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副球孢子菌病发病机制中的口服途径:对感染巴西副球孢子菌分生孢子的BALB/c小鼠的实验研究

The oral route in the pathogenesis of paracoccidioidomycosis: an experimental study in BALB/c mice infected with P. brasiliensis conidia.

作者信息

Roldán J C, Tabares A M, Gómez B L, Aristizábal B E, Cock A M, Restrepo A

机构信息

Corporación para Investigaciones Biológicas (CIB), Carrera, Medellín, Colombia.

出版信息

Mycopathologia. 2001;151(2):57-62. doi: 10.1023/a:1010961514974.

Abstract

Due to the high frequency of oral mucosal lesions observed in paracoccidioidomycosis patients, it was advocated that the infection was acquired by the traumatic implantation of the etiologic agent Paracoccidioides brasiliensis. Although at present this theory is considered invalid, it has not yet been excluded in experimental studies. In order to determine if intra-oral inoculation could explain the pathogenesis of paracoccidioidomycosis, 64 BALB/c mice were inoculated intra-orally with 850.000 viable P. brasiliensis conidia into the mandibular body. Animals were sacrificed at various time intervals up to 20 weeks and cultures were made from gingiva, lungs, spleen, and liver. Additionally, histopathological studies of the mandibular body were also performed. P. brasiliensis was isolated from all gingival tissues during the interval 24-72 h, indicating that the infection was active. During the 5-10 week period, the infection appeared to have been controlled at the inoculation site as cultures showed a significant reduction in colony forming units (CFU); however, at the 15-20 week period such control was lost and the fungus was recovered once more. Dissemination to other body sites was rare; thus, the lungs were involved in just one animal (2%), the liver in two (3%) and the spleen in seven (11%). The infection became established as proven by positive organ cultures, but the dissemination pattern did not correspond to the one observed in humans. Based on these findings, the intra-oral traumatic route does not appear to mimic the natural history of paracoccidioidomycosis.

摘要

由于在副球孢子菌病患者中观察到口腔黏膜病变的频率很高,有人主张该感染是由病原体巴西副球孢子菌经创伤植入而获得的。尽管目前这一理论被认为是无效的,但在实验研究中尚未被排除。为了确定口腔内接种是否可以解释副球孢子菌病的发病机制,将64只BALB/c小鼠的下颌体内接种850,000个活的巴西副球孢子菌分生孢子。在长达20周的不同时间间隔处死动物,并从牙龈、肺、脾和肝进行培养。此外,还对下颌体进行了组织病理学研究。在24 - 72小时内,从所有牙龈组织中分离出巴西副球孢子菌,表明感染处于活跃状态。在5 - 10周期间,接种部位的感染似乎得到了控制,因为培养显示菌落形成单位(CFU)显著减少;然而,在15 - 20周期间,这种控制丧失,真菌再次被检出。向身体其他部位的播散很少见;因此,只有一只动物(2%)的肺部受累,两只动物(3%)的肝脏受累,七只动物(11%)的脾脏受累。通过器官培养阳性证明感染已经确立,但播散模式与在人类中观察到的不同。基于这些发现,口腔内创伤途径似乎无法模拟副球孢子菌病的自然病程。

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