|Year : 2014 | Volume
| Issue : 2 | Page : 207-208
Is low virulence Acinetobacter baumannii acquiring virulence?
GK Badave, VA Agarwal, NG Deogade
Department of Microbiology, Government Medical College Nagpur, Maharashtra, India
|Date of Submission||14-Aug-2013|
|Date of Acceptance||18-Nov-2013|
|Date of Web Publication||2-Apr-2014|
G K Badave
Department of Microbiology, Government Medical College Nagpur, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Badave G K, Agarwal V A, Deogade N G. Is low virulence Acinetobacter baumannii acquiring virulence?. Indian J Med Microbiol 2014;32:207-8
|How to cite this URL:|
Badave G K, Agarwal V A, Deogade N G. Is low virulence Acinetobacter baumannii acquiring virulence?. Indian J Med Microbiol [serial online] 2014 [cited 2019 Oct 14];32:207-8. Available from: http://www.ijmm.org/text.asp?2014/32/2/207/129860
The image of Acinetobacter baumannii as a low virulence pathogen is under extreme scrutiny. Genes encoding for resistance to anti-microbials, heavy metals and antiseptics have been identified.  In non mammalian mutants genes encoding for transcription factors, multidrug efflux transport[TAG:2][/TAG:2]
system and a urease have also been identified,  although the virulence of these mutants was not assessed in mammalian models. Studies on virulence determinants in clinical isolates of A. baumannii are scanty. ,, We attempted identification of five virulence determinants selected on the basis of published information, in 72 non-duplicate isolates of A. baumannii identified by conventional methods and obtained from sputum (15), urine (12), pus (11), blood and wound swab (9 each), vaginal swab (4), cerebrospinal fluid (CSF) (3), conjuctival swab, ascitic fluid, pleural fluid (2each), catheter tip, peritoneal dialysis fluid and tracheal aspirate (1 each).
We found that 65 (90.3%) isolates were multidrug resistant (MDR, [Table 1]), a property that confers survival advantage in the presence of drugs. Biofilm formers were 45 (62.5%) which are known to be phenotypically MDR as long as the organism is in the biofilm due to excessive secretion of exopolysaccharide preventing anti-microbial penetration. In all 40 of 45 biofilm formers were genotypically MDR as demonstrated by disc diffusion test. Surface components like structural haemagglutinins lead to adhesion and initiate biofilm formation while bacterial enzymes facilitate invasion resulting in destruction of host components. Eleven of 14 haemagglutinators and ten of 12 urease producers were MDR, while 12 of 14 haemagglutinators and 9 of 12 urease producers were biofilm formers. A combination of virulence determinants may synergistically enhance pathogenicity. Gelatinase activity was not present in any isolate.
Our study is a preliminary effort that identified the existence of four out of five virulence determinants in clinically isolated A. baumannii. Larger studies are needed to identify these and other virulence determinants and perhaps their origin also which may be from highly pathogenic bacteria.
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