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.
A 64-year-old male had experienced a paroxysmal pain in the frontal region and left nose radiating to the occipital region for 7 months. The patient also reported progressive paresthesia on the left cheek and rapidly decreasing visual acuity in the left eye. Neurological examination revealed a left-sided ptosis as the only new finding. Interestingly, body temperature (axillary) fluctuated between 36.1 °C and 38.4 °C. The patient denied a history of other diseases. Physical examination showed no light perception or reflex was detected in the left eye. His pupils were 3 mm on the right and 4 mm on the left. CT showed an isodense lesion in the region of the left cavernous sinus, left orbital apex, left optic nerve canal, and sphenoid sinus. Bone destruction was seen in the left wall of the sphenoid sinus (Fig. a). MRI showed a 33 × 16 mm isointense lesion in both T1WI and T2WI of the left optic canal region and extending into the orbit. Enhanced-MRI showed ring enhancement of the lesion. Lesions with hyperintense T2-weighted signal were seen in paranasal sinuses (Fig. b–d). The patient was self-treated with anti-infectious medication but his headache increased in intensity, frequency, and duration. The patient underwent mass excision of the mass via pterional craniotomy. Cream-like liquid amidst a gray growth was observed in the left cavernous sinus. A biopsy was performed immediately, and histopathologic examination revealed an Aspergillus species (Fig. e). Post-operative images indicated the resection of mass (Fig. f). The patient received voriconazole after surgery. However, he was lost to follow-up.