Medication Summary
Owing to the propensity of Acinetobacter to develop resistance to antibiotics, current treatment strategies remain limited. Beta-lactam antibiotics are the preferred antibacterial choices for susceptible A baumannii infections. Because of increasing resistance, carbapenems have become an increasingly critical therapeutic option for Acinetobacter infections; however, carbapenem resistance rates for A baumannii have been rising dramatically, both in the United States and globally. [1] Minocycline may retain antimicrobial activity even against strains resistant to other tetracyclines (including tigecycline), although cross-resistance has been reported. [1] In cases of nonbacteremic drug-resistant Acinetobacter pneumonia, the addition of inhaled colistin can be considered. This approach may minimize toxicity and increase antibiotic delivery to the lung. [1]
A baumannii is intrinsically multidrug resistant. Relatively few antibiotics are active against this organism. [6, 7, 8] Avoid treating colonization, but infection should be treated.
Medications to which Acinetobacter is usually sensitive include the following [5, 9, 10, 11, 12] :
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Meropenem
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Colistin
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Polymyxin B
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Amikacin
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Rifampin
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Minocycline
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Tigecycline
In general, first-, second-, and third-generation cephalosporins, macrolides, and penicillins have little or no anti-Acinetobacter activity, and their use may predispose to Acinetobacter colonization. Some strains are sensitive to cefepime, ceftazidime, and sulbactam-containing beta-lactam/beta-lactamase–inhibitor drugs.
Monotherapy and combination therapy has been used successfully (eg, amikacin, minocycline, or colistin ± rifampin). Combination therapy is often discussed and suggested, but data proving lower failure rates or lower rates for the development of resistance are inconclusive. Combination therapy can be considered for empiric therapy when the local rates of antimicrobial resistance to certain antibiotics are high or when the isolate is resistant to several classes of antibiotics.
Antibiotics
Class Summary
Empiric antimicrobial therapy should include one of the agents listed below.
Colistimethate sodium (Coly-Mycin M)
Hydrolyzed to colistin, which acts as cationic detergent that can damage bacterial cytoplasmic membrane, causing leaking of intracellular substances and cell death.
Meropenem (Merrem)
Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negative bacteria and slightly decreased activity against staphylococci and streptococci compared with imipenem.
Amikacin
Irreversibly binds to 30S subunit of bacterial ribosomes; blocks recognition step in protein synthesis; causes growth inhibition. For gram-negative bacterial coverage of infections resistant to gentamicin and tobramycin. Effective against P aeruginosa.
Use patient's IBW for dosage calculation. The same principles of drug monitoring for gentamicin apply to amikacin.
Polymyxin B
Binds to phospholipids, alters permeability, and damages bacterial cytoplasmic membrane.
Tigecycline (Tygacil)
A glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. Inhibits bacterial protein translation by binding to 30S ribosomal subunit and blocks entry of amino-acyl tRNA molecules in ribosome A site. Indicated for complicated skin and skin structure infections caused by E coli, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible and -resistant isolates), S agalactiae, S anginosus group (includes S anginosus, S intermedius, and S constellatus), S pyogenes, and B fragilis.
Rifampin (Rifadin)
Inhibits RNA synthesis in bacteria by binding to beta subunit of DNA-dependent RNA polymerase, which in turn blocks RNA transcription.
Minocycline (Minocin, Solodyn)
Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma.
