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6 - Role of pili in Haemophilus influenzae adherence, colonization and disease

Published online by Cambridge University Press:  08 October 2009

Michael Wilson
Affiliation:
University College London
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Summary

INTRODUCTION

Haemophilus influenzae is a Gram-negative bacillus that causes significant human disease. This organism is classified on the basis of the presence and serological specificity (serotypes a through f) of its polysaccharide capsule. Systemic infections such as bacteraemia, meningitis, septic arthritis and pneumonia in young children are caused primarily by H. influenzae possessing the type b capsule (Hib), while respiratory infections such as pneumonia in patients with chronic pulmonary disease, otitis media, sinusitis, and bronchitis are caused primarily by non-encapsulated strains (the socalled non-typeable H. influenzae).

The organism lives exclusively on human mucosal surfaces, most commonly in the nasopharynx and occasionally on the conjunctivae or in the female genital tract, where it is carried asymptomatically. Respiratory tract colonization rates in children vary between 30% and 100% (Gratten et al., 1989; Trottier et al., 1989; Harabuchi et al., 1994; Faden et al., 1995; Fontanals et al., 2000; St Sauver et al., 2000), with point prevalence rates of about 25% (Bou et al., 2000) to 77–84% (St Sauver et al., 2000), and are higher among children as compared with adults (Turk, 1984).

The pathogenesis of H. influenzae infections is a complex, and incompletely understood, process. Transmission to new hosts is presumed to be via infected respiratory droplets, and the bacterial factors important in successful transmission are poorly defined (Lipsitch and Moxon, 1997). Upon entry into a new host, the organism adheres to respiratory tract structures by means of a number of adhesins that prevent removal of the bacteria by respiratory tract cleansing mechanisms such as mucin trapping and ciliary action.

Type
Chapter
Information
Bacterial Adhesion to Host Tissues
Mechanisms and Consequences
, pp. 139 - 162
Publisher: Cambridge University Press
Print publication year: 2002

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