Introduction

Abstract

Meningitis and encephalitis may be caused by various etiologies, including viruses, bacteria, fungi, protozoa, and helminthes [1, 2]. In addition, numerous noninfectious causes may account for syndromes that mimic central nervous system (CNS) infections [1–3]. These include autoimmune disorders, neoplastic and paraneoplastic diseases, medications, collagen vascular disorders, and other systemic illnesses. CNS infections usually present with cerebrospinal fluid (CSF) pleocytosis and high CSF protein levels due to disruption of the blood brain barrier (BBB) but up to 8% may present without pleocytosis [4]. Despite the availability of microbiological tools, serologies and nucleic acid amplification tests such as single or multiplex polymerase chain reaction (PCR) for the most common infectious agents, the majority of CNS infections currently still remain with an unknown etiology [1, 3, 5]. Meningitis and encephalitis may be associated with significant morbidity and mortality, sometimes requiring emergent neurosurgical interventions or early adjunctive steroids to improve clinical outcomes [1, 3]. Furthermore, CNS infections may also have long-term neurological and neurocognitive sequelae that affect quality of life and activities of daily living. A prompt etiological diagnosis with targeted therapy can improve or prevent several of these adverse clinical outcomes in those with urgent treatable etiologies [1].