Epidemiological study of sulfonamide and trimethoprim resistance genes in Enterobacteriaceae
- PMID: 2237584
Epidemiological study of sulfonamide and trimethoprim resistance genes in Enterobacteriaceae
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.
Similar articles
-
Pneumocystis carinii dihydropteroate synthase but not dihydrofolate reductase gene mutations correlate with prior trimethoprim-sulfamethoxazole or dapsone use.J Infect Dis. 1999 Dec;180(6):1969-78. doi: 10.1086/315148. J Infect Dis. 1999. PMID: 10558954
-
Associations of antifolate resistance in vitro and point mutations in dihydrofolate reductase and dihydropteroate synthetase genes of Plasmodium falciparum.J Postgrad Med. 2004 Jan-Mar;50(1):17-20. J Postgrad Med. 2004. PMID: 15047993
-
Molecular epidemiology of resistance to trimethoprim in enterobacteria isolated in a Parisian hospital.Ann Inst Pasteur Microbiol (1985). 1986 May-Jun;137A(3):239-51. doi: 10.1016/s0769-2609(86)80031-x. Ann Inst Pasteur Microbiol (1985). 1986. PMID: 3322170
-
Resistance to trimethoprim and sulfonamides.Vet Res. 2001 May-Aug;32(3-4):261-73. doi: 10.1051/vetres:2001123. Vet Res. 2001. PMID: 11432417 Review.
-
The changing pattern of trimethoprim resistance in Paris, with a review of worldwide experience.Rev Infect Dis. 1986 Sep-Oct;8(5):725-37. doi: 10.1093/clinids/8.5.725. Rev Infect Dis. 1986. PMID: 3024291 Review.
Cited by
-
Prevalence and trends of aminoglycoside resistance in Shigella worldwide, 1999-2010.J Biomed Res. 2013 Mar;27(2):103-15. doi: 10.7555/JBR.27.20120125. Epub 2013 Feb 28. J Biomed Res. 2013. PMID: 23554801 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Medical
Miscellaneous