2株贝氏隐孢子虫鸡源分离株对雏鸡的致病性比较

为了解不同地区鸡源贝氏隐孢子虫的致病特点,对收集到的郑州、林州两地区鸡源贝氏隐孢子虫卵囊经雏鸡传代扩增纯化后,分别以1×106个卵囊量接种3日龄罗曼公雏鸡,从其排卵囊情况、临床症状和病理学变化比较了2个分离株的致病情况。结果表明:2个隐孢子虫分离株均主要引起雏鸡呼吸道症状和法氏囊炎病变;接种雏鸡均于感染后第4天开始排卵囊,林州株和郑州株排卵囊持续期分别为23 d和13 d;排卵囊高峰期均为感染后第8~12天。雏鸡感染2个地区鸡源贝氏隐孢子虫分离株后,排卵囊量及排卵囊规律存在差异。     

固始鸡源隐孢子虫人工感染试验

为了解来源于地方鸡品种的隐孢子虫分离株致病特点,对收集到的河南固始鸡源隐孢子虫经鹌鹑传代纯化后,进行动物感染。结果:固始鸡源隐孢子虫分离株无论在正常还是免疫抑制情况下均不能感染小鼠,但能成功感染海兰雏鸡,出现明显的呼吸道症状及法氏囊病变。剖检发现虫体主要寄生在法氏囊、气管和泄殖腔等部位。根据卵囊形态学及寄生部位等特点,本试验分离的隐孢子虫种类鉴定为贝氏隐孢子虫(Crypto-sporidium baileyi)。增大感染剂量,可使雏鸡排卵囊高峰期提前,排卵囊量增大,持续期延长;免疫抑制剂的使用也可使高峰期提前,持续期延长,但会造成试验动物死亡率增高。雏鸡临床症状、剖检病变和增重减少均与感染剂量呈正相关,免疫抑制剂的使用会加重此影响。     

贝氏隐孢子虫不同感染剂量对樱桃谷鸭的致病性

为了确定贝氏隐孢子虫对鸭的致病性,本试验分为2×105、4×105、8×105、16×105、32×105、64×105个卵囊剂量组,实验感染2日龄樱桃谷品种雏鸭。从感染鸭的排卵囊情况、临床症状、组织病理学变化、病理形态学变化比较了不同剂量组的致病情况。结果表明,贝氏隐孢子虫主要引起呼吸困难症状,气管炎和法氏囊炎病变。其致病性与剂量有明显的相关性。贝氏隐孢子虫有较强致病性,而且病程较长,但其致死率较低。     

广东鸡,鸭隐孢子虫种类鉴定与致病性研究

从有患轻微呼吸道症状的鸡和鸭的粪便中分离到隐孢子虫卵囊，并在其组织切片中观察到隐孢子虫。根据卵囊的形态和大小、虫体寄生部位，确定鸡、鸭均为贝氏隐孢子虫感染。用上述鸡、鸭粪便中分离的卵囊，分别经口感染２日龄鸡和鸭各１５只以探索其致病性。感染鸡出现明显呼吸道症状，将引起死亡，气管、支气管、气囊、肺和法氏囊出现大体与显微病变。感染鸭则症状和病变都较鸡轻。结果表明：鸭对贝氏隐孢子虫感染的抵抗力比鸡强。     

贝氏隐孢子虫对丝毛乌骨鸡的致病性试验

２ 日龄丝毛乌骨鸡经口接种贝氏隐孢子虫（ Ｃｒｙｐｔｏｓｐｏｒｉｄｉｕｍ ｂａｉｌｅｙｉ）卵囊２×１０６ 个／只，潜隐期４ｄ，排卵囊开放期１８ｄ，排卵囊高峰期为感染后（ Ｐ Ｉ Ｄ）７～１４ｄ。呼吸道症状出现于 Ｐ Ｉ Ｄ１０，死亡率为１３３％ （２／１５）。扫描电镜观察发现气管纤毛脱落，寄生有各阶段发育虫体及杆形细菌和渗出的红细胞；法氏囊也寄生有大量虫体，粘膜上皮细胞肥大，微绒毛脱落， Ｐ Ｉ Ｄ２０ 在法氏囊粘膜表面见有许多虫体逸出后留下的带虫空泡。试验证明丝毛乌骨鸡为贝氏隐孢子虫的新宿主。使用扫描电镜系统观察了贝氏隐孢子虫感染引起的组织形态学病理变化。     

