Varicella and herpes zoster — branching viva

Opening question

Examiner: Take me through this child. What is the diagnosis, and what is your frame for managing him? [1]

Candidate: The diagnosis is primary varicella. The combination of fever, a generalised vesicular rash with lesions of all stages — papules, vesicles, pustules and crusts — and a sibling with chickenpox two weeks ago makes the clinical diagnosis. The critical point is that this child is on maintenance chemotherapy, so he is a high-risk host in whom the disease can disseminate to the lungs, liver and brain. My frame is to treat him as high-risk from the first minute: admit, start intravenous aciclovir promptly, and run the public-health response to protect his contacts. [1] [4]

Examiner: Why is he at particular risk? [1]

Candidate: Because his cell-mediated immunity is suppressed by the chemotherapy, and it is cell-mediated immunity rather than antibody that holds varicella-zoster virus in check. In a host who cannot contain replication, the virus disseminates, producing fulminant pneumonia, hepatitis and encephalitis. The biology is the same as in a healthy child; the host turns a self-limiting illness into a life-threatening one. [1]

Branch 1 — pathophysiology and latency

Examiner: Explain the pathophysiology of the rash, and the connection to herpes zoster. [3]

Candidate: Varicella-zoster virus enters via the respiratory mucosa and spreads through primary then secondary viraemia to seed the skin and, importantly, the sensory ganglia of the dorsal roots and cranial nerves. In the skin, each lesion runs from papule to a clear vesicle on an erythematous base — the dewdrop on a rose petal — to pustule to crust. Because successive crops appear over days, lesions of all stages are present at once, which is the clinical signature. Crucially, the virus that reached the ganglia establishes lifelong latency there, held by cell-mediated immunity. Decades later, if that immunity wanes, it reactivates down a single dermatome to produce herpes zoster. [3] [1]

Examiner: So the same virus causes two diseases? [3]

Candidate: Exactly. Primary varicella is the first encounter; herpes zoster is the reactivation of the same virus from ganglionic latency, usually decades later. This is why waning cell-mediated immunity from ageing or immunosuppression triggers zoster, and why antibody alone does not prevent it. [3]

Branch 2 — diagnosis and investigations

Examiner: How will you confirm the diagnosis here? [1]

Candidate: In a classic presentation like this, the diagnosis is clinical. But because he is a high-risk host and I want to confirm and characterise the virus, I would send PCR of vesicle fluid or a lesion-base swab, which is sensitive and specific and can distinguish wild-type from vaccine-strain virus. I would also request a chest X-ray because of his tachypnoea to look for varicella pneumonia, and liver function tests and a coagulation screen to assess for dissemination. I would not delay treatment while waiting for results. [1]

Examiner: When would you use serology instead? [1]

Candidate: Serology has a more limited role. IgG determines past immunity and susceptibility — useful for a pregnant woman or high-risk contact after an exposure, or for checking immune status before vaccination. IgM can support recent infection but is less reliable than PCR for an acute case. So PCR is the acute diagnostic tool, and serology is the immune-status tool. [1] [2]

Branch 3 — treatment and the risk-tier question

Examiner: What treatment will you give this child, and how does it differ from a healthy child? [4]

Candidate: I will start intravenous aciclovir promptly, because he is a high-risk host. The risk-tier principle is that the healthy child gets supportive care, the at-risk child may get oral aciclovir, and the high-risk host — immunocompromised, neonate, or pregnant — gets intravenous aciclovir. Applying the supportive default to this child would be the dangerous error. I would maintain hydration carefully to protect against aciclovir nephrotoxicity, and I would treat any complication — pneumonia, secondary bacterial infection, invasive group A strep — as it arises. [4] [1]

Examiner: Does aciclovir help in the healthy child? [4]

Candidate: Modestly, and only if started within twenty-four hours of rash onset. The Cochrane review found aciclovir shortened fever and reduced the maximum number of lesions, but the benefit was small and there was no evidence it prevented serious complications. So routine aciclovir for every healthy child is not recommended, though it retains a role for the child with chronic skin or lung disease, an adolescent, or a high-risk household contact. The point is that the treatment is tiered by host risk, not applied uniformly. [4]

Branch 4 — public-health layer

Examiner: Walk me through the infection-control and public-health response. [2]

Candidate: I would place him under airborne plus contact precautions, because the virus spreads by both routes. I would notify public health, because varicella is notifiable, and the notification triggers the contact response. I would identify all household and close contacts and flag who is high-risk — any pregnant woman, any neonate, any immunocompromised person, and any non-immune sibling or classmate. [2] [1]

Examiner: Who gets post-exposure prophylaxis, and with what? [2]

Candidate: For contacts in whom the live vaccine is not contraindicated, I give varicella vaccine within three to five days of exposure, which can prevent or modify disease. For the high-risk contact in whom the live vaccine is contraindicated — a pregnant woman, a neonate, an immunocompromised person — I give varicella-zoster immune globulin instead, to prevent or attenuate severe disease. The aim is always to protect the contact who cannot safely be vaccinated and who cannot safely afford to catch wild-type varicella. The child is excluded until every lesion has crusted, which is the endpoint of contagiousness. [2] [6]

Branch 5 — herpes zoster and prevention

Examiner: Tell me about herpes zoster in a child, and its prevention. [3]

Candidate: Childhood zoster is uncommon but occurs, especially in immunocompromised children or those who had primary varicella in infancy. It presents as a unilateral, painful, dermatomal vesicular rash that stops at the midline, often preceded by tingling. Ophthalmic zoster threatens vision and needs urgent ophthalmology. In an immunocompromised child with zoster I would assess for dissemination and treat with aciclovir. For prevention of zoster in adults, the adjuvanted recombinant zoster vaccine is highly effective at preventing zoster and post-herpetic neuralgia, and its place is in the older and immunocompromised adult population. [3]

Examiner: And prevention of primary varicella itself? [1]

Candidate: The two-dose live-attenuated varicella vaccine, given in early childhood. The vaccine is highly effective; breakthrough disease, when it occurs, is milder, with fewer lesions, less fever and lower contagiousness. This child's brother was unvaccinated, which is exactly why the household exposure happened — under-vaccination is the dominant risk factor. The lesson is that completing the two-dose schedule is the durable protection, for the individual and for the household. [1] [5]

Wrap

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

Candidate: Recognise the clinical signature of all stages at once, risk-stratify by host — supportive for the healthy child, intravenous aciclovir for the immunocompromised, neonate and pregnant — confirm with PCR when atypical or severe, isolate and exclude until every lesion has crusted, notify and protect high-risk contacts with vaccine or VZIG, and prevent the disease with the two-dose live varicella vaccine, remembering that the same virus reactivates decades later as zoster. [1] [3]