Paediatrics chapters
Pertussis
Whooping cough caused by Bordetella pertussis: how it spreads, the three stages, why infants present with apnoea instead of a whoop, the striking lymphocytosis, complications, macrolide treatment and prevention of contacts.
- Pertussis is a highly infectious Bordetella pertussis infection with three stages of about 2 weeks each: catarrhal (most infectious), paroxysmal (bouts of cough ending in a whoop and vomiting) and convalescent.
- Young infants may have apnoea and cyanosis without a whoop; the blood shows marked lymphocytosis of small mature cells; pneumonia is the commonest complication and main cause of death.
- Treat with a macrolide (azithromycin, erythromycin, clarithromycin), give the same to close contacts, and prevent with DPT in the EPI schedule.
On this page
Overview
Pertussis ("intense cough") or whooping cough is an acute respiratory infection caused by Bordetella pertussis. It produces weeks of violent coughing fits. It is most severe in infants under 1 year, who may stop breathing rather than whoop. It is preventable with the DPT (pentavalent) vaccine of the EPI, so most cases now occur in unvaccinated or partly vaccinated children.
Aetiology
- Bordetella pertussis: a small gram-negative coccobacillus with fussy growth needs; infects only humans.
- A milder, shorter pertussis-like illness (pertussoid syndrome) can be caused by B. parapertussis (about 5%), B. bronchiseptica and adenovirus; also Mycoplasma, Chlamydia and RSV (Nelson).
- There is no cross-immunity between these agents, which explains apparent second attacks.
Epidemiology
- Spread by droplets from coughing; attack rates in susceptible contacts approach 100%.
- Incubation: Akbar 3-12 days (mean 6); Nelson 7-10 days.
- Infectious for about 4 weeks; most infectious in the catarrhal stage, before the diagnosis is obvious.
- Most common and severe under 5 years; deaths are highest in infants under 1 year.
- No transplacental protection: young babies are fully susceptible.
- Immunity after vaccine wanes in 3-5 years and is gone by about 12 years; even natural disease does not give lifelong immunity. Older children and adults get an atypical prolonged cough and pass it on to infants in the family.
Pathogenesis
- Bacteria attach to ciliated respiratory epithelium and multiply there without invading the blood.
- Toxins damage the lining and cause patchy necrosis of the surface epithelium: pertussis toxin is the main virulence factor and causes the lymphocytosis. Other antigens (filamentous haemagglutinin, pertactin, fimbriae) are used in acellular vaccines.
- Thick, sticky mucopurulent exudate plugs bronchioles, causing atelectasis, patchy emphysema and later bronchiectasis.
- Peri-hilar inflammation gives the "shaggy heart border" on chest X-ray.
Clinical features
Classic disease runs 6-8 weeks in three stages of about 2 weeks each.
| Stage | Duration | Features |
|---|---|---|
| Catarrhal | 1-2 weeks | Like a cold: runny nose, sneezing, watery red eyes, low-grade fever, mild cough. Most infectious; diagnosis hard |
| Paroxysmal | 2-4 weeks | Bursts of many short coughs in one breath, face red or blue, eyes bulging, neck veins full; then a forced in-breath that makes the whoop; vomiting after coughing; exhaustion. Child looks well between bouts. Chest usually clear |
| Convalescent | 1-2 weeks or more | Bouts less frequent and milder, whoop fades; cough may return with later colds for months |
A cough lasting more than 2 weeks that comes in paroxysms with a whoop or post-tussive vomiting, in a child without much fever, is pertussis until proven otherwise.
Age differences
- Infants under 3-6 months: often no whoop; present with apnoea, choking, cyanotic spells or seizures; may look completely well between episodes yet be at risk of death.
- Immunised children, adolescents and adults: a mild, prolonged cough without whoop.
No whoop does not exclude pertussis. Infants present with apnoea; adolescents with a long dry cough.
A temperature above about 38.3 °C suggests a secondary bacterial infection or another illness, not pertussis itself.
Investigations
| Test | Finding |
|---|---|
| Blood count | Leucocytosis, often 15,000-100,000/mm3, with 70-80% lymphocytes (absolute lymphocytosis) in the late catarrhal and paroxysmal stages. The lymphocytes are small, mature cells, unlike the atypical cells of viral illness. Can mimic leukaemia (leukaemoid reaction). May be absent in young or partly immunised infants |
| Nasopharyngeal swab culture | On Bordet-Gengou medium, plated at once; positive in about 90% early, falling to about 50% by week 3-4, rarely positive later |
| PCR of nasopharyngeal sample | Rapid; about as sensitive as culture (Nelson) |
| Chest X-ray | Peri-hilar infiltrates, shaggy heart border, atelectasis or emphysema; excludes complications |
| Serology | Helpful only later, for confirmation |
Lymphocytosis of normal-looking small lymphocytes is the classic blood finding, driven by pertussis toxin. A shift to neutrophils suggests secondary pneumonia.
