Childhood Infections


Three bacterial species, Hemophilus influenzae, Bordetella pertussis, and Corynebacterium diphtheriae, preferentially infect children after maternal antibody protection has been lost and before contact with these and other bacteria has generated some level of self-protection. Adults only occasionally suffer infection, largely those predisposed by viral illness, alcoholism, or chronic disease. At the turn of the century, 80% of all United States children contracted whooping cough; diphtheria was also quite common, with a 35% mortality rate. Routine administration of vaccine at 1 year of age has ended these pandemics but has not completely eradicated either disease. Hemophilus influenzae is currently the biggest problem, especially in children under 1 year of age not protected completely by vaccine; it is also a true tissue invader, whereas B. pertussis and C. diphtheriae infect only luminal surfaces, causing disease mainly by their toxin production.

Whooping Cough

Whooping cough is an acute, highly communicable, usually self-terminating childhood disease characterized by violent coughing paroxysms followed by a loud inspiratory whoop. It is caused by B. pertussis, a small, pleomorphic, gram-negative coccobacillus. Milder forms of the disease may resemble a trivial attack of acute bronchitis; conversely, whooping episodes occasionally occur during adenoviral infections or other URIs. Wide use of the diphtheria-pertussis-tetanus (DPT) vaccine has reduced the prevalence of whooping cough in the United States to less than 12,000 cases per year, but no one expects it to disappear entirely.

The causative organism, B. pertussis, has strong tropism for the brush border of the bronchial epithelium with which its growing colonies become entangled without actually invading tissue. Diffusion of exotoxin from this source is thought to account for most of the characteristic disease manifestations (i.e., for the enhanced cough reflex, peripheral lymphocytosis, malaise, and frequent weight loss despite relatively mild fever). These features may persist after the bacteria themselves have disappeared until all intracellular toxin is inactivated. The key to recovery and to immune protection is secretory antibodies of the IgA class that inhibit the adhesion step essential for bacterial proliferation.

The respiratory lesions of established whooping cough resemble those of other forms of laryngotracheobronchitis. In severe cases there is bronchial mucosal erosion, hyperemia, and copious mucopurulent exudate but, unless superinfected, the lung alveoli remain open and intact. In parallel with the striking peripheral lymphocytosis (up to 90%), hypercellularity and enlargement of the mucosal lymph follicles and peribronchial lymph nodes have been observed.

After seven to ten days´ incubation, the disease passes through a catarrhal period of coughing and sneezing, followed by the onset of the characteristic paroxysms. Violent coughing may cause leakage of air from distended airways, resulting in subcutaneous emphysema; more frequently, convulsions are set off by the hypoxia and by the constant, tiring coughing effort; coughing spells may drag on after fever subsides but in most cases, with or without treatment, normality gradually returns over several days. The role of whooping cough in promoting adult chronic obstructive lung disease has long been debated, but supporting evidence is scant. Usually, whooping cough leaves no sequelae.

Seasonal incidence of Bordetella pertussis infection in a 1996 Vermont study.

Variation in confirmed Pertussis morbidity by age group.

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