A solitary intracranial rich focus with early meningeal involvement: A correlative image

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•Rich foci are caseating brain tuberculous (TB) granulomas surrounding the immigrated TB bacilli.•Rich foci are hypothesized as an underlying pathological mechanism of TB meningitis.•The hypothesis is based on necropsy studies and has rarely been depicted in vivo.•Ruptured foci discharge their contents into the neighboring subarachnoid space.•Discharged contents trigger a T cell response, leading to inflammatory meningitis. A 24-year-old man presented to the emergency department with a 2-day history of fever and headache, not responsive to over-the-counter medications. He reported a previous history of latent tuberculosis, for which he received antitubercular therapy a couple of years ago. Positive results were obtained from interferon-γ release and adenosine deaminase (ADA) assays, but chest computed tomography (CT) was unremarkable. The patient had unremarkable general and neurologic examinations. Brain CT demonstrated a left-sided focal lesion that delineates perfectly post-contrast administration, besides an adjacent area of meningeal enhancement at the Sylvian sulcus (Figure 1). Cerebrospinal fluid analysis revealed monocytic pleocytosis, an elevated protein level, marked hypoglycorrhachia, and positive ADA activity. Based on the data obtained thus far, we concluded that the patient had an early focal tuberculous meningitis (TBM) caused by a rupturing rich focus, consistent with the natural history of TBM that has rarely been confirmed in vivo (Supplement 1) [1Rich AR McCordock HA. Evidence for the presence of ribonucleic acid in the cytoplasmic bodies that appear in the hepatic and adrenal epithelial cells of man in acute infection.Bull Johns Hopkins Hosp. 1933; 52: 5-37Google Scholar, 2Donald PR Schaaf HS Schoeman JF. Tuberculous meningitis and miliary tuberculosis: the Rich focus revisited.J Infect. 2005; 50: 193-195https://doi.org/10.1016/j.jinf.2004.02.010Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar, 3Be NA Kim KS Bishai WR Jain SK. Pathogenesis of central nervous system tuberculosis.Curr Mol Med. 2009; 9: 94-99https://doi.org/10.2174/156652409787581655Crossref PubMed Scopus (100) Google Scholar]. Subsequently, the patient was started on antitubercular treatment using INH, RIF, PZA, and EMB for 2 months. After which, PZA and EMB were discontinued, while INH and RIF were continued for an additional nine months. The focus with the associated TBM resolved substantially following treatment with no evidence of recurrence over a 2-year follow-up.