Etiology and Epidemiology
The causative agent of the infection is the whooping cough bacterium (Bordetella pertussis). It is a Gram-negative, non-motile bacterium and an obligate aerobe. It has 4 serological variants differing in virulence. The pathogen is extremely unstable in the external environment: it lives for no more than a couple of hours in dried sputum and is rapidly killed by disinfectants and UV rays.
Pertussis is a typical anthroponosis, with humans being the sole reservoir of infection. Patients with mild or atypical forms pose the greatest hidden threat in groups. The infection is transmitted via airborne droplets (aerosols) during close contact (up to 2 meters). Susceptibility is very high (about 70–90%), especially in children under 5 years old. An autumn-winter seasonal rise is characteristic, and lifelong immunity is formed after the disease.
Pathogenesis: how the cough develops
The development of the disease is clearly linked to the pathogenicity factors of the bacterium. The pathogen attaches to the ciliated columnar epithelial cells of the respiratory tract. Its toxins paralyze the cilia, causing local inflammation, impaired drainage function, and local immunosuppression.
Pertussis toxin plays a key role in the transition of the disease to the spasmodic stage:
- Constantly irritates bronchial receptors.
- Entering the bloodstream, it reduces the tissue threshold of sensitivity to histamine.
- Forms a persistent focus of excitation in the medulla oblongata — the cough determinant.
As a result, a spasm of the small bronchi occurs, drastically complicating the evacuation of sputum and the passage of air.
Clinical stages and severity assessment
After the incubation period (on average 5–8 days), the disease lasts 6–8 weeks, passing through three mandatory stages:
- Catarrhal stage (1–2 weeks): gradual onset with low-grade fever and scanty rhinitis. The main marker is a progressive cough that does not respond to standard treatment.
- Spasmodic stage (2–4 weeks): a series of short expiratory jerks is replaced by a whoop (deep whistling inspiration). The attack ends with the discharge of vitreous sputum or vomiting. The face turns cyanotic, and hemorrhages in the sclera are possible. A characteristic sign is an ulcer on the frenulum of the tongue from friction against the teeth.
- Convalescence stage (1–3 weeks): paroxysms become less frequent, but a residual cough can persist for months.
In the inter-ictal period, dissociation is observed: despite the severity of the paroxysms, the child's well-being remains quite normal, and the temperature does not rise.
The severity of the peak period is classified by the number of attacks:
| Morphology | Number of attacks per day |
|---|---|
| Mild | 10–15 |
| Moderate | 15–20 |
| Severe | From 30 to 60 and more |
Features in infants and complications
In infants under one year of age, pertussis is extremely severe. The catarrhal stage may be absent, and during an attack, instead of the classic whoop, apnea (cessation of breathing) occurs. This rapidly leads to cyanosis and hypoxia.
Complications are divided into three groups:
- Hypoxic: encephalopathy, convulsive syndrome, loss of consciousness.
- Bronchopulmonary: atelectasis and secondary pneumonia.
- Mechanical (from high pressure): spontaneous pneumothorax, umbilical hernias, rectal prolapse, petechiae.
Diagnostics and treatment
It is clinically difficult to suspect pertussis during the catarrhal period. Key reference points are typical paroxysms and changes in the CBC (leukocytosis + lymphocytosis with normal ESR). For verification, bacteriological culture ("cough plate" method) and nasopharyngeal swab PCR are used — these methods are informative only up to the 2nd week of the spasmodic stage.
Treatment is mostly outpatient. Patients need fresh air (walks reduce the risk of attacks). Antibacterial therapy (macrolides, amoxicillin) is useful only in the early stages, while the pathogen is actively multiplying. In the spasmodic stage, when the cough is maintained by the determinant in the brain, antibiotics no longer affect the frequency of attacks.
To memorize the structure of the attack, use the rule "COUGH": Cough expiratory jerks $\rightarrow$ Origin of whoop (inspiration) $\rightarrow$ Unpleasant cyanosis (face color change) $\rightarrow$ Glue-like sputum/vomiting at the end.
Class and exam questions
Why are antibiotics ineffective for pertussis at the peak of the disease?
In the spasmodic stage, cough paroxysms are caused not by the bacteria themselves, but by the cough determinant (focus of excitation) in the medulla oblongata already formed under the action of toxins.
How to suspect pertussis using a complete blood count?
A typical reaction is marked leukocytosis with lymphocytosis, while the erythrocyte sedimentation rate (ESR) remains within normal limits or is decreased.
Why is pertussis dangerous for children under one year old?
In infants, instead of a deep inspiration (whoop) during an attack, apnea often occurs — a short-term cessation of breathing, which leads to severe hypoxia and the risk of seizures.
What else to study on this topic
- Mechanisms of action of specific pertussis toxins
- Differential diagnosis with parapertussis and respiratory mycoplasmosis
- Atypical and mild forms of infection in adults
- Types of post-vaccination reactions and neurological risks
- Differences between whole-cell (DTwP) and acellular (Pentaxim) vaccines
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