How Staph Infections Start In Your Nose
    By News Staff | December 31st 2012 01:03 PM | 1 comment | Print | E-mail | Track Comments

    Researchers have identified a mechanism by which the bacterium Staphylococcus aureus (S. aureus) colonizes our nasal passages, showing for the first time that a protein located on the bacterial surface called clumping factor B (ClfB) has high affinity for the skin protein loricrin.

    S. aureus is a major human pathogen - everyone has heard of staph infections - with the potential to cause severe invasive diseases. It is a major cause for concern in hospitals and healthcare facilities where many infections are caused by strains (MRSA) resistant to commonly used antibiotics. S. aureus persistently colonizes about 20% of the human population by binding to skin-like cells within the nasal cavity and being colonized predisposes an individual towards becoming infected.  

    ClfB was previously shown to promote S. aureus colonization in a human nasal colonization volunteer study. The new paper identifies the mechanism by which ClfB facilitates S. aureus nasal colonization. Purified ClfB bound loricrin with high affinity and this interaction was shown to be crucial for successful colonization of the nose in a mouse model.

    A knockout mouse lacking loricrin in its skin cells allowed fewer bacterial cells to colonize its nasal passages than a normal mouse. When S. aureus strains that lacked ClfB were used nasal colonization could not be achieved at all.  Finally it was shown that soluble loricrin could reduce binding of S. aureus to human nasal skin cells and that nasal administration of loricrin reduced S. aureus colonization of mice.

    Rachel McLoughlin, the study's corresponding author and Lecturer at the School of Biochemistry and Immunology at Trinity College Dublin concludes, "Loricrin is a major determinant of S. aureus nasal colonization." This discovery therefore opens new avenues for developing therapeutic strategies to reduce the burden of nasal carriage and consequently infections with this bacterium. This is particularly important given the difficulties associated with treating MRSA infections.

    Citation: Mulcahy ME, Geoghegan JA, Monk IR, O'Keeffe KM, Walsh EJ, et al. (2012) Nasal Colonisation by Staphylococcus aureus Depends upon Clumping Factor B Binding to the Squamous Epithelial Cell Envelope Protein Loricrin. PLoS Pathog 8(12): e1003092. doi:10.1371/journal.ppat.1003092


    Gerhard Adam
    S. aureus is a major human pathogen - everyone has heard of staph infections - with the potential to cause severe invasive diseases.
    I have a problem with this type of characterization because it portrays "staph" as being a generic pathogen without appreciating the complexity of the bacterial relationship with the hosts.  Just to be clear, I don't have a problem with the research, but rather with the journalistic portrayal of these bacteria.

    It should be understood that ALL bacteria represent a major risk if introduced into a sterile host environment [i.e. blood stream].   Staphylococcus bacteria are skin commensals and are present and harmless in almost 25% of the population.  Certainly they can be a major risk factor in any situation where the skin has been breached [i.e. surgery] and because of their prevalence on the skin and nasal passages, a clear avenue of introduction can occur [especially in those carrying a large bacterial load].

    One of the primary problems today is Methicillin-Resistant Staphylococcus aureus (MRSA) in hospital environments.  Again, illustrating the relationship between bacteria by exchanging antibiotic resistant traits amongst themselves.

    So the point isn't to simplistically identify bacteria as "good" or "bad" but to recognize that the situation is considerably more complex.  Even if staphylococcus was eliminated, the corresponding question one should ask is what bacterial colonist will replace it?

    There is no question that when these infections occur, they are extremely dangerous and life-threatening, but as the researchers indicate, the point isn't to eliminate the bacteria, but rather to control the load carried by individuals and to mitigate against the paths for introduction into vulnerable environments.

    As a quick note regarding S. aureus as a pathogen.  Consider that many carriers of this bacteria may well infect themselves in a hospital type setting.  However, those that are carriers may also have partial protection because of immune system sensitivity to the bacteria.  Non-carriers are at much higher risk when infected.  So, hopefully, people can see that addressing these kinds of problems extend well beyond "good" and "bad".  This becomes especially important given many people's germophobia, which may result in more commensals being impacted than the pathogens they're so frightened of.

    Anyway ... end of rant.
    Mundus vult decipi