[Enterobacter cloacae. In vivo emergence of a variant resistant to new beta-lactams during treatment with lamoxactam-gentamicin].

In a patient recently operated for an abdominal gun wound, and given gentamicin-cephalosporin (cefoxitin for one day, then moxalactam) for 11 days, treatment failed as a result of emergence of a E. cloacae variant resistant to beta-lactams only, i.e. carbenicillin, mezlocillin, cefamandole (CFM), cefoperazone (CPZ), cefotaxim (CTX) and moxalactam ( MOX ). The initial susceptible strains isolated from blood cultures (SH1, SH2) and the resistant ones isolated 11 days later from pancreatic pus (RP) and blood cultures ( RH1 , RH2 ) shared the same chemotype. MICs of CFM, CPZ, CTX, and MOX were much higher (1 000 to 4 000 fold) for RH1 than for SH1. The biochemical mechanism of resistance showed the six following features: loss of antimicrobial activity of CFM, CTX and MOX added to RH1 cultures; much higher (1 500 fold) beta-lactamase activity for RH1 than for SH1 (iodometric and microacidimetric methods); beta-lactamases focusing at the same pl (greater than 8) produced by RH1 , RP and also, but only after induction, SH1 and SH2; cephalosporinase-type beta-lactamase according to the enzymatic activity profile; restoration of RH1 's susceptibility to CFM, CTX and MOX merely by adding cloxacillin; apparently unchanged crypticity for RH1 . The enzymatic mechanism (cephalosporinase hyperproducing variant) seems very likely.