左肺泡状棘球蚴病1例报告

棘球蚴病分二种类型,一是多见的由细粒棘球绦虫所引起的棘球蚴病;二是较少见的由多房性棘球绦虫所致的泡状棘球蚴病。泡状棘球蚴病以发生在肝脏多见,但少数原发性病变也可发生在脑、肺、脾、肾等处。我院于去年曾收住1例肺泡状棘球蚴病,现报     

三维适形调强放疗对鼠骨细粒棘球蚴生发细胞凋亡及caspase-3表达的影响

目的 探讨三维适形调强放疗(intensity modulated radiation therapy,IMRT)的放射线对鼠骨细粒棘球蚴生发细胞生长及凋亡的影响。方法 骨细粒棘球蚴病子午沙鼠20只,将骨细粒棘球蚴内囊中的生发细胞进行分离,并进行体外培养,对体外培养成功的骨细粒棘球蚴生发细胞分为IMRT放疗组和空白对照组。IMRT放疗组给予总剂量为40Gy的IMRT放疗,对照组仅给予假照射。于放疗结束24h后采用流式细胞仪检测骨细粒棘球蚴生发细胞凋亡率,采用Western blot法检测骨棘球蚴生发细胞中凋亡相关蛋白caspase-3蛋白表达情况,采用RT-PCR法定量检测骨棘球蚴生发细胞caspase-3mRNA表达水平。结果 IMRT作用24h后,IMRT放疗组骨细粒棘球蚴生发细胞凋亡率、caspase-3蛋白及mRNA表达灰度值((67.21±14.40)%、7.761±1.447、59.44±19.28)明显高于对照组((2.91±0.51)%、0.129±0.054、1.17±0.50),差异均有统计学意义(P<0.05)。结论 IMRT对骨细粒棘球蚴生发细胞生长有明显诱导凋亡作用,其作用机制可能是通过调节凋亡相关蛋白caspase-3而实现的。     

泡状棘球蚴病

泡状棘球蚴病是一种罕见的寄生虫传染性疾病。成虫寄生在狐、狗、狼的小肠内即终末宿主;蚴虫多寄生于小啮齿类动物中为中间宿主。人误食含卵粪便也可成为中间宿主。因本病多发于我国西北部,较为罕见,病理医师对寄人虫的生活史和感染组织的病理形态认识不够,易误诊。故对其流行病学、寄生虫的生活史、蚴虫在中间宿主组织内的病理形态、器官感染分布、临床太和体征以及诊断与治疗等作一全面介绍。     

脑泡状棘球蚴病7例临床病理分析

目的研究和探讨脑泡状棘球蚴病的临床和病理学特征及鉴别诊断。方法对7例脑泡状棘球蚴病标本进行光镜观察，对其临床及组织形态学资料进行分析对比。结果脑泡状棘球蚴病对人脑组织破坏性强，有向周围组织浸润性生长的生物学行为。结论脑泡状棘球蚴病在临床易误诊为胶质瘤、转移瘤及其他寄生虫病，需靠病理诊断确诊。     

肝棘球蚴病12例诊治分析

目的：分析肝棘球蚴病的临床特点及诊治体会，提高对肝棘球蚴病的认识。方法：对1999～2007年，我院收治的12例肝棘球蚴患者进行回顾性分析。结果：全部患者无一例误诊，术后均治愈，随访至今，无一例复发。结论：肝棘球蚴病的临床诊断主要依靠B超检查及CT检查，治疗主要以手术为主。     

实时B型超声诊断肝包虫探讨

肝包虫病或称棘球蚴病,因吞食棘球绦虫卵后,其幼虫在人体内脏器寄生所致。分为细粒棘球蚴及泡状棘球蚴两类。临床上以前者尤为常见,在我国西北各省、内蒙、西藏等地发病率很高,是牧区的一种常见病。我院自1988年～1993年1月,用实时B型超声(下称B超检查)诊断腹部和盆腔病变共2000余例,从中选择了经综合诊断证实的37例肝包虫病,分析如下。     

细粒棘球蚴病的免疫逃逸机制探讨

细粒棘球蚴病(echinococcosis granulosa)是一种慢性、繁杂性、无临床症状的地方区域性寄生虫传染病。细粒棘球蚴病主要的致病是在其幼虫阶段,通过粪口途径传播。目前细粒棘球蚴绦虫分布在全世界除南极洲以外的每个大陆,这也导致全世界有大量人口感染。本文主要研究细粒棘球蚴病在感染人体后,机体免疫状态和细粒棘球蚴免疫逃逸机制的探讨,提出免疫细胞能量代谢在检测细粒棘球病新思路。     

