Pertussis

Pertussis is an acute respiratory infection caused by Bordetella pertussis, characterized by paroxysmal spasmodic cough ending in a crowing inspiratory whoop. The course lasts weeks to ~3 months. Mostly under-5s; infants risk asphyxia, pneumonia, encephalopathy with high mortality. Sources are patients, asymptomatic infections, and carriers; infectivity is strongest from late incubation to 2-3 weeks after onset. Transmission is by respiratory droplets. Typical course is 6-8 weeks in 3 stages: (1) catarrhal stage 1-2 weeks; (2) spasmodic paroxysmal cough stage 2-4+ weeks; (3) convalescence 1-2 weeks. Peripheral WBC is markedly elevated with lymphocyte predominance. Must be distinguished from foreign body and hilar lymph node TB. Infantile and adult cases are rising.

Common Symptoms

Inspiratory stridor; spasmodic cough; chest tightness; lung yin deficiency; convulsions; low fever; Yan Penghui; convulsion

Causes and Pathogenesis

(1) Etiology: B. pertussis (Bordetella) is 1.0-1.5 × 0.3-0.5 µm, encapsulated, non-motile, Gram-negative, aerobic, non-spore, non-flagellate, with deeply stained ends on toluidine blue; requires 15-25% blood (Bordet-Gengou medium: blood/glycerol/potato). Slow growth (3-7 days at 35-37°C); smooth S-phase colonies are virulent/encapsulated; rough R-phase are avirulent. Five toxins: (1) PT (pertussis toxin, formerly LPF/HSF/IAP), a 5-subunit A-B toxin; S1 ADP-ribosylates Gi, disrupting signaling and causing lymphocytosis/hyperinsulinemia; (2) heat-stable endotoxin (inactivated at 180°C) causing fever/spasmodic cough; (3) heat-labile toxin (destroyed 55°C/30 min); (4) tracheal cytotoxin damaging ciliated epithelium; (5) adenylate cyclase toxin activated by calmodulin, inhibiting phagocytosis. Major protective antigens: filamentous hemagglutinin (FHA, fimbrial, mediates adhesion) and agglutinogens (AGG-1 species-specific, AGG-2/3 type-specific). B. pertussis is killed at 55°C/30 min, sensitive to disinfectants/UV, but survives 0-10°C. (2) Pathogenesis: FHA mediates ciliary adhesion from pharynx to bronchioles; local toxins cause ciliary paralysis, epithelial necrosis, mucus retention irritating cough reflexes; CD4+/Th1 cytokines are important. Pathology: congested nasopharyngeal/tracheal/bronchial mucosa with neutrophil/monocyte infiltration; mucus plugging causes atelectasis/bronchiectasis/bronchopneumonia; encephalopathy shows cerebral edema, petechiae, cortical atrophy, fatty liver.

Treatment

Drug therapy, supportive therapy

Preventive Measures

1. Control sources: early antibiotics for prodromal symptoms in epidemic seasons. 2. Cut transmission: B. pertussis is fragile—no special disinfection needed, but ventilate rooms, sun bedding, disinfect sputum/oral secretions.

Department to Visit

It is recommended to visit the Pediatrics department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.