• C G Adair, S P Gorman, B M Feron, L M Byers, D S Jones, C E Goldsmith, J E Moore, J R Kerr, M D Curran, G Hogg, C H Webb, G J McCarthy, and K R Milligan.
• Northern Ireland Regional Immunogenetics Laboratory.
• Intensive Care Med. 1999 Oct 1;25(10):1072-6.

ObjectiveTo determine the relationship between, and antibiotic resistance of, endotracheal tube (ET) biofilm and pulmonary pathogens in ventilator-associated pneumonia (VAP).SettingGeneral intensive care units in two university teaching hospitals.DesignThe microbiology of ET biofilm and tracheal samples from patients with and without VAP were compared. For individual patients, matching pairs of pathogens were confirmed as identical and characterised for antibiotic susceptibility.Patients40 intensive care unit patients - 20 with VAP, 20 without VAP as control. The duration of intubation (median and range) was 6.5 days (3-17) and 5 days (2-10), respectively.Measurements And ResultsSamples of tracheal secretions were taken during ventilation for bacteriological culture. Following extubation, ETs were examined for the presence of biofilm. Isolates of high pathogenic potential included Staphylococcus aureus, enterococci, Enterobacteriaceae, pseudomonads and Candida spp. Where the same microorganism was found on tracheal and ET samples by phenotyping, these were confirmed as identical by genotyping and characterised for antibiotic susceptibility in both the free floating and biofilm forms. Seventy per cent of patients with VAP had identical pathogens isolated from both ET biofilm and tracheal secretions. No pairing of pathogens was observed in control patients (p < 0.005). Susceptibility data for these pairs show that the ET acts as a reservoir for infecting microorganisms which exhibit significantly greater antibiotic resistance than their tracheal counterparts.ConclusionThis investigation provides further evidence for the role of ET biofilm in VAP. The difficulty in eradicating an established microbial biofilm using antibiotics implies that increased attention must be directed towards modification of the ET to prevent or substantially reduce biofilm formation.

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