I thank Dr. Perischetti et al. for their analysis of the distribution of the icaA and icaD operons in relation to the presence of capsular contracture in patients undergoing second-stage breast reconstruction.
The ica cluster contains all the genes necessary for the production of the polysaccharide intercellular adhesin, one of two polysaccharides produced by Staphylococcus epidermidis that help it to accumulate biofilm once initial attachment has occurred to a surface. There are four open reading frames (icaA, icaD, icaB, and icaC) and a regulator (icaR) located upstream from the start codon that contribute to the successful production and activation of polysaccharide intercellular adhesin.1
Initial studies did show a competitive advantage in that strains with ica activity were more capable of forming attachment to medical prosthetics and more likely to cause invasive infection.2,3 More recent analysis, however, has shown that ica-negative strains are able to overcome their disadvantage and are also responsible for clinical infection. Investigation in knockout mutants has revealed no conclusive result, with three of four reports demonstrating no significant reduction in virulence in ica-inactive strains.4 Furthermore, recent studies examining isolates from prosthetic joints and patients with neurosurgical meningitis have shown that ica-negative strains are also capable of causing invasive biofilm infection.5,6 These observations have been attributed to the presence of alternative polysaccharide intercellular adhesion–independent mechanisms of biofilm accumulation such as the biofilm-associated protein that may be able to overcome deficiencies in ica expression.
In summary, the presence or absence of ica operon activity does not necessarily impact on the ability of S. epidermidis to cause clinical biofilm disease. It is therefore not possible to draw conclusions about the apparent random distribution of icaA/icaD activity in patients with capsular contracture from this patient sample.
Anand K. Deva, M.D.
Macquarie Cosmetic and Plastic Surgery
Macquarie University Clinic
Suite 301, Level 3
2 Technology Place
New South Wales 2109, Australia
1. Heilman C, Schweitzer O, Gerke C, Vannitanakom N, Mack D, Gotz F. Molecular basis of intercellular adhesion in the biofilm forming Staphylococcus epidermidis
. Mol Microbiol
2. Ziehbur W, Heilman C, Gotz F, et al. Detection of the intercellular adhesion gene cluster (ica) and phase variation in Staphylococcus epidermidis
blood culture strains and mucosal isolates. Infect Immun.
3. Frebourg NB, Lefebvre S, Baert S, Lemeland JF. PCR based assay for discrimination between invasive and contaminating Staphylococcus epidermidis
strains. J Clin Microbiol.
4. Rohde H, Mack D, Christner M, Burdelski C, Franke G, Knobloch JKM. Pathogenesis of staphylococcal device-related infections: From basic science to new diagnostic, therapeutic and prophylactic approaches. Rev Med Microbiol.
5. Stevens NT, Tharmabala M, Dillane T, Greene C, O'Gara JP, Humphreys H. Biofilm and the role of the ica operon and aap in Staphylococcus epidermidis
isolates causing neurosurgical meningitis. Clin Microbiol Infect.
6. Koskela A, Nilsdotter-Augustinsson A, Persson L, Soderquist B. Prevalence of the ica operon and insertion sequence IS256 among Staphylococcus epidermidis
prosthetic joint infection isolates. Eur J Clin Microbiol Infect Dis
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