Trimethoprim-resistant Shigella and enterotoxigenic Escherichia coli strains in children in Thailand

Abstract

The percentage of Shigella and enterotoxigenic Escherichia coli (ETEC) strains resistant to trimethoprim (TMP)-sulfamethoxazole isolated from children with diarrhea at the outpatient department of the Children's Hospital in Bangkok increased from 3 and 0%, respectively, in 1982 to 29% and 25% in 1986. One hundred thirty-nine Shigella and 22 ETEC strains resistant to > 1024 μg/ml of trimethoprim (TMP_r) isolated from children with diarrhea in Bangkok in 1984 and 1985 were analyzed for the presence of type I, II and III plasmid-specific dihydrofolate reductase (DHFR) genes. Thirty-two percent (45 of 139) of TMP_RShigella had genes encoding type II and 9% (13 of 139) had genes encoding type I DHFR genes. Fifty percent (11 of 22) of TMP_R ETEC had type II and 14% (3 of 22) had type I DHFR genes.Plasmids encoding DHFR were identified by the Southern technique in 24% (14 of 58) of Shigella and 1 of 14 ETEC that contained genes encoding DHFR. Plasmids coding for type II DHFR were transferred to E. coli K12 by conjugation from 13 of 14 Shigella and a plasmid coding for type I DHFR was transferred from the single ETEC containing a plasmid coding for type I DHFR. Genes coding for DHFR were presumably situated on the chromosome in 76% (44 of 58) of Shigella and 93% (13 of 14) of ETEC that contained genes encoding DHFR. Since 58% (81 of 139) of TMP_RShigella and 36% (8 of 22) of TMP_R ETEC strains examined did not contain genes encoding type I, II or III DHFR, high level TMP resistance was presumably caused by other types of DHFR genes. Additional studies should be performed to characterize mechanisms of TMP resistance in Shigella and ETEC in Thailand. TMP-sulfamethoxazole may no longer be efficacious in the treatment of Shigella and ETEC infections in Thailand.