Fungal infections in immunocompetent and immunocompromised children — formative SAQs

SAQ 1 (10 marks)

A 7-year-old boy with acute lymphoblastic leukaemia is on day 12 of induction chemotherapy. His absolute neutrophil count is 0.1, and he has a central venous catheter in situ. He has been febrile for six days despite appropriate broad-spectrum anti-pseudomonal beta-lactam therapy; blood cultures remain negative. He now reports pleuritic chest pain. [1]

Question: Outline your assessment and management of this child, including the differential diagnosis, the investigations, the empirical and definitive therapy, and the principles of source control and prophylaxis. (10 marks) [14]

Model answer

Differential diagnosis and risk framing (2 marks). Persistent febrile neutropenia beyond four to seven days on appropriate broad-spectrum antibiotics, in a profoundly neutropenic child with a central line, raises invasive fungal disease to the top of the differential — invasive candidiasis, invasive pulmonary aspergillosis, and mucormycosis — alongside unresolving bacterial infection and viral reactivation. The pleuritic chest pain points toward an invasive pulmonary mould process. The error to avoid is attributing the persistent fever to bacterial infection alone; the day-four-to-seven persistent fever is the trigger to add empirical antifungal therapy and to image the chest and sinuses. [14] [1]

Investigations (3 marks). Send blood cultures from a peripheral site and from each lumen of the central line, a serum galactomannan (Aspergillus) and a serum beta-D-glucan (Candida and Pneumocystis). Obtain an urgent high-resolution chest computed tomogram, looking for pulmonary nodules with the halo sign (early invasive aspergillosis) or the reversed-halo sign (mucormycosis) — a plain chest radiograph is insensitive in the neutropenic patient. Pursue bronchoalveolar-lavage galactomannan and, where feasible, biopsy histopathology for tissue invasion by hyphae. The principle is to investigate before, not instead of, empirical therapy. [2] [14]

Empirical and definitive therapy (3 marks). Start empirical antifungal therapy without delay — an echinocandin (caspofungin or micafungin) or liposomal amphotericin B, selected by the suspected organism and the local mould epidemiology; if invasive aspergillosis is confirmed, voriconazole becomes first-line, and if mucormycosis is confirmed, high-dose liposomal amphotericin B is the backbone. Give a minimum of two weeks of therapy after the first negative culture in candidaemia, maintain hydration and electrolytes (amphotericin nephrotoxicity), and arrange therapeutic drug monitoring for voriconazole or posaconazole given the interactions with chemotherapy and calcineurin inhibitors. [2] [14]

Source control, reversal of immunosuppression and prophylaxis (2 marks). Remove the central line if candidaemia is confirmed — line removal shortens the bacteraemia and reduces metastatic seeding. Reverse the immunosuppression where possible, and treat the underlying graft-versus-host disease or the haematological malignancy. For the next cycle, consider antifungal prophylaxis — fluconazole or caspofungin in acute myeloid leukaemia induction (the Fisher JAMA trial showed caspofungin reduced invasive fungal disease versus fluconazole), or posaconazole in graft-versus-host disease. The lesson is that host-tier recognition, empirical cover and source control together determine survival in this child. [1] [14]

SAQ 2 (10 marks)

A 5-year-old boy presents with a three-week history of an itchy, scaly, bald patch on his scalp, with occipital lymphadenopathy. His mother has been applying a topical steroid cream prescribed for her own eczema, which initially improved the itch but the patch has enlarged. On examination there is now a boggy, tender, purulent mass overlying the area. [12]

Question: (a) What is the diagnosis, and what is the name of the inflammatory variant now present? (b) Why did topical therapy fail, and what is the name of the error the mother made? (c) Outline the definitive management. (10 marks) [8]

Model answer

(a) The diagnosis and the inflammatory variant (3 marks). The diagnosis is tinea capitis — the commonest cause of hair loss in prepubertal children — caused by a dermatophyte (Trichophyton or Microsporum species) infecting the hair follicle and the keratin of the hair shaft. The scaling, the black-dot broken hairs, the occipital lymphadenopathy and the boggy, tender, purulent mass together mark the inflammatory variant known as a kerion. A kerion is a hypersensitivity reaction to the dermatophyte, not a bacterial abscess, and it must not be incised and drained. [12] [8]

(b) Why topical therapy failed, and the error (3 marks). Topical antifungal therapy fails in tinea capitis because the fungus lives in the hair follicle and the hair shaft, which topical agents cannot reach — the disease requires systemic (oral) therapy. The mother's error is the tinea-incognito trap: applying a topical steroid to an undiagnosed annular lesion. The steroid abolishes the scale and the itch (so the lesion "improves" symptomatically), masks the diagnosis, and lets the fungus spread unchecked. The safeguard is to confirm tinea with a skin scraping and potassium hydroxide preparation for hyphae, or a fungal culture, before reaching for a steroid. [8] [12]

(c) Definitive management (4 marks). Treat with an oral antifungal for six to eight weeks. The traditional first-line is oral griseofulvin; the Fleece meta-analysis found terbinafine at least as effective for Trichophyton species with a shorter course, while griseofulvin remains preferred for Microsporum infections. Add a selenium sulfide or ketoconazole shampoo to reduce contagious shedding of spores, and exclude the child from school until treatment has begun. The kerion is treated with the same oral antifungal — never incision and drainage — and a short course of oral prednisolone is sometimes added for severe inflammation, alongside the antifungal, to reduce scarring. Check household contacts for tinea, treat infected pets if an animal source is identified, and review at the end of therapy to confirm mycological cure. [8] [12]