A 69-year-old male was admitted with a progressive frontal paroxysmal headache accompanied with mild vomiting, diplopia, and visual disturbance for 1 month, without fever. Visual acuity was 0.6 in the left eye and 0.9 in the right eye without visual field loss. Other neurologic and clinical findings were normal. He was healthy other than a 10-year history of well-controlled hypertension and coronary heart disease. The patient reported no history of fungal infection or a history of contact with unusual infectious sources. CT scan showed a mass in the sphenoid sinus and clival region. Bone destruction was observed in both regions (Fig. a). MRI showed a hypointense signal on T2-weighted images (T2WI) in the lesions and an isointense signal on T1 weighted images (T2WI) with heterogeneous gadolinium-enhancement in the sphenoid sinus, both cavernous sinuses, bilateral ethmoid sinuses, and maxillary sinus (Fig. b–d). This patient underwent trans-sphenoidal lesion debridement. Purulence was observed during the operation. A biopsy was performed immediately and histopathology examination revealed Aspergillus species (Fig. e). The patient was administered fluconazole after surgery. Post-operative neurological examination showed obvious improvement of headache, vomiting, vision, and diplopia. Post-operative images indicated the resection of the mass (Fig. f). Examination after a follow-up period of 24 months showed no clinical symptoms, and no additional therapy was required.
A 59-year-old male having HIV positive illness for around 10 years, without any documented evidence of adhering to specific antiretroviral therapy regimen, presented to our hospital with history of low-grade fever, reduced appetite, and weight loss over 2 months followed by headache for about 2 weeks with recent worsening in the form of development of left-sided focal seizure with secondary generalization followed by altered sensorium for 3 days. He was started on empirical antitubercular medicines for last 2 weeks by a private practitioner before presenting to us. On presentation, he was febrile and drowsy. He had left hemiparesis with generalized brisk reflexes, extensor plantar response, and positive meningeal signs. Other systemic examination was unremarkable. A diagnosis of chronic meningitis in an immunocompromised individual was considered. Chronic meningitis in an immunocompromised patient has multiple differentials as enlisted in .\nOn investigations, he had pancytopenia (hemoglobin 6.8 g/dl, total leukocyte counts 3100/mm3, absolute neutrophil counts 2200/mm3, platelet counts 62,000/mm3) with normal glucose, electrolytes, and renal and hepatic functions. His chest X-ray showed right middle zone and left upper zone consolidation. Radiological differential diagnoses of this type of consolidation are bacterial pneumonia, tuberculosis, atypical mycobacterial infection, fungal infection, and lymphomatous or other neoplasm. He needed a CECT thorax and bronchoscopy-guided biopsy was advised but could not be done due to financial constraints and because the relatives declined any invasive procedure. His CECT head was normal []. CSF was acellular with normal glucose and protein level. CSF Gram stain, acid-fast bacillus stain, potassium hydroxide mount, India ink and cryptococcal antigen tests, and cytology for malignant cells were negative. CSF mycobacterial and fungal culture was also sent at the same time. As his focal deficits were not explained by a normal CECT head, magnetic resonance imaging (MRI) brain was done which revealed small, fairly defined, multiple altered signal intensity areas in the posterior aspect of right temporal lobe, posterolateral aspects of both the occipital lobes and anteroinferior portion of right frontal lobe on the gray-white matter junction, showing blooming on gradient images and peripheral enhancement on contrast-enhanced study associated with minimal to mild surrounding edema with normal MR angiogram, suggestive of hemorrhagic infarcts secondary to vasculitis. A differential diagnosis of this imaging feature in an immunocompromised is enumerated in .\nHe was treated with broad-spectrum antibiotics, empirical antitubercular drugs, antiepileptic drugs, and other supportive measures without any significant clinical improvement or deterioration. His toxoplasma antibodies were negative. His blood sample was sent for CD4 count analysis, but we could not get countable CD4 cells on flow cytometry despite doing the test twice in two different laboratories. The method used for detection of CD4 cells in flow cytometry was pan-leukocyte (CD45+) gating strategy by single platform technique. To get final diagnosis, CT scan chest, bronchoscopy, galactomannan test, and brain biopsy were considered but could not be done due to financial constraints. Considering febrile encephalopathy in a patient with HIV, febrile neutropenia and no response to 2 weeks of antibiotics and antitubercular drugs given before coming to our hospital, empiric broad-spectrum antibiotics in the form of meropenem, vancomycin with voriconazole and amphotericin B were started. In developing countries like India, upper lobe consolidation with clinical spectrum of chronic meningitis in immunocompromised individuals like HIV, tuberculosis remains one of the important differential diagnoses. Hence, antitubercular therapy was continued in his case due to high index of suspicion, which was already started 2 weeks before his presenting to us, pending reports of sputum and blood culture. Despite the above therapy for 4 days of hospitalization, there was no major improvement in his condition. Due to financial and social reasons, patient took discharge against medical advice 4 days after hospitalization. Due to our keen interest in the condition of the patient as well as the atypical MRI brain and CSF findings, we continued with our efforts to find the cause of his condition by serial observing his blood and CSF cultures. After 10 days, his CSF culture showed growth of A. niger. We got aware of his death on following up later with the family.