贝氏隐孢子虫鸡胚和雏鸡增殖模型筛选抗隐孢子虫药物试验

为探讨复方磺胺对甲氧嘧啶、磺胺二甲基嘧啶、地克珠利和阿奇霉素4种药物对鸡胚和雏鸡人工感染模型中鸡源贝氏隐孢子虫的作用,筛选有效防治隐孢子虫药物,采用鸡胚培养和人工感染雏鸡模型,分别以各组鸡胚发育状况、鸡胚中卵囊量、雏鸡精神状态、排卵囊规律、体质量变化、发病率、死亡率等为观察指标,考察这4种药物对隐孢子虫的作用。结果显示,使用复方磺胺对甲氧嘧啶、磺胺二甲基嘧啶、地克珠利、阿奇霉素组鸡胚中虫体数分别为阳性对照组的15.05%、88.71%、77.42%、68.82%。复方磺胺对甲氧嘧啶可缓解人工感染雏鸡隐孢子虫病临床症状,感染雏鸡发病率降低20%,死亡率降低13.13%,且可使排卵囊强度降低。结果表明,复方磺胺对甲氧嘧啶以一定剂量连续使用一定时间对雏鸡贝氏隐孢子虫病有潜在治疗作用。     

贝氏隐孢子虫对樱桃谷鸭的致病性试验

隐孢子虫病是一种全球性的人畜共患原虫病；禽类隐孢子虫发现于鸡、火鸡、鹌鹑、鹅、孔雀等，有关鸭隐孢子虫病的报道较少，特别是不同剂量感染的致病性差异未见报道，本试验采用鸭源贝氏隐孢子虫卵囊，雏鸡传代后，经口感染2日龄樱桃谷鸭，通过临床症状观察和病理变化观察，旨在探讨河南省鸭源贝氏隐孢子虫的致病性及不同剂量的卵囊接种后所引起的临床症状和病理变化的差异。     

不同禽源贝氏隐孢子虫分离株对鹌鹑致病性的比较研究

本研究旨在观察不同禽源贝氏隐孢子虫(Cryptosporidium baileyi)对鹌鹑的致病性差异。采用光镜、扫描电镜等技术研究了鸡源、鸭源、鹌鹑源、白文鸟源、鸵鸟源贝氏隐孢子虫分离株对10日龄鹌鹑的致病性。结果表明,感染鹌鹑均出现腹泻和呼吸道症状,排卵囊持续期11~18 d,虫体寄生于喉头、气管、法氏囊和泄殖腔。其中鸭源C.baileyi感染组鹌鹑发病率和死亡率分别为82.5%、25%,鸡源C.baileyi(郑州株)感染组发病率和死亡率分别为77.5%、12.5%,鹌鹑源C.baileyi感染组发病率、死亡率分别为37.5%和17.5%。本研究结果提示,不同禽源C.baileyi对鹌鹑有一定致病性,其致病性强弱存在差异。     

河南省规模化鸡场隐孢子虫感染情况调查

隐孢子虫（Cryptosporidium）是一种引起人兽共患病的机会性原虫,能感染包括人在内的240多种动物,引起动物机体不同程度的消化道和呼吸道症状。目前已鉴定出16个有效种,40多个基因型。感染禽类的隐孢子虫主要有3个种：贝氏隐孢子虫（C.baileyi）、火鸡隐孢子虫（C．meleagridis）和鸡隐孢子虫（C．galli）。其中C．baileyi为感染鸡的优势虫种,主要寄生在鸡的喉头、气管、法氏囊、泄殖腔等部位;C．meleagridis主要寄生于小肠,属于人兽共患病原;     

