A 56 year old male with no significant medical history presented with 40 Ib weight loss, fever, chills, night sweats, loss of appetite, fatigue and dry cough for the past few weeks. He was an active smoker, originally from Trinidad and came back from a 3 month trip to Trinidad 2 weeks ago. He worked at construction sites and denied any other travels or sick contacts. He was found to be tachycardic to 115 beats/min and febrile to 103.1  F. On physical exaimination he was cachectic with supraclavicular lymphadenopathy as well as diffuse wheezing and rales on lung auscultation.
Initial laboratory results demonstrated a white blood cell count of 4.3 K/uL, neutrophils: 88%, bands: 2%, lymphocytes: 6%, sodium: 129 mmol/L, potassium: 5.6 mmol/L, blood urea nitrogen: 22 mg/dL, creatinine: 1.23 mg/dL, alkaline phosphatase: 59, aspartate aminotransferase (AST): 87, alanine aminotransferase: 52, lactate dehydrogenase: 794 U/L.
Chest X-ray showed right upper lobe opacity with nodular opacities in the remainder of the lungs suggestive of miliary nodules. Chest CT scan showed right upper lobe opacities with innumerable sub centimeter and miliary pulmonary nodules in a random distribution, mediastinal, axillary and subclavicular lymphadenopathy, necrotic paratracheal and centrilobular emphysema (Fig. 1, Fig 2). The patient was admitted to rule out any malignancy, or infections such as Mycobacterium tuberculosis (TB).
Further work up revealed negative blood and urine culture, negative AFB smear of sputum, negative hepatitis serology but was positive HIV 1 antibody. HIV viral load was 33862 copies/mL with absolute CD4 count of 4 cells/uL. At this point the patient was started on prophylactic trimetoprim/sulfamethoaxazole, azithromycin and fluconazole for oral thrush.
Abdomen/Pelvis CT scan showed innumerable hypodense splenic lesions and calcifications of seminal vesicles which could be due to a granulomatous infection. Quantiferon gold was checked, which was indeterminate. Serum antigen for Cryptococcus was also negative. He then underwent bronchoscopy for definitive diagnosis.
During his stay the urine antigen for histoplasma was reported to be positive with a level >23 and the patient was started on amphotericin B with a presumptive diagnosis of histoplasmosis. Histoplasma capsulatum yeast antibody was negative <1:8 but the Histoplasma capsulatum mycelical antibody was positive to 1: 16. His symptoms improved gradually and he became afebrile.
Patient was discharged on voriconazole and his bronchial fungal culture eventually started growing a mold. He was also started on abacavir/lamivudine/dolutegravir for HIV management. Clinically, the patient continued to improve after discharge, gained weight and no longer had night sweats or cough. However, after 4 weeks, the mold in the BAL culture was identified as Acremonium species.
Although the sputum for AFB smear was negative, specimens grew MAI after two weeks but we did not consider MAI as the real pathogen and its significance is unclear.
The urine antigen for histoplasma became negative after 3 months of therapy and in view of his travel history to Trinidad; we consider this a co-infection with histoplasma and acremonium sp. leading to pneumonia.