Pestana ACNR*, Diniz CG, Farias LM, & Carvaiho MAR
Laboratório de Microbiologia Oral e Anaerébios, Depto. Micorbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Brasil

Antimicrobial resistance in bacteria has been reported as widely diffused and it is cause of concern that, in a coming future, infectious diseases become impossible to be treated with availiable drugs. This problem led CDC to elaborate a surveillance program to detect resistance in relevant pathogens, biochemistry and genetics of resistance and its transfer among bacteria, including B. fragilis group. In this work, we tried to establish relations between drug resistance and presence of plasmid bands in B. fragilis group strains. We studied 24 strains isolated from human (n=12) and marmoset (n=12) stool, previously described as resistant to penicillin G and/or clindamycin by the agar dilution method. Reference strain B. fragilis ATCC 25285 was included as control. Plasmid isolations were performed as described by Welch & Macrina, 1981, modified in our Laboratory. Extracts were analysed by conventional agarosis gel electrophoresis. Marmoset strains didn't show plasmid bands. 5 human strains showed plasmid bands, possibly related to resistance to clindamycin and/or penicillin G. These strains were submitted to plasmid curing. Among different methods tested to obtain cured colonies (elevation of incubation temperature, the use of sodium duodecyl sulfate, and the use of intercalating dyes, as acridin orange and ethidium bromide), the use of acridin orange was the only one that provided cured colonies of B. vulgatus "A25" strain, originally resistant to both drugs. Cured colonies became susceptible to clindamycin and penicillin G, suggesting, with strong evidence, that resistance to both drugs can be mediated by plasmid genes.

Supported by CAPES, CNPq, FAPEMIG, PRPq/UFMG