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Editor,—A 26 year old, previously fit and well Afro-Caribbean man, presented with a 5 week history of a “flu-like” illness. Initially treated with antibiotics, the patient deteriorated, developing a cough, haemoptysis, progressive breathlessness, intermittent blurring of vision, and a rash. Investigations indicated he was HIV positive.
On examination, though orientated, he looked unwell and was febrile. He had an extensive papulonodular rash on his face, trunk, and limbs. Many of these lesions were centrally umbilicated with areas of associated haemorrhage (fig 1). Respiratory examination revealed decreased air entry in the right chest and coarse inspiratory bi-basal crackles. Funduscopy demonstrated retinal pallor, congested optic discs, and bilateral soft exudates associated with haemorrhages. He had no focal neurological signs.
Full blood count, urea and electrolytes, and clotting screen were normal. Arterial blood gases on 35% oxygen revealed a pH of 7.44, Pao2 9.4 kPa, Paco2 2.7 kPa, base excess −8.2. Chest radiograph demonstrated bilateral infiltrates with a right sided pleural effusion.
The patient had been treated for a presumed diagnosis of severe community acquired pneumonia and/or Pneumocystis carinii pneumonia plus Molluscum contagiosum of the skin. In view of the patient's clinical findings, additional therapy was commenced with anticytomegalovirus (CMV) and anticryptococcal agents.
Urgent blood and pleural fluid cryptococcal reactive antigen testing (CRAG) were strongly positive at a titre of >1:2048. Blood CMV PCR was negative. The patient could not tolerate a lumbar puncture. Despite initial improvement, he developed progressive respiratory failure and died. The post mortem revealed disseminated cryptococcal disease with involvement of brain, skin, lung, heart, liver, spleen, kidneys, pancreas, thyroid, bowel, adrenal glands, and testes.
Disseminated cryptococcal infection has a >80% mortality when associated with respiratory failure.1 Cutaneous lesions occur in 5–10% of cases.2 These include subcutaneous nodules, ulcers, and cellulitis. These may mimic pyoderma gangrenosum, Kaposi's sarcoma, and Molluscum contagiosum. Clinically, cryptococcal disease may be distinguished from Molluscum contagiosum by a more acute onset of numerous papules, which often have a tiny central haemorrhagic crust.3
Our patient was unwell and had skin lesions that were too extensive for simple Molluscum contagiosum. While Pneumocystis carinii remains the commonest cause of severe respiratory disease in HIV infected individuals not on chemoprophylaxis, pleural effusions are rare in this condition. CMV would be unlikely to produce such acute systemic illness by itself. Hence, cryptococcal disease was a reasonable working diagnosis that required urgent treatment.4 A recent report has highlighted diagnostic delay as a major factor contributing to its high associated mortality.1 The CRAG test provides a rapid method of confirming the diagnosis of cryptococcosis.5 It will be positive in blood in infected individuals in up to 95% of cases. The result can then be verified on culture of suitable body fluids.
We recommend early consideration of disseminated cryptococcosis in HIV positive patients with respiratory features suggestive of pneumonia or pleural effusion and atypical skin lesions. The use of rapid diagnostic tests may help to improve the poor outcome in this patient population.
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