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Whooping cough is
caused by Bordetella pertussis, a nonmotile, gram-negative
coccobacillus that forms a capsule in its virulent state. Humans
provide the only reservoir.
B. pertussis
produces a heat-labile toxin, a heat-stable endotoxin, and a
lymphocytosis-producing factor also called histamine-sensitizing
factor.
Pertussis is
worldwide and passes from person to person in moist droplets
containing B. pertussis. Nearly all susceptible contacts become
infected.
B. pertussis
has a remarkable ability, probably enhanced by its pili, to attach to
ciliated bronchial epithelium. Here the organisms proliferate, remain
on the surface epithelium , and accumulate in great numbers. The
bacteria stimulate the bronchial cells to produce a profuse, tenacious
mucus that slows ciliary action and inhibits the bronchopulmonary
toilet. Secondary bacterial infections and epithelial necrosis follow.
A catarrhal
stage begins 7 to 10 day after exposure and may last 1 to 2 weeks.
There is low-grade fever, rhinorrhea and conjunctivitis.
During the
catarrhal stage, when the patient is most infectious, B. pertussis
proliferates, forms entangled masses mixed with the cilia, and elicits
a neutrophilic exudate.
Cough
progresses to severe paroxysms terminating in a gasping, strident,
inspiratory effort. During inspiration, air is forcibly drawn through
a narrow glottis, giving the characterisitic "whoop".
This
paroxysmal stage begins 2 - 3 weeks after inoculation, lasts days to
weeks and is marked by as many as 50 paroxysms per day.
The necrotic
bronchial epithelium is covered by a thick mucopurulent exudate.
The
convalescent stage lasts weeks or (rarely) months.
The death rate
is highest in infancy.
B. pertussis
infections in infancy are frequently associated with apneic spells,
which are occasionally life-threatening and, if leading to death,
might be reported as SIDS.
Immunity is
conferred by IgA antibody, which prevents bacterial attachment.
Second attacks
can occur but are caused by B. parapertussis ,which may cause 20% of
all whooping cough infections.
Vaccination
protects against B. pertussis , but not against B. parapertussis.
Morphological findings:
Morphologic
changes, in the uncomplicated case, are mostly limited to the air
passages and lung.
Findings
include laryngitis, tracheitis,
bronchitis and the
bronchiolitis . The
changes are most noticeable in the bronchi.
Bacterial
stains reveal many of the specific organisms contained within the
mucopurulent exudate that overlies the mucosa and is intertwined and
tangled with the cilia of the columnar epithelium.
Occasionally,
areas of superficial necrosis and erosion are evident.
Hyperemia and
excessive production of mucus occur.
The smaller
bronchi may contain dense plugs of mucus and these will include a few
inflammatory cells and many organisms.
Peribronchitis
and interstitial pneumonitis , especially around small bronchi are
characterisitic findings but are not pathognomonic, since they are
seen also in other disease.
Little exudate
is to be found in alveoli unless there is secondary
bronchopneumonia.
Emphysema is
almost always evident microscopically.
Peribronchial
lymph nodes are hyperemic and exhibit moderate hyperplasia.
B. pertussis
may be cultured from the posterior nasopharynx during the first 2
weeks. Smears from nasopharyngeal swabs can be tested with
fluorescent-labeled antipertussis serum.
A combination
of culture and fluorescent-labeled smears gives the greatest
diagnostic accuracy.
Erythromycin
is effective in the catarrhal stage and should be given to all
contacts with positive nasopharyngeal smears.
Antibiotics
begun after the paroxysmal stage begins do not alter the clinical
course.
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