Differential diagnosis
- Bronchiolitis and viral pneumonia
- Chlamydial or other atypical pneumonia
- Foreign body inhalation
- Tuberculosis, or intrathoracic nodes pressing on the airway
- Cystic fibrosis, asthma
- Pertussis-like illness from parapertussis or adenovirus
Complications
| Group | Complications |
|---|---|
| Respiratory | Bronchopneumonia (in about 25%; from B. pertussis itself or secondary H. influenzae, pneumococcus, Staph. aureus): the commonest complication and cause of over 90% of infant deaths; atelectasis from mucus plugs; later bronchiectasis; otitis media; reactivation of TB |
| Pressure effects of coughing | Pneumothorax, pneumomediastinum, subcutaneous emphysema; subconjunctival haemorrhage, epistaxis, retinal and intracranial bleeds; ulcer of the tongue frenulum; rectal prolapse, umbilical and inguinal hernia |
| Nervous system | Convulsions (about 4% of infants) from hypoxia or alkalosis; encephalopathy (about 1%), the main cause of permanent damage |
| Nutritional/metabolic | Malnutrition and weight loss from vomiting and poor feeding; dehydration; metabolic alkalosis |
| Infants | Apnoea and sudden death during a bout |
Management
Antibiotics
| Drug | Regimen (Akbar) | Notes |
|---|---|---|
| Azithromycin | 10 mg/kg once daily for 5 days | Preferred in neonates (Nelson) |
| Erythromycin | 30-50 mg/kg/day, split three times daily (maximum 2 g/day), for 14 days | Shorter courses risk relapse; in newborns it is linked to pyloric stenosis |
| Clarithromycin | 15 mg/kg/day in 2 doses for 7 days | Equally effective |
| Co-trimoxazole | Alternative after 2 months of age (Nelson) | For macrolide intolerance |
- Given in the catarrhal stage, a macrolide clears the organism in a few days and may shorten and soften the illness.
- Given in the paroxysmal stage, it does not change the course but makes the child non-infectious and protects others.
- Secondary pneumonia needs a separate antibiotic aimed at the usual bacteria.
- Akbar advises isoniazid prophylaxis for about 3 months because pertussis can reactivate dormant TB.
Macrolides are the drugs of choice; their main value after the cough starts is to stop spread.
Supportive care
- Admit infants, especially those under 6 months: monitor for apnoea and hypoxia.
- Oxygen and gentle suction of thick secretions; position to drain secretions.
- Small, frequent feeds; nasogastric feeds or IV fluids if vomiting is severe.
- Avoid mist tents; cough mixtures and sedatives help little.
- Treat convulsions with diazepam or phenobarbitone.
- Akbar notes that corticosteroids and nebulised salbutamol may help in severe cases.
- Isolate the child for the first 5 days of antibiotic treatment.
Prevention
- Vaccination: Akbar's EPI table gives pentavalent vaccine (pertussis with diphtheria and tetanus, plus hepatitis B and Hib) at 6, 10 and 14 weeks. Check the current national schedule at EPI Pakistan (checked 8 Nov 2026). Nelson describes acellular pertussis vaccine (DTaP) at 2, 4, 6 and 15-18 months with a preschool booster.
- Contraindication to further pertussis vaccine: encephalopathy within 7 days of a previous dose, or anaphylaxis. Progressive neurological disease delays it until stable.
- Contacts: every close contact, whatever their vaccination status, receives a macrolide (Akbar: erythromycin for 10-14 days; Nelson: azithromycin for 5 days).
- Contacts under 7 years who are fully vaccinated but have not had a dose for 3 years get a booster; under-vaccinated contacts complete their doses.
"Catarrh, Cough-whoop, Calm", about 2 weeks each, and "Catarrh = most Catching".
Prognosis
- Overall mortality is under 1%, but in infants under about 5 months it can be very high (Akbar: up to 40% in endemic settings).
- Most children regain normal lung function; lasting damage is mainly from hypoxic brain injury.
Expect: B. pertussis as a gram-negative coccobacillus; the three stages and that the catarrhal stage is most infectious; whoop mechanism and post-tussive vomiting; apnoea without whoop in young infants; lymphocytosis of small mature cells from pertussis toxin; Bordet-Gengou medium and nasopharyngeal swab; bronchopneumonia as the commonest complication and killer; pressure complications (subconjunctival haemorrhage, frenulum ulcer, hernia, prolapse); macrolide treatment and its stage-dependent benefit; azithromycin in neonates; contact prophylaxis and DPT in the EPI.
Quick revision
- B. pertussis; droplets; incubation about 1 week; no maternal protection.
- Catarrhal (most infectious), paroxysmal (whoop, vomiting), convalescent (months of cough).
- Infants: apnoea, cyanosis, no whoop.
- WBC very high with small mature lymphocytes; neutrophilia = secondary pneumonia.
- Culture on Bordet-Gengou; PCR; X-ray shaggy heart border.
- Pneumonia: commonest complication and killer; encephalopathy causes permanent harm.
- Azithromycin 10 mg/kg for 5 days; erythromycin 14 days; all close contacts treated.
- Pentavalent at 6, 10 and 14 weeks.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Why do young babies with pertussis often not whoop?
They lack the strength to take the deep forceful breath after a coughing bout, so they choke, turn blue or stop breathing instead.
If antibiotics do not shorten the paroxysmal stage, why give them?
They clear the organism within days, so the child stops infecting others, especially vulnerable infants at home.
Why is the white count so high?
Pertussis toxin keeps lymphocytes in the circulation, giving very high counts of small, mature lymphocytes.
Does having pertussis give lifelong immunity?
No. Both natural disease and vaccination give immunity that fades, so older children and adults can be infected again, usually mildly.