A 50-year-old female was admitted with a paroxysmal boring pain in the left parietal and left frontal region for 9 months, accompanied by progressive vomiting and decreasing of visual acuity and proptosis in the left eye. Headache could be relieved by diclofenac sodium. Two months prior to presentation, her headache worsened extending to the whole left side of the face, accompanied by numbness. No light perception or reflex was detected in the left eye. Horizontal movement was limited in the left eye. Pre-operative CT showed a 29 × 20 mm isodense lesion with heterogeneously enhancement in the region of the left cavernous sinus, left orbital apex, left optic nerve canal, and sphenoid sinus. Bone destruction could be seen in the left wall of the sphenoid sinus. The optic nerve could not be distinguished from the lesion (Fig. a). MRI showed a 21 × 26 mm patchy lesion that was isointense on T1WI and hyperintense on T2WI in the left cavernous sinus region (Fig. b, c). Enhanced-MRI showed noticeable enhancement of the lesion. The lesion was closely related to the dura mater and extended to the sphenoid sinus and optic apex, partly surrounding the left internal carotid artery (Fig. d). MRA suggested stenosis in the cavernous segment of the left internal carotid artery and A1 segment of the left anterior cerebral artery. The patient underwent partial mass excision via a pterional craniotomy due to its close attachment to the ophthalmic branch and maxillary branch of the trigeminal nerve. The lesion was partly fibrotic and partly a milk-white viscous substance. A biopsy was performed immediately and histopathologic examination revealed Aspergillus species (Fig. e). The patient was administered voriconazole after surgery. Post-operative images indicated the resection of the mass (Fig. f). Examination after a follow-up of 15 months showed a complete resolution of the headache. Her vision of the left eye was not regained.
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.