Other meanings of Acinetobacter baumannii
Microbiology
Acinetobacter baumannii is a Gram-negative, strictly aerobic, non-fermenting coccobacillus that has emerged as a leading cause of hospital-acquired infections, particularly ventilator-associated pneumonia and bloodstream infections in intensive care units. Its remarkable ability to survive on dry surfaces and acquire multidrug resistance has made it a global health threat, classified by the World Health Organization as a critical priority pathogen for the development of new antibiotics.1
A. baumannii is a short, plump rod that often appears as diplococci, staining Gram-negative. It is oxidase-negative, catalase-positive, and non-motile, with an optimal growth temperature of 37°C, though it can grow at 44°C, a trait used in its identification. On MacConkey agar it forms pale, non-lactose-fermenting colonies, and it is distinguished from other Acinetobacter species by its ability to grow at 44°C and its inability to hemolyze sheep blood.2 Molecular methods, such as 16S rRNA gene sequencing and MALDI-TOF mass spectrometry, are now the gold standard for definitive species identification, as phenotypic tests can misidentify closely related species like A. pittii and A. nosocomialis.
A. baumannii causes a spectrum of infections, most commonly ventilator-associated pneumonia, catheter-related bloodstream infections, wound infections, and urinary tract infections, predominantly in critically ill patients. It rarely infects healthy individuals, but outbreaks in intensive care units are frequent due to its persistence on medical equipment and environmental surfaces. The organism's ability to form biofilms on abiotic surfaces, such as catheters and ventilators, facilitates its spread and resistance to disinfection.3 Mortality rates in bloodstream infections range from 30% to 50%, with higher rates when the isolate is resistant to carbapenems.4
A. baumannii is notorious for its multidrug resistance, often leaving clinicians with few therapeutic options. Resistance arises through multiple mechanisms: β-lactamases (including carbapenemases like OXA-23 and NDM-1), efflux pumps, porin loss, and target modifications. The organism's genome is highly plastic, acquiring resistance genes via horizontal gene transfer, particularly through plasmids and transposons.5 Colistin and tigecycline are often the last-resort drugs, but resistance to colistin is emerging, driven by mutations in the pmrAB two-component system that modify lipid A.
Beyond its clinical notoriety, A. baumannii has several lesser-known facets. It is naturally competent, allowing it to take up DNA from the environment, which contributes to its rapid evolution. It can survive desiccation for up to 30 days on inanimate surfaces, a trait linked to its ability to form biofilms and produce capsular polysaccharides. The species name honors the bacteriologist Paul Baumann, who contributed to its taxonomy in the 1960s. In 2017, the WHO listed it as a critical priority for antibiotic research, yet it also shows promise in bioremediation: some strains can degrade aromatic compounds, such as phenol, in contaminated soils.
This article focuses on the clinical and microbiological aspects of Acinetobacter baumannii as a pathogen.
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