Description

An 18-month-old girl presented with a history of choking episodes and nasal regurgitation of feeds for a month. In the past, she had recurrent episodes of diarrhoea with oral thrush, which were treated at a local healthcare facility with topical medications. She had been failing to thrive and gain age-appropriate motor and mental milestones. On examination, she was pale with tachypnoea, tachycardia and hypoxaemia. She had wasting (weight for height below third centile), generalised lymphadenopathy, bilateral crepitations and hepatosplenomegaly. Oral cavity examination showed a 1×1 cm perforation in the hard palate with an erythematous margin around it (figure 1). Laboratory investigations showed haemoglobin of 67 g/L, total leucocyte count of 5.95×10⁹/L, thrombocyte count of 87×10⁹/L and C reactive protein of 64 mg/L. She had hypoalbuminaemia with normal renal and liver function parameters. She was investigated for HIV infection, which was found to be positive with CD4+ T cell count of 195 cells/µL. Her parents were also later tested to be seropositive. A swab from perforated palatal ulcer showed the growth of Candida albicans, which was treated with intravenous amphotericin-B. Chest X-ray showed evidence of bilateral pneumonia and was initiated on broad-spectrum antibiotics, along with amphotericin-B and co-trimoxazole. According to the National AIDS Control Organisation guidelines, workup was being done to rule out opportunistic infections before starting antiretroviral therapy. Over the next week, however, respiratory illness progressed and she succumbed to the illness despite supportive care.

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Figure 1

The oral cavity of the child showing perforation of the hard palate.

Oral thrush in infancy and childhood must prompt evaluation of underlying immunodeficiency. In this poorly treated HIV-infected infant, Candida infection progressed and led to palatal perforation. Other causes of palatal perforation in infancy are infections (eg, leprosy, tuberculosis, syphilis and blastomycosis), autoimmune disease (eg, systemic lupus erythematosus and granulomatosis with polyangiitis), while in older children and adults, antineutrophilic cytoplasmic antibodies associated vasculitis, chronic rhinosinusitis and neoplasia are the frequent causes. Aetiologies previously described for palatal ulcers and perforation in adult patients with AIDS are Histoplasma, Candida,1 Mucor 2 and Toxoplasma.3

This case is unique as palatal perforation in childhood AIDS is an uncommon occurrence. The index patient had an aggressive locally invasive Candida disease. Oral Candida colonisation can progress and result in local tissue damage, oral ulcerations and perforation in immunocompromised patients, especially HIV-positive patients. Impaired local immunological factors like decreased salivary IgA levels, impairment of mucosal CD4 T cells, altered cytokine secretions and a shift to Th2 cytokine expression in saliva contribute to predisposition to candidal disease in HIV-infected patients.

This image report highlights the importance of oral cavity examination for palatal ulcer and perforation in children with immunodeficiency as it may alert the physician to prevent further grievous complication. Candidal perforation of the hard palate in HIV-positive children is uncommon and may lead to fatal aspiration pneumonia.