[2] It can be an opportunistic pathogen in humans, affecting people with compromised immune systems, and is becoming increasingly important as a hospital-derived (nosocomial) infection.

[5] Bacteria of this genus lack flagella but exhibit twitching or swarming motility, likely mediated by type IV pili.

Motility in A. baumannii may also be due to the excretion of exopolysaccharide, creating a film of high-molecular-weight sugar chains behind the bacterium to move forward.

[10] Colloquially, A. baumannii is referred to as "Iraqibacter" due to its seemingly sudden emergence in military treatment facilities during the Iraq War.

Multidrug-resistant A. baumannii has spread to civilian hospitals in part due to the transport of infected soldiers through multiple medical facilities.

The ability to attach to host cells allows bacteria to interact with them in various ways, whether by type III secretion system or simply by holding on against the prevailing movement of fluids.

[21] A. baumannii has been shown to produce at least one beta-lactamase, which is an enzyme responsible for cleaving the four-atom lactam ring typical of beta-lactam antibiotics.

[23] A. baumannii has been noted for its apparent ability to survive on artificial surfaces for an extended period of time, therefore allowing it to persist in the hospital environment.

Further, disruption of the putative pili chaperone and usher genes csuC and csuE were shown to inhibit biofilm formation.

[4][26] In general, biofilm formation has been linked so far with BfmRS TCS (two-component system) regulating Csu pili, Csu expression regulated by the GacSA TCS, biofilm-associated proteins BapAb, synthesis of the exopolysaccharide poly-β-1,6-N-acetylglucosamine PNAG, acyl-homoserine lactones through AbaR receptor, and AbaI autoinducer synthase.

Moreover, inactivation of adeRS operon negatively affects biofilm formation and prompts decreased expression of AdeABC.

Disruption of abaF has displayed an increase in fosfomycin susceptibility and a decrease in biofilm formation and virulence, suggesting a major role for this pump.

[12] The formation of biofilm involves cell attachment, a fundamental process typically triggered by environmental metabolites.

When vanillic acid enters the cell through VanP and VanK porins it binds to the VanR regulator, which is usually bound to PvanABKP and Pcsu promoters.

[30] Symptoms of A. baumannii infections in turn range from fevers and chills, rash, confusion and/or altered mental states, pain or burning sensations when urinating, strong urge to urinate frequently, sensitivity to bright light, nausea (with or without vomiting), muscle and chest pains, breathing problems, and cough (with or without yellow, green, or bloody mucus).

[44][45] American and other western soldiers in Iraq and Afghanistan were at risk of traumatic injury due to gunfire and improvised explosive devices.

Depending on the severity of the injury, the soldiers might then be transferred to a level-II facility, which consists of a forward surgical team, for additional stabilization.

Depending on the logistics of the locality, the injured soldiers might be transfer between these facilities several times before finally being taken to a major hospital within the combat zone (level III).

Generally after 1–3 days, when the patients were stabilized, they were transferred by air to a regional facility (level IV) for additional treatment.

Multidrug-resistant A. baumannii is a major factor in complicating the treatment and rehabilitation of injured soldiers, and has led to additional deaths.

Due to its ability to survive on artificial surfaces and resist desiccation, it can remain and possibly infect new patients for some time.

[53] In a study of European intensive care units in 2009, A. baumannii was found to be responsible for 19.1% of ventilator-associated pneumonia cases.