ABSTRACT
Meningitis is a potentially life-threatening infection characterised by the inflammation of the leptomeningeal membranes. The estimated annual prevalence of 8.7 million cases globally and the disease is caused by many different viral, bacterial, and fungal pathogens. Although several genera of fungi are capable of causing infections in the central nervous system (CNS), the most significant number of registered cases have, as causal agents, yeasts of the genus Cryptococcus. The relevance of cryptococcal meningitis has changed in the last decades, mainly due to the increase in the number of people living with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) and medications that impair the immune responses. In this context, coronavirus disease 19 (COVID-19) has also emerged as a risk factor for invasive fungal infections (IFI), including fungal meningitis (FM), due to severe COVID-19 disease is associated with increased pro-inflammatory cytokines, interleukin (IL)-1, IL-6, and tumour necrosis factor-alpha, reduced CD4-interferon-gamma expression, CD4 and CD8 T cells. The gold standard technique for fungal identification is isolating fungi in the culture of the biological material, including cerebrospinal fluid (CSF). However, this methodology has as its main disadvantage the slow or null growth of some fungal species in culture, which makes it difficult to finalise the diagnosis. In conclusions, this article, in the first place, point that it is necessary to accurately identify the etiological agent in order to assist in the choice of the therapeutic regimen for the patients, including the implementation of actions that promote the reduction of the incidence, lethality, and fungal morbidity, which includes what is healthy in the CNS.
ABSTRACT
RESUMEN INTRODUCCIÓN: Las infecciones por hongos en el sistema nervioso central son cada vez más frecuentes debido al aumento de las poblaciones en riesgo; son principalmente de carácter oportunista y poco comunes en pacientes sin inmunocompromiso. PRESENTACIÓN DE CASO: Un hombre de 28 años, sin antecedentes medicoquirúrgicos de importancia, consultó al servicio de urgencias por cefalea refractaria, precedida de picos febriles y signos meníngeos, se le hizo punción lumbar con posterior hallazgo microbiológico de Candida glabrata en líquido cefalorraquídeo. Se descartó previamente causal de inmunocompromiso incluyendo coinfección por VIH, colagenosis, neoplasias e incluso falta de inmunización durante la infancia. DISCUSIÓN: Se estiman cerca de 70.000 especies de hongos formalmente descritas, de las cuales 300 podrían mostrar virulencia en los humanos, con múltiples formas de presentación en sistema nervioso central, principalmente meningitis, encefalitis, hidrocéfalo, absceso cerebral e ictus, todos condicionados por un factor predisponente u estado inmunológico del hospedero, planteándose incluso algún grado de inmunodeficiencia sobre receptores tipo Toll like, que limiten la unión a PAMPs y posterior progresión de infección.
SUMMARY INTRODUCTION: Fungal infections of the central nervous system are increasingly frequent due to the increase in populations at risk. They are mainly opportunistic, and uncommon in non-immunocompromise patients. CASE PRESENTATION: A 28-year-old man, without a significant medical and surgical history, consulted the emergency department for refractory headache, accompanied by fever and meningeal signs, a lumbar puncture lead to the subsequent microbiological finding of Candida glabrata in cerebrospinal fluid. Immunocompromise was ruled out, including HIV coinfection, collagen, neoplasms and even lack of immunization during childhood. DISCUSSION: About 70,000 formally described fungal species are estimated, of which 300 could show virulence in humans, with multiple forms of presentation in the central nervous system, mainly meningitis, encephalitis, hydrocephalus, brain abscess and stroke, all conditioned due to a predisposing factor or immune status of the host, even considering some degree of immunodeficiency on Toll like receptors, which limit the binding to PAMPs and subsequent progression of infection at the height of the CNS.