微孢子虫病化学治疗的研究进展

微孢子虫是一类专营细胞内寄生的真核生物，它是一种关系到农业生产和人类健康的病原微生物。本文主要针对国内外有关应用多菌灵、夫马洁林、阿苯哒唑等药剂对微孢子虫病的研究进展进行了综述，希望为微粒子病的化学治疗提供新思路。     

家蚕微孢子虫病研究进展

家蚕微孢子虫病是由微孢子虫Microsporidia(微粒子原虫类 )寄生蚕体引起的一种古老的、分布较广的传染性病害,因其经卵传染性而被世界各养蚕国家和地区列为蚕种生产的惟一检疫对象.多年来,广大学者对其病原、检测技术及防治方法等方面进行了大量的研究,取得了较大进展.现综述如下: 1 家蚕微孢子虫病病原的研究     

兔隐孢子虫病研究进展

<正>隐孢子虫是动物常见的机会致病性原虫,对哺乳动物主要引起以腹泻为主要症状的隐孢子虫病。随着人们生活水平的提高,兔作为经济动物和宠物与人类的关系日益密切,逐渐融入到人类的日常生活中,在部分地区发挥着很重要的作用。但近年来研究发现,兔可传播流行性人兽共患肠道寄生虫病,防治不及时就会对人类的健康造成很大的威胁。     

隐孢子虫病免疫学研究进展

隐孢子虫病（Cryptosporidiosis）是一种全球性的人畜共患病。其病原体为一种寄生性原虫，即隐孢子虫。隐孢子虫属于真球虫目、隐孢科、隐孢属，目前认为其有效种有6个，即感染鱼类的鼻隐抱子虫（C．nasorum）、感染爬行类的响尾蛇隐池子虫（C．crotati）、感染鸟类的火鸡隐抱子虫（C．meleagridis）和贝氏隐抱子虫（C．baileyi）、感染哺乳动物的鼠隐抱子虫（C．muris）和小隐子虫（C．parvum）。现已发现隐抱子虫可寄生于多种脊椎动物，下面就其引起的局部病理变化、免疫器官的反应、免疫反应和免疫诊断等方面述之。1寄生部位与所引起…     

脑炎微孢子虫属3种微孢子虫的虫株未能感染食用动物

研究了脑炎微孢子虫属最常见的3种微孢子虫的虫株对于食用动物包括猪,牛,鸡,和火鸡的感染力.动物经口接种孢子后用2种方法来检测是否被感染,一种方法是在每日粪样中检测孢子,另一种方法是在动物接种21d后的器官组织学检查.尽管每种虫种的接种量高迭2×10~6至2×10~7个孢子,但是在每种动物都没有检测到感染.结果表明,本试验中所用的脑炎微孢子虫属的3种微孢子虫虫株缺乏对猪,牛,鸠和火鸡的感染力.     

兔脑炎原虫病防制研究进展

兔脑炎原虫病是由兔脑炎原虫引起的一种人畜共患的寄生虫病 ,该虫可感染各种动物和人。其中以兔的感染较为严重 ,且多为隐性或慢性感染。因此对兔脑炎原虫病的诊断、预防及治疗显得非常重要。过去对此病的诊断通常采用病理组织学检查法或血清学等方法 ,而且没有有效防治该病的措施。随着近年来国际上对此病研究的深入 ,出现了一些新型的诊断技术如 PCR技术和透射电镜术等 ,并能用一些药物进行防治 ,如阿苯达唑和多胺等。文章重点就诊断和防治两方面进行了概述     

隐孢子虫病免疫学研究进展

隐孢子虫病（Cryptosxporidiosis）是一种全球性的人畜共患病。现已发现隐抱子虫可寄生于多种脊椎动物，其中包括哺乳动物、乌类、爬行类和鱼类。隐强子虫属于真球虫目、隐抱科、隐抱属，目前认为其有效种有6个，即感染鱼类的鼻隐抱子虫（C．nasorum）、感染爬行类的响尾蛇隐抱子虫（C．crotatN、感染鸟类的火鸡隐抱子虫（C。meleagrZdZs）和贝氏隐梅子虫（C．baileyi）、感染哺乳动物的鼠隐抱子虫（C。。urZs）和小隐掴寸一虫（C．parvu。）。下面就其引起的局部病理变化、兔疫器官的反应。免疫反应和免疫诊断等方面综述之。】．寄生…     

