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INTRODUCTION

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Despite relatively high coverage with an effective vaccine, pertussis continues to cause morbidity and mortality worldwide. The World Health Organization estimated in 2014 that approximately 89,000 children died from pertussis. The United States has seen a steady rise in case incidence to the highest levels in 60 years. The reemergence of pertussis in the United States and elsewhere punctuates the need for pediatricians to be aware of pertussis epidemiology and presentation in all ages. Early recognition of disease allows implementation of effective measures to prevent spread and further harm.

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PATHOGENESIS AND EPIDEMIOLOGY

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Bordetella are small, fastidious, aerobic, gram-negative coccobacilli that require enriched media for isolation. B pertussis is a respiratory pathogen of humans only and is the sole cause of epidemic pertussis. B parapertussis is a closely related species that accounts for less than 5% of clinical pertussis. B bronchiseptica occasionally causes disease in the immunocompromised host but is better recognized as a veterinary pathogen. Less related genetically, B holmesii has been reported to cause respiratory illness and rarely joint infection in normal hosts and invasive infection in asplenic and immunocompromised patients.

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B pertussis produces numerous virulence factors, including toxins and attachment agents, many of which are antigenic and included in the acellular vaccine. The link of each virulence factor to clinical illness has been difficult to elucidate due to lack of an animal model for experimentation. However, a recently developed model in infant baboons has the potential to address unanswered questions. The bacteria attach to ciliated epithelial cells of the respiratory tract, induce ciliary paralysis and local inflammation, and thicken and decrease clearance of secretions. B pertussis is not invasive. Pertussis toxin, necessary but not sufficient to cause clinical pertussis, is secreted by the bacteria and affects G-protein function, which prevents migration of lymphocytes to the area of infection, and inhibits the function of neutrophils, macrophages, monocytes, and lymphocytes. Adenylate cyclase toxin invades phagocytes and induces high levels of cyclic adenosine monophosphate (AMP), which impairs immune cell function and induces apoptosis. Other cell-surface proteins, including filamentous hemagglutinin, pertactin, and fimbrial agglutinogens, are involved in bacterial attachment to ciliated respiratory epithelium. Pertactin-deficient B pertussis strains have been described and hypothesized to evade vaccine immunity, although this has not borne out in surveillance studies. The function of additional factors, including tracheal cytotoxin, surface lipooligosaccharide, and cytoplasmic heat-labile toxin, is less well characterized.

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Pertussis occurs year-round in the United States, although the disease usually peaks in the summer and fall in most locations and occurs in 3- to 5-year epidemic cycles. Humans are the only reservoir for the causative agent, B pertussis, which does not cause prolonged colonization or persist in the environment. Thus, transmission occurs from person to person via respiratory droplets. Higher transmission rates among close household versus community (eg, school) contacts have been reported, with attack rates following household exposure as high as 90% for unimmunized children ...

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