Parasitic infections in children: Viva

Branch 1: Recognising the diagnosis and its clinical pattern

The candidate should immediately recognise this as scabies based on the classic clinical triad of intense pruritus worse at night, burrows in the characteristic distribution of finger webs and wrists, and a household contact with the same itch. The mite Sarcoptes scabiei burrows into the stratum corneum, and the pruritus is a type four hypersensitivity response to mite products that typically develops two to six weeks after first infestation, though reinfestation provokes symptoms within days. [1]

The candidate should describe the distribution that distinguishes scabies from other pruritic conditions. In older children and adults, the burrows and papules favour the finger webs, flexor surfaces of the wrists, axillae, waistline, and genitalia. In infants and young children, the distribution is broader and includes the palms, soles, head, and neck, which is a key difference from the adult pattern. The presence of a household contact with itch, the nocturnal predominance, and the characteristic burrows make the diagnosis clinical, and a skin scraping showing mites, eggs, or scybala confirms it when there is doubt. [1]

The examiner will probe the differential diagnosis. The candidate should distinguish scabies from atopic dermatitis, which favours the flexural creases of elbows and knees and is associated with a personal or family atopic history; from contact dermatitis, which follows a pattern related to the offending agent; and from papular urticaria from insect bites. The keys to scabies are the household contact, the nocturnal predominance, and the burrows in finger webs. [2]

Branch 2: Treatment and the household principle

The candidate should prescribe permethrin five per cent cream applied to the entire body from the neck down and washed off after eight to fourteen hours, with a repeat application after one to two weeks to kill mites hatched from eggs surviving the first dose. Oral ivermectin is an alternative for crusted scabies, immunocompromised children, or when topical therapy fails, and is given as two doses one to two weeks apart. [1]

The examiner will test whether the candidate understands the single most important treatment principle: all household and close contacts must be treated simultaneously, regardless of whether they have symptoms. Asymptomatic carriers within the household perpetuate the cycle of reinfestation, and treating only the symptomatic child is the most common reason for apparent treatment failure. The systematic review evidence shows that most treatment failures are reinfestation from untreated contacts rather than drug resistance. Bedding and clothing should be washed in hot water or bagged for several days to kill mites and eggs. [1]

The candidate should address the post-treatment itch, which can persist for two to four weeks after successful treatment due to ongoing hypersensitivity to dying mites and their products. This is not a sign of treatment failure if no new burrows appear, and symptomatic treatment with antihistamines or topical corticosteroids may be needed. The family should be warned about this to prevent unnecessary re-treatment. [2]

Branch 3: Public health, Indigenous communities, and the Streptococcus connection

The examiner will broaden the discussion to public health. The candidate should explain that scabies is disproportionately prevalent in remote Indigenous Australian communities, where historical prevalence in children has exceeded fifty per cent. The link between scabies, group A streptococcal pyoderma, acute post-streptococcal glomerulonephritis, and acute rheumatic fever is one of the most important parasitic connections in Australian paediatrics. Community-based scabies control programmes, including mass drug administration with ivermectin or permethrin, have reduced scabies prevalence and the downstream burden of streptococcal disease. [2]

The candidate should describe crusted scabies as a severe variant seen in immunocompromised, disabled, or Down syndrome children, in which an inadequate cellular immune response allows millions of mites to proliferate. The child presents with thick, scaly, hyperkeratotic crusts over the extremities and trunk, is extraordinarily infectious, and requires admission for isolation, oral ivermectin combined with topical permethrin, and prolonged treatment. [2]

The examiner may then ask about other parasitic screening before immunosuppression. The candidate should flag Strongyloides stercoralis as the other critical pre-immunosuppression parasitic concern: any child with tropical exposure must be screened with serology and treated with ivermectin before corticosteroids, because untreated Strongyloides can cause fatal hyperinfection under immunosuppression. This principle of screening before immunosuppression applies to both scabies contacts and Strongyloides, and is a recurring high-yield exam theme. [3]