• 대한임상독성학회지
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• 제4권2호
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• pp.131-136
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• 2006

Metronidazole is an antimicrobial drug widely used against various types of infectious agents, including protozoa, amoeba, Helicobacter pylori, and anaerobes. Metronidazole may produce some adverse effects on hematologic, immunologic, neurologic and other systems. We report a case of reversible metronidazole-induced encephalopathy. The toxic dose of metronidazole and the onset of encephalopathy were variable. Two patients showed abnormally high signal intensity in the bilateral dentate nucleus of cerebellum, and characteristic abnormalities were detected by brain magnetic resonance imaging (MRI) and T2-weighted images, fluid-attenuated inversion recovery images and/or diffusion weighted imaging (DWI). Discontinuation of metronidazole resulted in the improvement of the neurologic symptoms over a period of two to three weeks. We followed up the brain MRI with DWI in one case following obvious clinical improvement, and the previously detected lesion had disappeared.

• Parasites, Hosts and Diseases
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• 제22권2호
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• pp.253-258
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• 1984

Naegleria fowleri를 마우스 비강을 통하여 감염시킨 뒤 P.A.M. 발생율 및 발병후 생존기간을 마우스 주별 체중별, 성별, 접종아메 바수에 따라 비교하여 다음과 같은 성적을 얻었다. 1. N. fewleri를 감염시킨후 P.A.M. 발생은 ICR마우스보다 BALB/C마우스에서 많았으며 감염후 평균생존기간은 차이가 없었다. 2. 마우스 성별에 따른 N. fowleri감염후 P.A.M.발생율 및 발병후 평균생존기간은 차이가 없었다. 3. 체중이 다른 여러 실험군에서 P.A.M. 발생율 및 사망율은 차이가 없었으나 발병후 마우스의 평균생존 기간은 체중이 가벼운 실험군에서 짧았다. 4. 감염시킨 아메 바수에 따른 P.A.M. 발생율은 영양형 Ix104이상 감염 군에서는 차이가 없었으나 0.5x104인 경우 P.A.M 발생이 현저히 감소하였다.

• 응용통계연구
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• 제22권3호
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• pp.569-584
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• 2009

영상에서 에지검출은 영상처리시스템과 컴퓨터비전에서 매우 중요한 단계이다. 지금까지 형태학적 에지검출은 고정된 구조적 요소를 사용한 형태학적 연산 토대 하에서 수행되어왔다. 본 논문에서는 잡음영상에서 에지검출을 위해 영상의 다양한 형태에 맞춰 다이내믹하게 모양이 변하는 아메바라는 구조적 요소를 사용하고자 한다. 제안된 에지검출 방법의 성능을 시각적인 방법뿐만 아니라 객관적인 척도인 PFOM과 ROC 곡선을 사용하여 정성적, 정량적으로 모두 평가하였다. 영상 설험 결과 고정된 구조적 요소를 이용하는 기존의 방법보다 잡음에 덜 민감하였으며 미세한 에지까지도 검출하는 뛰어난 성능을 보여주었다.

• Parasites, Hosts and Diseases
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• 제43권1호
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• pp.7-13
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• 2005

The taxonomy of Acanthamoeba spp., an amphizoic amoeba which causes granulomatous amoebic encephalitis and chronic amoebic keratitis, has been revised many times. The taxonomic validity of some species has yet to be assessed. In this paper, we analyzed the morphological characteristics, nuclear 18s rDNA and mitochondrial 16s rDNA sequences and the Mt DNA RFLP of the type strains of four Acanthamoeba species, which had been previously designated as A. divionensis, A. parasidionensis, A. mauritaniensis, and A. rhysodes. The four isolates revealed characteristic group II morphology. They exhibited 18S rDNA sequence differences of $0.2-1.1\%$ with each other, but more than $2\%$ difference from the other compared reference strains. Four isolates formed a different clade from that of A. castellanii Castellani and the other strains in morphological group lion the phylogenetic tree. In light of these results, A. paradivionensis, A. divionensis, and A. mauritaniensis should be regarded as synonyms for A. rhysodes.

