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a short period of time. A variety of stimuli, including feeding, sucking, or crying, can trigger an attack. Very young infants tend to have apneic spells rather than paroxysms of cough.

The convalescent stage, which usually begins 4 to 6 weeks after the onset of disease, is characterized by a gradually diminishing frequency and severity of paroxysms. The whoop soon disappears, although a nonparoxysmal cough may persist for several months.


B. pertussis can be cultured by inoculation of nasopharyngeal mucus, obtained by swab, on special agar such as Bordet-Gengou with added methicillin or Regan-Lowe with added cephalexin. A positive culture is diagnostic. False-negative cultures are common, particularly in persons receiving antibiotics (Berkow, 1987). B. pertussis can also be detected by direct immunofluorescence, although the test has been hampered by relatively frequent false-positive and false-negative results (Wirsing von König et al., 1990). Serologic tests, including enzyme-linked immunosorbent assays, to detect antibody to filamentous hemagglutinin (FHA) and other B. pertussis components are being developed for diagnostic purposes (Berkow, 1987; Storsaeter et al., 1990; Wirsing von König et al., 1990). Probing for Bordetella DNA, either directly or after preliminary amplification by the polymerase chain reaction or culture, may provide another useful means of detection (Wirsing von König et al., 1990).


Minor complications of pertussis include subconjunctival hemorrhages and epistaxis secondary to the paroxysmal coughing. Suppurative otitis media is a frequent complication, especially in infants (Mortimer, 1988).

Major complications of pertussis can be fatal. They are divided into three general categories: respiratory, central nervous system (CNS), and nutritional. The most common are respiratory, including asphyxia in infants. Other severe respiratory complications include bronchopneumonia, a frequent complication in elderly people, atelectasis, bronchiectasis, interstitial and subcutaneous emphysema, and pneumothorax.

CNS complications following pertussis include acute encephalitis that can progress to convulsions, stupor, and coma. Pathologic findings reveal cerebral hemorrhage and edema (Dolgopol, 1941). Long-term sequelae include spastic paralysis, mental retardation, or other permanent neurologic disorders. Rates of CNS complications differ widely among studies. For example, 1.7 to 7 percent or more of pertussis cases in large series of hospitalized children developed CNS complications (Zellweger, 1959), whereas

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