• 제목/요약/키워드: eosinophilic meningitis

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Infectious Causes of Eosinophilic Meningitis in Korean Patients: A Single-Institution Retrospective Chart Review from 2004 to 2018

  • Park, Sunghee;Jung, Jiwon;Chong, Yong Pil;Kim, Sung-Han;Lee, Sang-Oh;Choi, Sang-Ho;Kim, Yang Soo;Kim, Min Jae
    • Parasites, Hosts and Diseases
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    • 제59권3호
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    • pp.227-233
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    • 2021
  • 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.

단일기관에서 소아 호산구성 수막염의 임상특징 분석 (Clinical Manifestation of Eosinophilic Meningitis in Korean Children: A Single Institution's Experience)

  • 변정희;최성열;김동수;김기환
    • Pediatric Infection and Vaccine
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    • 제22권1호
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    • pp.23-28
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    • 2015
  • 목적: 호산구성 수막염은 척수액에서 호산구가 ${\geq}10/mm^3$ 또는 백혈구 중 10% 이상인 것으로 정의하며, 기생충에 의한 신경계 감염으로 주로 보고된다. 기생충에 의한 감염이 흔한 국가 외에서는 호산구성 수막염에 관한 소아에 대한 국내외 보고는 드물다. 이 연구는 국내 단일기관에서 소아 호산구성 수막염 임상특징 분석하고자 한다. 방법: 2007년 1월에서 2012년 7월까지 5년간 세브란스 어린이병원을 방문한(입원, 외래) 18세 미만의 환자들 총 6,335명을 스크리닝했고, 그 중 호산구성 수막염에 맞는 39명을 대상으로 의무기록을 바탕으로 후향적으로 분석하였다. 결과: 뇌척수액 검사상 호산구성 수막염으로 진단된 환자는 39명(0.6%)이었으며, 평균연령은 6세(생후 7일-18세)였고, 남녀의 비는 1.3:1이었다. 혈액검사에서 호산구 증가가 동반되는 경우가 18례(46%) 있었다. 기저질환 및 과거력으로 신경계 질환 36례(92%) 있었다. 항경련제를 복용한 경우는 22례가 있었고, 이외 다른 약물의 복용이 1례 있었다. 뇌수술 이후에 발생한 경우가 35례(90%)였다. 증상은 주로 발열(50%), 두통(20%), 구토(15%), 경련(10%), 어지러움증(5%) 등이 있었다. 뇌척수액의 단백 수치는 평균 180 mg/dL (16-633 mg/dL)로 상승된 값을 보였다. 증상 지속시간은 평균 5일로 치료는 정맥 항생제 및 스테로이드를 투여하였다. 세균배양 된 예가 1례, 애완동물을 기른 예가 1례 있었고 이외에 기생충 관련된 정보는 없었다. 결론: 국내 소아 호산구성 수막염은 기생충 감염보다는 중추신경계의 수술과 관련 있거나 약제에 의한 것으로 생각된다. 따라서 호산구성 수막염의 원인을 잘 고려하여 불필요한 검사나 치료를 줄일 수 있을 것이며, 향후 다기관을 통한 분석이 필요하다.

Dexamethasone Downregulates Expressions of 14-3-3β and γ-Isoforms in Mice with Eosinophilic Meningitis Caused by Angiostrongylus cantonensis Infection

  • Tsai, Hung-Chin;Chen, Yu-Hsin;Yen, Chuan-Min;Chung, Li-Yu;Wann, Shue-Ren;Lee, Susan Shin-Jung;Chen, Yao-Shen
    • Parasites, Hosts and Diseases
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    • 제57권3호
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    • pp.249-256
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    • 2019
  • Steroids are commonly used in patients with eosinophilic meningitis caused by A. cantonensis infections. The mechanism steroids act on eosinophilic meningitis remains unclear. In this mouse experiments, expressions of 14-3-3 isoform ${\beta}$ and ${\gamma}$ proteins significantly increased in the CSF 2-3 weeks after the infection, but not increasedin the dexamethasone-treated group. Expression of 14-3-3 ${\beta}$, ${\gamma}$, ${\varepsilon}$, and ${\theta}$ isoforms increased in brain meninges over the 3-week period after infection and decreased due to dexamethasone treatment. In conclusion, administration of dexamethasone in mice with eosinophilic meningitis decreased expressions of 14-3-3 isoform proteins in the CSF and in brain meninges.

