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To identify Escherichia coli that cause infantile diarrhea in Bangkok, Thailand, E. coli isolated in a year-long study of infantile diarrhea were examined for O and H serotypes and virulence determinants. Classic enteropathogenic E. coli (EPEC) were isolated from 28 of 509 infants with diarrhea (cases) and 11 of 509 age-matched controls (P = .009; odds ratio [OR], 2.64). Most of this difference was attributable to EPEC adherence factor (EAF)-positive EPEC that produced an attachment and effacement lesion, as identified in the fluorescence actin staining assay, isolated from 13 cases and 1 control (P = .003; OR, 13.3). EAF-EPEC was isolated from 15 cases and 10 controls (P = .418; OR, 1.52) and EAF+ non-EPEC from 17 cases and 10 controls (P = .242; OR, 1.72). EAF+EPEC that caused an attachment and effacement lesion was found in 3% of children less than 6 months old with diarrhea who were studied in an outpatient clinic in Bangkok in 1988.

A double blind study of daily doxycycline (100 mg) vs. weekly mefloquine (250 mg) was performed on United States soldiers training in Thailand to assess the effect of doxycycline malaria prophylaxis on the incidence of gastrointestinal infections. During a 5 week period, 49% (58/119) of soldiers receiving doxycycline and 48% (64/134) of soldiers receiving mefloquine reported an episode of diarrhea. Infection with bacterial enteric pathogens was identified in 39% (47/119) of soldiers taking doxycycline and 46% (62/134) of soldiers taking mefloquine. Forty-four percent (59/134) of soldiers receiving mefloquine and 36% (43/119) of soldiers receiving doxycycline were infected with enterotoxigenic Escherichia coli (ETEC), while 9% (12/134) of soldiers receiving mefloquine and 4% of soldiers receiving doxycycline were infected with Campylobacter. Side effects from either medication were minimal. After 5 weeks in Thailand, the percent of non-ETEC strains resistant to greater than or equal to 2 antibiotics increased from 65% (77/119) to 86% (95/111) in soldiers on mefloquine and from 79% (84/106) to 93% (88/95) in soldiers on doxycycline. Doxycycline prophylaxis did not prevent or increase diarrheal disease in soldiers deployed to Thailand where ETEC and other bacterial pathogens are often resistant to tetracyclines.

Specific DNA probes were used to identify Shiga-like toxin I (SLT I)- and SLT II-producing Escherichia coli in vegetables, meats, cattle, and farm animals in Thailand. SLT-producing E. coli was isolated from 9% of market beef specimens, from 8 to 28% of fresh beef specimens at slaughterhouses, and from 11 to 84% of fecal specimens from cattle. Animals were frequently infected with several different SLT-producing E. coli types that hybridized with either the SLT I, SLT II, or both SLT probes. Of 119 SLT-producing E. coli isolates, 24% hybridized with the SLT I probe, 31% hybridized with the SLT II probe, and 44% hybridized with both SLT probes. The enterohemorrhagic E. coli plasmid probe hybridized with 64% (68 of 106) of SLT-producing E. coli isolates from food and cattle and with 8% (17 of 201) of E. coli isolates from pigs. No SLT-producing E. coli was detected in pigs. Seventy-six percent (26 of 34) of E. coli isolates that hybridized with the SLT II probe were cytotoxic to Vero but not to HeLa cells, suggesting that they produced the variant of SLT II. The high prevalence of SLT-producing E. coli in beef-producing animals suggests that exposure to animals and eating beef may pose a health risk for acquiring enterohemorrhagic E. coli infections in Thailand.

