ACINETOBACTER BAUMANNII

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ACINETOBACTER BAUMANNII

  

Acinetobacter baumannii is a rod shaped, almost round (coccobacillus)gram negative bacterium, named after the bacteriologist Paul Baumann. It is important as a hospital-derived(nosocomial) infection. It is often found in soil samples, but become resistant to antibiotics in hospital environments. Its natural habitat is still not known.

These bacteria lack flagella, may be due to the activity of type IV pili. motility in these bacteria may also be due to the excretion of exopolysaccharide, creating a film of high- molecular weight sugar chains behind the bacterium to move forward. 

Acinetobacter has similar morphology from other Moraxellaceae, hence it can be differentiated by performing Oxidase test, as Acinetobacter species are the only members of the Moraxellaceae, to lack cytochrome c oxidases.

Mechanisms of antibiotic resistance can be categorized into three groups. First, resistance can be achieved by reducing membrane permeability or increasing efflux of the antibiotic and thus preventing access to the target. Second, bacteria can protect the antibiotic target through genetic mutation or post-translational modification, and last, antibiotics can be directly inactivated by hydrolysis or modification. One of the most important weapons in the armory of Acinetobacter is its impressive genetic plasticity, facilitating rapid genetic mutations and rearrangements as well as integration of foreign determinants carried by mobile genetic elements. Of these, insertion sequences are considered one of the key forces shaping bacterial genomes and ultimately evolution.

Bacterial small RNAs are noncoding RNAs that regulate various cellular processes. Three sRNAs, AbsR11, AbsR25, and AbsR28, have been experimentally validated in the MTCC 1425 (ATCC15308) strain, which is a (multidrug-resistant) strain showing resistance to 12 antibiotics. AbsR25 sRNA could play a role in the efflux pump regulation and drug resistance

A. baumannii has been noted for its apparent ability to survive on artificial surfaces for an extended period of time, therefore allowing it to persist in the hospital environment. This is thought to be due to its ability to form biofilms. For many biofilm-forming bacteria, the process is mediated by flagella. However, for A. baumannii, this process seems to be mediated by pili. Further, disruption of the putative pili chaperone and usher genes csuC and csuE were shown to inhibit biofilm formation. The formation of biofilms has been shown to alter the metabolism of microorganisms within the biofilm, consequently reducing their sensitivity to antibiotics. This may be because fewer nutrients are available deeper within the biofilm. A slower metabolism can prevent the bacteria from taking up an antibiotic or performing a vital function fast enough for particular antibiotics to have an effect. They also provide a physical barrier against larger molecules and may prevent desiccation of the bacteria. In general, biofilm formation has been linked so far with BfmRS TCS (two-component system) regulating Csu pili, Csu expression regulated by the GacSA TCS, biofilm-associated proteins BapAb, synthesis of the exopolysaccharide poly-β-1,6-N-acetylglucosamine PNAG, acyl-homoserine lactones through AbaR receptor, and AbaI autoinducer synthase. Moreover, inactivation of adeRS operon negatively affects biofilm formation and prompts decreased expression of AdeABC. Disruption of abaF has displayed an increase in fosfomycin susceptibility and a decrease in biofilm formation and virulence, suggesting a major role for this pump.