To the Editors:
I would like to comment on the interesting article by van Schayck and Smit 1, which documents time trends in the prevalence of childhood asthma in a Dutch general practice registry and corresponding data from repeated cross-sectional surveys in another venue within the same country. While they and others have described an apparent levelling off and/or decline in asthma prevalence, a recent report from Denmark describes an increasing prevalence, particularly for nonatopic asthma in young females and adolescents 2. No satisfactory explanation for these time trends has been offered. I would like to propose a theory that: 1) explains these geographical and temporal variations in asthma; 2) accounts for genetic susceptibility; and 3) offers the real possibility of prevention, improved treatment and even a potential “cure” for asthma and other related chronic obstructive lung diseases.
Strachan 3 has pointed out that time trends in asthma incidence and prevalence can only be accounted for by extremely strong environmental factor(s), among which infectious disease pandemics must be acknowledged. For example, country-wide epidemics and the increasing seroprevalence of Chlamydia pneumoniae infection in Finland 4 have been accompanied by corresponding country-wide increased asthma medication use in both males and females and all age groups 5. The growing body of clinical, epidemiological and therapeutic evidence implicating acute, reactivated and chronic infection by C. pneumoniae in asthma 6, 7 forms the basis for proposing the theory that a now waning, geographically heterogeneous worldwide C. pneumoniae pandemic is responsible for the recent unexplained observations.
According to this theory, genetic susceptibility involves polymorphisms influencing innate/adaptive immunity and other critical functions (e.g. attachment receptors, etc.) that affect host response to C. pneumoniae infection to promote asthma and lung remodelling. As an example, in a case–control study, Nagy et al. 8 reported a strong and significant interaction between C. pneumoniae immunoglobulin A antibody, a putative marker for chronic infection, and mannose-binding lectin (MBL) allele polymorphisms producing MBL deficiency in children with asthma. C. pneumoniae has been detected in more than half of bronchoalveolar lavage fluids of another group of asthmatic children 9, confirming that the organism is actually present. MBL deficiencies affect up to one quarter of human populations and, perhaps not coincidentally, 20–25% is the apparent “upper limit” of wheezing prevalence in epidemiological studies.
Acute primary C. pneumoniae infections have been documented to trigger new-onset asthma, which can be successfully rendered asymptomatic after antibiotic treatment 10, raising the possibility of early detection and prevention. Asthma is a strong risk factor for developing chronic obstructive pulmonary disease (COPD) 11 and chronic C. pneumoniae infection is also implicated in COPD 12, further suggesting the possibility of prevention of COPD by early recognition and treatment.
The Chlamydia-asthma theory is receiving growing attention among a segment of the public that is acutely aware of current limitations in asthma treatment (www.asthmastory.com). I suggest that now is the time for asthma researchers to promote the widespread critical evaluation that the Chlamydia-asthma theory deserves.
- © ERS Journals Ltd
References