• 미생물학회지
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• 제32권4호
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• pp.280-284
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• 1994

공생 아메바에서 리소솜과 공생낭 간에 융합이 저해되는 이유로서는 먼저 이들 공생낭의 막에 어떤 특별한 인자가 존재하여 융합을 저해하거나 또는 융합 과정에 필수적인 어떤 요소가 이들 공생막에는 부족하여 융합이 일어나지 않는다고 유추해 볼 수 있다. 단일 클론 항체를 추적물질로 사용하여 이들 인자나 구성요소를 알아내는 과정에서, lipopolysaccharides가 공생 박테리아에 의하여 생산되어 공생낭의 막에 삽입된다는 것을 확인하였으며 이들이 공생막상에서도 세포질 방향으로 노출되어 있다는 것을 알아내었다. 따라서 이들 lipopolysaccharides가 리소솜과 공생낭간의 융합 저해에 간여하는 가를 알아보기 위하여 이들에 대한 단일 크론 항체를 공생 아메자의 세포질에 미세주사하여 보았다. 주사된 아메바에서는 공생낭과 리소솜간의 융합이 일어나는 것으로 미루어 보아, 아마도 lipopolysaccharides는 융합저해 요소 중의 하나로 사료되어 진다.

• Parasites, Hosts and Diseases
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• 제59권5호
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• pp.501-505
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• 2021

The pathogenic free-living amoeba Naegleria fowleri causes primary amoebic meningoencephalitis, a fatal infection, by penetrating the nasal mucosa and migrating to the brain via the olfactory nerves. N. fowleri can induce host cell death via lytic necrosis. Similar to phosphorylation, O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is involved in various cell-signaling processes, including apoptosis and proliferation, with O-GlcNAc addition and removal regulated by O-GlcNAc transferase and O-GlcNAcase (OGA), respectively. However, the detailed mechanism of host cell death induced by N. fowleri is unknown. In this study, we investigated whether N. fowleri can induce the modulation of O-GlcNAcylated proteins during cell death in Jurkat T cells. Co-incubation with live N. fowleri trophozoites increased DNA fragmentation. In addition, incubation with N. fowleri induced a dramatic reduction in O-GlcNAcylated protein levels in 30 min. Moreover, pretreatment of Jurkat T cells with the OGA inhibitor PUGNAc prevented N. fowleri-induced O-deGlcNAcylation and DNA fragmentation. These results suggest that O-deGlcNAcylation is an important signaling process that occurs during Jurkat T cell death induced by N. fowleri.

• Parasites, Hosts and Diseases
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• 제57권3호
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• pp.291-294
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• 2019

Primary amebic encephalitis (PAM) is a devastating central nervous system infection caused by Naegleria fowleri, a free-living amoeba, which can survive in soil and warm fresh water. Here, a 43-year-old healthy male was exposed to warm freshwater 5 days before the symptom onset. He rapidly developed severe cerebral edema before the diagnosis of PAM and was treated with intravenous conventional amphotericin B while died of terminal cerebral hernia finally. Comparing the patients with PAM who has similar clinical symptoms to those with other common types of meningoencephalitis, this infection is probably curable if treated early and aggressively. PAM should be considered in the differential diagnosis of purulent meningoencephalitis, especially in patients with recent freshwater-related activities during the hot season.