雏鸡贝氏隐孢子虫人工感染试验

作者对69只2日龄雏鸡进行了隐孢子虫的人工感染试验。试验分3组,每只口服贝氏隐孢子虫钝种卵囊分别为1.73×10~7、8.5×10~6和1.94×10~6个。于接种后第3天粪便中首次出现卵囊,第9—17天为排卵囊高峰期,排卵囊可长达35天。人工感染隐孢子虫后雏鸡的严重发病与死亡多见于接种后第14—21天。临床上出现严重的呼吸道症状。主要表现为:呼吸严重困难、气喘、伸颈、张口呼吸和打喷嚏。病鸡精神沉郁,眼半闭,翅下垂,站立不稳或独卧一侧,严重者则饮、食欲废绝,并于发病后2—3日内死亡,共死亡35只,死亡率为50.8%。病理剖检可见喉头与气管水肿,渗出物增多。有时气管内可见到块状的纤维素性渗出物,严重者在气管内形成一灰白色的凝固物。肺充血发炎、表面湿润,泡沫状渗出物增多。肺腹侧多有灰白色硬斑,气囊混浊,渗出物增多。肾灰白色肿胀。刮取气管及法氏囊粘膜作成涂片,经染色后可见到大量各发育期的隐孢子虫虫体。病理组织学观察可在喉头、气管、肺脏、直肠、泄殖腔及法氏囊粘膜表面找到大量的球形虫体。用透射电镜及扫描电镜观察发现鸡隐孢子虫均寄生在粘膜上皮细胞的表面,并不进入上皮细胞内部。在虫体寄生部位的粘膜绒毛层受害严重,大量上皮细胞脱落和破损,呼吸道有明显的炎性病变。     

Performance and oocyst shedding in broiler chickens orally infected with Cryptosporidium baileyi and Cryptosporidium meleagridis

To study effects of experimental cryptosporidiosis, broiler chickens were infected per os with 5 x 10(5) oocysts of Cryptosporidium baileyi and Cryptosporidium meleagridis. In the first experiment, chickens were infected with oocysts of C. baileyi at the age of 7, 14, and 21 days. In the second experiment, chickens were infected with oocysts of C. baileyi, C. meleagridis, or both cryptosporidial species at the age of 7 days. Although clinical signs of infection were apparent, neither final live weight nor mortality was significanty influenced in chickens infected with a single Cryptosporidium species. In chickens infected with C. meleagridis, the growth retardation was observed in the 2-wk period after infection. The compensatory growth, however, started when the oocyst shedding had ceased. The number of oocysts in excreta specimens of chickens infected with C. meleagridis was two to three times lower than in excreta of chickens infected with C. baileyi. Chickens infected with both C. baileyi and C. meleagridis (5 x 10(5) oocysts of each) had significantly lower final live weight and worse feed efficiency than chickens of other groups. Concurrent infection did not influence individual C. baileyi or C. meleagridis oocyst shedding.     

Cryptosporidium baileyi: effects of intra-abdominal and intravenous inoculation of oocysts on infectivity and site of development in broiler chickens

Developmental stages of Cryptosporidium baileyi were observed on the epithelium of the larynx, trachea, primary and secondary bronchi, air sacs, bursa of Fabricius, and cloaca of 12 chickens inoculated intra-abdominally with oocysts. All 12 birds inoculated intra-abdominally developed clinical signs of respiratory disease and had gross lesions of airsacculitis at necropsy. Developmental stages of C. baileyi and clinical signs of disease were not observed in 12 chickens inoculated intravenously with oocysts. The response of chickens to intra-abdominal inoculation of oocysts was similar to responses recorded following intratracheal inoculation of oocysts in previous studies.     

Interaction of reovirus and Cryptosporidium baileyi in experimentally infected chickens

No clinical signs, gross lesions, or increased mortality were observed in specific-pathogen-free chickens orally inoculated at 5 days of age with Cryptosporidium baileyi, reovirus 2035, reovirus 2408, or combinations of these agents. Weight gain of chickens inoculated with only reovirus 2408 was depressed 0-8 days postinoculation (PI) (P less than 0.01) but not for the 21-day period PI. Weight gain of chickens inoculated with only reovirus 2035 was not affected. Cryptosporidium baileyi infection significantly depressed weight gain 8-14 days PI but not for the entire 21-day period PI. Weight gain of chickens infected with both C. baileyi and reovirus 2035 was significantly depressed 0-14 days PI and for the entire 21-day period PI. Dual infection with C. baileyi and either reovirus appeared to promote shedding of both agents. Cryptosporidia were found principally in the rectum 2-10 days PI and in the bursa of Fabricius 6-10 days PI. Reovirus infection did not cause any microscopic lesions and did not modify lesions caused by C. baileyi infection.     

