Enteropathogenic Escherichia coli (EPEC) produces a lesion on epithelial cells called the attaching and effacing (AE) lesion. All genes necessary for AE are encoded within the locus of enterocyte effacement (LEE). EPEC also adheres in a characteristic pattern to epithelial cells by forming microcolonies, usually referred to as localized adherence (LA). LA is mediated by the bundle-forming pilus and flagella. The LEE genes are directly activated by the LEE-encoded regulator (Ler). Transcription of Ler is under the control of Per, integration host factor, Fis, BipA, and quorum sensing (QS), specifically through the luxS system. QS activates expression of the LEE genes in EPEC, with QseA activating transcription of ler. Here we report that transcription of the LEE genes and type III secretion are diminished in both luxS and qseA mutants. Transcription of the LEE genes is affected in both mutants mostly during the mid-exponential phase of growth. Transcription of qseA itself is diminished throughout growth in a luxS mutant and is under autorepression. Furthermore, QS activation of type III secretion is independent of per, given that QseA still activates type III secretion in a per mutant strain. Both mutants are deficient in adherence to epithelial cells and form smaller microcolonies. Several factors may contribute to this abnormal behavior: transcription of LEE genes and type III secretion are diminished, and expression of flagella and Per is altered in both mutants. These results suggest that QS is involved in modulating the regulation of the EPEC virulence genes.Enteropathogenic Escherichia coli (EPEC) is a major cause of diarrhea in children in developing countries (29). EPEC is part of a group of pathogens that includes enterohemorrhagic E. coli (EHEC), Citrobacter rodentium, and Hafnia alvei, all of which are able to cause a lesion on the intestinal epithelial cells named the attaching and effacing (AE) lesion. This lesion is characterized by the destruction of the microvilli and rearrangement of the cytoskeleton to form a pedestal-like structure which cups the bacteria individually (21,28,48). The genes involved in the formation of the AE lesion are encoded within a chromosomal pathogenicity island named the locus of enterocyte effacement (LEE) (25). The LEE region contains five major operons, i.e., LEE1, LEE2, LEE3, tir (LEE5), and LEE4

Resistance of Escherichia coli to trimethoprim (TMP)-sulfamethoxazole remains at 3%-8% at many medical centers within the United States. In this study a 44% resistance rate was observed among E. coli isolated at a pediatric hospital in Santiago, Chile, and a 40% resistance rate at a general teaching hospital in Bangkok, Thailand. Most isolates were from urinary tract infections and showed high-level resistance (minimal inhibitory concentration of TMP greater than 1,000 micrograms/ml). Nineteen of 35 isolates tested transferred resistance to TMP; most cotransferred resistance to streptomycin and sulfonamides. Dihydrofolate reductase type I was detected by gene probing in 14 of 35 strains. Subsequent investigations in Brazil, Honduras, and Costa Rica revealed that this high rate of resistance was not an isolated phenomenon.

Escherichia coli strains belonging to serotype 0128ac:H12 and producing heatstable enterotoxin (ST) and colonization factor CFA/I were found in Sao Paulo in children with diarrhea, but not in normal children. Segregants occurred in such strains with a frequency of about 10%, which have lost the ability to produce ST and CFA/I at the same time. From one strain, both properties were transferred jointly in matings to an E. coli K-12 strain. All such ST' CFA/I+ progeny had

A total of 102 Escherichia coli strains belonging to serogroups O127 and O142 were examined for genotypic and phenotypic characteristics. The most frequent serotypes found were O127:H21, O127:H40 and O142:H34. The virulence properties were evaluated by adhesion to HeLa cells and hybridization with gene probes for diarrhoeagenic E. coli. Most strains in the two serogroups were categorized as enteropathogenic E. coli, but enteroaggregative E. coli was also detected in both serogroups. All strains that carried the eae sequence presented the LEE region inserted in selC. Five ribotypes were detected in serogroup O127 and four in serogroup O142 and a correlation between serotypes and ribotypes was observed mainly in serogroup O142.

Heat-stable enterotoxin I (STI) can be assayed in intestinal loops of pigs and rabbits and in the gut of infant mice. To produce a simpler and more discriminating assay procedure, we used three gene probes corresponding to three forms of STI called STIa, STIb, and STIc. We tested 159 Brazilian isolates, of which 40 were positive in the infant mouse assay. The STIb and STIc probes are similar (93% DNA homology) and are both different from the STIa probe (70% DNA homology). Of 33 strains that were still active for STI 3 years after their isolation, 25 reacted with both the STIb and STIc probes, 4 reacted with the STIc probe only, and 7 reacted strongly with the STIa probe and weakly or not at all with the other probes. Two strains reacted with all three probes. Further analysis showed that each of these two strains contains a small plasmid that reacts with the STIa probe and a large plasmid that reacts with the STIc probe in one strain and weakly with both the STIa and STIc probes in the other strain. It was also shown that the STIa probe reacts with the cloning vehicle pACYC184 used for the cloning of STIc. We conclude that the gene probes used can identify most STI-producing strains and that in cases of positive responses with several probes careful scrutiny is necessary for analysis.