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Epidemiological study of sulfonamide and trimethoprim resistance genes in Enterobacteriaceae
W Panbangred1, P Jayanetra, A Pilantanapak
1Department of Microbiology, Faculty of Science, Mahidol University, Bangkok, Thailand.
Abstract:
Sulfonamide (Su) and trimethoprim (Tp) resistance are known to caused by the production of drug resistant dihydropteroate synthase (DHPS) and dihydrofolate reductase (DHFR), respectively. Sulfonamide and trimethoprim are often used in combination under the name cotrimoxazole. Cotrimoxazole resistance in various enteric bacteria isolated at Ramathibodi Hospital was studied. The rate of resistance from 1984-1989 of many genera was rather constant at 40%-60% except in Shigella spp in which the rate increased rapidly in 1987 till 1989. Seventy-five percent of Su-Tp resistant (Sur-Tpr) bacteria were also found to be resistant to other drugs such as ampicillin, aminoglycosides, tetracycline and chloramphenicol in addition to cotrimoxazole. Two hundred and forty Su-Tp resistant strains were analysed for the presence of type I and II dihydropteroate synthase as well as type I and V dihydrofolate reductase genes by hybridization with the corresponding gene probes. Type I DHPS gene predominated in Su-Tp resistant bacteria at 60.8% whereas type II DHPS was found in only 25%. Some strains (11.7%) had both genotypes but 2.5% did not have any. In the trimethoprim resistance study, the DHFR type I gene was also found more frequently (30%) whereas type V DHFR was only 19%. The remaining of Tp resistance (51%) was unclassified. The coexistence of Su and Tp resistance genes of each type was investigated among 118 Su and Tp resistant strains. It was found that type I DHPS gene was found together with either type I or V DHFR gene and type II DHPS was found with type I DHFR gene at about the same rate (28.9%, 27.1% and 26.3%, respectively). However, the presence of type II DHPS together with type V DHFR was rather low, only 5.9% of isolates were found to have both types of genes.
Insights
Cotrimoxazole resistance in enteric bacteria is linked to specific drug-resistant genes. Type I dihydropteroate synthase (DHPS) and type I dihydrofolate reductase (DHFR) genes were most common, often co-occurring.
Area of Science:
- Microbiology
- Molecular Biology
- Antimicrobial Resistance
Background:
- Sulfonamide (Su) and trimethoprim (Tp) resistance in enteric bacteria are primarily caused by mutations in dihydropteroate synthase (DHPS) and dihydrofolate reductase (DHFR) genes, respectively.
- Cotrimoxazole, a combination of Su and Tp, is widely used, making resistance a significant public health concern.
- Previous studies indicated a concerning but relatively stable rate of cotrimoxazole resistance (40%-60%) in various enteric bacteria between 1984-1989, with a notable increase in Shigella spp.
Purpose of the Study:
- To investigate the prevalence and genetic basis of cotrimoxazole resistance in enteric bacteria isolated at Ramathibodi Hospital.
- To determine the specific types of DHPS and DHFR genes responsible for sulfonamide and trimethoprim resistance.
- To analyze the co-occurrence patterns of these resistance genes within resistant bacterial strains.
Main Methods:
- Phenotypic characterization of cotrimoxazole resistance in enteric bacteria isolated from clinical samples.
- Molecular analysis using gene hybridization with specific probes to detect the presence of type I and II DHPS genes and type I and V DHFR genes.
- Investigation of the coexistence of different DHPS and DHFR gene types in cotrimoxazole-resistant strains.
Main Results:
- A high proportion (75%) of sulfonamide-trimethoprim resistant (Su-Tpr) bacteria exhibited co-resistance to other antibiotics, including ampicillin, aminoglycosides, tetracycline, and chloramphenicol.
- Among 240 Su-Tpr strains, type I DHPS was the predominant genotype (60.8%), followed by type II DHPS (25%). Some strains (11.7%) possessed both, while 2.5% had neither.
- For trimethoprim resistance, DHFR type I was more frequent (30%) than type V (19%), with 51% of resistance remaining unclassified. Type I DHPS frequently coexisted with either DHFR type I or V, and type II DHPS commonly coexisted with DHFR type I.
Conclusions:
- The study highlights the significant role of specific DHPS and DHFR gene types in conferring cotrimoxazole resistance among enteric bacteria.
- The predominance of type I DHPS and type I DHFR genes, and their frequent co-occurrence, suggests a significant genetic mechanism driving cotrimoxazole resistance.
- Understanding these genetic underpinnings is crucial for developing effective strategies to combat the rising threat of antimicrobial resistance in clinical settings.