Acinetobacter [asz−in−ée−toe–back−ter] is a genus of Gram-negative bacteria belonging to the Gammaproteobacteria. Acinetobacter species are non-motile and oxidase-negative, and occur in pairs under magnification.
They are important soil organisms, where they contribute to the mineralization of, for example, aromatic compounds. Acinetobacter are a key source of infection in debilitated patients in the hospital, in particular the species Acinetobacter baumannii.
Acinetobacter is a compound word from scientific Greek, meaning 'nonmotile/immobile rod'. The first element acineto- is an unusual transliteration of the Greek ακινητο-; the usual romanization in English is akineto-, as in akinetic.
Species of the genus Acinetobacter are strictly aerobic nonfermentative Gram-negative bacilli. They show preponderantly a coccobacillary morphology on nonselective agar. Rods predominate in fluid media, especially during early growth.
Most strains of Acinetobacter, except some of the A. lwoffii strain, grow well on MacConkey agar (without salt). Although officially classified as nonlactose-fermenting, they are often partially lactose-fermenting when grown on MacConkey agar. They are oxidase-negative, nonmotile, and usually nitrate negative.
However, because routine identification in the clinical microbiology laboratory is not (yet) possible, they are divided and grouped into three main complexes:
- Acinetobacter calcoaceticus-baumanii complex: glucose-oxidising nonhemolytic, (A.baumannii can be identified by OXA-51 typing)
- Acinetobacter lwoffii: glucose-negative nonhemolytic
- Acinetobacter haemolyticus: hemolytic
The other reliable identification test at genus level is chromosomal DNA transformation assay (CTA): In this assay, a naturally competent tryptophan auxotrophic mutant of Acinetobacter baylyi (BD4 trpE27) is transformed with the total DNA of a putative Acinetobacter isolate and the transformation mixture plated on a brain heart infusion agar (BHI). The growth is then harvested after incubation for 24 h at 30°C, plating on an Acinetobacter minimal agar (AMM), and incubating at 30°C for 108 h. Growth on the minimal agar medium indicates a positive transformation assay and confirmes the isolate as a member of the genus Acinetobacter. E. coli HB101 and A. calcoaceticus MTCC1921T can be used as the negative and positive controls, respectively.
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Acinetobacter are widely distributed in nature, and commonly occur in soil. They can survive on moist and dry surfaces, including in a hospital environment. Some strains have been isolated from foodstuffs. In drinking water, they have been shown to aggregate bacteria that otherwise do not form aggregates.
Acinetobacter is frequently isolated in nosocomial infections, and is especially prevalent in intensive care units, where both sporadic cases as well as epidemic and endemic occurrence is common. A. baumannii is a frequent cause of nosocomial pneumonia, especially of late-onset ventilator associated pneumonia. It can cause various other infections including skin and wound infections, bacteremia, and meningitis, but A. lwoffi is mostly responsible for the latter. A. baumannii can survive on the human skin or dry surfaces for weeks.
Epidemiologic evidence indicates that Acinetobacter biofilms play a role in infectious diseases such as cystic fibrosis, periodontitis, bloodstream infections, and urinary tract infections, because of the bacteria's ability to colonize indwelling medical devices (such as catheters). Antibiotic resistance markers are often plasmid-borne, and plasmids present in Acinetobacter strains can be transferred to other pathogenic bacteria via horizontal gene transfer. The ability of Acinetobacter species to adhere to surfaces, to form biofilms, and to display antibiotic resistance and gene transfer motivates research into the factors responsible for their spread.
Since the start of the Iraq War, more than 700 U.S. soldiers have been infected with A. baumannii. Four civilians undergoing treatment for serious illnesses at Walter Reed Army Medical Center in Washington, D.C. contracted A. baumannii infections and died. At Landstuhl Regional Medical Center, a U.S. military hospital in Germany, another civilian under treatment, a 63-year-old German woman, contracted the same strain of A. baumannii infecting troops in the facility and also died. These infections appear to have been hospital-acquired. Based on genotyping of A. baumannii cultured from patients prior to the start of the Iraq War, one can presume that it is likely the soldiers contracted the infections while hospitalized for treatment in Europe.
Acinetobacter species are innately resistant to many classes of antibiotics, including penicillin, chloramphenicol, and often aminoglycosides. Resistance to fluoroquinolones has been reported during therapy, which has also resulted in increased resistance to other drug classes mediated through active drug efflux. A dramatic increase in antibiotic resistance in Acinetobacter strains has been reported by the CDC and the carbapenems are recognised as the gold-standard and treatment of last resort. Acinetobacter species are unusual in that they are sensitive to sulbactam; sulbactam is most commonly used to inhibit bacterial beta-lactamase, but this is an example of the antibacterial property of sulbactam itself.
In November, 2004, the CDC reported an increasing number of A. baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom (OIF) and in Afghanistan during Operation Enduring Freedom (OEF) were treated. Most of these were multidrug-resistant. Among one set of isolates from Walter Reed Army Medical Center, 13 (35%) were susceptible to imipenem only, and two (4%) were resistant to all drugs tested. One antimicrobial agent, colistin (polymyxin E), has been used to treat infections with multidrug-resistant A. baumannii; however, antimicrobial susceptibility testing for colistin was not performed on isolates described in this report. Because A. baumannii can survive on dry surfaces for up to 20 days, they pose a high risk of spread and contamination in hospitals, potentially putting immune-compromised and other patients at risk for drug-resistant infections that are often fatal and, in general, expensive to treat.
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