We read with great interest the article by Tamboto, Vickery, and Deva in the September of 2010 issue of the Journal on the role of subclinical infection and biofilm in capsular fibrosis.1 The methods used and the animal model developed are very interesting and are certainly an approximation of use in humans. We are interested in the fact that for the first time someone has shown a direct causal link between the presence of biofilm and capsular contracture in vivo in an animal model. However, our experience in humans shows quite different results.
We performed a study aimed to genotype Staphylococcus epidermidis isolates from subclinical periprosthetic infections with samples taken in a sterile field from four different foci: capsule, intraprosthetic liquid, periprosthetic liquid, and prothesis. The implants removed were textured surface expanders in 10 patients subjected to a second heterologous breast reconstruction. All samples were plated onto selective media (blood agar/colistin–nalidixic acid blood agar, MacConkey agar), nonselective media (blood agar, chocolate) in aerobic atmosphere or carboxyphylia, and in anaerobic conditions (Centers for Disease Control and Prevention agar); the genotypic analysis was performed by polymerase chain reaction to detect the presence of icaA and icaD genes, as a part of the ica operon, essential among S. epidermidis isolates in the biofilm formation. In particular, this operon encodes for different enzymes, including N-acetylglucosamine transferase, essential for the production of the biofilm.
A total of three of 10 S. epidermidis isolates studied showed both icaA and icaD genes (30 percent), whereas the remaining seven strains were polymerase chain reaction–negative for both of these genes (70 percent).
The three icaA-negative and icaD-positive strains were isolated from three patients, two of whom had a Baker grade II capsular contracture and one of whom had a Baker grade III capsular contracture. The seven strains negative for ica were isolated from patients who had a Baker grade II capsular contracture (n = 4), a Baker grade III capsular contracture (n = 2), or a Baker grade IV capsular contracture (n = 1) (Table 1).
Although the limited number of cases analyzed (10 cases) makes any speculation difficult to be inferred, it is interesting to notice a likely random distribution between the Baker grade of capsular contracture and the genetic profile of icaA and icaD, responsible for the biofilm formation, among S. epidermidis isolates surveyed in this study, with only three S. epidermidis strains positive for both icaA and icaD genes. According to our results, we may conclude that the grade of capsular fibrosis seems to be independent of the production of biofilm.
Paolo Persichetti, M.D., Ph.D.
Giuseppe Angelo Giovanni Lombardo, M.D.
Giovanni Francesco Marangi, M.D.
Giovanni Gherardi, Ph.D.
Giordano Dicuonzo, M.D., Ph.D.
“Campus Bio-Medico di Roma” University
1. Tamboto H, Vickery K, Deva AK. Subclinical (biofilm) infection causes capsular contracture in a porcine model following augmentation mammaplasty. Plast Reconstr Surg
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