Escherichia coli strains isolated from adults with diarrhea in Bangkok, Thailand, were examined for hybridization with DNA probes for genes that code for Shiga-like toxin (SLT)-I, SLT-II, and serogroup O157 enterhemorrhagic E. coli (EHEC) fimbriae. Seven isolates that hybridized with the SLT-I, SLT-II, and O157 EHEC fimbria probes and produced verocytotoxin (VT; group A) were isolated from two patients with diarrhea. Two strains that hybridized with only the SLT-II probe and the O157 EHEC fimbria probe and were VT+ (group B) were isolated from two patients with diarrhea, 7 strains that hybridized with only the SLT-II probe and were VT+ (group C) were isolated from two patients with diarrhea, and 26 strains that hybridized with only the O157 EHEC fimbria probe and were VT- (group D) were isolated from four patients with diarrhea. Seven strains in group A had serotypes O2:H1 (n = 1), O110:H19 (n = 1), and Ont:H8 (n = 5); 2 strains in group B were O112ab:H21 (n = 1) and O113:H21 (n = 1); 7 strains in group C were O6:H28 (n = 1), O22:H16 (n = 1), O52:H25 (n = 1), O112ab:H21 (n = 1), OR:H45 (n = 2), and OR:H11 (n = 1); and 26 strains in group D were O76:H7 (n = 18), O146:H3 (n = 2), O146:H10 (n = 1), O146:Hnt (n = 1), OR:H16 (n = 1), Ont:H2 (n = 1), Ont:H8 (n = 1) and Ont:H16 (n = 1). In Thailand, E. coli strains that hybridized with SLT-I, SLT-II, and O157 EHEC fimbria probes were of a variety of serotypes, none of which were O157:H7.

Outbreaks of Shigella dysenteriae I occurred in northeastern Thailand in the fall of 1986 and again in the spring and fall of 1987 for the first time in over 20 years. The epidemic strain of S. dysenteriae I was resistant to tetracycline, streptomycin, chloramphenicol, and trimethoprim-sulfamethoxazole, but susceptible to ampicillin. Trimethoprim resistance was chromosomally encoded by type I dihydrofolate reductase. In Ubon Province, where 10,000 cases of dysentery were reported, there were 3-5 cases of dysentery per 1,000 residents during the peak months, with 2-5 hospitalizations per 100 cases of reported dysentery. There were 2 deaths among 101 hospitalized, culture-confirmed cases. The overall case-fatality rate among reported cases of dysentery in this province was 0.9%. In contrast to S. flexneri infections, which occurred predominantly among children less than 5 years old, S. dysenteriae I infections occurred in all age groups. The large number of susceptibles appeared to be important in allowing rapid spread of S. dysenteriae I. In 1 village, 46% of 434 villagers reported dysentery; S. dysenteriae I was isolated from 24 out of 81 (30%) individuals cultured. Based on the prevalence of IgG antibody to S. dysenteriae I lipopolysaccharide, it was estimated that 76% of the villagers had been infected.

Specific DNA probes were used to identify Shiga-like-toxin (SLT) I- and II-producing Escherichia coli from children less than 5 years of age with bloody diarrhea, in infants with diarrhea, and in controls of the same age without diarrhea in Thailand. At one hospital, SLT-producing E. coli was identified in 4 (7%) of 54 children with bloody diarrhea from whom other enteric pathogens were not identified and from 3 (6%) of 50 children without diarrhea. In the positive specimens, SLT-producing E. coli constituted only 0.3 to 4% of the 100 to 300 colonies on the replica blots. Non-toxin-encoding 933J and 933W bacteriophagelike DNA sequences were detected by colony hybridization with E. coli isolates from 18 (33%) of 54 children with bloody diarrhea and 23 (46%) of 50 controls. At another hospital, SLT-producing E. coli was not identified in 115 infants with diarrhea and 119 controls without diarrhea. One infant with diarrhea was infected with E. coli O76:H7 that hybridized with the enterohemorrhagic E. coli probe but not with the SLT probes. E. coli producing SLT I or SLT II was isolated in small numbers from a similar proportion of Thai children with bloody diarrhea in whom no other enteric pathogen was identified and from controls without diarrhea.

When Shigella species, Escherichia coli, and five other bacterial enteric pathogens isolated from children with diarrhea in Thailand were tested for hybridization under stringent conditions with probes for Shiga-like toxins I and II, only 30 Shigella dysenteriae 1 hybridized with the Shiga-like toxin I probe.