ANTIBIOTIC RESISTANCE |[lpar]|AbR|[rpar]| OF HEMOPHILUS INFLUENZAE |[lpar]|Hi|[rpar]||[period]| 1971|[ndash]|76

The prevalence, basis and epidemiology of AbR in the 283 Hi causing essentially all Hi disease at CHMC has been studied. AbR by year, no. of strains and patterns of resistance to 10 Ab were: 1971-1972. 81, 0: 1973. 42, 2 AmpR: 1974, 50, 0: 1975, 87, 13 AmpR. 1 AmpTcR, 2 TcR, 1 TcCmR; 1976-77, 21 AmpR, 2 TcR. Patients with AbR and AbS Hi did not differ significantly in prior antibiotic exposure, type of disease, or clinical course. The incidence of AbR was greater among non-typeable than type b Hi. Amp and CmR were mediated by Ab-inacting enzymes. Plasmids capable of conjugal transfer to Hi in vitro mediated AmpR in 34 of 36 resistant Hi and all AmpTcR, TcR and TcCmR. Arsenite resistance (ArsR) was found in 60% of Hi independent of year of isolation or AbR. It was mediated by a previous unrecognized, conjugally fertile plasmid(s). Genes mediating AbR in 90% of resistant Hi were associated with an ArsR plasmid. Plasmids differed widely in the kinetics of conjugal transfer. Properties, i.e., amount of capsule, of donor and recipient Hi also affected plasmid transfer. These data provide important insights into the present and future of AbR in Hi: it involves more Ab than previously recognized and is mediated by genes which apparently have only recently become associated with native, occult Hi plasmids. The genetics of Hi and its plasmids appears to hold the key to the natural prevalence and patterns of AbR.