北京鸭菲莱氏温扬球虫内生发育的研究

作者对北京鸭菲莱氏温扬球虫 Wenyonella philiplevinei 的内生发育进行了研究,所得结果如下:1.雏鸭感染后36～48小时发现第一代裂殖体,寄生于卵黄蒂前后和回肠肠绒毛顶端上皮细胞内,位于核的上方或下方。裂殖体和殖裂子都比 Leibovitz(1968)所报告的偏小,出现的时间偏后,该作者在雏鸭感染后24小时观察到第一代裂殖体。2.在雏鸭感染后54～72小时发现第二代裂殖体,寄生于卵黄蒂前后肠段、回肠和盲肠的肠绒毛上皮细胞和固有层中,比 Laibovitz(1968)所报道的偏小,出现的时间偏后,该作者报道出现于感染后49小时。3.感染后78～108小时发现第三代裂殖体,寄生于卵黄肇前后、回肠和盲肠肠绒毛上段上皮细胞内和固有层中,亦较 Leibovitz(1968)所报道的偏小,出现的时间偏后,该作者说出现于感染后74小时。4.感染后84小时见到配子体,91～120小时在卵黄蒂前后肠段、回肠和盲肠见到成熟的大小配子体,比 Leibovitz(1968)所见到的偏小,出现的时间略偏前,该作者在感染后93小时见到大小配子体。5.感染后91小时在回肠肠绒毛上皮细胞内发现卵囊,延续至120小时;到132小时仍能在回肠绒毛固有层中见到极个别的囊。到144小时即未再见到卵囊。人工感染的潜在期为95小时,Leibovitz(1968)报道为93小时。6.内生发育阶段寄生于卵黄蒂前后、回肠、盲肠和直肠肠绒毛上段的上皮细胞内和固有层中,曾在极个别患者的12指肠和空肠发现虫体,与 Leibovitz(1968)的观察基本相似,但他报道在盲肠12指肠和空肠未见到虫体。7.感染78至98小时之间,在卵黄蒂前后段、回肠和盲肠,见有不同程度的肠绒毛上皮脱落,水肿,固有层充血,和成纤维细胞增多等变化。肉眼病变不显著。所见病变比 Leibovitz(1968)所描述的偏轻。     

北京鸭毁灭泰泽球虫Tyzzeria perniciosa内生发育的研究

作者对北京鸭毁灭泰泽球虫的内生发育进行了研究,所得结果如下: 1.感染后48小时发现第一代裂殖体,寄生在肠绒毛远端部上皮细胞核的上方。肠绒毛的基部、肠腺和固有层中未发现虫体。在第一代裂殖体出现的最早时间上,我们的结果和Allen(1936)的报道不同,该作者于感染后24小时见到第一代裂殖体。而和Versenyi(1967)的报道相一致,该作者亦于感染后48小时发现第一代裂殖体。但Versenyi所报道的裂殖体偏大,寄生于粘膜间质细胞中。 2.感染后96小时发现第二代裂殖体,比Allen(1936)和Versenyi(1967)所报道的偏小。 3.Allen(1936)认为毁灭泰泽球虫内生发育的无性世代,至少有三代,Versenyi(1967)认为不大可能多于两代。我们认为最大可能是两代:第一代裂殖体最早出现于感染后48小时,延续到84小时,寄生于肠绒毛上皮细胞核的上方,个别的在核下方,靠近固有层;第二代裂殖体最早发现于感染后96小时,延续至120小时,寄生于肠绒毛上皮细胞核的下方和固有层以及肠腺腺细胞核的内侧。 4.感染后96小时发现大小配子体,延续到120小时以后,直至143小时仍能在12指肠和卵黄蒂前后肠段绒毛固有层中见到大配子。Allen报道感染后48小时出现大小配子体;Versenyi(1967)报道最早于感染后96小时出现配子细胞。 5.感染后104—120小时发现卵囊;到感染后144—216小时,即不再发现裂殖体和大、小配子体,亦未见卵囊。感染后第五天(118小时),随粪便排出卵囊。 6.内生阶段的虫体寄生于12指肠、空肠和回肠(整个小肠),尤以卵黄蒂前后段受侵害最为严重。感染严重时,盲肠和直肠也见有虫体。     

