Fatal invasive pulmonary aspergillosis due to Aspergillus pseudodeflectus in a liver transplant patient: first case report

Françoise Botterel Chartier


Background: Liver transplant recipients are a   population at risk for developing invasive aspergillosis and Aspergillus fumigatus  is the most common species. However, other non-fumigatusAspergillusspecies can be involved with reduced sensitivity to antifungal drugs. Accurate identification associated to antifungal susceptibility testing is essential for therapy adjustment. We report  a  case  of invasive pulmonary aspergillosis due to Aspergilluspseudodeflectusin  a    liver transplant  recipient. To  our knowledge, this is the first reported case of invasive aspergillosis due to this species. 

Case report: In May 2013, a   64 year-old woman with drug-induced fulminant hepatitis underwent livertransplantation in our  University Hospital (Créteil, France). Prophylactic treatment with  caspofungin was introduced due to aspergillosis risk factors consisting in    hemodialysis and fulminant hepatitis. Six weeks after transplantation, CT scan showed a right pulmonary opacity associated with an increase of galactomannan (index 5.4 (Nl<0,5, Platelia Aspergillus®, Biorad))andβ-D-glucan(236 pg/ml (Nl<80,Fungitell®, Cape Cod). Direct examination   of BAL showedAspergillus-like branching   hyphae. Caspofungin was then switched to voriconazole. Culture of BAL grew with several colonies of a white to brown filamentous  fungus with a    velvety appearance. Microscopic examination of the colonies showed Aspergillus  biseriate conidial heads with curved conidiophores. The  antifungal susceptibility tests (Etest®)   revealed low MICs to echinocandins (0,016 and 0,5 mg/L for micafungin and caspofungin respectively) and amphotericin B    (0,75 mg/L) but high MICs to azoles (4, 12 and 6   mg/L for voriconazole, itraconazole and posaconazole,  respectively). After these  results, voriconazole was switched to liposomal  amphotericin  B. The patient  died  one month after diagnosis from a   refractory septic shock with multiple organ failure. No autopsy had been performed. A molecular identification of isolate, based on partial β-tubulinand calmodulin genes, was performed. A  BLAST search in MycoBank revealed an  identity of 99.8%  to reference sequencesof A.   pseudodeflectusstrain CBS596.65 with a   query coverage of 99.9%. This species belongs to Aspergillussection Usti and is very close to Aspergillus calidoustus previously reported in human pathology.

Conclusions: Our case reports an invasive pulmonary aspergillosis in    a   liver transplant recipient due to a    species newly described in human pathology:A. pseudodeflectus.  This species has loweredsusceptibility to azoles.



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European Congress of Clinical Microbiology and Infectious Diseases
    • ECCMID 26th (2016)