Acinetobacter baumannii

by Caitlin Deseve and Jessika Marquis-Hrabe

Introduction

Acinetobacter baumannii (see Figure 1) is a multi-drug resistant pathogen that has become of great concern to medical facilities around the world. It causes various infections of the blood, brain, lungs, urinary tracts, and open wounds. The species was first identified in 1911 in soil samples, but became prevalent among returning soldiers who were treated in field hospitals of Iraq – thus earning it the common name ‘Iraqibacter’. Its natural habitat is still unknown.

Figure 1: Computer-generated image of Acinetobacter baumanii based on scanning electron microscopy. Source: Public Health Image Library, Center for Disease Control, James Archer, U.S. Centers for Disease Control and Prevention 2013.

Disease

Acinetobacter baumannii is a nosocomial bacterial pathogen, meaning it originates from hospital settings. The pathogen is capable of growing at various temperatures and pH conditions, which permits A. baumannii to persist in diverse environments. It causes a range of symptoms once it breaches the skin – from skin infections to pneumonia. It is most common in intensive care units, and in patients in hospital stays longer than 90 days with open wounds and invasive devices.

The most common symptoms of A. baumannii are ventilator-associated pneumonia (VAP) and bloodstream infections. VAP develops when pathogens transmit from external equipment and colonize the patient’s airways. Mortality rates due to A. baumannii-associated pneumonia range from 30 to 75%, with VAP responsible for the higher end. The most reported infections are encountered in the respiratory tract, wounds and catheter insertion sites.

Epidemiology

The United States has suffered several outbreaks, mostly associated with the return of military placed in Iraq and Afghanistan. The pathogen is often transmitted by contact to inanimate surface in field hospitals. Improper isolation and disinfecting treatments permitted the transfer of A. baumannii to US hospitals.  In 2004, 83% A. baumannii bloodstream infections were identified in the casualties injured. Infections in military personnel have also been reported in Canada and the United Kingdom.

Additionally, A. baumannii outbreaks have been identified in Europe since the 1980s. In most instances, transmission was caused by transfer of infected patients between hospitals; only one or two epidemic strains were recorded in hospitals. However, the outbreaks were not only limited to the hospitals, but spread internationally through airline travel.

The pathogens` prolonged survival in clinical settings contributes to its continuing outbreaks. Furthermore,  A. baumannii mortality rates are suspected to be associated with warmer temperature conditions, as pathogen colonization appears to be higher in tropical regions.

Virulence Factors

A. baumannii is highly capable of adhering to surfaces using hair-like appendages called pili. Specifically, A. baumannii employs Type IV pili on its surface, which function not only in adherence, but also in motility by extending and retracting. It has become of great concern due to its potential to produce biofilms. Communities of A. baumanni form by sticking together in a slimy extracellular matrix on both skin and hospital equipment. Formation of biofilms (see Figure 2) is a key virulence factor that provides resistance to antibiotics and allows persistence in unfavourable environmental conditions, such as low nutrient availability and desiccation.

Figure 2: Biofilm formation on a surface by Acinetobacter baumannii. 1, Attachment of free cells; 2, cell-cell adhesion in extracellular matrix; 3, dividing cells (proliferation) and cell growth; 4, cells spread and colonize new surfaces.

The presence of competence genes comFECB and comQLONM allow A. baumannii to uptake DNA from the environment and integrate it into its genome through a process called transformation. This factor enables A. baumannii to develop new traits rapidly, such as developing lower susceptibility to antibiotics. Moreover, the pathogen can produce antimicrobial-inactivating enzymes, such as Beta-lactamases. These enzymes destroy antibiotics like penicillins, to render them ineffective.  Finally, A. baumannii has a capsule that surrounds the outer membrane of the bacteria to serve as a protective barrier. Its presence helps the pathogen to evade the human immune response, ultimately making it more persistent in infection sites.

Treatment

A. baumannii is resistant to disinfectants and known antibiotics. Therefore, sufficient control is the current aim in hospitals. To prevent infection, environmental samples, especially from medical equipment, should be cultured and sources of contamination discarded. Additionally, hygiene control could prevent contamination between surface contact or direct person-person interaction. Should patients be infected, they should be isolated until infection has passed. Antibiotic selection is strenuous due to varying strains acquiring different antibiotic resistance. Discerning application of antibiotics in hospitalized patients is important to minimize drug resistance through pathogen evolution. Therefore, the treatment considered should be determined case-by-case.

References

Eliopoulos GM, Maragakis LL, Perl ™. Acinetobacter baumannii: Epidemiology, Antimicrobial Resistance, and Treatment Options. Clinical Infectious Diseases. 46(8): 1254–1263. Available from: https://academic.oup.com/cid/article-lookup/doi/10.1086/529198

Gaddy JA, Actis LA. 2009. Regulation of Acinetobacter baumannii biofilm formation. Future Microbiology. 4: 273-278. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724675/

Geisinger E, Isberg RR. 2015. Antibiotic Modulation of Capsular Exopolysaccharide and Virulence in Acinetobacter baumannii. PLoS Pathog. 11(2): e1004691. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334535/

Piepenbrink KH, Lillehoj E, Harding CM, Labonte JW, Zuo X, Rapp CA, Munson RS, Goldblum SE, Feldman MF, Gray JJ, Sundberg EJ. 2016. Structural Diversity in the Type IV Pili of Multidrug-resistant Acinetobacter. Journal of Biological Chemistry. 291: 22924-22935. Available from: http://www.jbc.org/content/291/44/22924.full

Peleg AY, Seifert H, Paterson DL. 2008. Acinetobacter baumannii: Emergence of a Successful Pathogen. Clinical Microbiology Reviews. 21(3): 538-582. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493088/

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