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One hundred and twenty chicken samples from feces (n = 80), the carcass surface at slaughter at 2 meat chicken farms (n = 20), and retail chicken meat from 5 markets (n = 20) collected during 2018 and 2019 were examined for the prevalence of plasmid-mediated quinolone resistance (PMQR) in Escherichia coli. We detected qnrS-positive E. coli in a total of 74 samples from feces (n = 59), the carcass surface (n = 7), and retail meat (n = 8). These 74 qnrS-positive isolates were tested for antimicrobial susceptibility to determine the minimum inhibitory concentrations (MICs) of certain antimicrobials and genetically characterized. Ampicillin-resistance accounted for 71 of the 74 isolates (96%), followed by resistance to oxytetracycline (57/74; 77%), enrofloxacin (ERFX) (56/74; 76%), sulfisoxazole (SUL) (56/74; 76%), trimethoprim (TMP) (49/74; 66%), and dihydrostreptomycin (48/74; 65%). All farm-borne SUL- and TMP-resistant isolates except one were obtained from samples from farm A where a combination of sulfadiazine and TMP was administered to the chickens. Concentrations of ERFX at which 50 and 90% of isolates were inhibited were 2 μg/mL and 32 μg/mL, respectively. Diverse pulsed-field gel electrophoresis (PFGE) patterns of XbaI-digested genomic DNA were observed in the qnrS-positive isolates from fecal samples. Several isolates from feces and the carcass surface had identical XbaI-digested PFGE patterns. S1-nuclease PFGE and Southern blot analysis demonstrated that 7 of 11 dfrA13-positive fecal isolates carried both the qnrS and dfrA13 genes on the same plasmid, and 2 of 3 dfrA1-positive isolates similarly carried both qnrS and dfrA1 on the same plasmid, although the PFGE patterns of XbaI-digested genomic DNA of the isolates were different. These results suggest that the qnrS gene is prevalent in chicken farms via horizontal transfer of plasmids and may partly be co-selected under the use of TMP., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

The recent emergence of colistin (COL) resistance, particularly mcr-1 plasmid-mediated COL resistance in Gram-negative bacteria, has led to renewed interest in antibiotic combinations to overcome clinical therapeutic impasses. The aim of this study was to evaluate the potential of the synergistic and bactericidal activity of COL in combination with sulphonamide compounds, including sulfadiazine (SDI), sulfamethoxazole (SMX) and trimethoprim/sulfamethoxazole (SXT), as well as trimethoprim (TMP) against clinical COL-resistant bacterial strains, including strains with the plasmid-encoded mcr-1 gene. A collection of 55 COL-resistant and -susceptible strains from different origins (Laos, Thailand and France) was used in this study. Several in vitro methods were used to determine the potential of the synergistic activity of these combinations, including Etest on agar pre-treated plates, the Etest cross method and the chequerboard assay. A time-kill assay was performed to evaluate the potential bactericidal activity of combinations in addition to synergistic activity. Significant synergistic activity was observed with all combinations tested. The combination of COL + SDI presented the highest synergistic effect against the various species of COL-resistant strains (92.7%). For the other combinations, a synergistic effect was also observed but with lower frequency for COL + SMX (33.3%), COL + TMP (47.3%) and COL + SXT (31.5%). Synergy was observed independently of the COL resistance mechanism. These in vitro results suggest that the combination of COL + SDI would appear to be justifiable in patients with multidrug-resistant bacterial infections that cannot be treated with COL monotherapy., (Copyright © 2018 Elsevier B.V. and International Society of Chemotherapy. All rights reserved.)

Administration of antimicrobials to food-producing animals increases the risk of higher antimicrobial resistance in the normal intestinal flora of these animals. The present cross-sectional study was conducted to investigate antimicrobial susceptibility and extended-spectrum β-lactamase (ESBL)-producing strains and to characterize class 1 integrons in Escherichia coli in healthy swine in Thailand. All 122 of the tested isolates had drug-resistant phenotypes. High resistance was found to ampicillin (98.4% of isolates), chloramphenicol (95.9%), gentamicin (78.7%), streptomycin (77.9%), tetracycline (74.6%), and cefotaxime (72.1%). Fifty-four (44.3%) of the E. coli isolates were confirmed as ESBL-producing strains. Among them, blaCTX-M (45 isolates) and blaTEM (41 isolates) were detected. Of the blaCTX-M-positive E. coli isolates, 37 carried the blaCTX-M-1 cluster, 12 carried the blaCTX-M-9 cluster, and 5 carried both clusters. Sequence analysis revealed blaTEM-1, blaTEM-135, and blaTEM-175 in 38, 2, and 1 isolate, respectively. Eighty-seven (71%) of the 122isolates carried class 1 integrons, and eight distinct drug-resistance gene cassettes with seven different integron profiles were identified in 43 of these isolates. Gene cassettes were associated with resistance to aminoglycosides (aadA1, aadA2, aadA22, or aadA23), trimethoprim (dfrA5, dfrA12, or dfrA17), and lincosamide (linF). Genes encoding β-lactamases were not found in class 1 integrons. This study is the first to report ESBL-producing E. coli with a class 1 integron carrying the linF gene cassette in swine in Thailand. Our findings confirm that swine can be a reservoir of ESBL-producing E. coli harboring class 1 integrons, which may become a potential health risk if these integrons are transmitted to humans. Intensive analyses of animal, human, and environmental isolates are needed to control the spread of ESBL-producing E. coli strains.

