Of the total, 46 isolates were E. faecalis and 54 E. faecium, of which 70% (32 E. faecalis and 38 E. faecium) were HLGRE and 7% (1 E. faecalis and 6 E. faecium) were VRE. Haemolysin and gelatinase production, haemagglutination and biofilm formation was seen in 29%, 17%, 39% 34%, respectively. Virulence factors were more in E. faecalis (P > 0.05). asa1 and gelE were the most prevalent virulence genes [ Figure 1]. None harboured all the virulent genes and 10 isolates did not show any virulence factors. Majority of the strong biofilm producers possessed either asa1 or gelE gene. On statistical analysis, decreasing expression and possession of virulence genes was seen with increasing drug resistance (P < 0.05). Acquisition of vancomycin resistance resulted in this decrease (P < 0.05).We found that just as increase in one aspect of survival fitness reduces the other, as seen in community and hospital acquired Methicillin-resistant Staphylococcus aureus (MRSA), [5] acquisition of plasmids for drug resistance might have led to loss of virulence due to fitness cost benefits relating to VRE. Figure 1: CLI induction testing of S. aureus by disk diffusion. E: ERY disk (15 µg); CD: CLI disk (2 µg). MS Phenotype (a), Constitutive MLSB Phenotype (b), S phenotype (c) b a c [Downloaded free from http://www.ijmm.org on Saturday, June 13, 2015, IP: 61.16.135.116]
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