This thesis describes studies investigating the biological properties of B. cepacia, in particular those which may contribute to the organism's role as an opportunist pathogen and considers the host-bacterium interaction in CF including factors involved in early colonisation and the host immune response to B. cepacia colonisation. Emphasis is placed on studies of a highly transmissible or epidemic strain isolated in Edinburgh in 1989 and responsible for colonisation of CF patients in other regional CF centres. B. cepacia adhesion to respiratory mucin was measured in an ELISA-based mucin adherence assay. The majority of B. cepacia strains did not adhere to purified respiratory mucin. Interestingly, the epidemic strain exhibited the greatest degree of mucin adherence. Adhesion of B. cepacia to buccal epithelial cells studied by fluorescent labelling and flow cytometry also showed that the epidemic strain demonstrated greatest adhesion. The humoral immune response in CF patients colonised with B. cepacia was investigated by ELISA, incorporating B. cepacia LPS and by immunoblotting against LPS, flagella and outer membrane protein antigens. Elevated levels of specific anti-B. cepacia IgG, IgA and IgM were observed in patients chronically colonised by B. cepacia, especially in those patients colonised by the epidemic strain. Detection of anti-B. cepacia antibodies may aid in early diagnosis of B. cepacia colonisation, but as yet does not appear to have prognostic value. Evidence presented in this thesis indicates that B. cepacia persists in the CF respiratory tract despite a specific humoral immune response and causes bacteraemia despite being serum sensitive. These factors together with the intractability of B. cepacia to antimicrobial therapy and the close taxonomic relationship with the highly virulent Burkholderia pseudomallei, allows speculation that the association B. cepacia with CF may involve a stage of intracellular growth for survival.