Survival ofAcinetobacteron Three Clinically Related Inanimate Surfaces

Webster, Carol; Towner, K. J.; Humphreys, H.

doi:10.1086/503214

Cited by 55 publications

(32 citation statements)

References 5 publications

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“…Patients can carry the microorganism for months, and their skin and mucosa can act as a source of cross contamination. Furthermore, the hands of healthcare workers may act as direct vectors for spread, while a contaminated environ- 325 ment may serve as a secondary source (15). In our study, the epidemic strain was not recovered from the hands of the healthcare workers but was found on the surface of a serum container located in the room of an outbreak patient.…”

mentioning

confidence: 64%

Outbreak of Multiresistant OXA-24- and OXA-51-Producing Acinetobacter baumannii in an Internal Medicine Ward

Tena

Martínez

Oteo³

et al. 2013

Jpn J Infect Dis

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SUMMARY:Here we describe the clinical, microbiological, epidemiological, and molecular characterization of an outbreak of multidrug-resistant Acinetobacter baumannii (MRAB) involving 5 patients admitted to the internal medicine ward of our hospital. Over a 6-week period, 5 MRAB isolates were recovered from 5 patients, including 1 with fatal meningitis, 3 with skin and soft tissue infections, and 1 with respiratory colonization. One sample obtained during environmental monitoring in the ward was A. baumannii-positive. According to the pulsed-field gel electrophoresis typing results, the strains isolated from all patients and the environmental sample belonged to a single clone, identified as ST79 by multilocus sequence typing. The bla OXA-24 and bla OXA-51 carbapenemases were detected in all isolates. Four patients died, but only the death of the meningitis patient was probably related to the A. baumannii infection. The infection source was probably the hands of the healthcare workers because the outbreak strain was isolated from the surface of a serum container. The results of the present study revealed the importance of strict adherence to control measures by all healthcare workers because the consequences of noncompliance can be very serious.

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mentioning

confidence: 64%

Outbreak of Multiresistant OXA-24- and OXA-51-Producing Acinetobacter baumannii in an Internal Medicine Ward

Tena

Martínez

Oteo³

et al. 2013

Jpn J Infect Dis

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“…This Gram-negative, aerobic, coccobacillus is responsible for a significant number of hospital-acquired infections, including those of the skin and bloodstream, as well as pneumonia and meningitis (5,6,18,34,47). Importantly, A. baumannii is able to persist on hospital surfaces for weeks to months, providing an environmental reservoir for its transmission (44)(45)(46). Compounding this problem, multidrug-resistant (MDR) strains of A. baumannii have been isolated with increasing frequency, and strains with pan-drug resistance (PDR) have been described as well, particularly among vulnerable patients within intensive care units or military hospitals (3,11,15,33,36,39,41).…”

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confidence: 99%

Rapid Killing of Acinetobacter baumannii by Polymyxins Is Mediated by a Hydroxyl Radical Death Pathway

Sampson

Liu

Schroeder

et al. 2012

Antimicrob Agents Chemother

172

137

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Acinetobacter baumannii is an opportunistic pathogen that is a cause of clinically significant nosocomial infections. Increasingly, clinical isolates of A. baumannii are extensively resistant to numerous antibiotics, and the use of polymyxin antibiotics against these infections is often the final treatment option. Historically, the polymyxins have been thought to kill bacteria through membrane lysis. Here, we present an alternative mechanism based on data demonstrating that polymyxins induce rapid cell death through hydroxyl radical production. Supporting this notion, we found that inhibition of radical production delays the ability of polymyxins to kill A. baumannii. Notably, we demonstrate that this mechanism of killing occurs in multidrug-resistant clinical isolates of A. baumannii and that this response is not induced in a polymyxin-resistant isolate. This study is the first to demonstrate that polymyxins induce rapid killing of A. baumannii and other Gram-negatives through hydroxyl radical production. This significantly augments our understanding of the mechanism of polymyxin action, which is critical knowledge toward the development of adjunctive therapies, particularly given the increasing necessity for treatment with these antibiotics in the clinical setting.

