Abstract

Acinetobacter baumannii is an important opportunistic pathogen due to its capabilities for developing mechanisms of resistance to a wide range of antimicrobial agents including carbapenems. This review described the risk factors, antimicrobial susceptibility and mechanisms of carbapenem resistance of A. baumannii from different geographical regions of Saudi Arabia. Several factors including complexity of intensive care unit (ICU) environments, increased numbers of patients with serious diseases, wide spread gastrointestinal colonization and extensive use of antimicrobial drugs led to a wide prevalence of A. baumannii infections in hospitals in Saudi Arabia. A. baumannii has been noted to be less susceptible to antimicrobials agents, including carbapenems, over time, resulting in the evolution of multidrug-resistant (MDR) strains. Dissemination of MDR A. baumannii is attributed to the extreme use of wide-spectrum antimicrobial drugs in hospitals, cross infection between inpatients, invasive ICU procedures, and hospitalized patients with diabetic and cancer those are under frequent invasive diagnostic and therapeutic interventions. Although an increasing prevalence of colistin and tigecycline resistance has been reported in many hospitals, combinations of these agents with carbapenems or other antibiotics remain the best therapeutic choice and reasonably safe to treat patients with MDR A. baumannii infections. The wide distribution of carbapenem resistant A. baumannii (CRAB) due to several mechanisms with diverse genetic determinants has been documented. Although OXA-23 β-lactamase and OXA-51 β-lactamase are the most common genes responsible for CRAB, other novel genes such as blaVIM, PER-1-like and GES-5 have been discovered in carbapenem resistant strains. The high rates of MDR A. baumannii in Saudi hospitals indicate that extensive investigation into the molecular basis of MDR and developing new therapies of CRAB is needed. Moreover, the development of a local antibiogram database coupled with a nationwide antimicrobial stewardship and infection prevention program might help to improve our knowledge of the resistance patterns of A. baumannii, and in developing a treatment protocol for decreasing the infection burden in Saudi Arabia.

Highlights

  • Over the last few years, Acinetobacter baumannii (A. baumannii) has become an important opportunistic pathogen that is widespread in hospitals and other healthcare settings [1,2,3]

  • Multiple complex factors related to the hospital environment, patient co morbidities, duration of hospital admission, intensive care unit (ICU) complexity, intercurrent illness and the usage of antimicrobial agents contribute to the spread of A. baumannii

  • The high rates of resistant A. baumannii in Saudi Arabia call for comprehensive surveillance programs to understand the origins and extent of the A. baumannii problem in depth

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Summary

Background

Over the last few years, Acinetobacter baumannii (A. baumannii) has become an important opportunistic pathogen that is widespread in hospitals and other healthcare settings [1,2,3]. Gastrointestinal colonization by A. baumannii in ICU patients is a significant risk factor for spreading antimicrobial resistance, increases disease severity and provides an important reservoir for clinical infections and hospital outbreaks [27]. Numerous studies indicated that the severity of underlying disease, broad-spectrum antimicrobial use, prolonged hospitalization, ICU stays, the presence of invasive devices, and prolonged mechanical ventilation were risk factors for acquisition of multi-drug resistant A. baumannii strains [7, 25, 34]. Between 2006 and 2007, clinical samples were collected from different sites of infection of hospitalized and community patients at major hospitals and medical center across Saudi Arabia, and the A. baumannii isolates were all highly resistant to the most common antimicrobial agents [37]. Another study found that 96% of A. baumannii were resistant amoxicillin/clavulanic acid, 93% were resistant

East South
Sources of isolates Setting
Tracheal aspirate
Findings
Conclusions

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