Acinetobacter baumannii: An Emerging Multidrug-resistant Threat

Thomas D Gootz; Andrea Marra

Disclosures

Expert Rev Anti Infect Ther. 2008;6(3):309-325. 

In This Article

Acinetobacter Origins

There has been a great deal of taxonomic confusion regarding the genus Acinetobacter, which is characterized as a strictly aerobic, non-motile, Gram-negative, nonfermentative, oxidase-negative, catalase-positive organism.[1,2] The designation of Acinetobacter taxonomy as being distinct from the Moraxellaceae was established in the 1970s and was changed again in the mid-1980s.[3] There are currently 32 Acinetobacter named and un-named species.[2,4]Acinetobacter baumannii, also referred to as Acinetobacter calcoaceticus-A. baumannii complex, encompasses these two species, plus two other un-named species, 3 and 13TU, due to the close relatedness of these strains[4] and is primarily responsible for clinical pathogenesis.[1,5,6] Genomic characterization methods have proven useful for following the dissemination of clonal outbreak strains in the hospital environment, as well as for detecting specific antibiotic-resistance genes and their regulation. Definitions of pan- and multidrug resistant (MDR) A. baumannii are not consistent in the literature[7]; typically MDR A. baumannii are resistant to aminoglycosides, antipseudomonal penicillins, carbapenems, cephalosporins and quinolones. Genomic typing information has provided insight into the origin and spread of MDR strains across local and global hospital environments.[8] Acinetobacter spp. have been isolated from a broad range of environmental samples but A. baumannii has been found to a more limited degree in soil, water, sewage, animals, humans and produce for human consumption.[1,9,10,11] Despite the ubiquity of this organism in the environment, a r-eservoir for infection has not been identified.

A. baumannii is a remarkably hardy organism, tolerant to wide ranges in temperature, pH and humidity. It has been shown to be able to survive on dry surfaces for 5 months, posing a challenge to hospital infection control measures.[12] It has been isolated from hospital equipment, bedding, furniture and staff.[4] Furthermore, contamination of hospital devices with MDR A. baumannii isolates has been documented for ventilator tubing, suction catheters, humidifiers, multidose vials of medication, potable water, bedding and improperly sterilized arterial pressure transducers.[13] One study found that a significant correlation existed between the number of monthly environmental isolations of A. baumannii obtained and the incidence of patient colonization and/or infection with the same strain over the course of the study period.[14] Thorough cleaning of hospital rooms with sodium hypochlorite 1000 ppm solution reduced both environmental contamination and patient colonization with this organism. Acinetobacter shares this survival tactic with other important Gram-negative nosocomial pathogens, such as Escherichia coli, Klebsiella spp., Pseudomonas aeruginosa and Shigella spp..[12] An extensive review of 1561 reported hospital epidemics, occurring over the past 40 years, indicated that ward closure and cleaning was necessary to control an outbreak in 22.9% of wards involving Acinetobacter versus 11.7% of wards containing other epidemic pathogens.[15]

Some literature reports suggest a level of carriage of A. baumannii in the general population that may be related to hospital infection rates, but this suggestion is not universally accepted. Carriage rates for Acinetobacter spp. have been reported up to 50%[16]; other reports find that actual A. baumannii carriage is considerably lower, nearer 1-3%.[4,17,18] Several Acinetobacter spp. can colonize human skin and such colonization can serve as a major source for infection, including those of the urinary and respiratory tracts, endocarditis, wounds, septicemia and meningitis.[8] Carriage with MDR A. baumannii, however, appears to be rare. One recent study compared hospital and community isolates and found that environmental or carriage-related isolates are generally susceptible to antibiotics (0% were MDR), in contrast to A. baumannii strains associated with nosocomial infections, with MDR rates of 36.6%.[19] This finding, in combination with the ability of A. baumannii to remain viable on hospital surfaces for extended time periods, indicates that the hospital is the probable reservoir for MDR A. baumannii infections.

The available data suggest that while A. baumannii remains an opportunistic pathogen, critically ill patients in acute care hospitals have a high incidence of colonization with MDR strains. In a 2-year duration outbreak study, A. baumannii was isolated from 229 patients.[20] Of these, 66% were colonized with clonal MDR isolates. Other studies have indicated that A. baumannii is not frequently found in feces from healthy subjects in the community,[21] suggesting that persistent colonization of the hospital environment provides the main source of patient infection. To this end, studies indicate that antibiotic use in the hospital may provide selective pressure that promotes fecal carriage of MDR A. baumannii for inpatients.[22] This, in turn, appears to promote the recolonization of the hospital environment, as well as providing an initial source of MDR strains that increase patient infection rates.[22,23] One study suggests that infection rates with MDR strains are higher in intensive-care unit (ICU) patients in some European and Asian hospitals compared with the USA and, if true, this may reflect a difference in global antibiotic use.[23] Persistence in the hospital environment probably promotes colonization of tracheobronchial secretions with A. baumannii, leading to ventilator-associated pneumonia with acinetobacters. Paterson has recently reviewed some of the epidemiological data associated with infections caused by panresistant acinetobacters (defined as clones resistant to all ß-lactam and fluoroquinolone antibiotics recommended for empirical therapy of ventilator-associated pneumonia).[13,24] It is clear that many outbreaks with MDR strains are clonal in nature, and that such strains may only be susceptible to agents such as tigecycline, polymyxin B and colistin. Unfortunately, dosing regimens that demonstrate efficacy with some of these drugs are not well defined.

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