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ceftazidime, ceftriaxone, gentamicin, imipenem, piperacillin/ tazobactam, tobramycin and trimethoprim/sulfamethoxazole, with intermediate susceptibility to ticarcillin/clavulanic acid. On hospital days 11 and 13 the CSF Gram stains and cultures demonstrated persistent Acinetobacter, with susceptibility to imipenem, ampicillin/sulbactam and ticarcillin/clavulanic acid. Rifampicin susceptibility testing by disc diffusion (5 mg disc on Mueller–Hinton agar with a 0.5 McFarland inoculum incubated for 24 h at 32–36 C in ambient air) revealed an 11 mm zone of inhibition. On hospital day 13, rifampicin at a dose of 600 mg intravenously daily was added to the meropenem, and gentamicin and metronidazole were stopped. On hospital day 16, the patient defervesced, and CSF analysis demonstrated marked improvement with negative cultures (Table 1). Rifampicin and meropenem were continued for 2 more weeks. The ventriculostomy was removed on hospital day 23. The patient was discharged from the hospital ambulating with minimal assistance 30 days after admission. Nosocomial meningitis due to A. calcoaceticus-baumannii complex carries a 20–25% mortality. Acinetobacter may be resistant to multiple antibiotics at the time of initial infection, or may rapidly develop resistance during therapy. Susceptibility testing by rapid automated systems, such as the Vitek system in use at our hospital, may erroneously report resistance in Acinetobacter species. This is one potential explanation for the MDR Acinetobacter isolated on hospital day 9 in our patient. We made the decision to add rifampicin based on our patient’s unimproved clinical status and believe that rifampicin in combination with meropenem provided a cure of meningitis due to Acinetobacter in this patient. Additional in vitro, animal and clinical studies of rifampicin and carbapenem combinations for Acinetobacter are necessary.

Antibiotics for childhood community-acquired pneumonia in a region with a high prevalence of penicillin non-susceptible Streptococcus pneumoniae