Knowledge of the mechanisms of antimicrobial resistance and resistance transfer in anaerobic bacteria has been gained over the past several years. There is widespread resistance to the beta-lactam antibiotics in the B. fragilis group of organisms and there is emerging penicillin resistance in other Bacteroides species. These resistances are usually mediated by chromosomal beta-lactamases. There have been two new beta-lactamases described in Bacteroides; a penicillinase which inactivates ureidopenicillins and another that inactivates cefoxitin. The transfer of the common beta-lactamase, penicillinase, and cefoxitin resistance has been documented in B. fragilis. The mechanism of tetracycline resistance in B. fragilis is the lack of accumulation of intracellular drug; the resistance is widespread in anaerobic bacteria and is seen in two-thirds of the B. fragilis strains. The transfer of tetracycline resistance is common, however, no transfer factor has yet been isolated. Clindamycin-erythromycin resistance in Bacteroides was first recognized in the mid-1970s and transferable resistance was described in 1979. The mechanism of resistance is probably similar to macrolide-lincosamide-streptinogramin-resistance seen in aerobic bacteria. Two clindamycin resistance transfer factors, pBFTM10 and pIP410 (pBF4) have been described. A common resistance determinant found both on plasmids and chromosomes is widely distributed in nature and it probably resides on a transposon. DNA homology studies indicate that there is more than one type of clindamycin resistance in Bacteroides; a newly recognized clindamycin resistance determinant is transferable. Local outbreaks of clindamycin resistance have been noted in the United States and in Europe. The susceptibility of Bacteroides in the United States in 1983 from a multi-center study reveals a 5% incidence of resistance in B. fragilis and 1% in Bacteroides species. The rate of clindamycin resistance has remained steady over the past three years in the Bacteroides fragilis group.