Pertussis — branching viva

Opening question

Examiner: Take me through this infant. What is the most likely diagnosis, and what is your frame for managing it? [8]

Candidate: The most likely diagnosis is pertussis. The combination of apnoea and cyanosis in a ten-week-old, a three-week household cough contact in the mother, and the infant being between doses of the DTaP schedule is classic for infant pertussis — and the whoop is often absent at this age, so apnoea may be the only sign. My frame is two-layered: support and protect this infant now, and run the public-health response to stop transmission to other vulnerable contacts. I would admit for monitoring, confirm with PCR, start a macrolide, isolate, notify and trace contacts. [8] [1]

Examiner: Why is the infant at particular risk? [8]

Candidate: Infants under six months carry the highest morbidity and mortality in pertussis. They are often too young to have completed the primary series, so they depend on maternal antibody and the immunity of the people around them. Their small airways and limited respiratory reserve turn the same toxin-mediated injury that causes a prolonged cough in an older child into apnoea, cyanosis, pneumonia and, through hypoxia, encephalopathy. The biology is the same; the host turns it lethal. [8]

Branch 1 — pathophysiology

Examiner: Explain the pathophysiology of the paroxysmal cough. [1]

Candidate: Bordetella pertussis is inhaled and adheres to the ciliated epithelium of the nasopharynx and upper airways via adhesins such as filamentous haemagglutinin, pertactin and fimbriae. It then secretes toxins — pertussis toxin, adenylate cyclase toxin and tracheal cytotoxin — that paralyse the cilia and injure the epithelial cells. With the mucociliary escalator stopped, secretions and debris pool in the airway, and the cough reflex fires explosively and repeatedly to clear them. That is the paroxysm. [1]

Examiner: Does the organism invade? [1]

Candidate: Not deeply — it is a surface, toxin-mediated infection. The baboon-model histopathology shows the organism localised to the airway surface with ciliated-epithelial damage and inflammatory exudate, rather than tissue invasion. This is also why the cough can persist for weeks after the bacteria are cleared: the injury and inflammation outlast the infection, producing the prolonged convalescent phase. [1]

Branch 2 — diagnosis

Examiner: How will you confirm pertussis in this infant? [1]

Candidate: I would send a nasopharyngeal aspirate or flocked nasopharyngeal swab for pertussis PCR, which is the test of choice early in the illness — the first three to four weeks, when the organism is most abundant and sensitivity is highest. PCR has largely replaced culture for routine diagnosis because it is faster and more sensitive. I would not delay management while waiting for the result. [1]

Examiner: And if the presentation were a six-week cough in an adult? [1]

Candidate: Then PCR sensitivity would have fallen as the organism was cleared, so I would use serology — a single high-titre anti-pertussis-toxin IgG can support the diagnosis in a late presentation. The choice between PCR and serology is governed by the duration of illness at presentation. I would also note that a full-blood count may show a marked lymphocytosis, driven by pertussis toxin, and in an infant with apnoea and a cough contact that strengthens the case while the PCR is pending. [1]

Branch 3 — treatment and the macrolide question

Examiner: What treatment will you give this infant, and what is the macrolide actually for? [4]

Candidate: I will start a macrolide — azithromycin first-line, for five days. Its principal role is to limit the infectious period and protect contacts; it rarely shortens the paroxysmal course once it is established. The Cochrane review of antibiotics for whooping cough found that macrolides eradicate the organism and reduce infectiousness, but the evidence that they shorten the paroxysmal course is weak. So I frame the macrolide honestly to the family as a public-health measure, not a cough cure. [4]

Examiner: Any caution about the choice of macrolide? [4]

Candidate: Yes — erythromycin carries a risk of infantile hypertrophic pyloric stenosis when given to neonates in the first weeks of life, so azithromycin is preferred in that age group. In this ten-week-old infant azithromycin is the straightforward first choice, but the principle is to match the macrolide to the age. [4]

Branch 4 — public-health layer

Examiner: Walk me through the infection-control and public-health response. [10]

Candidate: I would place the infant under droplet precautions and exclude until five days of effective antibiotic have been completed — or, if untreated, for three weeks from the onset of paroxysms. I would notify public health according to local requirements, because pertussis is notifiable, and the notification triggers the contact-tracing and prophylaxis response. I would identify all household and close contacts, and flag who is high-risk: any infant under twelve months, any pregnant woman, and any unvaccinated or under-vaccinated contact. [10] [1]

Examiner: Who gets chemoprophylaxis? [10]

Candidate: High-risk contacts should receive a macrolide promptly after exposure — infants under twelve months, pregnant women, and unvaccinated or under-vaccinated household contacts. A household study of azithromycin prophylaxis supports its use to prevent pertussis in exposed contacts, and the aim is to protect the youngest, least-protected member of the household. I would also give catch-up vaccination to any under-immunised contacts, completing the cocoon around the vulnerable infant. [10]

Branch 5 — prevention and resurgence

Examiner: This infant was between doses. How do we prevent the next infant case? [8]

Candidate: The single most effective current protection for the newborn is maternal Tdap in every pregnancy, optimally between 28 and 38 weeks, because transplacental antibody transfer protects the infant through the first months before the primary series is complete. The US infant-pertussis-incidence trends study showed maternal Tdap implementation was associated with reduced infant incidence and hospitalisation. Around that, the childhood DTaP schedule, an adolescent Tdap booster, and cocooning of household contacts complete the strategy. [8]

Examiner: Why does pertussis resurge if we have a vaccine? [2]

Candidate: Because immunity after the acellular vaccine wanes faster than after the whole-cell vaccine. The acellular-vaccine efficacy trial in adolescents and adults established that the vaccine works in this transmission-sustaining group, but baboon-model work comparing whole-cell and acellular vaccines showed that while acellular vaccines prevent disease, they may not block colonisation and transmission as effectively. Waning immunity plus under-vaccinated pockets produces the cyclical resurgence we see every few years — which is why boosters, the maternal programme and high coverage all matter. [2] [6]

Wrap

Examiner: Summarise the pertussis stance in one sentence. [1]

Candidate: Recognise the apnoeic infant early and support them, confirm with PCR early or serology late, treat with a macrolide to limit infectiousness, isolate and notify, prophylax the high-risk contacts, and prevent the next case with maternal Tdap in every pregnancy, the full childhood schedule, an adolescent booster and cocooning — because pertussis kills infants, and every layer of the strategy exists to protect them. [8] [1]