Resistance to ß-lactam drugs has been shown to be caused by both ß-lactamases and modification of penicillin-binding proteins. These genes may be present together or separately in the organism. Some non-toxigenic C. diphtheriae have been shown to be susceptible to penicillin by MIC method but further studies after treatment failure indicated a high level of tolerance to penicillin. The Minimum Bactericidal Concentration (MBC) was shown to be much higher for these strains indicating that the organism was not being killed by the antibiotic. Another interesting tolerance to oxacillin was shown in other Corynebacterium species where the ability to survive treatment with oxacillin was due to two genes expressing resistance to tetracycline (tetA and tetB). The activated pumping mechanism of these genes also helped to remove the oxacillin and it ceased to be effective even though the MIC value was low.
Erythromycin and clindamycin resistance is generally attributed to the ermX or the ermB gene whereas resistance to quinolones has been observed due to mutations in gyrA. If the gyrA gene mutation is present in a C. macginleyi isolate recovered from an ophthalmic infection, it may be more difficult to treat with the fluoroquinolone eye drops commonly prescribed.
Note: Corynebacterium isolates with higher levels of resistance tend to be found in hospital-acquired infections rather than in isolates recovered from patients outside of the hospital setting. The potential for multi-drug-resistant Corynebacterium may be correlated with gene transfer of resistant genes from other bacteria.
