Virulence Factor and Biofilm Formation in Clinical Enterococcal Isolates of the West of Iran

Abstract

Background: Enterococcus spp., a part of the normal flora of the human intestine, possess several virulence factors that can develop biofilms to endure harsh environments. Their ability to cause nosocomial infections makes them as critical opportunistic pathogens in hospital settings. Objectives: The current study aimed at determining the occurrence of 6 genes coding virulence factors and their ability to develop biofilms, and conducting phenotypical assessments of haemolysin and gelatinase in clinical enterococci isolated from the West of Iran. Methods: A total of 126 isolates were screened for harbouring the following genes: aggregation substance (asa1), cytolysin (cylABM), enterococcal surface protein (esp), and gelatinase (gelE). Isolates were tested for haemolysin and gelatinase expression phenotypically and for biofilm production quantitatively, using the microtiter method.Results: Of the 126 tested isolates, 95 (73%) were Enterococcus faecalis and 28 (21%) were E. faecium. The total frequency of virulence gene was cylA 92 (73%), cylB 85 (67%), cylM 57 (45%), asa1 26 (21%), gelE 64 (51%), and esp 66 (53%); while 98 (75%) of the isolates were able to form biofilm. A total of 74 (58%) and 46 (35%) isolates could secret haemolysin and gelatinase. Conclusions: There was a significant difference between the frequency of virulence gene in E. faecalis and E. faecium. Enterococcus faecium isolates lacked the gelE and asa1 genes and the frequency of cylABM genes were lower than that of E. faecalis isolates. Enterococcus faecalis isolates were relatively rich in virulence factors; no association was observed between biofilm formation and the presence of specific virulence genes.

Phenotype–Genotype Correlations and Distribution of Key Virulence Factors in Enterococcus faecalis Isolated from Patients with Urinary Tract Infections

“… 30 , 39 , 40 Despite this high frequency of detection of gelE , only 22% of the isolates expressed a phenotypic gelatinase activity, consistent with prior findings. 18 , 41 Other studies stated that expression of gelE is regulated by the fsr locus and does not merely depend on gelE , 15 , 42 which is congruent with our findings here, as a significant and strong correlation between the presence of fsrA, fsrB, fsrC and the gelatinase activity was found. As in prior work from our laboratory, 18 fsrA or fsrB can be a sufficient biomarker for gelatinase activity; however, fsrB remains the single strongest predictor ( Figure 3 and Table 4 ) of that activity.…”

Investigation of the relationship between virulence factors and antibiotic resistance of Enterococci isolates

“…It was determined gelatinase enzymatic activity is a prerequisite for biofilm formation (19). In previous studies, gelE positivity varies between 19.6 % and 80.4 % (14,18,20,21). In this study gelE gene positivity was observed at 22.8 %, and ampicilin resistance in gelE gene positive E. faecalis was significantly higher compared to isolates that did not contain these genes.…”

Improved detection of esp, hyl, asa1, gelE, cylA virulence genes among clinical isolates of Enterococci

“…Nevertheless, the presence of virulence determinants in the clinical isolates might contribute to increased severity as they could be expressed under optimum conditions in vivo. Metadata of the previous studies on the detection of virulence genes of enterococci by multiplex/duplex/simplex PCR is depicted in Additional file 1: Table S1 [18,27,29,[33][34][35][36][37][38][39][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59].…”