Deep Dive: How Nose Picking Affects Nasal Carriage of Staph
Abstract & Commentary
By Joseph F. John, Jr., MD, FACP, FIDSA, FSHEA, Associate Chief of Staff for Education, Ralph H. Johnson Veterans Administration Medical Center; Professor of Medicine, Medical University of South Carolina, Charleston. Dr. John does research for Merck, is a consultant for Cubist, Roche, and bioMerieux, and is on the speaker's bureau for Pharmacia, GSK, Merck, Bayer, and Wyeth.
Synopsis: Overcoming the habit of nose picking may aid S. aureus decolonization strategies.
Source: Wertheim HF, et al. Nose picking and nasal carriage of Staphylococcus aureus. Infect Control Hosp Epidemiol. 2006;27:863-867.
Nouwen and colleagues at Erasmus University in Rotterdam, have a long and sophisticated interest in staphylococcal infection and, in particular, the role of carriage, and subsequent infection with S. aureus.1 In this report, part of Heiman Wertheim's PhD thesis — whether nose picking and S. aureus nasal carriage are associated — was examined. In 2004, the Erasmus group established the concept of a culture rule, a rule that tried to distinguish among persistent carriage, intermittent carriage, and non-carriage. In that paper, it was shown that qualitative and quantitative data from 2 consecutive studies was predictive for persistent carriage, with a reliability of 93.6%.
This current study was done in 2001 and 2002 with Dutch speaking patients > 18 years of age. Patients were asked to document conditions of the nasal such as rhinitis, nasal crusts, and runny nose. They also had to say if they were cigarettes smokers, if they rubbed their noses externally, and if they picked their nose. To be considered a nose picker, the subjects had to say they picked their noses (on a 5-point scale) and had to have physical evidence of nasal trauma due to picking.
There were 2 groups of subjects: one group of healthy volunteers and one group of patients who visited an ENT physician. Patients in the latter group were excluded if they had rhinitis. ENT patients had one nasal culture, and healthy subjects had 5 nasal cultures.
In the patient group, 97 of 238 (41%) were S. aureus carriers and 29% were nose pickers. Nose pickers had a relative risk of 1.51 of being carriers. Put simply, 59% of patients who were nose pickers were carriers compared to 35% of those who were not. With regard to quantitation of carriage, nose-picking patients carried a mean of 1.9 colony forming units, compared to only 0.9 cfu of patients who never pick (P = .02).
Of the 86 healthy persons studied, 38.4% were non carriers, 25.6% were occasional carriers, 10.5% were moderate carriers, and 25% were frequent carriers. Subjects were more likely to be carriers if they self-reported nose picking. Carriers harbored a few colonies, up to a total of log 3.5 colonies. People who said they never picked their noses, indeed, had very low or absent colony counts.
Commentary
Well, where do we go with these data? The most obvious place is to relate nose pickers with the likelihood that they have more staphylococcal infections, or that by reducing the picking rate, infections would, in turn, be decreased. The Erasmus group, which is always on the cutting edge of staphylococcal infections, may one day be able to take us to that conclusion, but not yet. In the meantime, the data may help us advise patients who have had recurrent staphylococcal infection. In such cases, we can advise those patients that nose picking may increase their likelihood of recurrent infection.
Why do people pick their noses? Wertheim and colleagues think nose picking is initiated by nasal crusts. Indeed, self reporting of nose picking is associated with self reporting of nasal crusts. Perhaps, but in my experience, it is a small percentage of the population that actually reports nasal crusts, and almost everyone picks his or her nose at some point. More work clearly has to be done on more diverse populations to determine self-reporting of crusts, findings of crust on exam, and the character of nasal carriage, including the genomic content and protein expression by colonizing strains.
From this study we know that if you pick your nose you are more likely to be a S. aureus carrier, but what we don't know is, is if you are already a carrier, whether the carriage predisposes to nose picking. There are components of nasal mucus and the nasal cytokine response that relate to adherence to nasal mucosa by S. aureus through the cell-wall teichoic acids of this bacterium. Intense work is now underway to understand that adhesion, work that has shown so far that wall teichoic acid is necessary, though perhaps not sufficient, for nasal adhesion and thus carriage.
There are several topical and systemic chemotherapeutic products that reduce, at least temporarily, the burden of nasal carriage. Even though there's a plethora of nasal decolonization studies, these studies have not studied the frequency of nose picking before and after decolonization. Further studies are needed to determine if reduction of the nasal load can result in reduced nose picking. Such an observation may add to the value of nasal decolonization, even if transient, in patients at risk for invasive S. aureus infection. Perhaps a cycle of colonization, inflammation, trigger-response nose picking increased carriage and increased quantitation. As Wertheim et al state, "It remains to be resolved if nose picking is a cause or a consequence of S. aureus nasal carriage.
The Erasmus group deserves superlatives for their long, persistent, and creative pursuit of the nasal connection and invasive S. aureus disease. We look forward to further elucidation of those microbiologic and immunologic factors that promote nose picking, factors which may be ameliorated by chemotherapeutic, psychologic, or genetic manipulation.
Reference
1. Nouwen JL, et al. Predicting the Staphylococcus aureus nasal carrier state: Derivation and validation of a "culture role". Clin Infect Dis. 2004;39:806-811.
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