Acinetobacter Pneumonia: A Review

Joshua D. Hartzell, MD, Andrew S. Kim, MD, Mark G. Kortepeter, MD, MPH, Kimberly A. Moran, MD

Disclosures
In This Article

Epidemiology

Acinetobacter grow easily in nature and have been isolated from many sources throughout the world.[12] In nature, Acinetobacter are most commonly found in soil and water, but have been isolated from animals as well.[5,18,19] It was recently found in human body lice of homeless people in France.[20] It has also been isolated from food (including hospital food), ventilator equipment, suctioning equipment, infusion pumps, sinks, stainless steel trolleys, pillows, mattresses, tap water, bed rails, humidifiers, soap dispensers, and other sources.[11,18,21,22,23,24,25,26,27,28,29]

In humans, Acinetobacter have been isolated from all culturable sites.[18] Up to 40% of healthy adults can have skin colonization, with higher rates among hospital personnel and patients.[18,30,31] Skin colonization is common among injured military personnel returning from OIF -- an average of 15% are colonized on admission to Walter Reed Army Medical Center (WRAMC). At Brooke Army Medical Center, skin, soft tissue, and orthopedic infections caused by Acinetobacter are 10 times more common than bacteremia.[32] A study of healthy troops, most of whom had not deployed, revealed colonization rates of 17%, with Acinetobacter strains genotypically and phenotypically different from those of infected or colonized soldiers returning from OIF.[33]

The respiratory tract is an important site of colonization and is the most frequent site of infection.[18,34] Acinetobacter colonization has been reported from the nares, nasopharynx, and tracheostomy sites.[34,35] Rates of colonization increase during ICU stays.[35,36] The frequency of nasal colonization among healthy persons has been variable. A recent study showed no nasal colonization among 293 healthy, nondeployed US soldiers.[37] Ongoing studies in soldiers returning from OIF and OEF may show different results. Whether nasal colonization is a risk factor for pneumonia remains to be determined.

The prevalence of Abc infections is increasing.[16] The risk factors for Acinetobacter hospital-acquired pneumonia (AHAP) and Acinetobacter ventilator-associated pneumonia (AVAP) published in the literature are derived from studies with small sample sizes. Husni and colleagues assessed 15 patients in a case-control study and identified prior ceftazidime treatment as a risk factor by univariate analysis.[38] Baraibar and coworkers reported on 12 intubated patients and, using logistic regression, identified risk factors for AVAP, including previous neurosurgery, head trauma, and large-volume pulmonary aspiration.[39]

A recent study by Garnacho-Montero and coworkers has better characterized risk factors for AVAP and imipenem-resistant AVAP.[40] This study compared 41 cases of AVAP with 40 cases of VAP secondary to other pathogens. The univariate analysis showed prior sepsis, previous antibiotic use, reintubation, length of hospital stay, length of mechanical ventilation, imipenem exposure, and fluoroquinolone exposure as potential risk factors for AVAP. The multivariate analysis, however, only showed prior antibiotic exposure as a risk factor. Patients with a history of antibiotic use were more likely to develop AVAP (odds ratio [OR], 14; 95% confidence interval [CI], 4.1-91; P < .0001). The authors reported that previous exposure to imipenem was the only variable by multivariate analysis that was associated with AVAP secondary to imipenem-resistant Acinetobacter (OR, 4; CI, 1.1-29.8; P < .005).[40] This study and others have shown that inappropriate empirical use of antibiotics results in worse outcomes in AVAP cases, which has implications for treatment.[40,41]

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