A 68-year-old male patient, presented to us with history of progressive loss of vision in the right eye and persistent right-sided retro-orbital pain and headache for 2 months which started immediately after the cataract surgery of the right eye (Phacoemulsification under topical anaesthesia using lignocaine 2% eye drops) with intra-ocular lens implantation. The pre-operative visual acuity was 6/60 in the right eye and 1/60 in the left eye. The patient reported initial improvement in vision, but it was followed by rapid deterioration, for which he attended his ophthalmologist, who diagnosed it as a case of optic neuritis, as a complication of cataract surgery. He was started on oral methyl-prednisolone. There was no improvement in the symptoms and then the patient attended our out-patient department clinic. He had no history of diplopia, redness, watering, proptosis or floaters. There was no history of trauma or symptoms suggestive of meningitis or encephalitis. There was no history of cough, dyspnoea or haemoptysis.\nOn examination, the patient was conscious and oriented, with non-tender paranasal sinuses and bilaterally palpable temporal arteries. Neurological examination revealed complete right-sided ophthalmoplegia with mydriasis, hypoalgesia and diminished right corneal reflex. Ophthalmological examination revealed right and left visual acuity of 3/60 and 1/60, respectively. Right pupil was dilated and fixed, whereas the left pupil was reactive to light. Fundoscopy revealed oedema and pallor of right disc, whereas the left disc was normal.\nLaboratory investigations revealed haemoglobin of 12 g/dl (Normal:12–16 g/dl) and fasting blood sugar of 105 mg/dl (normal: 60–100 mg/dl). Serum angiotensin-converting enzyme and thyroid function tests were within their normal limits. Serum immuno-inflammatory markers were within normal limits. He was negative for HIV, hepatitis B and C and had normal levels of cluster of differentiation (CD)-4 and CD-8.\nThe first T1-weighted axial magnetic resonance imaging (MRI) of brain (Fig. A) showed minimal soft tissue at the right orbital apex which was abutting the right-sided optic nerve suggestive of OAS. In view of clinical examination and MRI report, a presumptive diagnosis of pseudotumor (inflammatory versus infectious aetiology) was made and the patient was started on ceftriaxone and vancomycin in meningitis dosage with tapering course of dexamethasone. Even after 10 days of this treatment, there was no improvement in symptoms. Instead, the visual acuity in the right eye decreased to perception of light only with development of right-sided proptosis.\nRepeat T1-weighted axial MRI scan of head (Fig. B) revealed an increase in the size of the mass with bony erosion of sphenoid sinus which was suggestive of infectious aetiology. Biopsy of the lesion was deferred in view of the proximity of the mass to the major neuro-vascular bundle in the orbital apex and cavernous sinus and the major risk involved in the procedure relative to its yield. The patient was empirically started on liposomal amphotericin-B in view of possibility of fungal infection.\nEven after 21 days of liposomal amphotericin-B, there was further increase in proptosis and the visual acuity in right eye diminished to ‘No light perception’ with increased intensity of peri-orbital and retro-orbital pain. A repeat T1-weighted axial MRI of head (Fig. C) revealed further destruction of the local anatomic sites with increase in mass lesion to 19 × 16 × 14 mm. Serum galactomannan antigen level was 0.5 index (Borderline).\nBy virtue of its size and extension, the mass was now accessible for biopsy. Under general anaesthesia, endoscopic navigation-assisted biopsy was taken from seven different sites. Review of histological specimen from posterior ethmoid mucosa, posterior ethmoid tissue near optic nerve and sphenoid sinus mucosa (Fig. ) showed fungal hyphae (Fig. A and B) morphologically compatible with Aspergillus species.\nHe was subsequently started on injectible voriconazole which was continued for 10 days. Now the patient showed dramatic improvement in his headache which resolved completely in 5 more days. Right eye movements began. The patient was then discharged on oral voriconazole.\nThe patient was completely free of symptoms with completely resolved ophthalmoplegia with repeat T2-weighted axial MRI revealing decrease in the size of the mass (Fig. D), after 7 months of oral voriconazole. But unfortunately, the patient had no recovery of vision in his right eye.
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.