A 59 year-old man was admitted with complaints of productive cough and dyspnea. He was healthy until approximately 2 months earlier when he experienced fever, chills and productive cough during a trip to the north of Iran. Non-massive hemoptysis occurred soon after initial presentation. His symptoms worsened despite outpatient management of pneumonia with ceftriaxone and azithromycin. He also developed night sweat and purulent sputum.
Due to progressive symptoms and significant weight loss as well as chest imaging findings (Figure 1), bronchoscopy was performed without remarkable findings. Due to antibiotic treatment failure, he had been treated with standard anti-tuberculosis regimen for 6 weeks in another center without any response.
He lived with his wife and three healthy children and worked as a manager of a service company. He reported smoking 3 cigarettes per day since 20 years ago and occasionally inhaled opiates. He was diabetic since 19 years ago controlled with oral medications. He was otherwise healthy. He did not recall any contact with birds and animals nor with chemical agents.
On admission, he was febrile (38.5 C oral temperature) and normotensive with a respiratory rate of 20 breaths/minute and oxygen saturation rate of 91% with ambient air.
Physical examination was normal except for pallor of conjunctiva.
Further investigations revealed normochromic normocytic anemia (hemoglobin 9.5 mg/dl), leukocytosis (12400 cells/mm3, polymorphonuclears: 76%, eosinophils: 4%), thrombocytosis (536,000/mm3), elevated erythrocyte sedimentation rate (130 mm/1st hr.), normal liver biochemistry and renal function tests. Urinalysis was normal. Antinuclear antibodies (ANA) and antineutrophil cytoplasmic antibodies (ANCA) were negative. Glycosylated hemoglobin (HbA1C) and fasting plasma glucose (FPG) were 6.9% and 115 mg/dl, respectively. Level of immunoglobulins and lymphocytes, flow cytometric analysis and nitroblue tetrazolium test as well as human immune deficiency virus serology were unremarkable. Moreover, scar of the bacille Calmette-Guerin (BCG) vaccine was evident.
Echocardiography was normal. Repeated bronchoscopy in our center revealed mucosal secretion without endobronchial lesion. Transbronchial lung biopsy as well as bronchoalveolar lavage specimens were negative for pathogenic bacteria, fungi and mycobacterial agents by smears, cultures and polymerase chain reaction.
Based on his progressive condition and negative investigations (Figure 2), CT-guided biopsy of the lung lesion was performed, which revealed alveolated lung parenchyma with interstitial thickening due to infiltration of lymphoplasma cells as well as some eosinophils and a few ill-defined hyaline septate hyphae. After a few days, white yellow colonies grew in Sabouraud dextrose agar. As observed microscopically, it was hyaline mold producing conidia in clusters compatible with Acremonium spp. The conidia were elongated and arranged in loose clusters in a crisscross formation at the tip of a long, slender, delicate conidiophore (Figures 3 and 4). Biochemical analysis confirmed the morphological diagnosis of the cultured microorganism to be Acremonium spp.
Itraconazole 200 mg twice daily was initiated and within a week, respiratory symptoms ameliorated and after a couple of weeks he was symptom-free and chest-X-ray was completely normal (Figure 5). The patient continued taking itraconazole for a period of 6 months.
Chest CT revealed alveolar consolidation and adjacent ground glass opacity in the right lower lobe.