A 46-year-old Guinea-Bissau born male, living in Portugal for 16 years, was admitted to our institution because of vomiting, hiccups, weight loss (about 16 kg), occasional nocturnal sweating, and dry cough, lasting for 1 month. He had a past medical history of recurrent episodes of intestinal worm infection and excessive alcohol consumption (100-120 g/day). He was screened for tuberculosis due to prior contact with pulmonar tuberculosis. Laboratory blood tests were normal except for a high sedimentation rate (79 mmh). A bilateral bronchial reinforcement was observed on chest X-ray. Mediastinal enlarged lymph nodes and a nodular lesion at inferior left pulmonary lobe were noted on chest CT (computerized tomography) scan. A brain CT showed a small corticosubcortical ring-enhancing lesion in the right frontal lobe. He was diagnosed with HIV-1 infection (323/8,3% T-CD4 + lymphocytes/muL) and HBV chronic infection (AgHBs positive, Ac anti-HBc positive, and AgHBe negative).
Inspection revealed good general condition, with papular lesions scattered throughout the body. On brain MRI a single round lesion with 7 mm was seen, with perilesional oedema, suggesting tuberculoma (Figures 1(a)-1(b)).
Cerebrospinal fluid (CSF) cytochemical evaluation was normal. Bronchoscopy showed nonspecific inflammatory findings. Bacteriological and mycobacteriological (direct and cultural examination) analysis of respiratory products tested negative. Bronchial histology showed inflammatory infiltrate, with no granuloma or neoplastic tissue. Patient was discharged from hospital clinically stable, with no signs of infection.
One month later he manifested persistent deterioration of general condition, with vomiting, abdominal pain in the right upper quadrant, myalgias, and fever. Laboratory tests revealed leukocytosis, C-reactive protein 12,2 mg/dL, and sedimentation rate >120 mmh. On chest CT scan a bulky right adrenal gland mass was disclosed. Abdominal sepsis was considered and treatment with intravenous (IV) ceftriaxone (1 g bid) was empirically started. Blood, urine, and stool cultural exams were negative, as well as Schistosoma spp. and Taenia solium serology. He completed a 14-day cycle of antibiotic treatment with clinical and analytical improvement. He was also treated with oral fluconazole (200 mg id) during 14 days for esophageal candidiasis. One week after ceftriaxone suspension a worsening of headache and inaugural seizures were observed. MRI brain-scan presented multiple well-defined annular lesions. Nocardia versusfungal abscesses was hypothesized (Figures 1(c)-1(d)). Empirical treatment with IV ceftriaxone (2 g bid), liposomal B amphotericin (4 mg/Kg id), and valproic acid was started. Adrenal mass was punctured; culture of purulent material revealed Nocardia spp. Characterization of bacterial species and antimicrobial susceptibility testing were not possible, neither by microbiologic methods nor by protein chain reaction (the sample was deteriorated when it arrived at reference laboratory; in Portugal, characterization of Nocardia spp. and antimicrobial susceptibility testing are made at reference laboratory, National Health Institute, Dr. Ricardo Jorge). ACTH and cortisol were within normal limits. As skin nodules persisted, a skin biopsy was performed; histology revealed superficial acute folliculitis and no microorganisms were seen with special stains; microbiological study was missed. The diagnosis of disseminated nocardiosis with brain, adrenal, and possibly lung and skin involvement was assumed. Based on literature, IV treatment was started with cotrimoxazole 1440 mg 8/8 h, amikacin (dosage adjusted to the serum levels), and ceftriaxone (2 g bid); liposomal B amphotericin was stopped.
Two months later the patient showed clinical and laboratory improvement. His CD4 + cell count was then 207 (7,1%)/muL and viral load was 491640 cp/mL (genotypic resistance test was negative); HBV viral load was 777873717 UI/mL. An antiretroviral scheme with HBV activity was initiated with lopinavir/ritonavir (LPV/RTV) and tenofovir/emtricitabine (TDF/FTC). Four weeks later there was deterioration of renal function (GFR 69,2 mL/min). Amikacin was stopped. As renal failure went on worsening (GFR 37,7 mL/min), TDF/FTC was replaced by abacavir/lamivudine (ABC/3TC) and then cotrimoxazole was also stopped. Attempting to maintain a sulfonamide on the antibiotic regimen, dapsone was introduced. A significant transaminases elevation (AST 513 U/L; ALT 622 U/L with normal bilirubin) was interpreted as hepatotoxicity and dapsone was discontinued. The possibility of reactivation of HBV infection regarding the replacement of TDF/FTC for ABC/3TC was also considered. HBV viral load was still detectable (782 UI/mL), but at a lower level, so entecavir was added. Treatment with IV ceftriaxone (2 g bid) was kept for 1 year. Reassessment with Brain-MRI showed remaining lesions (Figures 1(e)-1(f)) and abdominal-CT scan showed resolution of adrenal abscess; HIV viral load was on the threshold of detectability (54 cp/mL) as well as HVB viral load (16 UI/mL).
Currently, six months after stopping ceftriaxone, the patient is asymptomatic and presents a good recovery of renal function (GFR 80 mL/min). He is under valproic acid (800 mg bid) and antiretrovirals, with virologic suppression of HIV and HBV and improvement of immune status (306/12% T-CD4 + lymphocytes/muL).