鹅艾美球虫对雏鹅的致病性及病理学研究

用纯种鹅艾美球虫孢子化卵囊分别人工感染9日龄和18日龄雏鹅,进行致病性与病理学研究.以0.01×104个/只、0.1×104个/只、1.0 × 104个/只剂量感染9日龄雏鹅,死亡率分别为0、10%和60%;以0.5×104个/只、3.0×104个/只剂量感染18日龄雏鹅,死亡率分别为20%和75%.雏鹅发病的临床症状和死亡鹅的病理变化基本一致,潜伏期5 d～5.5 d,病程3.5 d～4 d.病变主要在小肠下段,尤其是空肠后段与回肠前段最严重,呈急性出血-坏死性或出血-卡他性肠炎.大量配子体或卵囊寄生在肠绒毛基部尤其是肠腺上皮细胞中,引起肠黏膜上皮坏死、脱落以及肠壁水肿、出血和炎性细胞浸润等.结果表明:鹅艾美球虫对雏鹅有很强的致病性;致病性主要发生在配子生殖阶段,是由大量的配子体或卵囊在肠腺上皮细胞内发育破坏了肠道黏膜组织结构与功能所致.     

柔嫩艾美耳球与鸡体的相互作用

鸡吞食柔嫩艾美耳球虫卵囊后感染，子孢子穿过绒毛上皮和固有层，进入隐窝上皮细胞，经数次无性生殖和有性生殖，形成裂殖子和配子体。大配子被小配子受精后发育成卵囊并脱落到粪便中，鸡感染球虫后，鸡体免疫系统抑制球虫的发育有三个时期：子孢子寻找穿透位点时；子孢在子绒毛上皮时；子孢子穿过固有层时。     

柔嫩艾美耳球虫与鸡体的相互作用

鸡吞食柔嫩艾美耳球虫卵囊后感染,子孢子穿过绒毛上皮和固有层,进入隐窝上皮细胞,经数次无性生殖和有性生殖,形成裂殖子和配子体。大配子被小配子受精后发育成卵囊,并脱落到粪便中,鸡感染球虫后,鸡体免疫系统抑制球虫的发育有三个时期：子孢子寻找穿透位点时;子孢子在绒毛上皮时;子孢子穿过固有层时。据此,我们研究了抗球虫免疫中诱导和效应阶段的决定因素。结果表明,子孢子在固有层中的穿透诱导了免疫;子孢子是免疫有关的最重要的发育阶段;细胞毒性Ｔ细胞对抑制球虫发育是必需的。     

巨型艾美耳球虫地方株的分离与鉴定

本文报道对巨型艾美耳球虫长春株的分离鉴定。主要鉴定指标如下:虫体寄生于小肠中段的空肠与回肠,配子体寄生于上皮下。病理变化主要表现为肠管充血、黄染、臌气,粘液性稀便以及肠粘膜针尖大小出血点。卵囊大小为31.5±0.26×23.1±0.15微米。最大裂殖体为9.2微米,潜隐期126±0.15小时,卵囊最短孢子发育时间为28小时。     

不同发育期两种艾美耳球虫在鸡消化道内的分布

对柔嫩艾美耳球虫Eimeria teenlla和巨型艾美耳球虫Eimeria maxima的卵囊、孢子囊和子孢子在鸡消化道和粪便中的分布情况进行了研究。口服接种柔嫩艾美耳球虫卵囊第1小时后,盲肠内孢子囊数为3.4×10~8、以后则逐渐减少;而子孢子数增加且直到接种后第12小时仍保持一个高水平。其它肠段只有少量的孢子囊和子孢子。在接种巨型艾美耳球虫卵囊后的第2小时,主要在空肠内发现有大量的子孢子。研究发现,柔嫩艾美耳球虫和巨型艾美耳球虫的绝大多数子孢子分别寄居在盲肠和空肠内,表明每种球虫子孢子侵袭部位的特异性在侵袭发生前就确定了。     

