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Chapter: Medical Microbiology: An Introduction to Infectious Diseases: Haemophilus and Bordetella

Pertussis : Clinical Aspects

After an incubation period of 7 to 10 days, pertussis follows a prolonged course consist-ing of three overlapping stages: (1) catarrhal, (2) paroxysmal, and (3) convalescent.



After an incubation period of 7 to 10 days, pertussis follows a prolonged course consist-ing of three overlapping stages: (1) catarrhal, (2) paroxysmal, and (3) convalescent. In the catarrhal stage, the primary feature is a profuse and mucoid rhinorrhea that persists for 1 to 2 weeks. Nonspecific findings such as malaise, fever, sneezing, and anorexia may also be present. The disease is most communicable at this stage, because large numbers of or-ganisms are present in the nasopharynx and the mucoid secretions.

The appearance of a persistent cough marks the transition from the catarrhal to the paroxysmal coughing stage. At this time, episodes of paroxysmal coughing occur up to 50 times a day for 2 to 4 weeks. 

The characteristic inspiratory whoop follows a series of coughs as air is rapidly drawn through the narrowed glottis. Vomiting frequently follows the whoop. The combination of mucoid secretions, whooping cough, and vomiting pro-duces a miserable, exhausted child barely able to breathe. Apnea may follow such episodes, particularly in infants. Marked lymphocytosis reaches its peak at this time, with absolute lymphocyte counts of up to 40,000/mm3.


During the 3- to 4-week convalescent stage, the frequency and severity of paroxysmal coughing and other features of the disease gradually fade. Partially immune persons and infants under 6 months of age may not show all the typical features of pertussis. Some evolution through the three stages is usually seen, but paroxysmal coughing and lympho-cytosis may be absent.

The most common complication of pertussis is pneumonia caused by a superinfecting organism such as S. pneumoniae. Atelectasis is also common but may be recognized only by radiologic examination. Other complications, including convulsions and subconjuncti-val or cerebral bleeding, are related to the venous pressure effects of the paroxysmal coughing and the anoxia produced by inadequate ventilation and apneic spells.


A clinical diagnosis of pertussis is best confirmed by isolation of B. pertussis from na-sopharyngeal secretions or swabs. Throat swabs are not suitable, because the cilia to which the organism attaches are not found there. Specimens collected early in the course of disease (during the catarrhal or early paroxysmal stage) provide the greatest chance of successful isolation. Unfortunately, the diagnosis is frequently not considered until parox-ysmal coughing has been present for some time, and the number of organisms has de-creased significantly. The nasopharyngeal specimens are plated onto a special charcoal blood agar medium made selective by the addition of a cephalosporin. This allows the slow-growing B. pertussis to be isolated in the presence of more rapidly growing mem-bers of the normal upper respiratory flora. The characteristic colonies appear after 3 to 7 days of incubation and look like tiny drops of mercury. Immunologic methods (aggluti-nation, immuofluorescence) are required for specific identification.

A direct immunofluorescent antibody (DFA) technique has been successfully applied to nasopharyngeal smears for rapid diagnosis of pertussis. DFA is particularly helpful in pertussis because of the many days required for culture results. Because the sensitivity and specificity of DFA can vary with the quality of the reagents, these results should al-ways be confirmed by culture, if possible. Serologic and molecular diagnostic methods have been developed but are not widely used for clinical diagnosis.


Once the paroxysmal coughing stage has been reached, the treatment of pertussis is primarily supportive. Antimicrobial therapy is useful at earlier stages and for limiting spread to other susceptible individuals. Of a number of antimicrobics active in vitro against B. pertussis, erythromycin or clarithromycin are preferred because of their clini-cal effectiveness and relative lack of toxicity.


Active immunization is the primary method of preventing pertussis. The original vaccine, which produced a 99% reduction in disease, was prepared from inactivated whole cell sus-pensions and given together with diphtheria and tetanus toxoids as DTP. The undoubted ef-ficacy of this vaccine was colored by a high rate of side effects due to the crude nature of the whole cell preparation. These included local inflammation, fever and, rarely, febrile seizures. Although permanent neurologic sequelae were never convincingly linked to pertussis immunization, there were those who argued that the vaccine was worse than the disease. This led to the development of acellular vaccines, guided by knowledge of the vir-ulence factors involved in the pathogenesis of pertussis. One type of vaccine is made by purification of virulence factors from whole cell preparations followed by formaldehyde inactivation where appropriate. Another vaccine strategy is the production of recombinant components, genetically engineered to be immunogenic but nontoxic.

The multiple acellular vaccines licensed in the United States have different combina-tions of virulence factors. All contain PT toxoid and Fha and some add pertactin or pili (vaccine manufacturers use the term fimbriae). The efficacy of these vaccines has now been established and all have dramatically lower frequencies of side effects. They have been combined with diphtheria and tetanus toxoids as DTaP replacing the whole cell DTP. This vaccine is now recommended for the full primary immunization (2, 4, and 6 months) and boosters (15 – 18 months, 4 – 6 years). Additional boosters are recom-mended every 10 years after the last dose.

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