Medication Summary
Vancomycin has been used to treat nonneonatal Elizabethkingia meningitis in the past, but it has a high minimum inhibitory concentration (MIC). Vancomycin has been used in combination with other agents, including rifampin; however, its usefulness has been questioned. [15]
Elizabethkingia shows some susceptibility to fluoroquinolones, whereas its susceptibility to doxycycline and trimethoprim varies. This often leads to an inappropriate choice of antibiotics for initial empiric therapy and results in treatment failures. It is resistant to multiple antibiotics, especially beta-lactams, as it produces two beta-lactamases, extended-spectrum beta-lactamase and a carbapenem-hydrolyzing metallo beta-lactamase, conferring resistance to many extended-spectrum beta-lactam antibiotics, aztreonam, and carbapenems. However, various studies have found E meningoseptica to be sensitive to piperacillin and piperacillin/tazobactam. [16, 17, 18] Antimicrobial resistance may vary depending on the species and region and time of bacterial isolation.
The 2015/2016 Elizabethkingia infections in Wisconsin, Michigan, and Illinois were found to be susceptible to several antibiotics, including fluoroquinolones, minocycline, rifampin, and trimethoprim/sulfamethoxazole. If possible, combination treatment is recommended over monotherapy.
An extensive 2017 survey by Han et al, from Seoul, Republic of Korea, studied 86 isolates of Elizabethkingia species, of which 17 were E meningoseptica, 18 were E miricola, and 51 were E anophelis. Over 90% of E meningoseptica and E anophelis isolates were susceptible to piperacillin-tazobactam and rifampin. In contrast, all E miricola isolates were susceptible to fluoroquinolones except ciprofloxacin. [19]
This helps to summarize the potential empiric choices for each of the species described above.
Antibiotics
Class Summary
Antibiotics should be selected based on antimicrobial susceptibility testing on a case-by-case basis. [4] Combination antibiotic treatment is encouraged.
Levofloxacin (Levaquin)
Fluoroquinolone antibiotic that is the l-stereoisomer of ofloxacin. Inhibits DNA gyrase activity, which in turn promotes breakage of DNA strands.
Ciprofloxacin (Cipro, Cipro XR, ProQuin XR)
Fluoroquinolone antibiotic. It inhibits DNA gyrase in susceptible organisms, and therefore promotes breakage of double-stranded DNA.
Minocycline (Minocin)
Tetracycline antibiotic. It inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
Rifampin (Rifadin)
Inhibits DNA-dependent RNA polymerase by binding to beta subunit, which in turn blocks RNA transcription; potent enzyme inducer.
Trimethoprim/sulfamethoxazole (Bactrim, Cotrim)
Blocks 2 consecutive steps in the biosynthesis of nucleic acids and proteins essential to many bacteria. Trimethoprim inhibits dihydrofolate reductase, thereby blocking production of tetrahydrofolic acid from dihydrofolic acid. Sulfamethoxazole inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid.
