The Intercellular Adhesion ( ica ) Locus Is Present in Staphylococcus aureus and Is Required for Biofilm Formation

Abstract

Nosocomial infections that result in the formation of biofilms on the surfaces of biomedical implants are a leading cause of sepsis and are often associated with colonization of the implants byStaphylococcus epidermidis. Biofilm formation is thought to require two sequential steps: adhesion of cells to a solid substrate followed by cell-cell adhesion, creating multiple layers of cells. Intercellular adhesion requires the polysaccharide intercellular adhesin (PIA), which is composed of linear β-1,6-linked glucosaminylglycans and can be synthesized in vitro from UDP-N-acetylglucosamine by products of the intercellular adhesion (ica) locus. We have investigated a variety ofStaphylococcus aureus strains and find that all strains tested contain the ica locus and that several can form biofilms in vitro. Sequence comparison with the S. epidermidis ica genes revealed 59 to 78% amino acid identity. Deletion of the ica locus results in a loss of the ability to form biofilms, produce PIA, or mediateN-acetylglucosaminyltransferase activity in vitro. Cross-species hybridization experiments revealed the presence oficaA in several other Staphylococcus species, suggesting that cell-cell adhesion and the potential to form biofilms is conserved within this genus.

Investigation of biofilm production and icaA and icaD genes in Staphylococcus aureus isolated from heifers and cows with mastitis

“…In the present study, although 55.5% of the S. aureus isolates produced biofilms in vitro on CRA, the icaA gene was detected in 98.9% of the isolates by PCR and the icaD gene in 100%. According to Cramton et al (1999), despite the presence of the ica locus, biofilm formation may not occur in vitro or on inert surfaces since S. aureus strains are highly sensitive to the growth conditions, such as the amount of glucose or glucosamine available for matrix formation. Another hypothesis is that some capsular exopolysaccharides are not well expressed in the presence of oxygen, AMP, ampicillin (10 μg); CL, cephalexin (30 μg); CTF, ceftiofur (30 μg); FLF, florfenicol (30 μg); G, gentamicin (10 μg); K, kanamycin (30 μg); N, neomycin (30 μg); OX, oxacillin (1 μg); P, penicillin G 10 (IU).…”

An in vitro study on disinfection of titanium surfaces

“…Moreover, infection of medical devices is predominantly caused by coagulase-negative staphylococci (Tillander et al 2010). Specifically, the infections that are associated with S. aureus represent a serious clinical hazard due to the wide range of virulence pathogenic potential that it exhibits (Cramton et al 1999;Windolf et al 2014). Interestingly, S. aureus and other staphylococcal speciesfor example S. warneri (Eick et al 2015) have exhibited affinity for titanium surfaces colonisation and their contribution to the development of peri-implantitis has been reported in other studies as well (Rokadiya & Malden 2008;Salvi et al 2008).…”

icaand beyond: biofilm mechanisms and regulation inStaphylococcus epidermidisandStaphylococcus aureus

“…Recent in vitro studies have provided evidence that PIA/PNAG is also required for immune evasion and virulence in S. epidermidis (Vuong et al, 2004). Although the majority of clinical S. aureus isolates contain the ica operon (Cramton et al, 1999;Arciola et al, 2001;Fowler et al, 2001;Frank et al, 2004;Rohde et al, 2004;Fitzpatrick et al, 2005), expression of the ica operon and biofilm production is tightly controlled under in vitro conditions (Ammendolia et al, 1999;McKenney et al, 1999;Cramton et al, 2001;Stepanovic et al, 2003;Fitzpatrick et al, 2005Fitzpatrick et al, , 2006 but is apparently upregulated in the in vivo infection milieu (McKenney et al, 1999;Fluckiger et al, 2005).…”