蜜蜂微孢子虫病研究进展

本文叙述了国内外学者研究蜜蜂微孢子虫病的成果，包括：蜜蜂微孢子虫（Nosema apis)的生物学，发育周期，孢子虫病的流行规律及影响发病的因素，患病蜜的病理及孢子虫病的诊断防治。     

自然感染兔脑炎原虫獭兔肾上皮细胞凋亡的研究

运用透射电镜术、原位末端标记技术(TUNEL)和流式细胞术对11只自然感染兔脑炎原虫獭兔的肾脏进行了细胞凋亡研究，5只健康长耳白兔用作对照。结果表明．凋亡细胞多见于远曲小管和集合管的上皮细胞。用透射电镜观察，初期的凋亡细胞，其细胞核的染色质高度凝集，边缘化，粗面内质网增多、扩张呈泡状；后期的凋亡细胞，其细胞质浓缩．细胞膜起泡，细胞核分裂成块状，最后形成膜包裹的凋亡小体。TUNEL法检测，病变轻微的细胞，胞核微缩，胞膜增厚；病变严重的细胞，其胞核体积明显缩小，胞膜皱缩，最后形成膜包裹的凋亡小体。流式细胞术检测，病兔可呈现明显的亚“G1”峰，凋亡细胞百分比与对照兔相比差异极显著(P=0．01)，且病兔。肾细胞的周期也有所改变。结果表明，3种方法检测的病兔肾上皮细胞凋亡数均高于对照免。     

阿苯达唑对自发性兔脑炎原虫病的治疗

为了有效地治疗兔脑炎原虫病,本研究根据脑炎原虫的生物学特点和对组织损伤的特征选用阿苯达唑进行了治疗试验。将28只3～4月龄隐性感染的獭兔,随机分为对照组和治疗组进行试验。治疗组按30mg／kg剂量（首次给药量为50mg／kg）,每隔12h给药1次,连续用药10d,停药1周为1个治疗期,共治疗3个疗程。对照组按正常饲养。每1疗程之后,均采血和尿液进行ELISA检测和尿沉渣虫体检查。结果,治疗组的病兔用阿苯达唑治疗3个疗程后,ELISA检测的D值均低于标准值（〈0．044）,即抗脑炎原虫血清抗体呈阴性反应,从尿沉渣中也不能检出虫体。而对照组病免的D值则大大高于正常值．从尿沉渣中均易检出虫,并有1只对照兔出现典型的神经症状,剖检后从脑组织中检出脑炎原虫性肉芽肿。经方差分析,2组间差异非常显著（P〈0．01）。试验证明,阿苯达唑对兔脑炎原虫有良好治疗作用,用药的时机以脑炎原虫还未进入脑组织时最合适,用药的剂量一定要保持有效的杀虫浓度。     

细胞培养的脑炎原虫感染家兔实验

用在体外连续培养１０代的兔脑炎原虫，接种于１２只家兔，动态地观察了脑炎原虫对家免的感染情况。实验发现，肾脏产生的病变明显早于大脑，即感染３周后，用Ｇｒａｍ＇ｓ和Ｇｏｏｄｐａｓｔｕｒｅ＇ｓ染色，即可在髓袢和远曲小管内脱落的上皮细胞中发现兔脑炎原虫。６周后即可见到间质性肾炎变化，而脑组织于感染９～１２周时才见有细胞性肉芽肿的形成；脑炎原虫具有较强的抗原性，即在感染３周后，血液中的抗体含量足以进行诊断。     

扫描及负染电镜在兔脑炎原虫病诊断中的应用

12只临床表现头颈歪斜、昏睡、震颤、局部或全身轻瘫的可疑为兔脑炎原虫病的獭兔 ,对其肾脏皮髓交界和尿沉渣分别进行了扫描电镜和负染电镜观察 ,看到了大小为 1～ 1 .5× 1 .4～ 2 .5μm,形态呈卵圆形和杆状的兔脑炎原虫。阳性检出率为 1 0 0 %。说明扫描及负染电镜术是诊断兔脑炎原虫病的一种较为可靠的技术。     

兔脑炎原虫病肾脏病变的病理形态学观察

对97只患脑炎原虫病獭兔的肾脏病变做了系统的病理形态学研究.眼观,可将肾脏病变分为三型:皱缩型、凹陷型和斑点型;镜检,依结缔组织增生的数量、部位和肾组织结构的不同改变而分为贯通型、局灶型和肉芽肿型.     