Trimethoprim-sulfamethoxazole (co-trimoxazole) is the primary drug used for oral eradication therapy of Burkholderia pseudomallei infections (melioidosis). Here, we demonstrate that trimethoprim resistance is widespread in clinical and environmental isolates from northeast Thailand and northern Australia. This resistance was shown to be due to BpeEF-OprC efflux pump expression. No dihydrofolate reductase target mutations were involved, although frequent insertion of ISBma2 was noted within the putative folA transcriptional terminator. All isolates tested remained susceptible to trimethoprim-sulfamethoxazole, suggesting that resistance to trimethoprim alone in these strains probably does not affect the efficacy of co-trimoxazole therapy.

One hundred and eighty-nine Salmonella isolates from swine were tested for susceptibility to nine antimicrobial agents, presence of dfrA12 and class 1 integrons containing dfrA12-orfF-aadA2 cassette. All isolates were multidrug resistant and exhibited highest resistance prevalence to trimethoprim (93%). Most isolates (89%) were intll-positive and 107 isolates (57%) carried dfrA12, all of which were resistant to trimethoprim. Forty-eight dfrA12-harboring strains (45%) were intl1-positive together with dfrA12-aadA2 gene cassette. Fifteen isolates contained dfrA12 but not intl1 and dfrA12-aadA2 cassette. The results indicated a wide distribution of dfrA12 and its role in dissemination of trimethoprim resistance among Salmonella isolates from fattening pigs.

One hundred strains of Haemophilus ducreyi isolated in Thailand from patients with chancroid were tested by the agar dilution method against 10 antimicrobial agents and typed by outer membrane protein pattern by using sodium dodecyl sulfate gel electrophoresis. All strains produced beta-lactamase and were resistant to tetracycline, kanamycin, and sulfonamides. Most had a decreased susceptibility to trimethoprim (MIC for 50% of the strains [MIC50], 0.5 micrograms/ml) and chloramphenicol (MIC50, 8 micrograms/ml). Strains were susceptible to ciprofloxacin (MIC90, 0.001 micrograms/ml), ceftriaxone (MIC50, 0.0015 micrograms/ml), erythromycin (MIC50, 0.015 micrograms/ml), rosoxacin (MIC50, 0.03 micrograms/ml), and spectinomycin (MIC50, 8 micrograms/ml). The degree of antimicrobial resistance found in Thailand is higher than that reported for H. ducreyi isolated in other regions. Five different outer membrane protein patterns were found by analyzing proteins in the range of 29 to 61 kilodaltons, but 98% of the Thai strains fell into three patterns which did not differ greatly. Outer membrane protein patterns of Thai strains were also seen in strains from other geographic areas. A new outer membrane protein type was found among nine strains isolated in Singapore.

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 greater than 1024 micrograms/ml of trimethoprim (TMPr) 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 TMPR Shigella had genes encoding type II and 9% (13 of 139) had genes encoding type I DHFR genes. Fifty percent (11 of 22) of TMPR 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 TMPR Shigella and 36% (8 of 22) of TMPR 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.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

A single dose of ceftriaxone (250 mg) administered intramuscularly was compared with trimethoprim-sulfamethoxazole (TMP-SMZ; 160/800 mg) administered orally twice daily for seven days or with a single dose of TMP-SMZ (640/3,200 mg) administered orally for the treatment of chancroid in men in Thailand. Haemophilus ducreyi was isolated from 79 (48%) of 164 men with a clinical diagnosis of chancroid. For men with ulcers that were culture positive for H. ducreyi, rates of cure were 100% in 25 men treated with ceftriaxone, 87% in 23 men given TMP-SMZ for seven days, and 55% in 31 men given TMP-SMZ in a single dose. For men with ulcers that were culture negative for H. ducreyi, rates of cure were 100% in 29 men treated with ceftriaxone, 66% in 32 men given TMP-SMZ for seven days, and 63% in 24 men given TMP-SMZ in a single dose. The MIC50 of the three antibiotics for 94 isolates of H. ducreyi were as follows: 0.004 micrograms/ml for ceftriaxone, 16 micrograms/ml for trimethoprim, and greater than 512 micrograms/ml for sulfamethoxazole. Our study indicates that ceftriaxone in a single dose of 250 mg is effective, but that TMP-SMZ, even when given in a standard seven-day regimen, is not effective treatment for chancroid in Thailand.