Resistance to Different Antibiotics
The emergence of sulfonamide resistance in N. meningitidis, due to mutational or recombinational modification of the target dihydropteroate synthase, emerged in the early 1960s and is now widespread. Of greater concern today is the emergence of penicillin resistance. The MIC of penicillin for meningococci is usually <0.08 mg/L, but this may be increased in moderately susceptible isolates up to 0.5 mg/L. These strains were first reported in the 1960s but have increased in frequency in some countries, especially in Spain. This low-level penicillin resistance is due to alterations in PBP 2, with a mosaic gene structure arising as a result of transformation from commensal Neisseria species. In the 1990s, Spain suffered a clonal epidemic associated with a moderately susceptible penicillin strain that accounted for more than 60% of invasive serogroup C isolates. There are only scant clinical data indicating that meningitis with the moderately susceptible meningococcal strains may be associated with penicillin treatment failures. Third-generation cephalosporins remain very active on these strains.
In addition, β-lactamase production by meningococci has been reported in four cases and appears to be encoded on a gonococcal plasmid. Chloramphenicol resistance has been reported recently from Vietnam and was determined by a catP gene located on a defective transposon from Clostridium perfringens. Although up to 10% of carriers treated with rifampicin are subsequently found to harbor rifampicin-resistant meningococci, caused by a point mutation in the rpoB gene, such strains remain extremely rare in invasive disease. Four cases of meningococcal disease caused by ciprofloxacin- resistant N. meningitidis serogroup B have been reported in the USA. They were caused by the same strain which revealed a gyrA mutation that was possibly acquired by horizontal gene transfer from the commensal N. lactamica.
