Staphylococcus in the nose
Via the review journal Trends in Microbiology, authors from the University of Tubingen (Germany) have reviewed the major determinants that allow Staphylococcus aureus to colonize the human body. Previous epidemiological studies have examined the source of nosocomial infections by S. aureus, and have found that many of these infections occur by endogenous means, or from the patient’s own microbial flora as opposed to being introduced from other sources. Understanding the relationship between the host and the microbe then becomes essential for identifying means for controlling hospital acquired infections.
Previous genetic analysis of individuals with persistent (greater than several months) colonization by S. aureus has identified several possible, but no conclusive host traits that might explain why these individuals remain infected for so long. The role of a number of S. aureus surface determinants have also been identified from genomic studies, including a number of factors that aid in the attachment of the bacterium to nasal epithelial cells. Shedding of bacteria occurs constantly via the continual loss of epithelial cells and the action of mucous membranes, and consequently the bacterial reproductive rate in this environment is high. The bacterium also makes a number of potent immune system evasion factors, such as staphylokinase which in addition to promoting dissemination, also allows complement and bound IgG to be deactivated.
Individuals with long term colonization do appear to receive some benefit from the arrangement, should they avoid an unfortunate complication during hospital care. Competition by long term microbial residents such as S. aureus can prevent the colonization by other more virulent organisms via the process of microbial antagonism. One well documented study examined the protective effects of sensitive S. aureus in preventing acquisition of methicillin-resistant isolates. Additionally, individuals with these organisms also appear to make more antibodies against several important S. aureus virulence traits such as toxic shock syndrome toxin 1 (TSST-1) and staphylococcal enterotoxin.
The upshot of the review is that there exists a complicated interaction between the host and the microorganism, and a variety of determinants are critical for determining the effectiveness of the interaction. Genetic analysis of S. aureus isolates of human origin indicates that although there is heterogeneity in bacterial factors, by in large most isolates are relatively similar and equally able to colonize the human nose. Factors that are much more significant likely exist on the host side and are currently under study. However, the utility of unraveling the complexity of host factors in light of the generally more simplistic diversity of pathogen factors seems to be less important than devising mechanisms to block S. aureus determinants in the first place.