高强度聚焦超声波的两种辐照模式对棘球蚴杀伤效果的比较研究

目的比较不同高强度聚焦超声波辐照方式对细粒棘球蚴包囊的损伤作用的差异,探索高强度聚焦超声波用于治疗囊性病变的可行性。方法在声功率与辐照时间都相同的情况下,用曲线闭环扫描和直线扫描2种辐照方式处理配对分组的细粒棘球蚴包囊,从包囊囊壁组织病理学改变,囊液的温升变化以及囊内原头蚴死亡情况等方面比较2种辐照模式杀伤细粒棘球蚴包囊的效果。结果曲线闭环扫描方式能造成囊壁生发层和角质层断裂、脱落,其破坏囊壁生发层和角质层作用远比直线扫描方式强,而引起囊液的温度升高和原头蚴的死亡这两方面的效应均不如直线扫描方式。结论曲线闭环扫描方式主要破坏囊壁及生发层细胞,直线扫描方式杀伤囊内原头蚴效果优于曲线闭环扫描方式。     

46例肝泡性包虫病的手术配合及体会

包虫是人体内最大的寄生虫,属于自然疫源性疾病,人类作为中间宿主受害,主要流行在牧业发达地区,我国新疆是高发病流行地区之一,严重危害牧民及流行区居民的生命。肝泡性包虫病(肝泡棘球蚴病)的病理形态是由千万个小泡球蚴虫聚集成峰房状硬块,呈灰白色,触之坚硬如橡皮。临床体征与手术所见     

肝脏泡状棘球蚴病的CT诊断探讨

目的通过对肝脏泡状棘球蚴病患者CT检查、随访，探讨CT对肝脏泡状棘球蚴病的诊断价值。方法回顾性分析14例经生化检查、手术及病理检查结果证实的肝脏泡状棘球蚴病的CT表现。结果14例肝脏泡状棘球蚴病患者CT检查①平扫肝实质内均见低密度实性占位，边缘模糊。②病灶内均见散在颗粒状钙化，分布呈地图状、放射状，部分钙化灶可相互融合。散在颗粒状钙化征象在CT诊断泡状棘球蚴病中具有特异性。③CT增强检查病灶均无强化改变。具有②、③特征可对肝脏泡状棘球蚴病做出定性诊断。结论CT对肝脏泡状棘球蚴病的诊断有较大价值。     

In vitro cultivation of Wolbachia pipientis in an Aedes albopictus cell line

A continuous cell line, Aa23, was established from eggs of a strain of the Asian tiger mosquito, Aedes albopictus , naturally infected with the intracellular symbiont Wolbachia pipientis . The resulting cell line was shown to be persistently infected with the bacterial endosymbiont. Treatment with antibiotics cured the cells of the infection. In the course of establishing this cell line it was noticed that RFLPs in the PCR products of two Wolbachia genes from the parental mosquitoes were fixed in the infected cell line. This indicates that the mosquito host was naturally superinfected with different Wolbachia strains, whereas the infected cell line derived from these mosquitoes only contained one of the original Wolbachia strains. The development of an in vitro culture system for this fastidious microorganism should facilitate molecular analysis of the reproduction distorting phenotypes it induces in natural arthropod hosts.     

Selective sweep of Wolbachia and parthenogenetic host genomes – the example of the weevil Eusomus ovulum

Most parthenogenetic weevil species are postulated to have originated via hybridization, but Wolbachia has also been speculated to play a role via the induction of parthenogenesis. Here, we examine the molecular diversity of Wolbachia and parthenogenetic host genomes. The host species studied here, Eusomus ovulum, is known to be exclusively parthenogenetic and triploid. The E. ovulum populations that we examined had a low genetic diversity of mitochondrial (cytochrome oxidase I gene) and nuclear markers (internal transcribed spacer 2 and elongation factor 1‐ α gene), and they all were infected by only single bacteria strains (genotyped for five genes according to the multilocus sequence typing system). We found significant signs of linkage disequilibrium and a lack of recombination amongst all of the examined genomes (bacteria and host), which strongly indicates a selective sweep. The lack of heterozygosity in host nuclear genes, missing bisexual populations and selective sweep between the parthenogenetic host and bacteria genomes suggest that parthenogenesis in this species could have originated as a result of infection rather than hybridization. However, the finding that highly similar Wolbachia strains are also present in other parthenogenetic weevils from the same habitat suggests the opposite scenario: bacteria may have infected the already parthenogenetic lineage and taken advantage of the host's unisexual reproduction.     

