Pulmonary aspergillosis (PA) is a disease which usually occurs in immunocompromised hosts with an overall mortality around 60%.1 There have been some reports in the literature of invasive PA after pandemic influenza A (H1N1) infection.2,3 We present two cases of invasive aspergillosis after influenza A (H1N1) infection in patients without classical predisposing factors.
Case reportThe first patient is a 43-year old diabetic male, who was admitted to the intensive care unit (ICU) due to diabetic ketoacidosis, pneumococcal pneumonia and influenza A (H1N1). He received levofloxacin, ceftriaxone, oseltamivir and methylprednisolone (80mg/day/1wk). On day 12, fever and respiratory failure reappeared, invasive mechanical ventilation was required. The chest computed tomography (CT) scan showed a cavity of 6cm×5cm. Aspergillus fumigatus grew in a sputum sample and the galactomannan antigen (AGA) tested positive in BAL fluid. Intravenous voriconazole was started as well as corticosteroids due to respiratory distress syndrome. He was discharged after three months of hospitalization. The second case is a 56-year old diabetic man with alcoholic liver cirrhosis admitted to ICU due to alcoholic hepatitis, a methicillin sensitive Staphylococcus aureus bacteraemic pneumonia and influenza A (H1N1). He was started with oseltamivir, cloxacillin, meropenem and methylprednisolone (60mg/day/1 wk). On day 14, the patient developed right hemiparesis. Magnetic resonance imaging showed various parenchymatous lesions suggestive of brain abscesses. A chest CT had bilateral cavitated nodules. A. fumigatus grew in BAL fluid. Treatment was switched to voriconazole, anidulafungin and cloxacillin. The patient died on hospitalization day 21.
DiscussionWe present two cases of influenza A (H1N1) complicated by invasive aspergillosis. These patients had none of the risk factors traditionally related to IA but they fulfilled the criteria for proven Aspergillosis according to the EORT/MSG consensus group.4 The second patient developed a neurological deficit and it is difficult to determine if the cause was Aspergillus or S. aureus. However neurological impairment appeared when the bacteraemia had already cleared and the CT scan showed images suggestive of aspergillosis.
Influenza A (H1N1) virus infection may cause various immunological or respiratory tract disorders. Defects in cellular immunity, mucociliary transport as well as leukocyte dysfunction are among the described mechanisms.3 On the other hand, Influenza pneumonia may result in acute respiratory distress syndrome that requires high doses of corticosteroids.5 All of these can predispose to pulmonary aspergillosis.
Sporadic cases of invasive aspergillosis complicating influenza A have been reported since the 1990s.6 The question is whether infection by the current pandemic A (H1A1) virus is a stronger predisposing factor than infection by other strains. An affirmative answer is plausible based on the increased clinical and pathological morbidity associated with pandemic A (H1A1) virus infection, probably due to a broader range of susceptible respiratory cells.7 Invasive pulmonary aspergillosis should be considered as a possible complication in patients presenting with severe influenza A (H1A1) and who have received corticosteroids, even if they do not have classical immunocompromising conditions. Taking this into consideration may be helpful for an early diagnosis and treatment which could be valuable for a favourable outcome.
