The pathogenic bacterium Haemophilus influenzae causes meningitis, epiglottitis, pneumonia, otitis media and other infections. Irrespective of the presence or absence of the capsule, the first step in the pathogenesis of both respiratory and invasive H. influenzae infections is asymptomatic colonization of the nasopharynx. The infection is transmitted by droplets from infected (but not necessarily symptomatic) people. H. influenzae organisms are inhaled through the upper respiratory tract and, following initial interactions with respiratory mucus (Lipsitch et al., 1997, Virkola et al., 2000), utilize a number of adhesins on the bacterial surface to adhere to respiratory epithelial cells. Both H. influenzae possessing the type b capsule (Hib) and nontypeable H. influenzae (NTHi) adhere to respiratory cells by means of hemagglutinating pili, P5 fimbriae, lipo-oligosaccharide, H. influenzae adherence and penetration protein (Hap) , opacity-associated protein (OapA), and Haemophilus surface fibrils (Hsf). In addition to these adhesins, NTHi organisms, which are more genetically diverse than Hib, possess additional epithelial cell adhesins, including the high-molecular-weight (HMW) proteins HMW1 and HMW2 and H. influenzae adhesin (Hia), which is an allele of the Hsf of Hib (Ecevit at al., 2004).

H. influenzae adhesin (Hia), which is an allele of the Hsf of Hib (Ecevit at al., 2004). Pneumonia caused by H. influenzae type b is usually lobar or segmental, and is similar to such pneumonia caused by pneumococci in its clinical features (apart from age-range) and its radiological appearances. H. influenzae bacteraemia does not always give rise to localised disease, or even to illness sufficient to require hospital admission. In health the bronchi are self-sterilising; but in chronic bronchitis and related diseases they lose this capacity and are liable to bacterial colonisation, mainly by non-capsulated H. influenzae and by pneumococci. So long as the sputum remains mucoid these organisms are present (Turk., 1984).