THE SWINE LUNGWORM AS A RESERVOIR AND INTERMEDIATE HOST FOR SWINE INFLUENZA VIRUS : II. THE TRANSMISSION OF SWINE INFLUENZA VIRUS BY THE SWINE LUNGWORM

1. The swine lungworm can serve as intermediate host in transmitting swine influenza virus to swine. The virus is present in a masked non-infective form in the lungworm, however, and, to induce infection, must be rendered active by the application of a provocative stimulus to the swine it infests. Multiple intramuscular injections of H. influenzae suis furnish a means of provoking infection. Swine influenza infections can be provoked in properly prepared swine during the autumn, winter, and spring, but not during the summer. The phenomenon, while not regularly reproducible, occurs in well over half the experiments conducted outside the refractory period of summer. No explanation for the failures is apparent. 2. The virus can persist in its lungworm intermediate host for at least 2 years. 3. Swine infected with swine influenza virus by way of the lungworm intermediate host exhibit a more pronounced pneumonia of the posterior lobes of the lung than do animals infected intranasally with virus. The situation of the worms providing the virus will account for this. 4. Occasional swine infested with lungworms carrying influenza virus fail to become clinically ill after provocation but instead become immune. In these it is believed that lungworms containing the virus are localized outside the respiratory tract at the time of provocation. 5. It is believed that the experiments described furnish an explanation for the findings recorded in the preceding paper, in which swine influenza virus infections were induced in apparently normal swine by multiple injections of H. influenzae suis. 6. In a single experiment swine lungworms failed to transmit hog cholera virus.     

Localization of azithromycin in Toxoplasma gondii-infected cells.

Agents effective against intracellular pathogens must enter infected cells, crossing vacuolar membranes surrounding the organisms and then penetrating into the microbe and localizing to the microbial target site. We have characterized these parameters for azithromycin entry into Toxoplasma gondii-infected Chinese hamster ovary cells and murine macrophage-like J774 cells. Azithromycin uptake into infected host cells was concentrative and was dependent upon proton gradients. Subcellular fractionation of azithromycin-loaded infected CHO cells demonstrated > 95% intracellular drug in host cell lysosomes and cytosol, with < 5% associated with the parasite. Uptake of azithromycin into the T. gondii vacuole increased if parasites were coated with antibody prior to internalization by murine J774 cells, conditions which result in the formation of acidified phagolysosomes. No redistribution or retention of azithromycin in the parasite was observed when drug efflux from antibiotic-loaded infected CHO cells was monitored. Azithromycin entry into extracellular T. gondii was concentrative, was temperature and pH dependent, and was not different when azithromycin-sensitive and -resistant parasites were compared. These results demonstrate that azithromycin concentrates primarily in acidified compartments in parasites and host cells. The high concentration of azithromycin within these compartments may not be biologically relevant to inhibition of intracellular parasite growth by this agent.     

新型冠状病毒肺炎基本再生数的初步预测

目的预测新型冠状病毒感染肺炎(2019-nCoV)的基本再生数,为其防控和相关政策支持提供依据。方法基于包括"易感态-潜伏态-感染态-移除态"的SEIR仓室模型,假设2020年1月25日及以前出现症状的感染者均属于无干预自由传播期间感染的人员,结合截至1月26日凌晨已确诊和疑似病例数及国际同行预测的感染人数,参考SARS的流行病学关键参数,对新型冠状病毒感染肺炎的基本再生数进行估计。结果以《人民日报》和丁香园发布的新型冠状病毒感染肺炎疫情实时动态数据为基准,估计2019-nCoV的基本再生数在2.8~3.3之间;以国外同行预测的感染人数为基准,基本再生数在3.2~3.9之间。结论 2019-nCoV早期致病传播能力与SARS接近或略高于SARS,属于中高度传染性的传播疾病。迅速切断传播途径,采用及时有效的防控措施能够较快遏制2019-nCoV的进一步蔓延。     

Intracellular development of choleraphage phi 149 under permissive and nonpermissive conditions: an electron microscopic study

Intracellular development of choleraphage phi 149 following infection of Vibrio cholerae and Vibrio eltor cells under different conditions was examined by thin-section electron microscopy. Degradation of the host DNA following infection and formation of mature phage particles inside the infected cells were demonstrated. The concatemeric DNA intermediate formed during intracellular replication of phi 149 DNA in permissive hosts was resolved. In confirmation of biochemical evidence, no concatemeric DNA intermediate was observed for infection in high-phosphate medium.     

