A case of invasive pulmonary aspergillosis caused by Aspergillus terreus is described. The diagnosis was based on demonstration of branched septate hyphae in a sputum specimen and isolation of the fungus in culture. The diagnosis was further supported by detection of A. terreusspecific DNA, galactomannan (GM) and (1A3)-b-D-glucan (BDG) in consecutive serum specimens. The patient was treated for about 10 weeks with voriconazole. The decreasing levels of GM and BDG in serum samples were accompanied by symptomatic and radiological improvement. The report highlights the value of surrogate markers in the diagnosis and for monitoring the course of invasive aspergillosis during therapy.
IntroductionInvasive pulmonary aspergillosis (IPA) remains a significant cause of morbidity and mortality in immunocompromised patients (Sherif & Segal, 2010). Timely and accurate diagnosis is essential but remains challenging because of non-specific clinical and radiological findings. An important impediment for timely diagnosis is the low yield of positive cultures from respiratory specimens. Furthermore, the positive cultures may not always be indicative of Aspergillus infection (Vandewoude et al., 2006). To overcome these limitations, attempts have been made to develop alternative strategies for early and specific diagnosis (Ostrosky-Zeichner, 2008). Although the majority of IPA cases are caused by Aspergillus fumigatus, Aspergillus terreus has also emerged recently as a significant respiratory pathogen in some tertiary care centres (Baddley et al., 2003;Hachem et al., 2004;Steinbach et al., 2004; Lass-Flörl et al., 2005;Blum et al., 2008). About 85 % of the isolates of A. terreus exhibit an MIC of .1 mg ml 21 for amphotericin B, and thus may be refractory to treatment with this drug (Lass-Flörl et al., 2009). This case report highlights the value of detection of A. terreus-specific DNA along with galactomannan (GM) and (1A3)-b-D-glucan (BDG) in sequential serum samples as an adjunct to diagnosis of A. terreus infection and for monitoring the course of the disease during treatment with antifungal agents. , leading to suspicion of acute lymphoblastic leukaemia (ALL). The diagnosis of ALL was subsequently confirmed by bone marrow examination. Induction chemotherapy as per the UK-MRC-ALL-2003 protocol was started, followed by consolidation and maintenance chemotherapy regimens. While on maintenance therapy, he developed his first haematological relapse in January 2009 with complex cytogenetics along with positive Philadelphia chromosome. After necessary supportive therapy, he was started on induction chemotherapy with vincristine, epirubacin, dexamethasone, asparaginase, intrathecal Cytosar (cytarabine) and intrathecal methotrexate as per the UK-MRC bone marrow relapse protocol along with Gleevec (imatinib mesylate). About 10 days later, he developed Klebsiella pneumoniae septicaemia, pneumonia and signs of disseminated intravascular coagulopathy. With intensive supportive therapy, his condition improved. However, he continued to rema...