Virulence genes were investigated among all beta

Virulence A 779 were investigated among all beta-lactamase-producing isolates using PCR. There were 54% (n=54) isolates that had one or more than one type of all these six virulence factors. Among all the isolates, 40.74% (n=22) produced OprI (249 bp in size) and 29.62% (n=16) expressed OprL (504 bp) virulence genes. Furthermore, these isolates were evaluated for LasB (300 bp) and PlcH (307 bp) virulence factors, and 24% (n=13) and 18.5% (n=10), respectively, were found to be positive for these factors (Fig. 1 and Table 2). Subsequently, these isolates were screened for ExoS and ToxA, having a product size of 504 bp and 352 bp, respectively. The prevalence of ToxA isolates was 33.33% (n=18); ExoS had a higher prevalence of 37.03% (n=20) compared with ToxA. Coproduction of virulence factors was observed among all these isolates. A total of 42.59% (n=23) isolates produced more than one type of virulence factors. Among these isolates, 13 (24%) were determined to be positive for two virulence factors, five (9.25%) produced three virulence factors, four (7.4%) produced four virulence factors, and one expressed five virulence factors.
Discussion P. aeruginosa, one of the major human opportunistic pathogens secreting various toxins and involved in different types of infections, is considered to be a primary contributor in the pathogenesis of infected individuals. Production of virulence factors was analyzed in extended spectrum beta lactamases (ESBL)-producing P. aeruginosa, and it was established that a strong correlation exists between secretion of toxins and beta-lactamase producers. It was revealed that pigment production was more significantly associated with drug resistance than the production of virulence factors such as elastases and proteases in clinical isolates of P. aeruginosa. In another study, pigment production was consistent with our results. Biofilm formation was compared with previously reported cases of clinical isolates, and it was noted that the prevalence of biofilm formation was consistent with our study results, which implied that biofilm formation has a strong correlation with the drug resistance pattern. Biofilm formation can strengthen ESBL-carrying bacteria more pathogenically compared with non-ESBL producers, as in our case, where all were biofilm producers. There has been some measure of phenotypic diversity linked with biofilm formation which leads to mortality and morbidity. Therefore, exploration of the mechanistic details of biofilm formation will open up new therapeutic venues to control these pathogens. Distribution of virulence factor ExoS was higher compared with the data shown in another study previously. The ToxA prevalence was lower in our study than that in a previous study. Expression of virulence factors can be retarded using azithromycin, which inhibits autoinducers that are involved in the expression of these genes. Overall, expression levels of both ExoS and ToxA were lower in our study as compared with those in a previous study. When ExoS acts as a mitogen, it can promote activation of T lymphocytes leading to inflammation, which is the cause of pathogenesis in cystic fibrosis patients. An elevated incidence of ExoS was reported in drug resistance isolates in a study conducted in Iran. The expression of these virulence factors is required to cause infection in patients, particularly in those having pulmonary infection. LasB incidence was slightly higher in our isolates as compared with cases reported in another study, which involved the detection of virulence genes in pigment- and nonpigment-producing P. aeruginosa. ESBL-harboring bacteria have more LasB activity than non-ESBL-harboring bacteria, which highlights their strong interaction with the drug resistance pattern. Another study disclosed the occurrence of LasB and PlcH virulence factors in clinical isolates of P. aeruginosa, where the prevalence of both virulence factors was higher in contrast to our findings. Some inhibitors having interactions with quorum-sensing receptors such as LasR and RhlR can affect the pathogenicity of P. aeruginosa in humans, and it will be helpful in developing new therapeutic strategies in the future for patients having cystic fibrosis infections. Expression of virulence genes both in cystic and in noncystic fibrosis revealed that it might not have a strong link with the type of infection, but can have an impact on treatment strategies.