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Pertussis and Other Bordetella Infections

Chapter 165 | Part 5: Infectious Diseases

KEY CLINICAL POINTS

  • Pertussis is caused by Bordetella pertussis, characterized by paroxysmal coughing and whooping sound, with variable presentation across age groups
  • Diagnosis requires combination of clinical suspicion, PCR, culture, and serologic testing due to challenges with traditional methods
  • Antimicrobial therapy with macrolides (azithromycin/erythromycin) is first-line, with TMP-SMZ as alternative for allergic patients
  • Vaccination remains the cornerstone of prevention, with acellular vaccines recommended for adolescents and adults
  • Infants <1 year old have highest mortality risk, requiring hospitalization and strict infection control measures

1. DEFINITION & OVERVIEW

Pertussis is an acute respiratory tract infection caused by Bordetella pertussis, characterized by paroxysmal coughing with a distinctive 'whooping' sound. The disease presents variably by age group, with infants showing severe complications and adolescents/adults often presenting with atypical symptoms. Other Bordetella species (B. parapertussis, B. holmesii) cause similar but milder infections.

Table 165-1: Clinical Features of Pertussis by Age Group and Diagnostic Status

FEATURE PERCENTAGE OF PATIENTS ADOLESCENTS AND ADULTS INFANTS AND CHILDREN
Cough 70–99 89–93
Worse at night 61–87 41
Whoop 8–82 69–92
Post-tussive vomiting 17–65 48–60

Table 165-2: Antimicrobial Therapy for Pertussis

PATIENT AGE GROUP PRIMARY AGENTS ALTERNATE AGENT
<1 month AZITHROMYCIN (AZ) 10 mg/kg/day x5 days ERYTHROMYCIN (ER) 40–50 mg/kg/day x14 days
Infants (‡6 months) and children AZ 10 mg/kg/day x5 days ER 40–50 mg/kg/day x14 days
Adults AZ 500 mg/day x14 days ER 2 g/day x7 days
PATIENT AGE GROUP PRIMARY AGENTS ALTERNATE AGENT
All ages CLARITHROMYCIN 15 mg/kg/day x7 days TMP-SMZ 8 mg/kg TMP + 40 mg/kg SMZ x14 days

1.1 Microbiology

Bordetella species are gram-negative aerobic bacilli. B. pertussis is slow-growing and requires selective media. Key virulence factors include pertussis toxin, filamentous hemagglutinin, and pertactin. Pertactin-negative strains have emerged due to vaccine immunity pressure.

1.2 Pathogenesis

Infection begins with attachment to ciliated epithelium via adhesins. Pertussis toxin mediates immune evasion and cellular damage. The toxin causes lymphocytosis and airway inflammation, leading to the characteristic cough. Secondary bacterial pneumonia is common in infants.

2. EPIDEMIOLOGY

Pertussis is highly contagious with 80–100% attack rate among unimmunized contacts. Global incidence has declined but remains significant in developing countries (40 million cases/year). Infants <3 months have highest mortality (400,000 deaths/year). Outbreaks occur every 3–5 years despite vaccination. Immunity wanes rapidly after acellular vaccines.

2.1 Demographics

Infants <1 year old have highest morbidity/mortality. Adolescents and adults may have prolonged cough without classic whoop. School-age children are primary transmitters. Vaccination coverage globally is 84% (2021), but remains <50% in many developing nations.

2.2 Transmission

Spread via respiratory droplets. Incubation 7–10 days. High-risk settings include healthcare facilities, daycare centers, and households with infected members. Nosocomial outbreaks require water system disinfection (chlorine, copper-silver ionization).

3. ETIOLOGY & PATHOPHYSIOLOGY

B. pertussis produces pertussis toxin (ADP-ribosylates G proteins), filamentous hemagglutinin, and tracheal cytotoxin. These factors cause airway inflammation, lymphocytosis, and ciliary dysfunction. Pertactin-negative strains have emerged due to vaccine immunity pressure. B. holmesii causes 20% of pertussis-like syndromes.

