| dc.description | Trimethoprim-sulfamethoxazole (co-trimoxazole) is used frequently for people living with HIV/AIDS in Africa. In this study, the prevalence and mechanisms of resistance to sulfonamides and trimethoprim in commensal oral streptococci from Uganda were determined. Commensal streptococci from throat and nasal swabs of 34 HIV positive individuals taking co-trimoxazole prophylaxis and 18 individuals not on prophylaxis were cultured and analysed for species identity, antibiotic resistance profile and polymorphisms in the genes coding for dihydropteroate synthase (DHPS) and dihydrofolate reductase (DHFR). The majority were of the mitis group. Several Ugandan clinical isolates of S. pneumoniae were similarly analyzed concurrently. All were resistant to co-trimoxazole and oxacillin, while 83% were resistant to ciprofloxacin. Resistance to chloramphenicol was about 29% while less than 10% of isolates were resistant to ceftriaxone. There was considerable polymorphism in both DHPS and DHFR. In DHFR, the mutation 100Ile→Leu (I100L) was present in 20 of 21 sequenced isolates. A number of other mutations such as E20D, L135F, and different substitutions in D92 were very frequent. The most common DHPS variant had two serine residues between amino acid 60 and 61 or arginine and proline inserted between 59P and 60G. In addition, three new insertions/substitutions were found. There were no obvious differences between the mutation patterns in S. pneumoniae and viridans streptococci. Our results suggest that the chromosomal mutations we found have been acquired by transformational interchanges of DNA among related organisms and that resistance genes are freely transferred between commensal and pathogenic streptococci. | |
