particular set of characteristics that have successfully persisted in the host. According to the group of virulence determinants acquired, specific combinations were formed determining the currently known E. coli pathotypes, which are collectively known as diarrheagenic E. coli. In this review, we have gathered information on current definitions, serotypes, lineages, virulence mechanisms, epidemiology, and diagnosis of the major diarrheagenic E. coli pathotypes.

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Escherichia coli strains of nonenteropathogenic serogroups carrying eae but lacking the enteropathogenic E. coli adherence factor plasmid and Shiga toxin DNA probe sequences were isolated from patients (children, adults, and AIDS patients) with and without diarrhea in Brazil. Although diverse in phenotype and genotype, some strains are potentially diarrheagenic.

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The natural diversity of the elt operons, encoding the heat-labile toxin LT-I (LT), carried by enterotoxigenic Escherichia coli (ETEC) strains isolated from humans was investigated. For many years, LT was supposed to be represented by a rather conserved toxin, and one derivative, produced by the reference H10407 strain, was intensively studied either as a virulence factor or as a vaccine adjuvant. Enterotoxigenic Escherichia coli (ETEC)-associated diarrhea represents a major cause of mortality and morbidity among children and travelers, respectively, in most developing countries in Latin America, Africa, and Asia (3, 33). ETEC secretory diarrhea involves a rather straightforward pathogenesis plan, requiring first colonization of small intestine epithelial cells by means of filamentous adhesins collectively known as colonization factors (CFs) and, at a second stage, production of at least one out of two enterotoxin types, the heat-stable toxin (ST) and/or the heat-labile toxin (LT) (28, 36). One of the most complex aspects of ETEC pathogenesis is the remarkable antigen heterogeneity. At least 150 O:H serotypes have been found among ETEC strains isolated from humans, although a more restricted number of serotype combinations is detected among strains isolated from patients requiring medical intervention, also characterized, in some cases, by a conserved set of virulence-associated factors and a common clonal origin (29,30,46). Moreover, the ETEC phenotypic heterogeneity is also well illustrated by the encoded virulence-associated factors, including more than 20 known CFs and production of LT, ST, or both enterotoxins (10,33,46). Two types of ST, STa and STb (also known as ST-I and ST-II), have been differentiated based on biological and chemical features (7,11). Similarly, LTs produced by ETEC strains are also a heterogeneous group of toxins. Two major LT families have been identified, LT-I and LT-II. LT-II is rarely found among human-derived ETEC strains, but two natural variants have been reported, LT-IIa and LT-IIb, based on differences in the subunit sequences (14, 16). LT-I shows a rather high similarity with cholera toxin (CT) (over 80% amino acid identity), and both have been intensively studied as virulence factors and modulators of immune responses in mammalian species, including humans (18,28).The known natural variability of LT-I toxins expressed by ETEC strains has been mainly restricted to the differences detected between LTs produced by human (LTh)-and pig (LTp)-derived strains. Initial evidence based on the antigenicities and electrophoretic mobilities of LTh and LTp indicated that the toxins differ in their primary amino acid sequences (19,42). Sequencing of the elt operons encoding LTh and LTp revealed differences in the primary sequences of the toxins, which share over 95% identity along the complete amino acid sequence (45). Altogether, six amino acid replacements were detected between the A subunits (K4R, K213E, and N238D) and the B subunits (S4T, A46E, and E102K) of LTh and LTp derived from th...

Twenty-nine Shiga toxin-producingShiga toxin-producing Escherichia coli (STEC) can cause a broad spectrum of human illness ranging from uncomplicated diarrhea to hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS) (14). E. coli O157:H7 is by far the most important STEC serotype in the world and has been associated with numerous outbreaks and many sporadic cases of HC and HUS (20). However, infections with other non-O157 STEC serotypes have been increasingly reported in many countries (2,3,22). Currently more than 100 different non-O157 STEC serotypes have been isolated from human infections. Unlike with O157:H7, outbreaks caused by non-O157 STEC have rarely been reported, and these strains have been more frequently associated with sporadic cases of diarrhea, HC, and HUS. Moreover, in many countries, non-O157 strains are more commonly isolated from patients with diarrhea or HUS than are O157 STEC strains (3, 5, 23). The major virulence trait of these bacteria is the production of one or more Stx types (Stx1, Stx2, or Stx2 variants) (20). Additional factors, produced mainly by strains in straight association with human disease and collectively referred to as enterohemorrhagic E. coli (EHEC), include intimin and enterohemolysin (1,20). Other putative virulence factors include the enteroaggregative E. coli heat-stable enterotoxin (EAST-1), encoded by astA (25), particularly in O157:H7 and O26:H11 strains and in some other STEC serotypes. In Brazil, the studies conducted so far that searched for STEC in human diarrheal disease have investigated a limited number of strains and have described the isolation of a few non-O157 STEC strains (7,12,16). The isolation of O157:H7 strains from patients with bloody diarrhea as well as one with HUS related to O26:H11 infection was only recently reported in Brazil (15,19).The purpose of this study was to search for STEC in a collection of 2,607 E. coli isolates, most of them belonging to important serogroups increasingly associated with HUS and HC in other countries. The main virulence factors, biotypes, and susceptibility to antimicrobial agents of the STEC strains identified were characterized.The E. coli strains studied belonged to the collection of Instituto Adolfo Lutz, a Central Public Health Laboratory in São Paulo, Brazil, and national center for E. coli serotyping, and were isolated between 1976 and 1999, mainly from children (0 to 5 years old) with diarrhea (2,549 strains); the remaining 58 E. coli strains were isolated from immunocompromised adult patients with diarrhea (mainly human immunodeficiency virus positive) over the same period. Each strain was derived from one patient. Except for diarrhea, no other information regarding the clinical aspects of the patients were available. None of the strains belonging to the enteropathogenic E. coli (EPEC) serogroups carried the EAF sequence (EPEC adherence factor) as assayed by hybridization assays with a specific DNA probe (13). The remaining strains outside the EPEC serogroups did not belong to the enteroinvasive ...

h Shiga toxin-producing Escherichia coli strains of serotype O113:H21 have caused severe human diseases, but they are unusual in that they do not produce adherence factors coded by the locus of enterocyte effacement. Here, a PCR microarray was used to characterize 65 O113:H21 strains isolated from the environment, food, and clinical infections from various countries. In comparison to the pathogenic strains that were implicated in hemolytic-uremic syndrome in Australia, there were no clear differences between the pathogens and the environmental strains with respect to the 41 genetic markers tested. Furthermore, all of the strains carried only Shiga toxin subtypes associated with human infections, suggesting that the environmental strains have the potential to cause disease. Most of the O113:H21 strains were closely related and belonged in the same clonal group (ST-223), but CRISPR analysis showed a great degree of genetic diversity among the O113:H21 strains.