4. CLINICAL FEATURES

Classic presentation in infants: paroxysmal cough, whoop, post-tussive vomiting, and apnea. Older children/adults: prolonged cough without whoop, often with secondary bacterial pneumonia. Atypical features include weight loss, urinary incontinence, and cough syncope. Infants may develop subconjunctival hemorrhages and pneumothorax.

4.1 Age-Specific Manifestations

Infants: 84% of deaths, 2957 cases/year. School-age children: catarrhal phase (common cold-like symptoms). Adolescents/adults: prolonged cough, often without whoop. Post-vaccination resurgence in teens due to waning immunity.

5. DIFFERENTIAL DIAGNOSIS

Distinguish from viral bronchiolitis, RSV, Mycoplasma, Chlamydia, and reactive airway disease. In infants, differentiate from apnea of infancy. In adults, consider postnasal drip, GERD, and ACE inhibitor use. Lymphocytosis increases likelihood of B. pertussis.

6. INVESTIGATIONS & DIAGNOSIS

Nasopharyngeal PCR (gold standard) and culture (Bordet-Gengou medium). Serologic testing for IgA/IgG antibodies to pertussis toxin. PCR results available within hours; cultures positive by day 5. Nasopharyngeal cultures remain positive for 3 weeks post-infection.

6.1 Diagnostic Algorithms

PCR for suspected cases (especially in adolescents/adults). Culture for infants with pneumonia. Serologic testing for outbreak investigation. Use of Regan-Lowe medium for B. holmesii detection.

7. MANAGEMENT & TREATMENT

Macrolides (azithromycin/erythromycin) for 14–21 days. TMP-SMZ as alternative for allergic patients. Supportive care: humidified air, antipyretics, and isolation. Hospitalization for infants with complications. Post-exposure prophylaxis for contacts within 21 days of onset.

7.1 Antimicrobial Therapy

Azithromycin 10 mg/kg/day x5 days (infants) or 500 mg/day x14 days (adults). Erythromycin 40–50 mg/kg/day x14 days. Clarithromycin 15 mg/kg/day x7 days. TMP-SMZ 8 mg/kg TMP + 40 mg/kg SMZ x14 days.

7.2 Supportive Care

Maintain hydration, monitor for apnea, and use humidified air. Avoid cough suppressants. Hospitalize infants with pneumonia, apnea, or respiratory distress.

8. PROGNOSIS & COMPLICATIONS

Mortality: 0.3–0.5% in infants, 0.01% in adults. Complications: pneumonia (9.4% in infants), apnea, encephalopathy, and subconjunctival hemorrhages. Long-term sequelae include bronchial hyperreactivity and cough syncope.

8.1 Infant Mortality

Infants <3 months have 400,000 annual deaths. Pneumonia (22% in infants), apnea, and respiratory failure are leading causes. Postnatal corticosteroids may reduce mortality.

9. SPECIAL CONSIDERATIONS

Pregnant women should receive vaccine at 27–36 weeks for passive immunity. Adults require booster doses (Tdap). Immunocompromised patients may have prolonged shedding. Nosocomial outbreaks require water system disinfection and isolation protocols.

9.1 Vaccination Strategies

Infants: 3-dose series at 2, 4, 6 months with booster at 15–18 months. Adolescents/adults: Tdap booster. Pregnant women: Tdap at 27–36 weeks. WHO recommends acellular vaccines for all countries.

10. KEY POINTS & CLINICAL PEARLS

  • Pertussis is a reportable disease with high transmission risk in unvaccinated populations
  • PCR is preferred over culture for rapid diagnosis
  • Macrolides are first-line therapy, with TMP-SMZ as alternative
  • Infants <1 year require hospitalization for severe cases
  • Vaccination remains the most effective prevention strategy
  • Post-exposure prophylaxis is critical for contacts within 21 days