Experimental infection of lacertids with lizard erythrocytic viruses

OBJECTIVE: Lizard erythrocytic viruses (LEVs) produce inclusions in the cytoplasm of erythrocytes, but their impact on the infected host is poorly understood. This work reports on an experimental study of the infection process in Lacerta monticola and Lacerta schreiberi from Serra da Estrela Mountain, Portugal. METHODS: A time sequence light microscope and transmission electron microscope (TEM) study of the infection process was performed in peripheral blood erythrocytes of experimentally infected lizards. Virions were searched for by TEM in visceral organs and bone marrow of the animals. RESULTS: Infection was usually restricted to erythrocytes, but occasionally became systemic and induced disease. In the first case, a prevalence of infected erythrocytes of up to 98% followed by recovery was observed. In the latter, infection spread to leukocytes, leading to the death of the infected animals. CONCLUSIONS: The potential of LEVs to induce systemic infections was demonstrated. Sequential TEM examination of LEV-infected cells is described for the first time, demonstrating features such as dense inclusions related to virus nucleoid formation, intranuclear virions, intermediate structures in virion capsid morphogenesis and virus release by budding.     

Paclitaxel Arrests Growth of Intracellular Toxoplasma gondii

Addition of paclitaxel (Taxol) at a concentration of 1 μM to Toxoplasma gondii-infected human foreskin fibroblasts arrested parasite multiplication. Division of the T. gondii tachyzoite nucleus was inhibited, leading to syncytium-like parasite structures within the fibroblasts by 24 h after infection and treatment of the cultures. By 4 days after infection and treatment of the cultures with paclitaxel, this inhibition was irreversible, since the arrested intracellular form was incapable of leaving the host cell, infecting new cells, and initiating the growth of tachyzoites with normal morphology. Specifically, when paclitaxel was added to infected cells for 4 days and then removed by washing and the infected, paclitaxel-treated cells were cultured for 4 more days, there were no remaining T. gondii organisms with normal morphology. Syncytium-like structures in the cultures that were infected and treated with paclitaxel for 8 days were similar in appearance to those in preparations of infected paclitaxel-treated fibroblasts that had been cultured for 24 to 48 h. Pretreatment of the tachyzoites for 1 h with paclitaxel followed by the removal of the paclitaxel by repeatedly centrifuging and resuspending the parasites in fresh medium without paclitaxel and then adding fresh medium prior to culture of the parasites with fibroblasts did not prevent their invasion of fibroblasts but did affect their subsequent ability to replicate within fibroblasts. Pretreatment of the fibroblasts with paclitaxel also diminished subsequent replication of T. gondii in such host cells after 8 days. Thus, paclitaxel alters the ability of T. gondii to replicate in host cells. Inhibition of parasite microtubules by such compounds at concentrations which do not interfere with the function of host cell microtubules may be useful for development of novel medicines to treat T. gondii infections in the future.     

CELLULAR AND VASCULAR COMPONENTS OF THE ALLOGRAFT REACTION : EVIDENCE FROM RETURNED SKIN ALLOGRAFTS

In order to gain added insight into the mechanisms of allograft destruction, skin grafts were returned to their original donors after remaining as allografts long enough to induce immunity in the intermediate host but not long enough to cause destruction of the graft. Upon their return to unmodified donors, such grafts became revascularized and remained viable. An intense cellular infiltration was incited within the graft and its draining lymph node by the interaction between immunologically competent cells, some antigenically activated, that were transferred from the intermediate host with the graft, and those of the final host, the original donor. This immune interaction excited a nonspecific granulocytic and histiocytic response, which led to the destruction of the adjacent epithelium already re-accepted within its native habitat. This mechanism of epithelial destruction required vascular connection to permit the cellular infiltration, and was unlikely to have primarily involved circulating antibody. When similar grafts were returned to donors that had been sensitized to the intermediate host, vascularization and reacceptance of the graft did not occur. No cellular infiltration took place in the graft and no lymph node response was evoked. The returned grafts were cast off as full-thickness sloughs. Here the mechanism of graft rejection was apparently an interaction between the preformed antibody of the specifically sensitized host and the allogeneic cells transferred from the intermediate host; this interaction prevented the vascularization of the graft, even though the endothelia involved were autologous. In unmodified allografts, both the character and the variability of the histologic patterns can be accounted for by the superimposition, in differing rates and degrees, of humoral vascular effects upon cellular events already in progress.