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“…Specific inhibitors of the FAS-II pathway include triclosan and thiolactomycin. Triclosan, a specific inhibitor of FAS-II trans-2-enoyl-ACP reductase (ENR, also known as inhA or FabI) is effective against a broad spectrum of bacteria (20), including Escherichia coli (21,22), mycobacteria (23), and multidrug-resistant Staphylococcus aureus (24,25) and is widely used as an antimicrobial in household formulations, including soaps and toothpaste. Recently, triclosan was found to inhibit P. falciparum growth with an IC 50 of ϳ1 M (19,26).…”

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confidence: 99%

Structural Elucidation of the Specificity of the Antibacterial Agent Triclosan for Malarial Enoyl Acyl Carrier Protein Reductase

Perozzo

Kuo

Sidhu

et al. 2002

Journal of Biological Chemistry

202

228

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The human malaria parasite Plasmodium falciparum synthesizes fatty acids using a type II pathway that is absent in humans. The final step in fatty acid elongation is catalyzed by enoyl acyl carrier protein reductase, a validated antimicrobial drug target. Here, we report the cloning and expression of the P. falciparum enoyl acyl carrier protein reductase gene, which encodes a 50-kDa protein (PfENR) predicted to target to the unique parasite apicoplast. Purified PfENR was crystallized, and its structure resolved as a binary complex with NADH, a ternary complex with triclosan and NAD ؉ , and as ternary complexes bound to the triclosan analogs 1 and 2 with NADH. Novel structural features were identified in the PfENR binding loop region that most closely resembled bacterial homologs; elsewhere the protein was similar to ENR from the plant Brassica napus (root mean square for C␣s, 0.30 Å). Triclosan and its analogs 1 and 2 killed multidrug-resistant strains of intra-erythrocytic P. falciparum parasites at sub to low micromolar concentrations in vitro. These data define the structural basis of triclosan binding to PfENR and will facilitate structure-based optimization of PfENR inhibitors.Treatment of Plasmodium falciparum malaria has depended for decades on the use of the aminoquinoline chloroquine or the synergistic antifolate combination pyrimethamine-sulfadoxine. These drugs were characterized by their potency against the P. falciparum asexual intra-erythrocytic stages (responsible for malaria pathogenesis), their affordability and their safety. The occurrence and spread of drug-resistant strains of P. falciparum have largely contributed to a recent resurgence of malaria, which claims 1 to 3 million lives annually and which is endemic in inter-tropical areas representing 40% of the world's population (1). The current situation of antimalarial chemotherapy and resistance, in conjunction with the reappearance of malaria in formerly well-controlled areas, reinforces the need for new, highly potent antimalarials.Recent investigations into Apicomplexan parasites, including Plasmodium and Toxoplasma, have uncovered the existence of a unique organelle, the apicoplast (2-4). The finding that ciprofloxacin-mediated inhibition of plastid replication in Toxoplasma gondii tachyzoites blocked parasite propagation provided evidence for the indispensable nature of this nonphotosynthetic plastid organelle (5). Studies of plastid inhibitors and apicoplast mis-segregation mutants confirmed the essential requirement of this organelle for normal parasite development and indicated that inhibition of apicoplast function or loss of this organelle resulted in parasite death following reinvasion of host cells (5-7). This organelle appears to derive ultimately from a cyanobacterial endosymbiont (4,8,9) and as such was postulated to contain prokaryotic-type metabolic pathways, of significant interest from the perspective of developing antiparasitic drugs (10). Recent studies indicate that these pathways include fatty acid and isoprenoid bios...

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Survival ofAcinetobacteron Three Clinically Related Inanimate Surfaces

Cited by 55 publications

References 5 publications

Outbreak of Multiresistant OXA-24- and OXA-51-Producing <i>Acinetobacter baumannii</i> in an Internal Medicine Ward

Outbreak of Multiresistant OXA-24- and OXA-51-Producing <i>Acinetobacter baumannii</i> in an Internal Medicine Ward

Rapid Killing of Acinetobacter baumannii by Polymyxins Is Mediated by a Hydroxyl Radical Death Pathway

Structural Elucidation of the Specificity of the Antibacterial Agent Triclosan for Malarial Enoyl Acyl Carrier Protein Reductase

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