兔脑炎原虫的超微形态与发育

用电镜连续７代动态地观察了培养细胞中兔脑炎原虫的超微结构与发育状态。脑炎原虫含有细胞核，但无线粒体、内质网和高尔基复合体等细胞器，其表面有几根极丝。脑炎原虫在培养细胞中除二分裂增殖外，还有裂体增殖和配体增殖。由于脑炎原虫有３种增殖方式，故在光学显微镜下呈多形态结构。     

Brain and spinal cord lesions in encephalitozoonosis in mink

Central nervous system lesions were studied by light microscopy in 43 farmed mink, aged 5 months to 2 1/2 years, with spontaneous encephalitozoonosis and showing cataractous eye changes. Lesions were found in the brain and spinal cord of all animals examined but were generally mild and chronic. The lesions were consistent with those previously described in spontaneous encephalitozoonosis in other carnivores. Parasites in parasitophorous vacuoles and free or phagocytosed in necrotic and granulomatous lesions were demonstrated in animals aged 5 months to 1 year. The occurrence of arterial lesions of the polyarteritis nodosa type found in the youngest animals probably indicates fetal infection. In animals aged 1 1/2 and 2 1/2 years active lesions were usually lacking and the changes were characterized by arterial sclerosis, sometimes with aneurysmal formations, small perivascular lympho-plasmacytic cuffings and focal gliosis.     

Experimental Encephalitozoonosis in the Blue Fox: Transplacental Transmission of the Parasite

Spores of Encephalitozoon cuniculi were recovered from foetal and placental tissues from blue fox females orally inoculated with the parasite. The results provided evidence for transplacental transmission of the causative agent of fox encephalitozoonosis.     

Experimental Encephalitozoonosis in the Blue Fox: Neonatal Exposure to the Parasite

Newborn and young pups up to the age of 15 days were exposed to E. cuniculi, either by keeping the pups in cages together with orally inoculated foster-mothers and their offspring, or by oral inoculation with E. cuniculi spores. A majority of pups appeared sero-positive to E. cuniculi with the india-ink immuno-reaction from 35 to 87 days post exposure; spores of E. cuniculi were detected in organs of some of the animals. The non-inoculated pups kept together with the orally inoculated pups became seropositive from 49 to 129 days after the oral inoculations. However, the exposure of newborn and young pups failed to induce clinical encephalitozoo-nosis, and when killed at the time of pelting the body weights and fur quality appeared to be within the normal range in all exposed foxes. No macroscopic lesions were detected in the various organs. Histologically focal interstitial nephritis occurred in the great majority of the seropositive animals. Meningoencephalitis was seen in some of the foxes, whereas slightly thickened walls of some arteries, mainly in the myocardium, were found in a few animals. The lesions of the brain and kidneys seem to be very similar to those seen in chronic cases of rabbit encephalitozoonosis. Polyarteritis nodosa and severe encephalitis and interstitial nephritis with extensive proliferations of plasma cells, which are almost constant findings in cases of clinically diseased foxes, were not detected in any of the subclinically infected animals. Various factors that might be of significance in the pathogenesis of the disease are discussed, and it is concluded that intrauterine infection of the pups via the transplacental route appears to be an essential supposition for the establishment of clinical fox encephalitozoonosis.     

Experimental Encephalitozoonosis in the Blue Fox: Clinical and Serological Examinations of Affected Pups

Two groups of blue fox pups about 1½— 2 and 2½—3 months old, respectively, suffering from experimental encephalitozoonosis, were examined clinically and serologically. Antibodies to Encephalitozoon cuniouli were detected in all pups, the titres varying within the range 10–12,800. In addition to unspecific signs of disease the pups showed various neurological disturbances including ataxia, posterior weakness, lameness and circling behaviour, terminaiting in recumbency, paralysis or convulsions. Reduced sight or blindness was observed occasionally. Some of the pups appeared thirsty. Haematological examinations revealed pronounced leukocytosis without any conspicuous shift within the various groups of leukocytes. Biochemical examinations of serum showed significant elevated values of urea nitrogen, creatinine, and magnesium concentrations, reflecting renal dysfunction. Alanine aminotransferase was found significantly depressed in both groups. Raised levels of total protein were demonstrated due to pronounced hyperglobulinaemia. This finding, together with the common occurrence of generalized polyarteritis nodosa and proliferations of plasma cells in clinically affected pups, is probably a result of autoimmune disturbances initiated directly or indirectly by the protozoan infection.