A 54-year-old male presented to us with a history of headache for the past 3 months, which had gradually increased in severity over this period. It was associated with giddiness and blurring of vision. At the time of onset of the symptoms, he had visited his general practitioner, who had then done a full blood count, which had shown a low white cell count of 3.0/mm3(normal range being 4-11/mm3) with a low lymphocyte count of 0.6/mm3(normal range being 1-4/mm3). No further testing was done. This was diagnosed as a viral prodrome, and he was prescribed symptomatic therapy, but the symptoms still persisted for the next 2 and a half months. Fifteen days before presentation to our center, he was admitted to another hospital with severe headache, which lasted for 1 hour, which he described as an "unbearable headache." Magnetic resonance imaging (MRI) brain was done at that hospital, which was normal. Unable to find a cause at that hospital, and with no improvement in his symptoms, he was transferred to our hospital for further evaluation.
He did not have a history of fever, vomiting, weight loss, rash, or a loss of appetite. There was no episode of loss of consciousness, seizure activity, motor weakness, or bowel or bladder involvement. He did not reveal any history of trauma or of any high-risk sexual behavior, drug abuse, or blood transfusion. He gave a history of pulmonary tuberculosis 25 years back, for which received treatment for 9 months. He was a known hypertensive for 3 years, which was well controlled with medications. His pulse rate, blood pressure, and temperature were normal. Neurological examination did not reveal any focal deficit. The rest of the systemic examination was unremarkable. MRI brain showed meningeal enhancement in bilateral cerebellar regions [Figure 1] with leptomeningeal enhancement in the right temporal [Figure 2] and right temporo-occipital [Figure 3] regions. Full blood count revealed a low white cell count of 2.5/mm3(normal range being 4-11/mm3) with a low lymphocyte count of 0.5/mm3(normal range being 1-4/mm3). Lumbar puncture was done, and the cerebrospinal fluid (CSF) analysis revealed 980 cells (normally < 5 cells/mm3), with a predominance of lymphocytes (60%), glucose was 32 mg/dL (normal is 25-35 mg/dL), and protein was 27 mg/dL (normal is 18-45 mg/dL). CSF polymerase chain reaction (PCR) for tuberculosis was negative. CSF examination for cyptococcal antigen was positive. CSF for viral PCR (herpes simplex virus, varicella-zoster virus [VZV], cytomegalovirus [CMV], and John Cunningham [JC] virus was negative. Lymphocyte flow cytometry was done, and the subset estimation showed low levels of CD4 T-cells, which were at 16% (normal range is above 25%), absolute CD4 count was 200/mm3(normally between 500 and 1500/mm3), whereas CD8 cell count was normal (29%). We further investigated to look for any cause for his immunocompromised state. ELISA for HIV-1 and HIV-2 and PCR for HIV-1 and HIV-2 were negative. Serum PCR for CMV, Epstein-Barr virus, VZV, and parvovirus B19 were negative. Serum PCR for human T-cell lymphotropic virus 1 and 2 was negative. Immunoglobulin levels were normal. Autoimmune workup including antinuclear antibody, anti-dsDNA, extractable nuclear antigens, and antiphospholipid antibodies was negative. Complement levels were normal. The bone marrow examination was normal. There was no evidence of aplasia or myelodysplasia. Once the diagnosis of cryptococcal meningitis was made, the first and foremost differential was HIV infection, but that was ruled out. Severe combined immunodeficiency was another possibility. However, in this condition, immunodeficiency-related infections often start manifesting in childhood and early adulthood. In our patient, cryptococcal meningitis occurred at the age of 54 years. The detailed workup ruled out any autoimmune conditions that could have caused such a clinical picture. He was treated with liposomal amphotericin-B. Flucytosine could not be given in view of its unavailability. He had an episode of generalized tonic-clonic seizures during his hospitalization with the compromise of his airways, and hence he was put on mechanical ventilatory support. His neurological condition progressively deteriorated during the course of his hospitalization, along with hemodynamic instability. He was thus put on inotropic support. Unfortunately, there was no improvement, and he passed away with worsening shock.