Staphylococcal infections begin when the organism gains access to host tissues or the adjoining blood supply through breaches in the skin. More than 20% of healthy humans are natural carriers of S. aureus, 10%-20% of these carriers harbor multidrug-resistant strains, and the frequencies of both community-acquired and hospital-acquired staphylococcal infections continue to increase. Disturbingly, our stockpile of antibiotics is not evolving at a rate capable of quelling the uprising of resistance.
Determining whether an infection is contained or succeeds in spreading is a complex battle between defensive cells of the patient's immune system and the onslaught of the array of enzymes, toxins and other injurious factors released by the bacterium. During early stages of infection the S. aureus expresses proteins that enable its binding to, and colonization of, host tissue. Following establishment within the host, other toxins and enzymes help the staphylococci spread to nearby tissue and begin the process of colonization over and over again.
In the November 18 issue of the Journal of Clinical Investigation Eric Brown and colleagues from the Texas A&M University Health Science Center further investigate the role of another interesting member of the S. aureus artillery. The MHC class II Analog Protein (known as Map) was shown to interfere with the function of T cells, a patient's most specific defense against foreign intruders, which appeared to promote the persistence and survival of S. aureus in infected mice.