Experimental cryptosporidiosis and infectious bursal disease virus infection of specific-pathogen-free chickens

Specific-pathogen-free chickens orally inoculated at 4 days of age with a moderately pathogenic vaccine strain of infectious bursal disease virus (IBDV) and/or at 5 days of age with Cryptosporidium baileyi oocysts remained free of overt clinical signs throughout a 16-day period postinoculation (PI). The prepatency period for C. baileyi oocyst shedding was shorter in chickens receiving higher numbers of oocysts, but once shedding was detected, there were no obvious differences in shedding patterns among groups receiving 10(3) through 10(6) oocysts. On days 8 and 16 PI, cryptosporidia were located primarily in the bursae of Fabricius. IBDV exposure was associated with bursal follicle atrophy, whereas C. baileyi infection resulted in bursal epithelial hypertrophy and hyperplasia, mild follicle atrophy, and heterophil infiltration of the bursal mucosa. Examination of experimental groups of 30 birds each indicated that concurrent infection with both agents resulted in more severe bursal lesions, more infected birds, and greater numbers of cryptosporidia in infected tissues. At the termination of the trial, 16 days PI, Cryptosporidium infection was associated with a 6% decrease in mean body weight compared with controls.     

Experimental infections in domestic ducks with Cryptosporidium baileyi isolated from chickens

Oral inoculation of 13 ducks (Anas platyrhynchos) with 1 x 10(6) Cryptosporidium baileyi oocysts produced patent infections but no clinical signs of disease. Intratracheal inoculation of 13 ducks with 1 x 10(6) C. baileyi oocysts produced only mild clinical signs of respiratory disease, no deaths, and gross lesions of airsacculitis in only three ducks. The distribution of developmental stages of C. baileyi in ducks was similar to that observed in experimentally infected chickens and turkeys. Results of this study indicate that ducks are more resistant to experimentally induced respiratory cryptosporidiosis caused by C. baileyi than are chickens and turkeys.     

Experimentally induced infections in turkeys with Cryptosporidium baileyi isolated from chickens

Oocysts of Cryptosporidium baileyi isolated from chickens were inoculated by different routes into 3 groups of turkey poults. Intratracheal inoculation of oocysts produced clinical signs of respiratory tract disease, deaths, and gross lesions of airsacculitis. Parasites developed in the microvillous border of the nasopharynx, larynx, trachea, bronchi, and air sacs. Oral and intracloacal inoculations of oocysts caused no deaths or clinical signs of disease, but did produce patent infections. Respiratory tract infections limited to the nasopharynx, larynx, and trachea occurred in 3 orally inoculated poults. Respiratory tract infections were not observed in intracloacally inoculated poults. The mode of inoculation did not influence the distribution of C baileyi in the digestive tract. The cloaca was parasitized in 100% of the birds with intestinal infections, and the bursa of Fabricius was parasitized in 72.7%.     

Interaction of Marek's disease virus and Cryptosporidium baileyi in experimentally infected chickens

Histocompatible B13/B13 white specific-pathogen-free leghorn chickens were used to investigate the effect of coinfection with Cryptosporidium baileyi and the HPRS 16 strain of Marek's disease virus (MDV) in chickens and to assess the pathogenicity of C. baileyi when MDV is given before or after the parasite. Groups of chickens concurrently infected with C. baileyi orally inoculated at day (D)4 and MDV inoculated at hatching (C4M0 group) or at D8 (C4M8 group) were compared with relevant control groups inoculated with only C. baileyi at D4 (C4 group), only MDV at hatching (M0 group) or at D8 (M8 group), and an uninoculated control group (UC group). The chickens were kept in isolator units until the end of the experiment at D62. Our results showed a considerable synergistic effect in concurrently infected chickens and more severe consequences when chickens received MDV before C. baileyi infection. In fact, except for a slight transitory weakness, the chickens in C4 group remained free of overt clinical signs and there was no mortality. However, coinfection with both pathogens induced more lasting or permanent oocyst shedding. Severe clinical cryptosporidiosis with weakness, anorexia, depression, growth retardation, and chronic and severe respiratory disease causing death occurred in all chickens in the C4M0 group between D12 and D43 and in 67% of the chickens in the C4M8 group between D17 and D57. Eighty-two percent and 33%, respectively, died before the development of specific Marek's disease lesions. Mortality rates were 27% and 33% in the M0 and M8 groups, respectively. The presence of MDV enhanced the establishment of more lasting cryptosporidial infection in the respiratory tract, esophagus, crop, proventriculus, and kidneys (only in C4M0 group) as well as in bursa of Fabricius, ceca, and cloaca. Serologic analysis showed that chickens with chronic cryptosporidiosis in the C4M8 group had an increased level of C. baileyi-specific immunoglobulin A. Our results may explain some cases of mortality in chickens naturally infected with MDV and Cryptosporidium.