Methicillin-resistant and biofilm-forming
Staphylococcus aureus (MRSA) isolates have become a common clinical problem [
1]. In recent years, MRSA incidences seemed to be decreasing, and the focus of infection control specialists was multidrug-resistant Gram-negative bacteria [
2‐
4]. However, Public Health England recently reported an alarming 26% increase in MRSA bloodstream infections [
5]. Although the rise in numbers coincided with the Department of Health’s change in policy on screening for MRSA, from universal to targeted screening, it underlines the fact that MRSA cannot be considered “out of the picture”. The formation of biofilms as a reaction to therapeutic interventions, which can lead to increased antimicrobial resistance and a higher chance of treatment failure, is being increasingly recognized as an infection control problem [
6,
7]. Accordingly, treatment and decolonization failure occur more frequently when topical drugs like mupirocin are used against biofilm-forming microorganisms [
8‐
12].
The organization of bacteria into biofilms is the common mode of bacterial survival, since this form increases their ability to withstand antibiotics, disinfectants, and host responses. Biofilm formation is a multifarious, controlled bacterial process that induces many additional functional and phenotypic alterations, including loss of motility, reduced growth rate, increased surface adhesion, as well as an altered susceptibility to the host response [
13‐
17]. An association with biofilm formation has been reported for many hospital-acquired infections, such as urinary tract and catheter-related bloodstream infections as well as infections of implanted medical devices including indwelling catheters, artificial heart valves, orthopedic prostheses, or osteosynthesis materials [
7,
18‐
24]. Colonization with MRSA is associated with a high risk of acquiring an MRSA infection during hospital stays [
25,
26]. Decolonization may reduce the risk of MRSA infection in individual carriers and prevent transmission to other patients [
25]. However, the most commonly used agent for decolonization, mupirocin, comes with a considerable risk of resistance if widely employed [
26]. There have been many other attempts to eradicate carriage, mostly with topical agents, but success rates have not been consistent or applicable to all populations [
26], and even mupirocin decolonization success rates can be low [
25]. Many international guidelines (i.e., in Germany, Ireland, Netherlands, Slovenia) already state that attempts at decolonization are unlikely to be successful in patients with chronic skin conditions, ulcers, or in-dwelling catheters [
27‐
30]. Some studies, however, showed that decolonization can be effective in patients with lines and catheters [
25] and that the inability to decolonize was most closely associated with failure to use a standardized decolonization protocol [
31]. However, to our knowledge, no study has been able to identify a consistent subgroup of patients at higher risk for decolonization failure. Perhaps, the focus has been on the wrong variable in the equation, and the reason for decolonization failure is not the patient but the bacterium and its biofilm-forming capacities. Alarmingly, one study on biofilm formation among MRSA nasal carriers showed that all of the isolated MRSA had the ability to form biofilms [
7]. The goal of our study, therefore, was to evaluate the extent to which MRSA biofilms are influenced by the use of the topical decolonization antibiotic MUP and the widely used topical disinfectants, i.e., octenidine (OCT), chlorhexidine (CHG), polyhexanide (POL), and chloroxylenol (CLO).