The degree of virulence does not necessarily affect MRSA biofilm strength and response to photodynamic therapy

• Published in: Microbial pathogenesis 2016-02, Vol.91, p.54-60
• Main Authors: Abouelfetouh, Alaa A.Y., Nafee, Noha A., Moussa, Nihal K.
• Format: Article
• Language: English
• Subjects: agr; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Biofilm; Biofilms - radiation effects; cap; clfA; fnb; Humans; Hypericin; Methicillin-Resistant Staphylococcus aureus - pathogenicity; Methicillin-Resistant Staphylococcus aureus - physiology; Methicillin-Resistant Staphylococcus aureus - radiation effects; MRSA; nuc; PDT; Photochemotherapy; spa; Staphylococcal Infections - microbiology; Staphylococcal Infections - therapy; Virulence; Virulence Factors - genetics; Virulence Factors - metabolism
• ISSN: 0882-4010; 1096-1208
• DOI: 10.1016/j.micpath.2015.11.012

Biofilm formation transforms infections from acute to chronic, increasing patient mortality and significantly increasing healthcare costs. We are studying the prevalence of some virulence genes among methicillin resistant Staphylococcus aureus (MRSA) isolates relative to biofilm formation and the potential of photoactivated hypericin to treat these infections. Isolates were collected from three Egyptian governorates over seven months in 2011, 100 isolates were identified as MRSA. Biofilm formation was established using crystal violet staining and 2,3,5-triphenyl tetrazolium chloride reduction. Twenty two percent of the isolates formed biofilms, of which 68.2% were moderate to strong. The virulence genes were detected using polymerase chain reaction. spaX (x-region of protein A) was most prevalent. All biofilm-formers lacked cap5 (capsular polysaccharide 5), the other genes were: nuc (thermonuclease) > clfA (clumping factor) > spaIgG (IgG binding site of protein A), fnbA (fibronectin protein A), cap8 (capsular polysaccharide 8), agr (accessory-gene-regulator locus) > fnbB (fibronectin protein B). agr-locus was only found in 22.22% of moderate biofilm-formers, the remaining genes were almost equally prevalent among biofilm-formers and negative controls. Photoactivated hypericin efficiently inhibited 92.2–99.9% of biofilm viability, irrespective of the number of virulence genes. To conclude, biofilm formation, and treatment might be affected by a myriad of virulence factors rather than a single gene, however, photoactivated hypericin remains a potential antibiofilm approach.