The present investigation was deliberately aimed at evaluating the biofilm-forming ability of 63 clinical MRSA isolates recovered from pharyngitis patients through different phenotypic assays. The molecular detection of adhesion (icaA/icaD/icaB/icaC), adhesins (fnbA/fnbB, clfA, and cna), staphylococcal accessory regulator (sarA), and α-toxin (hla) genes was done by employing polymerase chain reaction (PCR). Out of 63 isolates, 49 (77.8%) were found slime positive by the Congo red agar (CRA) method and 44 (69.8%) as biofilm positive by the quantitative microtitre plate assays. The results of MATH assay showed that most of the test pathogens are hydrophilic in nature. The molecular investigation of biofilm-associated genes revealed that 84.13% (n = 53) of isolates were found positive for icaADBC genes. The fnbA and fnbB genes were present in 49 (77.8%) and 51 (81%) MRSA isolates, respectively. In addition, 58.7% (n = 37), 73% (n = 46), and 69.8% (n = 44) of the isolates harboured the clfA, cna, and hla genes, respectively. Further, nearly 81% (n = 51) of the isolates were found positive for the gene sarA and all the ica negative isolates were also negative for the gene. Furthermore, the results of in vivo adherence assay unveiled the factual commonness in the in vitro adherence method.

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The present study reports that Klebsiella pneumoniae (KP) killed the Caenorhabditis elegans as a consequence of an accumulation and proliferation of the pathogen inside the worms' intestine. The real-time PCR analysis of the genes responsible for vulval development (let-23) and egg laying (lin-29) in KP infected C. elegans confirmed the reproductive defects provoked by KP at the molecular level. In addition, the genetic analysis in N2 wild type, tol-1, sek-1 and pmk-1 mutants unveiled that KP attenuates the toll-dependent p38 mitogen-activated protein kinase (p38 MAPK) by chiefly inhibiting the production of antimicrobial factors such as nlp-29, lys-1 and C-type lectins. Conclusively, the surrendering of the host immune system appears to be attenuated by the toll-dependent p38 MAPK pathway regulation in C. elegans.

The current study explores the inhibitory efficacy of cyclo(l-leucyl-l-prolyl) (CLP), a cyclic dipeptide from Bacillus amyloliquefaciens on the biofilm and virulence production of methicillin-resistant Staphylococcus aureus (MRSA).