Clinical Manifestations of Eosinophilic Meningitis Due to Infection with Angiostrongylus cantonensis in Children

  • Sawanyawisuth, Kittisak;Chindaprasirt, Jarin;Senthong, Vichai;Limpawattana, Panita;Auvichayapat, Narong;Tassniyom, Sompon;Chotmongkol, Verajit;Maleewong, Wanchai;Intapan, Pewpan M.
    • Parasites, Hosts and Diseases
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    • 제51권6호
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    • pp.735-738
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    • 2013
  • Eosinophilic meningitis, caused by the nematode Angiostrongylus cantonensis, is prevalent in northeastern Thailand, most commonly in adults. Data regarding clinical manifestations of this condition in children is limited and may be different those in adults. A chart review was done on 19 eosinophilic meningitis patients aged less than 15 years in Srinagarind Hospital, Faculty of Medicine, Khon Kaen University, Thailand. Clinical manifestations and outcomes were reported using descriptive statistics. All patients had presented with severe headache. Most patients were males, had fever, nausea or vomiting, stiffness of the neck, and a history of snail ingestion. Six patients had papilledema or cranial nerve palsies. It was shown that the clinical manifestations of eosinophilic meningitis due to A. cantonensis in children are different from those in adult patients. Fever, nausea, vomiting, hepatomegaly, neck stiffness, and cranial nerve palsies were all more common in children than in adults.

Neuronal Apoptosis: Pathological Basis of Behavioral Dysfunctions Induced by Angiostrongylus cantonensis in Rodents Model

  • Luo, Shiqi;OuYang, Lisi;Wei, Jie;Wu, Feng;Wu, Zhongdao;Lei, Wanlong;Yuan, Dongjuan
    • Parasites, Hosts and Diseases
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    • 제55권3호
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    • pp.267-285
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    • 2017
  • 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.

앙고라 토끼의 급성폐사성질병(急性斃死性疾病)의 병인학적(病因學的) 연구(硏究) : 소위(所謂) 토끼의 바이러스성(性) 급사병(急死病) (Etiological Studies on the Acute Fatal Disease of Angora Rabbits : The So-Called Rabbit Viral Sudden Death)

  • 이차수;박청규
    • 대한수의학회지
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    • 제27권2호
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    • pp.277-290
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    • 1987
  • This paper dealt with etiological studies on the acute fatal disease of Angora rabbits occurring as a group in Korea. The disease was confirmed as an acute infectious disease caused by virus. The results obtained were summarized as follows: The disease produced a high morbidity in the rearing Angora rabbits and a high mortality in the infected rabbits, and was acute. The infected rabbits died soon without premonitory signs after inappetence. The body temperature of the affected rabbits rose to $40^{\circ}C$ and nearly all deaths occurred within 48 hours after inoculation. In many cases a bloody foam was visible from the nostrils after death. According to the progress of the disease the nervous signs, such as ataxia, paralysis of the legs, and torticollis could be recognized in the some cases. Rabbits that had recovered from the disease were severe emaciation, and bristly and sparse hairs. In macroscopical findings, there were hemorrhage and edema of the lung, hemorrhage or hyperemia of the tracheal and broncheal mucosae, appearance of blood-tinged effusion in the respiratory tract. The principal lesions were found in the liver. Usually the lobular necrosis of the liver cells was progressed, and focal necrosis and hemorrhagic spots of various sizes were often observed in the liver. Liver was as a whole pale. In chronic cases, however, there was a slight liver cirrhosis with the atrophy of the parenchymal cells. The other lesions encountered grossly consisted of swelling and petechiae of the kidney, hyperemia and hemorrhage of the spleen, catarrh of the small intestine, and hyperemia of the brain. The urinary bladder contained a lot of turbid urine or bloody urine and urinary cast, and was distended with the urine. In microscopical findings, the most striking lesions occurred in the liver and may be classified as viral hepatitis. The hepatic lesions were initially characterized by progression from periportal to peripheral necrosis of the lobules with the infiltration of mononuclear cells. Focal necrosis of various sizes, hemorrhage and hyperemia were often observed in the hepatic lobules. In chronic cases, there were intensive infiltration of lymphocytes, proliferation of fibroblasts, appearance of plasmal cells, and atrophy of parenchymal cells in the hepatic tissue. Perivascular lymphocytic infiltration and meningitis were seen in the brain and spinal cord. In the kidney, there were acute glomerulonephritis, hemorrhage, necrosis of the uriniferous tubules, and retention of eosinophilic substance within the renal tubules. Proliferation of fibroblasts and infiltration of mono-nuclear cells were found in the interstitial stroma of the kidney in chronic case. There were also hemorrhage and edema in the lung, hyperemia and hemorrhage in the trachea and bronchus, perivascular lymphocytic infiltration and focal myocardial necrosis in the heart, hyperemia and hemorrhage in the spleen, vacuolization and desquamation of mucous epithelia in the urinary bladder, catarrhal inflammation of the small intestine, hemorrhage in the adrenal cortex and hyperemia in the other organs. In the electron microscopical findings of the hepatic tissue, crystals of viral particles appeared in the cytoplasm of the hepatocytes and the sinusoidal endothelial cells, and the viral particles, were small in size and polygonal. The authors suppose the virus may belong to picornaviridae family of RNA viruses. Also immature virus-like particles, dilated rough endoplasmic reticulum and destruction of nuclear membrane were seen in the hepatocytes. From these results, it is concluded that the sudden death is an acute viral disease characterized by hepatitis and the affected rabbits may be died of viremia.

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