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首页> 外文期刊>The Internet Journal of Tropical Medicine >Clinical and Histopathological Presentation of Buruli Ulcer in Experimentally Infected Grasscutters (Thryonomys swinderianus)
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Clinical and Histopathological Presentation of Buruli Ulcer in Experimentally Infected Grasscutters (Thryonomys swinderianus)

机译：实验感染的草of（Thryonomys swinderianus）中布鲁氏溃疡的临床和组织病理学表现

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Buruli ulcer (BU) is a skin disease caused by Mycobacterium ulcerans, a toxin-producing mycobacterium. BU manifests as papule, plaque, nodule, oedema and undermined ulcer with accompanying complications such as contracture deformities and osteomyelitis. Its mode of transmission and pathogenesis are unclear and effective treatment is not available. Therefore animal modelling, among other strategies is being undertaken to elucidate the problems. This study investigated the grasscutter (Thryonomys swinderianus), a hystricomorph rodent as a BU animal model. Grasscutters were inoculated subcutaneously with Mycobacterium ulcerans and developed progressive skin lesions: erythema, papule, nodule, oedema, undermined ulcer and contracture. The lesions were accompanied by histopathological changes, specifically: coagulative necrosis, mixed inflammatory reactions, myolisis, perineuritis, neurogenic muscular atrophy and osteomyelitis; some of which were accompanied by extracellular and intravascular acid fast bacilli (AFBs). Our findings show that grasscutters are susceptible to Mycobacterium ulcerans; they develop clinical, microbiological and histopathological lesions that mimic BU in humans and therefore are potential BU animal models. Study Location Department of Animal Experimentation, Noguchi Memorial Institute for Medical ResearchSource of FundingNoguchi Memorial Institute for Medical Research Introduction Buruli ulcer (BU) is a poorly understood disease caused by Mycobacterium ulcerans, a toxin-producing mycobacterium (Krieg et al, 1974; Read et al, 1974) with predilection for the skin and its deeper tissues. It is the third most common mycobacteriosis of immunocompetent hosts after tuberculosis and leprosy (Meyers et al, 1996). BU is a disease of public health importance because the exact mode of its transmission is unclear, and its treatment with antimicrobials has not been very successful, thus resulting in its prevalence being higher than that of tuberculosis and leprosy in some communities (Amofah et al, 2002). BU manifests as papule, plaque, nodule, oedema and undermined ulcer with accompanying complications such as contracture deformities, osteomyelitis, amputation of limbs and involvement of the eye, breast and genitalia (Barneston, 1993; WHO, 2001a; WHO, 2001b). progresses slowly, is usually painless and patients are systemically well (Walsh et al, 1999; Johnson et al, 2005); these factors contribute to the late presentation of patients at hospitals with resultant massive ulceration of the skin, accompanying complications, fever and pain due to the secondary infection of the lesions (Thangaraj et al, 1999; Johnson et al, 2005). Furthermore, the absence of effective treatment worsens the prognosis because the complications lead to impairment of body functions with long-term socio-economic impact (WHO, 2001a; 2001b). Though some BU patients heal spontaneously (Walsh et al, 1999; Thangaraj et al, 1999; WHO, 2001; Johnson et al, 2005) and recent data also suggests that rifampicin, streptomycin and amikacin are effective in combination with surgery (WHO, 2004; Etuaful et al, 2005), 16-47% of the spontaneously and antibiotic healed patients relapse (WHO, 2001a; WHO, 2001b; Teelken et al, 2003), underscoring the difficulty associated with the control of BU. In the face of the enigma that BU presents, the World Health Organization (WHO) has recommended that animal studies should be undertaken worldwide to elucidate the pathogenesis and mode of transmission of the disease and to provide valuable new approaches for its diagnosis, treatment, management and general control (WHO, 2001c). Though mice, rats, guinea pigs and the nine-banded armadillo are BU animal models (Walsh et al, 1999), each of them has limitations in replicating the whole spectrum of features presented in humans, thus leaving a lot of gaps in knowledge on the pathogenesis, transmission, diagnosis, treatment and general control of BU (Pattyn & Royacker, 1965; Reed et
机译：布鲁氏溃疡（BU）是由产毒素的分枝杆菌溃疡分枝杆菌引起的皮肤疾病。 BU表现为丘疹，斑块，结节，水肿和溃疡破坏，并伴有诸如挛缩畸形和骨髓炎等并发症。其传播方式和发病机制尚不清楚，尚无有效的治疗方法。因此，正在采取动物建模以及其他策略来阐明这些问题。这项研究调查了草c（Thryonomys swinderianus），这是一种作为BU动物模型的拟变体啮齿动物。割草器皮下接种溃疡分枝杆菌，并发展为进行性皮肤损害：红斑，丘疹，结节，水肿，溃疡和挛缩。病变伴有组织病理学改变，特别是：凝固性坏死，混合性炎症反应，黑斑病，神经周炎，神经源性肌萎缩和骨髓炎。其中一些伴有细胞外和血管内耐酸杆菌（AFB）。我们的研究结果表明割草者易受溃疡分枝杆菌的侵害。他们发展出模仿人类BU的临床，微生物和组织病理学病变，因此是潜在的BU动物模型。野口纪念医学研究所动物实验研究室研究资金来源野口纪念医学研究所简介布鲁氏溃疡（BU）是由产分枝杆菌溃疡的分枝杆菌引起的一种鲜为人知的疾病（Krieg等，1974; Read et等（1974）等人，其偏爱于皮肤及其深层组织。它是具有免疫能力的宿主之后的第三大最常见的分枝杆菌病，仅次于结核和麻风病（Meyers等，1996）。 BU是一种具有重要公共卫生意义的疾病，因为尚不清楚其确切的传播方式，而且用抗生素治疗还不是很成功，因此导致某些地区的流行率高于结核病和麻风病的发生率（Amofah等， 2002）。 BU表现为丘疹，斑块，结节，水肿和溃疡破坏，并伴有诸如挛缩畸形，骨髓炎，四肢截肢以及眼睛，乳房和生殖器受累等并发症（Barneston，1993; WHO，2001a; WHO，2001b）。病情进展缓慢，通常无痛且患者全身健康（Walsh等，1999; Johnson等，2005）。这些因素导致患者在医院晚期出现皮肤溃疡，并伴随病变的继发感染而导致并发症，发烧和疼痛（Thangaraj等，1999; Johnson等，2005）。此外，缺乏有效治疗会使预后恶化，因为并发症会导致身体功能受损，并具有长期的社会经济影响（WHO，2001a; 2001b）。尽管一些BU患者自发he愈（Walsh等，1999; Thangaraj等，1999; WHO，2001; Johnson等，2005），但最近的数据也表明利福平，链霉素和丁胺卡那霉素与手术联合治疗是有效的（WHO，2004 ; Etuaful等，2005），自发和抗生素治愈的患者复发的比例为16-47％（WHO，2001a; WHO，2001b; Teelken等，2003），强调了控制BU的难度。面对BU提出的难题，世界卫生组织（WHO）建议在全球范围内进行动物研究，以阐明该疾病的发病机理和传播方式，并为其诊断，治疗，管理提供有价值的新方法和一般控制（WHO，2001c）。尽管小鼠，大鼠，豚鼠和九带犰狳是BU动物模型（Walsh等，1999），但是它们每个在复制人类呈现的全部特征方面都有局限性，因此在知识上还存在很多空白。 BU的发病机理，传播，诊断，治疗和一般控制（Pattyn＆Royacker，1965; Reed等

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