Plasmid-independent resistance of 'gray' colony variants of a strain of Serratia marcescens resistant to amikacin, cefotaxime and lamoxactam.

A multiple-drug-resistant strain of Serratia marcescens (serotype O14:H12; bacteriocin type 18), which was recovered repeatedly from the respiratory tract of an intensive care unit patient, yielded 'gray' colony phenotypic variants which were greater than or equal to four-fold less susceptible to amikacin, cefotaxime, and lamoxactam, but not to netilmicin and N-formimidoyl thienamycin, as compared with 'opaque' (wild-type) colony variants. The 'gray' variants proved phenotypically highly unstable and displayed comparable low virulence for NMRI mice (intraperitoneal route). The 'opaque' and 'gray' variants of this strain carried a nonconjugative, 46-megadalton resistance (R) plasmid, as determined by DNA agarose gel electrophoresis. The R-plasmid-mediated resistance against chloramphenicol, gentamicin, kanamycin, mezlocillin, piperacillin, triple sulfonamides, and cotrimoxazole, as demonstrated with 'curing' experiments. The mechanism of the novel amikacin-beta-lactam antibiotic resistance phenomenon remained undetermined.