Acinetobacter baumannii complex

Background

Contains Acinetobacter baumannii, Acinetobacter nosocomialis, and Acinetobacter pittii
Non-motile, non-fermenting Gram-negative bacillus

A number of mechanisms
Carbapenem resistance is usually mediated by acquisition of OXA-type class D carbapenemase
- Less common mechanisms include acquisition of class B (VIM, IMP, and NDM) carbapenemases, loss of outer membrane CarO protein, and modification of AdeABC efflux pump

Choice of antibiotic depends on susceptibility testing
Possible options include:
- Cefepime, ceftriaxone, and cefotaxime
- Cefiderocol
- Carbapenems
- Tigecycline
- Colistin and polymyxin B (though Acinetobacter junii has inherent resistance)
Aminoglycosides may not penetrate well into lungs and brain, so are usually avoided
Bacteriophages are promising

Infection must be distinguished from colonization of the airway or wound
Resistance may be mediated by a number of β-lactamases, including OXA-24/40-like carbapenemases, OCA-23-like carbapenemases, and metallo-β-lactamases, and often has sulbactam resistance
Often have concurrent aminoglycoside-modifying enzymes or 16S rRNA methyltransferases, which confer resistance to aminoglycosides including plazomicin
Single-agent treatment may be sufficient for mild infections
- High-dose ampicillin-sulbactam is preferred, at a dose of either 9 g IV q8h infused over 4 hours, or 27 g IV q24h continuous infusion
Combination treatment with at least two agents that have in vitro activity for most other infections
- Options include ampicillin-sulbactam (preferred), minocycline, tigecycline, polymyxin B, and cefidercocol
- Ampicillin-sulbactam may remain effective in non-susceptible isolates when used at high doses
- Fosfomycin and rifampin are not recommended
- After clinical improvement, step down to single-agent therapy