Epidemiology and Pathogenesis of Bordetella pertussis, Bordetella parapertussis, and Related Species
المؤلف:
Patricia M. Tille, PhD, MLS(ASCP)
المصدر:
Bailey & Scotts Diagnostic Microbiology
الجزء والصفحة:
13th Edition , p436-437
2025-08-18
502
Epidemiology
Before the introduction of the vaccine (and currently in nonimmunized populations), pertussis (whooping cough) periodically became an epidemic disease that cycled approximately every 2 to 5 years. Transmission occurs person to person through inhalation of respiratory droplets. Humans are the only known reservoir.
Pertussis is a highly contagious, acute infection of the upper respiratory tract caused primarily by B. pertussis and less commonly by B. parapertussis. The latter agent generally has a less severe clinical presentation both in duration of symptoms and in the percentage of identified cases. Recently, B. holmesii was reported to cause a pertussis-like illness, but little is known about the biology, virulence mechanisms, and pathogenic significance. Pertussis was first described in the sixteenth century and occurs worldwide, totaling about 48.5 million cases annually. Although the incidence has decreased significantly since vaccination became widespread, outbreaks of pertussis occur periodically. B. pertussis infections appear to be endemic in adults and adolescents, most likely because of waning vaccine-induced immunity; these infections may serve as the source of the epidemic cycles involving unvaccinated or partially immunized infants and children.
Pathogenesis
B. pertussis, the primary pathogen of whooping cough, uses several mechanisms to overcome the immune defenses of healthy individuals. The mechanisms are complex and involve the interplay of several virulence factors (Table 1). Some factors help establish infection; others are toxigenic to the host; and still others override specific components of the host’s mucosal defense system. For example, when B. pertussis reaches the host’s respiratory tract, its surface adhesins attach to respiratory ciliated epithelial cells and paralyze the beating cilia by producing a tracheal cytotoxin. A major virulence factor, pertussis toxin (PT), is produced by the attached organism. PT enters the bloodstream, subsequently binding to specific receptors on host cells. After binding, PT disrupts several host cell functions, such as initiation of host cell translation; inability of host cells to receive signals from the environment causes a generalized toxicity. The center membrane of B. pertussis blocks access of the host’s lysozyme to the bacterial cell wall via its outer membrane. B. pertussis and B. parapertussis share a nearly identical virulence control system encoded by the bvgAS locus that is responsive to variation in environ mental conditions. Because of this very complex system, Bordetella organisms appear to be able to alter phenotypic expression, enhancing transmission, colonization, and survival.
Table1. Major Virulence Determinants of Bordetella pertussis
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