A case of chronic cerebral paragonimiasis westermani

Kang, Sung-Soo; Kim, Tae-Kwon; Kim, Tae Yun; Ha, Young-Il; Choi, Sun-Wook; Song, Hong

doi:10.3347/kjp.2000.38.3.167

Cited by 27 publications

(15 citation statements)

References 9 publications

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“…1 Correlation between histologic stage of cerebral paragonimiasis and treatment outcomes is not well known; however, even chronic infection may be amenable to surgical resection if recognized in time. 10 …”

Section: Discussionmentioning

confidence: 99%

Cerebral Paragonimiasis Presenting with Sudden Death

Amaro

Cowell

Tuohy

et al. 2016

The American Journal of Tropical Medicine and Hygiene

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Abstract.A 58-year-old Korean-born woman with a history of seizures and psychiatric issues was found dead at home. Autopsy was notable for large, calcified nodules that had nearly replaced her right temporal lobe. Histologic examination revealed the presence of Paragonimus eggs. This case demonstrates a rare manifestation of an aberrantly migrated lung fluke that resulted in epilepsy and sudden death years after the initial infection.

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Section: Discussionmentioning

confidence: 99%

Cerebral Paragonimiasis Presenting with Sudden Death

Amaro

Cowell

Tuohy

et al. 2016

The American Journal of Tropical Medicine and Hygiene

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“…Other bacterial etiologies should also be considered, since CSF glucose levels are typically low (212). Cerebral involvement may include chronic silent lesions, detectable with image examination as multiple conglomerated iso-intensity or low-signal-intensity round nodules, with peripheral rim enhancement (39,50,141,277). Skin tests, CFA, immunodiffusion, hemagglutination, and other techniques have been used for anti-Paragonimus antibody detection, with variable results (49).…”

Section: Diagnosismentioning

confidence: 99%

“…Meningitis is secondary to parenchymal lesions, which progress chronically to granulomatous and fibrotic lesions (211,212). Eggs may be found in histological sections at the border of necrotic nodules (141).…”

Section: Diseasementioning

confidence: 99%

Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance

2009

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SUMMARY Eosinophilic meningoencephalitis is caused by a variety of helminthic infections. These worm-specific infections are named after the causative worm genera, the most common being angiostrongyliasis, gnathostomiasis, toxocariasis, cysticercosis, schistosomiasis, baylisascariasis, and paragonimiasis. Worm parasites enter an organism through ingestion of contaminated water or an intermediate host and can eventually affect the central nervous system (CNS). These infections are potentially serious events leading to sequelae or death, and diagnosis depends on currently limited molecular methods. Identification of parasites in fluids and tissues is rarely possible, while images and clinical examinations do not lead to a definitive diagnosis. Treatment usually requires the concomitant administration of corticoids and anthelminthic drugs, yet new compounds and their extensive and detailed clinical evaluation are much needed. Eosinophilia in fluids may be detected in other infectious and noninfectious conditions, such as neoplastic disease, drug use, and prosthesis reactions. Thus, distinctive identification of eosinophils in fluids is a necessary component in the etiologic diagnosis of CNS infections.

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“…In cases of extrapulmonary paragonimiasis, the central nervous system (CNS) is the most common locus of involvement [6, 7]. Cerebral paragonimiasis causes serious and often fatal neurological injury with sequelae of seizures, visual disorders, hemiplegia, and cerebral hemorrhage [7,8,9]. …”

Section: Introductionmentioning

confidence: 99%

“…Although chronic pulmonary disease is the most common result of Paragonimus infection, extrapulmonary infection does occur in brain, peritoneal and pelvic cavities, diaphragm, and subcutaneous tissues [4, 5]. In cases of extrapulmonary paragonimiasis, the central nervous system (CNS) is the most common locus of involvement [6, 7]. Cerebral paragonimiasis causes serious and often fatal neurological injury with sequelae of seizures, visual disorders, hemiplegia, and cerebral hemorrhage [7,8,9].…”

Section: Introductionmentioning

confidence: 99%

Excretory-Secretory Products Produced by <i>Paragonimus westermani</i> Differentially Regulate the Nitric Oxide Production and Viability of Microglial Cells

Jin

Lee²,

Choi³

et al. 2005

Int Arch Allergy Immunol

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Background:Tissue-invading helminth parasites secrete a large amount of cysteine proteases that may play critical roles in tissue invasion and immune modulation. However, roles of excretory-secretory products (ESP) secreted by Paragonimus westermani in the activation and death of microglial cells in brain are poorly understood. Objectives: In the present study, we investigated whether ESP could regulate microglial nitric oxide (NO) production and viability. Methods: The NO production and cell viability were assessed by respectively measuring the formation of nitrite and the release of lactate dehyrogenase. Results:At a low (0.2 µg/ml) concentration, ESP significantly stimulated NO production with no apparent cell injury or death in cultured microglial cells. However, at high (≧2 µg/ml) concentrations, ESP induced severe cell death. Inhibition of inducible NO synthase significantly reduced the NO productivity, but not cytotoxicity, of ESP. Similarly, inhibitors of the extracellular signal-regulated kinase, p38 and nuclear factor kappa B also blocked only the NO productivity of ESP. Interestingly, heat inactivation did not hamper the ability of ESP to stimulate microglial NO production. Similarly, pretreatment with thiol-crosslinking reagents dramatically reduced both proteolytic activity and cytotoxicity of ESP, but did not alter NO production in microglial cells. Interestingly, although cysteine protease competitive inhibitors and thiol-alkylating reagents markedly reduced the proteolytic activity of ESP, they did not influence the NO productivity and cytotoxicity of ESP. Conclusion: The present results indicate that the NO production and cytotoxicity by ESP may be differentially regulated via unknown mechanisms, not related with cysteine protease activity.

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A case of chronic cerebral paragonimiasis westermani

Cited by 27 publications

References 9 publications

Cerebral Paragonimiasis Presenting with Sudden Death

Cerebral Paragonimiasis Presenting with Sudden Death

Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance

Excretory-Secretory Products Produced by <i>Paragonimus westermani</i> Differentially Regulate the Nitric Oxide Production and Viability of Microglial Cells

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