Neither the presence of ica locus, nor in vitro-biofilm formation ability is a crucial parameter for some Staphylococcus epidermidis strains to maintain an infection in a guinea pig tissue cage model

The pathogenesis of Staphylococcus epidermidis is thought to be based on its capacity to colonize medical devices by forming a biofilm. Biofilm formation is in part mediated by the polysaccharide intercellular adhesin (PIA), which is encoded by the icaADBC operon. We have previously investigated in vitro the correlation existing between biofilm formation (B±), presence of ica locus (I±) and PIA production (P±) in some clinical isolates of coagulase-negative staphylococci (CoNS). Here, we used a guinea pig model of subcutaneous implanted tissue cages to assess the implication of B, I and P parameters in the capacity of nine S. epidermidis and one S. carnosus strains to develop and maintain an infection in vivo. Using clinical isolates and a model strain of S. epidermidis, we showed that the “B+, I+, P+” type confers the ability to maintain an infection in vivo. Surprisingly, the opposite type “B−, I−, P−” tested with clinical and commensal isolates, presented infection rates ranging from 25% to 60%. Other clinical isolates having a “B+, I+, P−” type, were not able to cause an infection in the present model. These results showed that, depending on the strains the capacity to colonize the tissue cage might be independent of the ability to form biofilm.