The two interesting but contrasting (and possibly confusing) papers on Pseudomonas serology in cystic fibrosis (CF) published in this issue of Thorax illustrate the controversy and challenge that have become increasingly important as very young patients are routinely diagnosed through newborn screening. Fortunately, such infants at diagnosis are typically free of Pseudomonas aeruginosa (PA) infection,¹ unlike about 30% of those diagnosed by traditional methods following signs/symptoms of CF.² The potential to eradicate non-mucoid PA, and even to delay transformation to mucoid species,¹ makes ascertainment of the initial PA infection one of the highest priorities in current clinical management. Yet, just as in the diagnosis of CF per se, traditional methods of PA identification (relying on microbiology) leave much to be desired in young children with CF. Thus, more attention has focused once again on the potential diagnostic value of Pseudomonas serology. In a recent review Rosenfeld et al³ stated that “limitations of serologic markers of P aeruginosa infection include lack of commercially available standardized assays and lack of specificity to the site of P aeruginosa infection (i.e. upper or lower airway)”.

The pioneering studies on Pseudomonas serology were published 2–3 decades ago when the research teams of Niels Hoiby and Gerd Doring developed the initial methodology and applied Pseudomonas antibody titre determinations to patients with CF.^4–,⁶ The first tests were based on detection of “precipitating antibodies” (precipitins) against a pool of sonicated extracts from common 0-antigen serotypes. Their evaluations showed that rising antibody titres correlated with PA respiratory infections. They also showed⁶ that, soon after the onset of PA lung infections, the numbers of individual precipitin bands rose and eventually became a sign of “poor prognosis”. Subsequently, Brett and co-workers⁷ published …