Indian Journal of Medical Microbiology Home 

CORRESPONDENCE
[Download PDF]
Year : 2014  |  Volume : 32  |  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

Correspondence Address:
G K Badave
Department of Microbiology, Government Medical College Nagpur, Maharashtra
India

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;32:207-208

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 2020 Feb 17 ];32:207-208
Available from: http://www.ijmm.org/text.asp?2014/32/2/207/129860

Full Text

Dear Editor,

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. [1] In non mammalian mutants genes encoding for transcription factors, multidrug efflux transport

 



system and a urease have also been identified, [2] although the virulence of these mutants was not assessed in mammalian models. Studies on virulence determinants in clinical isolates of A. baumannii are scanty. [3],[4],[5] 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.{Table 1}

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.

References

1Fournier PE, Vallenet D, Barbe V, Audic S, Ogata H, Poirel L et al. Comparative genomics of multidrug resistance in Acinetobacter baumannii. PLoS Genet 2006;2:e7.
2Smith MG, Gianoulis TA, Pukatzki S, Mekalanos JJ, Ornston LN, Gerstein M et al. New insights into Acinetobacter baumannii pathogenesis revealed by high-density pyrosequencing and transposon mutagenesis. Genes Dev 2007;21:601-14.
3Cevahir N, Demir M, Kaleli I, Gurbuz M, Tikvesli S. Evalution of biofilm production, gelatinase activity and mannose resistant hemagglutination in Acinetobacter baumannii strains. J Microbiol Immunol Infect 2008;41:513-18.
4Rao RS, Karthika RU, Singh SP, Shashikala P, Kanungo R, Jayachandran S, et al. Correlation between biofilm production and multiple drug resistance in imipenem resistant clinical isolates of Acinetobacter baumannii. Indian J Med Microbiol 2008;26:333-37.
5Peleg AY, Seifert H, Paterson DL. Acinetobacter baumannii: Emergence of a successful pathogen. Clin Microbiol Rev 2008;21:538-82.