Eosinophilic meningitis is defined as the presence of more than 10 eosinophils per μl in the cerebrospinal fluid (CSF), or eosinophils accounting for more than 10% of CSF leukocytes in patients with acute meningitis. Parasites are the most common cause of eosinophilic meningitis worldwide, but there is limited research on patients in Korea. Patients diagnosed with eosinophilic meningitis between January 2004 and June 2018 at a tertiary hospital in Seoul, Korea were retrospectively reviewed. The etiology and clinical characteristics of each patient were identified. Of the 22 patients included in the study, 11 (50%) had parasitic causes, of whom 8 (36%) were diagnosed as neurocysticercosis and 3 (14%) as Toxocara meningitis. Four (18%) patients were diagnosed with fungal meningitis, and underlying immunodeficiency was found in 2 of these patients. The etiology of another 4 (18%) patients was suspected to be tuberculosis, which is endemic in Korea. Viral and bacterial meningitis were relatively rare causes of eosinophilic meningitis, accounting for 2 (9%) and 1 (5%) patients, respectively. One patient with neurocysticercosis and 1 patient with fungal meningitis died, and 5 (23%) had neurologic sequelae. Parasite infections, especially neurocysticercosis and toxocariasis, were the most common cause of eosinophilic meningitis in Korean patients. Fungal meningitis, while relatively rare, is often aggressive and must be considered when searching for the cause of eosinophilic meningitis.
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Angiostrongylus cantonensis invades the central nervous system (CNS) of humans to induce eosinophilic meningitis and meningoencephalitis and leads to persistent headache, cognitive dysfunction, and ataxic gait. Infected mice (nonpermissive host), admittedly, suffer more serious pathological injuries than rats (permissive host). However, the pathological basis of these manifestations is incompletely elucidated. In this study, the behavioral test, histological and immunohistochemical techniques, and analysis of apoptotic gene expression, especially caspase-3, were conducted. The movement and motor coordination were investigated at week 2 post infection (PI) and week 3 PI in mice and rats, respectively. The cognitive impairs could be found in mice at week 2 PI but not in rats. The plaque-like lesion, perivascular cuffing of inflammatory cells, and dilated vessels within the cerebral cortex and hippocampus were more serious in mice than in rats at week 3 PI. Transcriptomic analysis showed activated extrinsic apoptotic pathway through increased expression of TNFR1 and caspase-8 in mice CNS. Immunohistochemical and double-labeling for NeuN and caspase-3 indicated the dramatically increased expression of caspase-3 in neuron of the cerebral cortex and hippocampus in mice but not in rats. Furthermore, western-blotting results showed high expression of cleaved caspase-3 proteins in mice but relatively low expression in rats. Thus, extrinsic apoptotic pathway participated in neuronal apoptosis might be the pathological basis of distinct behavioral dysfunctions in rodents with A. cantonensis infection. It provides the evidences of a primary molecular mechanism for the behavioral dysfunction and paves the ways to clinical diagnosis and therapy for A. cantonensis infection.
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