Meet the expert: microbiology case presentation

Abstract

A 63-year-old man of Cambodian descent presented to emergency department with history of fever, weight loss and loss of appetite, and right hypochondrial pain. He had been living in Australia for the last 17 years. He had a history of hypertension, hyperlipidaemia and tuberculosis (treatment details are uncertain). He also had a history of unspecified liver disease diagnosed 30 years ago. He was an ex-smoker and non-drinker. He had presented to the emergency department three times during 3 months prior to this admission, for colicky abdominal pain, followed by syncope and diarrhoea, with moderately abnormal liver function tests. ERCP arranged after one such admission detected choledocholithiasis. Two months prior to this admission he had a flu-like illness which was treated with Ostalmivir. Since then he had a persistent non-productive cough, orthopnoea, fever and anorexia and significant weight loss. On admission he was tachypnoeic, and tachycardic and had a fever of 38.3°C. Oxygen saturation was 94%. The abdomen was soft and had generalised tenderness. The rest of the examination was unremarkable. The white cell count was 46109/L, neutrophils 2.46109/L, and lymphocytes 0.4 6109/L. C-reactive protein was 29 and ESR was 140. Liver function tests were elevated with ALT 94 U/L, AST 365 U/L, ALP 410 U/L H and GGT 640 U/L. Bilateral opacities with areas of consolidation were seen in chest X-ray. CT of the chest showed a collapsed right upper lobe of the lung. Ceftriaxone was started empirically for likely community acquired pneumonia. Blood culture, sputum culture, direct ZN smears, mycobacterial cultures and TB PCR performed on admission were negative. HIV serology was repeatedly negative; serology for hepatitis B and C was negative. A bronchoalveolar lavage sample obtained in the second week of admission was positive for Pneumocystis jiroveci by direct fluorescent antigen test and by PCR and treatment with cotrimoxazole was commenced. As his immune status was further investigated peripheral blood WCC was 3.4 6109/L, lymphocytes 0.8 6 109/L, with absolute CD4 count of 50 with unaltered CD4:CD8 ratio. His IgG, IgA, and IgM levels were elevated. HTLV serology was negative. Despite treatment, his respiratory function further deteriorated and he was transferred to ICU and ventilated. Chest X-ray progressively worsened with new bilateral infiltrates, WCC and CRP increased up to 10.56109/L, and 185, respectively. Piperacillin tazobactam was commenced to broaden antifbacterial cover. Bronchoalveolar lavage and sputum sampled during the second week grew Scedosporium apiospermum sensitive to voriconazole MIC 0.05 mg/L. Intravenous voriconazole was commenced. At this point he was further investigated for the other opportunistic infections associated CD4 lymphopenia but none were detected. Even though bone marrow biopsy and liver biopsy was sought repeatedly, he remained too unwell for them. He continued to deteriorate and developed acute respiratory distress syndrome, liver failure, haemodynamic disturbances, thrombocytopenia and renal failure. A course of prednisolone and hydrocortisone was commenced. Voriconazole dose was reduced due to concerns regarding drug induced hepatotoxicity. Despite that his liver function remained abnormal and he was too unwell to undergo liver biopsy. Endotracheal aspirate became negative for Pneumocystis but continued to grow Scedosporium. After this initial stormy course he started to show progressive clinical improvement. At the moment he has completed 8 weeks of voriconazole. This patient has been a diagnostic dilemma as we were uncertain wheather he had pneumonia due to Scedosporium or Pneumocystis jiroveci. As he was too unwell to undergo liver biopsy we could not confirm our clinical suspicion as to whether he had disseminated Scedosporium including the liver. To date the aetiology and nature of his immune suppression has remained a mystery. Management of this patient has been hard as Scedosporium has been sensitive only to voriconazole, making it the only therapeutic option. When his liver function was worsening we did not know whether it was voriconazole induced or due to fungal infiltration of the liver or another unidentified cause. Furthermore, we were uncertain as to whether we should continue voriconazole to prevent the patient from dying from possible scedosporiasis or whether we should cease it to avoid liver failure.