• 대한의생명과학회지
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• 제24권4호
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• pp.435-438
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• 2018

Acanthamoeba culbertsoni is the causative agent of granulomatous amoebic encephalitis (GAE), a condition that predominantly occurs in immunocompromised individuals and which is typically fatal. A mannose-binding protein (MBP) among lectins was shown to have strong A. castellanii pathogenic potential when correlated with major virulence proteins. In this study, protective effects were analyzed using the monoclonal antibody to A. culbertsoni MBP by quantification and were also compared with other free-living amoebae. For the amoebial cytotoxicity to the target cell, amoeba trophozoites were incubated with Chinese hamster ovary (CHO) cells. For the protective effects of antibodies, amoebae were pre-incubated with them for 4 h and then added to the target cells. After 24 h, the supernatants were collected and examined for host cell cytotoxicity by measuring lactate dehydrogenase (LDH) release. The cytotoxicity of A. culbertsoni to the CHO cells showed about 87.4%. When the monoclonal antibody was pre-incubated with A. culbertsoni, the amoebial cytotoxicity was remarkably decreased as shown at LDH release (1.858 absorbance), which was represented with about 49.9%. Taken together, it suggested that the monoclonal antibody against MBP be important to inhibit the cytotoxicity of A. culbertsoni trophozoites to the target cell. The antibody will be applied into an in vivo functional analysis, which would help to develop therapeutics.

• Journal of Microbiology and Biotechnology
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• 제29권5호
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• pp.713-720
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• 2019

Acanthamoeba castellanii belonging to the T4 genotype may cause a fatal brain infection known as granulomatous amoebic encephalitis, and the vision-threatening eye infection Acanthamoeba keratitis. The aim of this study was to evaluate the antiamoebic effects of three clinically available antidiabetic drugs, Glimepiride, Vildagliptin and Repaglinide, against A. castellanii belonging to the T4 genotype. Furthermore, we attempted to conjugate these drugs with silver nanoparticles (AgNPs) to enhance their antiamoebic effects. Amoebicidal, encystation, excystation, and host cell cytotoxicity assays were performed to unravel any antiacanthamoebic effects. Vildagliptin conjugated silver nanoparticles (Vgt-AgNPs) characterized by spectroscopic techniques and atomic force microscopy were synthesized. All three drugs showed antiamoebic effects against A. castellanii and significantly blocked the encystation. These drugs also showed significant cysticidal effects and reduced host cell cytotoxicity caused by A. castellanii. Moreover, Vildagliptin-coated silver nanoparticles were successfully synthesized and are shown to enhance its antiacanthamoebic potency at significantly reduced concentration. The repurposed application of the tested antidiabetic drugs and their nanoparticles against free-living amoeba such as Acanthamoeba castellanii described here is a novel outcome that holds tremendous potential for future applications against devastating infection.

• Parasites, Hosts and Diseases
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• 제61권4호
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• pp.388-396
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• 2023

Entamoeba histolytica is an enteric tissue-invasive protozoan parasite causing amoebic colitis and liver abscesses in humans. Amoebic contact with host cells activates intracellular signaling pathways that lead to host cell death via generation of caspase-3, calpain, Ca²⁺ elevation, and reactive oxygen species (ROS). We previously reported that various NADPH oxidases (NOXs) are responsible for ROS-dependent death of various host cells induced by amoeba. In the present study, we investigated the specific NOX isoform involved in ROS-dependent death of hepatocytes induced by amoebas. Co-incubation of hepatoma HepG2 cells with live amoebic trophozoites resulted in remarkably increased DNA fragmentation compared to cells incubated with medium alone. HepG2 cells that adhered to amoebic trophozoites showed strong dichlorodihydrofluorescein diacetate (DCF-DA) fluorescence, suggesting intracellular ROS accumulation within host cells stimulated by amoebic trophozoites. Pretreatment of HepG2 cells with the general NOX inhibitor DPI or NOX2-specific inhibitor GSK 2795039 reduced Entamoeba-induced ROS generation. Similarly, Entamoeba-induced LDH release from HepG2 cells was effectively inhibited by pretreatment with DPI or GSK 2795039. In NOX2-silenced HepG2 cells, Entamoeba-induced LDH release was also significantly inhibited compared with controls. Taken together, the results support an important role of NOX2-derived ROS in hepatocyte death induced by E. histolytica.