Most deaths in tuberculous meningitis occur in the early part of the illness. We assessed the determinants of early deaths, occurring within 2 months of intensive therapy. We prospectively included consecutive newly diagnosed adults with HIV-negative tuberculous meningitis. Patients were given WHO-recommended antituberculosis treatment and were followed up for 9 months. We enrolled 152 patients. A total of 26 deaths were recorded during 2 months. The logistic regression analysis revealed that papilledema (P = 0.029, odds ratio (OR) = 4.8 [1.2–19.8]), increasing age (P = 0.001, OR = 1.07 [1.03–1.1]), stage-III disease (Glasgow coma scale score ≤ 10; P = 0.01, OR = 4.2 [1.4–12.3]), and hydrocephalus (P = 0.003, OR = 8.4 [2.1–33.6]) were independently associated with death. In addition, cerebral infarcts (P = 0.012, OR = 5.6 [1.5–21.3]), paraparesis (P = 0.004, OR = 8.8 [2.02–38.1]), and age (P = 0.005, OR = 1.05 [1.02–1.09]) were associated with poor functional outcome. In conclusion, disease severity predicts early deaths in tuberculous meningitis.

Subacute sclerosing panencephalitis (SSPE) is still a common disease in India which is characterized by a progressive mental decline, myoclonus, periodic encephalographic abnormalities, and raised anti-measles antibody titter in the cerebrospinal fluid. Acute fulminant SSPE is characterized by a rapid course of disease culminating in death, within 6 months. We report of a 10-year-old boy, who came with a 14-day history of continuous involuntary jerky movements of the left half of the body, including the head. There was a highly increased anti-measles IgG antibody titer, both in the cerebrospinal fluid and serum. We conclude that acute rapidly progressive SSPE can present as acute encephalitis syndrome.

Pediatric neurobrucellosis represents a common anthropozoonosis in endemic areas but only anecdotal reports are available till date. Using appropriate search terms in the database platforms of MEDLINE, SCOPUS and Web of Sciences, we performed a systematic review of all the cases of pediatric neurobrucellosis published in the medical literature till date, in the light of a case report. The protocol was registered under PROSPERO (CRD42022333907). Our search strategy yielded 187 citations of which 51 citations were included. A total of 119 cases were reviewed. Of these cases, eight of them had insufficient data. The most common presentation was meningitis with or without encephalitis (n = 79, 71.2%). A high prevalence of cranial neuropathies (n = 22, 20.7%) was observed in the pediatric population in which abducens palsy was the most common (n = 9, 8.1%). Diagnosis was based on multimodal investigations including standard agglutination test (n = 44, 39.6%), Rose Bengal test (n = 37, 33.3%), blood culture (n = 23, 20.7%), serology (n = 20, 18.0%) and cerebrospinal fluid (CSF) culture (n = 11, 9.9%). Rifampicin-based triple drug regimen was the most commonly employed (83/102, 81.4%). Pediatric neurobrucellosis was associated with greater frequency of sequalae (5.4%), deafness (2.7%) and mortality (2.7%), when compared to that of general population. Neurobrucellosis mimics neuro-tuberculosis in various aspects. The review highlights several unique aspects of this entity in children. A high index of suspicion can ensure prompt diagnosis, timely initiation of management and favorable outcomes.

We thank the author for his comments on the immune status in patients with tuberculous meningitis. 1 We agree that being tested negative for HIV infection does not mean that there is a perfect state of immunocompetence. 2 We believe that immune dysregulation in any form, primary or secondary, can alter the course of tuberculous meningitis and affect its outcome. In view of the paucity of literature in this area, we are currently studying the prevalence of primary immunodeficiencies in patients with tuberculous meningitis, after having ruled out the commoner secondary immunodeficiencies in addition to HIV infection, including hepatitis C virus and hepatitis B virus infections, diabetes mellitus, and hepatic dysfunction. 3,4 We are evaluating humoral (antibody and complement aberrancies) as well as cellular (T-cell and B-cell disorders) immune dysfunction. We expect that these studies will add to our understanding of immunodeficiency and tuberculous meningitis.