Hospital-acquired infections following the 1999 Marmara earthquake

Öncül, Oral; Keskın, Onur; Acar, H. Volkan; Küçükardalı, Yaşar; Evrenkaya, Rıfkı; Atasoyu, Enes Murat; Top, Cihan; Nalbant, Selim; Özkan, Sezai; Emekdaş, Gürol; Çavuşlu, Şaban; Us, Melih Hulusi; Pahsa, Alaattin; Gökben, Merih

doi:10.1053/jhin.2002.1205

Cited by 97 publications

(36 citation statements)

References 27 publications

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“…Similar infections have occurred in trauma victims after natural disasters, such as floods and earthquakes, or bystanders in areas of active military conflicts (209)(210)(211)(212)(213)(214)(215).…”

Section: Clinical Manifestationsmentioning

confidence: 73%

Clinical and Pathophysiological Overview of Acinetobacter Infections: a Century of Challenges

et al. 2017

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SUMMARY Acinetobacter is a complex genus, and historically, there has been confusion about the existence of multiple species. The species commonly cause nosocomial infections, predominantly aspiration pneumonia and catheter-associated bacteremia, but can also cause soft tissue and urinary tract infections. Community-acquired infections by Acinetobacter spp. are increasingly reported. Transmission of Acinetobacter and subsequent disease is facilitated by the organism's environmental tenacity, resistance to desiccation, and evasion of host immunity. The virulence properties demonstrated by Acinetobacter spp. primarily stem from evasion of rapid clearance by the innate immune system, effectively enabling high bacterial density that triggers lipopolysaccharide (LPS)–Toll-like receptor 4 (TLR4)-mediated sepsis. Capsular polysaccharide is a critical virulence factor that enables immune evasion, while LPS triggers septic shock. However, the primary driver of clinical outcome is antibiotic resistance. Administration of initially effective therapy is key to improving survival, reducing 30-day mortality threefold. Regrettably, due to the high frequency of this organism having an extreme drug resistance (XDR) phenotype, early initiation of effective therapy is a major clinical challenge. Given its high rate of antibiotic resistance and abysmal outcomes (up to 70% mortality rate from infections caused by XDR strains in some case series), new preventative and therapeutic options for Acinetobacter spp. are desperately needed.

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Section: Clinical Manifestationsmentioning

confidence: 73%

Clinical and Pathophysiological Overview of Acinetobacter Infections: a Century of Challenges

et al. 2017

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“…Despite the hospital and community acquired A. baumannii infections, its occurrence appeared to be also related to injuries in war conflicts in e.g. Afghanistan, Iraq and Syria [17,18] as well as natural disasters, such as earthquakes and tsunami [19,20]. Epidemic spread of A. baumannii in above-mentioned extreme situations is attributed by some authors to substantial pressure on hospital emergency wards, which may result in failure in infection control precautions [7].…”

Section: Introductionmentioning

confidence: 99%

Acinetobacter baumannii: biology and drug resistance — role of carbapenemases

Nowak

Paluchowska

2015

Folia Histochem Cytobiol.

107

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Acinetobacter baumannii is a Gram-negative, glucose-non-fermenting, oxidase-negative coccobacillus, most commonly associated with the hospital settings. The ability to survive in adverse environmental conditions as well as high level of natural and acquired antimicrobial resistance make A. baumannii one of the most important nosocomial pathogens. While carbapenems have long been considered as antimicrobials of last-resort, the rates of clinical A. baumannii strains resistant to these antibiotics are increasing worldwide. Carbapenem resistance among A. baumannii is conferred by coexisting mechanisms including: decrease in permeability of the outer membrane, efflux pumps, production of beta-lactamases, and modification of penicillin-binding proteins. The most prevalent mechanism of carbapenem resistance among A. baumannii is associated with carbapenem-hydrolysing enzymes that belong to Ambler class D and B beta-lactamases. In addition, there have also been reports of resistance mediated by selected Ambler class A carbapenemases among A. baumannii strains. Resistance determinants in A. baumannii are located on chromosome and plasmids, while acquisition of new mechanisms can be mediated by insertion sequences, integrons, transposons, and plasmids. Clinical relevance of carbapenem resistance among strains isolated from infected patients, carriers and hospital environment underlines the need for carbapenemase screening. Currently available methods vary in principle, accuracy and efficiency. The techniques that deserve particular attention belong to both easily accessible unsophisticated methods as well as advanced techniques based on mass spectrometry or molecular biology. While carbapenemases limit the therapeutic options in A. baumannii infections, studies concerning novel beta-lactamase inhibitors offer a new insight into effective therapy.

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“…Other hospital-acquired A. baumannii infections include urinary tract infections, wound infections, and meningitis (55). In addition, A. baumannii infections have been a recurrent problem during wars and natural disasters (53,76), and recently MDR A. baumannii has become a major pathogen found in combat-associated wounds in military personnel deployed to Iraq or Afghanistan (18,29). Problematically, 89% of Acinetobacter strains isolated from patients injured in Iraq and Afghanistan were resistant to at least two major classes of antibiotics (72).…”

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confidence: 99%

Identification of Ata, a Multifunctional Trimeric Autotransporter of Acinetobacter baumannii

et al. 2012

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Acinetobacter baumannii has recently emerged as a highly troublesome nosocomial pathogen, especially in patients in intensive care units and in those undergoing mechanical ventilation. We have identified a surface protein adhesin of A. baumannii, designated the Acinetobacter trimeric autotransporter (Ata), that contains all of the typical features of trimeric autotransporters (TA), including a long signal peptide followed by an N-terminal, surface-exposed passenger domain and a C-terminal domain encoding 4 ␤-strands. To demonstrate that Ata encoded a TA, we created a fusion protein in which we replaced the entire passenger domain of Ata with the epitope tag V5, which can be tracked with specific monoclonal antibodies, and demonstrated that the C-terminal 101 amino acids of Ata were capable of exporting the heterologous V5 tag to the surface of A. baumannii in a trimeric form. We found that Ata played a role in biofilm formation and bound to various extracellular matrix/basal membrane (ECM/ BM) components, including collagen types I, III, IV, and V and laminin. Moreover, Ata mediated the adhesion of whole A. baumannii cells to immobilized collagen type IV and played a role in the survival of A. baumannii in a lethal model of systemic infection in immunocompetent mice. Taken together, these results reveal that Ata is a TA of A. baumannii involved in virulence, including biofilm formation, binding to ECM/BM proteins, mediating the adhesion of A. baumannii cells to collagen type IV, and contributing to the survival of A. baumannii in a mouse model of lethal infection.

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Hospital-acquired infections following the 1999 Marmara earthquake

Cited by 97 publications

References 27 publications

Clinical and Pathophysiological Overview of Acinetobacter Infections: a Century of Challenges

Clinical and Pathophysiological Overview of Acinetobacter Infections: a Century of Challenges

Acinetobacter baumannii: biology and drug resistance — role of carbapenemases

Identification of Ata, a Multifunctional Trimeric Autotransporter of Acinetobacter baumannii

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