Case Reports: Tuesday, October 25, 2011 |

Invasive Aspergillosis in H1N1 Influenza A Pneumonia FREE TO VIEW

Peter Law, MD; Michael Gelfand, MD; Wael Nasser, MD; Mohammad Shokouh-Amiri, MD; Alan Boom, MD; Jose Yataco, MD
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University of Tennessee Health Science Center, Memphis, TN

Chest. 2011;140(4_MeetingAbstracts):103A. doi:10.1378/chest.1085959
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INTRODUCTION: In March 2009, a novel swine-origin influenza A virus (H1N1) was discovered in Mexico, and one month later, two cases were identified in California. The WHO declared a pandemic from June 2009 to August 2010. The CDC estimated 61 million cases; 274,000 hospitalizations; and 12,470 deaths in the United States. We report a case of invasive aspergillosis (IA) in a patient with H1N1 influenza A.

CASE PRESENTATION: A 31-year-old man without medical history presented with dizziness and syncope. He reported fevers, productive cough, dyspnea, and myalgias for four days. On exam, he was afebrile, normotensive, tachycardic 107 beats/min, tachypneic 24 breaths/min, oxygen saturation 92% on room air. BMI 29 kg/m2. Physical exam was unremarkable except bibasilar crackles. Laboratory values were as follows: carbon dioxide 20 mmol/L, creatinine 1.5 mg/dL, white-blood-cell count 4,100/mL with 87% neutrophils, hemoglobin 12.3 g/dL, platelet count 211,000/mL. HIV was negative. Arterial blood gas on room air was pH 7.39, PaCO2 29 mmHg, PaO2 52 mmHg, oxygen saturation 87%. Chest x-ray showed bibasilar atelectasis and left pleural effusion. The patient was admitted for pneumonia and treated with ceftriaxone, azithromycin, and oseltamivir. H1N1 was diagnosed by serum PCR. He became increasingly tachypneic, PaO2/FiO2 ratio fell to 111, and he was intubated. Chest x-ray showed worsening bilateral infiltrates. Antibiotics were changed to linezolid, piperacillin-tazobactam, and moxifloxacin. He developed septic shock, acute respiratory distress syndrome (ARDS), and acute kidney injury requiring hemodialysis. He received vasopressors, corticosteroids, and low-tidal volume and prone ventilation. Bronchoalveolar lavage (BAL) fluid grew resistant P. aeruginosa, and antibiotics were changed to imipenem-cilastatin, tobramycin, and ciprofloxacin. On hospital day 16, chest CT showed diffuse interstitial and alveolar infiltrates and no pulmonary embolus. On hospital day 19, the patient developed massive hemoptysis, cardiac arrest, and expired.

DISCUSSION: Autopsy revealed alveoli collapse and extensive organizing diffuse alveolar damage with hemorrhage. Suspected causes of death were bacterial coinfection, ARDS, and alveolar hemorrhage. A CDC report found coinfection in 29% of fatal H1N1 cases. Ventilator-associated Pseudomonas likely exacerbated his severe viral pneumonia. Additionally, reported H1N1 histopathological studies (1) showed diffuse alveolar damage, necrotizing bronchiolitis, alveolar hemorrhage, secondary infection, and focal alveolar necrosis. Alveolar hemorrhage is a known complication of influenza and has been described in H1N1 infection.(2) In our patient, section of the right middle lobe revealed necrosis with Aspergillus invading a large blood vessel. Blood and BAL cultures did not show fungal growth, so diagnosis of IA was made by histology only. Respiratory cultures have 30% sensitivity for aspergillosis, while galactomannan in BAL has 88% sensitivity and 87% specificity. Invasive aspergillosis seems the predominant cause of death in our patient and has been reported (3) during the H1N1 pandemic as well as in viral pneumonias including the severe acute respiratory syndrome outbreak. IA typically occurs in immunocompromised patients and can cause pulmonary hemorrhage. The mechanism and propensity of Aspergillus angioinvasion have been documented. For glucocorticoid-treated, non-neutropenic patients, there is more extensive necrosis, less angioinvasion, and lower fungal burden suggestive of an inflammation-driven pathology. Influenza itself may induce a glucocorticoid compromise of innate host defense, while H1N1 may cause immunodysregulation. For refractory shock, our patient received hydrocortisone 200 mg I.V. in divided doses which was tapered until his arrest 17 days later. Our non-neutropenic patient received caspofungin empirically, and he expired three days later. Caspofungin is approved for the treatment of IA in patients who cannot tolerate or are refractory to standard therapy. In one trial, caspofungin had an overall complete and partial response rate of 45%. Some trials and case reports note breakthrough rates between 1 and 13%.

CONCLUSIONS: We report a fatal case of invasive aspergillosis in a previously healthy man infected with H1N1 influenza. Given the rapid symptom-onset and deterioration, the clinician must be vigilant in promptly diagnosing and treating influenza-like illness. Antibiotics for bacterial coinfection and antifungal therapy should be considered. Finally, corticosteroids in patients with influenza may pose a risk for invasive fungal infections.

Reference #1 Mauad et al. Lung pathology in fatal novel human influenza A (H1N1) infections. Am J Respir Care Med Vol 181. pp 72-79, 2010.

Reference #2 Gilbert et al. Novel H1N1 influenza A viral infection complicated by alveolar hemorrhage. Respir Care. 2010 May;55(5):623-5.

Reference #3 Lat et al. Invasive aspergillosis after pandemic (H1N1) 2009. Emerg Infect Dis. 2010 Jun;16(6):971-3.

DISCLOSURE: The following authors have nothing to disclose: Peter Law, Michael Gelfand, Wael Nasser, Mohammad Shokouh-Amiri, Alan Boom, Jose Yataco

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