柔嫩艾美耳球虫病鸡盲肠上皮细胞凋亡的分析

从细胞凋亡的角度探讨柔嫩艾美耳球虫(E.tenella)对鸡盲肠黏膜的损伤机理,为鸡球虫病的防治提供理论依据.用E.tenella孢子化卵囊感染雏鸡,于感染后不同时间段取盲肠组织,运用常规病理组织学、超微病理学和原位末端标记技术对感染E.tenella病鸡肓肠黏膜上皮细胞和肠腺上皮细胞进行观察和分析.结果表明:鸡感染E.tenella的第2天,盲肠黏膜上皮细胞凋亡数即开始增加,感染后第4～6天是病变最严重且具有特征性的阶段,主要表现为中、后段盲肠黏膜深层严重出血,大最黏膜上皮脱落,严重者可见整个黏膜几乎完全脱落,肠腺破坏,其表面被覆盖大量脱落的变性、坏死的上皮细胞和红细胞,残存的黏膜上皮细胞和肠腺上皮细胞凋亡速度加快,大多数上皮细胞处于凋亡状态,凋亡指数极显著(P≤0.01)高于空白对照组,凋亡细胞体积缩小,细胞线粒体肿胀,严重时破裂成大空泡,染色质致密边集或断裂成核碎片,形成膜包裹性凋亡小体.结果提示E.tenella感染鸡后盲肠上皮细胞凋亡加重,以裂殖生殖阶段最为明项,且与损伤程度和病程密切相关.     

兔肠艾美尔球虫的致病性研究

为研究寄生在肠道内肠艾美耳球虫的致病性,文章使用不同剂量组的纯种卵囊去感染无球虫兔的方式,从临床及病理组织学等方面进行了试验。通过临床症状、体重、卵囊产量的变化及光镜对感染无球虫兔的致病性试验观察,除对照组外,每组在第6天,均出现临床症状,感染后8、9、10天最为明显,第9天出现死亡现象。组织学病变发生于空肠后部向下延及回肠至回盲口。结果表明,肠艾美耳球虫具有强致病性。     

长毛兔球虫病的综合防控措施

<正>兔球虫病是由艾美耳尔属的球虫引起,该属共有14个种,其中,斯氏艾美球虫可寄生于兔胆管上皮细胞内,其余各种都寄生于肠黏膜上皮细胞内,一般为混合感染。兔球虫卵囊在温度20℃,湿度55%~75%的外界环境中,经2~3d即可发育成为感染性卵囊。卵囊对化学消毒药物及低温的抵抗力很强,大多数卵囊可以越冬。但对日光和干燥很敏感,直射阳光在数小时内能杀死卵囊。该病流行于潮湿多雨季节,或冬季采用密封式温棚保温,     

Scanning electron microscopic observations on the intestinal villi in growing White Leghorn and broiler chickens from 1 to 30 days of age

1. To obtain intestinal morphological data demonstrating the faster growth rate in broiler (BR) than in White Leghorn (WL) chickens, villi of the duodenum, jejunum and ileum were examined from 1 to 30 d of age by scanning electron microscopy. 2. At the first day after hatching, villi of each intestinal segment showed a finger-like shape in both breeds. Villi developed to a plate-like shape in the duodenum, a wave-like shape in the jejunum and a tongue-like shape in the ileum at 30 d of age via the common plate-like villi at 10 d of age. The fundamental villous shape and arrangement seem to be accomplished by 10 d of age; two types of obliquely elongated plate-like villi showed a zigzag arrangement, adjoining at an angle of 40 degrees to 60 degrees like an oblique T-shape. It is suggested that such a villous arrangement would be more effective for nutrient absorption by inducing a long zigzag flow of ingesta. 3. Compared with WL, even at the first day after hatching BR had many more developed epithelial cell protrusions over the whole apical surface of the duodenal villi. In WL the protrusions were not so apparent and located only in the central area of the villous tip. Furthermore, at 10 d of age BR showed more developed and larger villi, many wider microvilli at the apical portion of villi and more active extrusions of epithelial cells from the tip of the duodenal and jejunal villi. 4. These morphological characteristics of villi in early life in BR suggest a greater absorptive surface area and a more active intestinal function, permitting the faster growth rate of BR immediately after hatching.     

Acute primary toxoplasmic hepatitis in an adult cat shedding Toxoplasma gondii oocysts

A 3-year-old 4-kg neutered male domestic shorthair cat died within 5 days after onset of fever and respiratory distress. At necropsy, all tissues were icteric, and the liver had a diffuse reticular pattern. Histologically, hepatitis and encephalitis were associated with Toxoplasma gondii tachyzoites. Toxoplasma gondii female gamonts and oocysts were found in epithelial cells of intact villi and in epithelial cells desquamated into the lumen. Finding of acute hepatitis and T gondii oocysts in an adult cat without detectable immunodeficiency is unusual, because adult cats rarely have clinical signs of toxoplasmosis during the oocyst-shedding phase.     

Distribution of the pores of epithelial basement membrane in the rat small intestine

The distribution and diameter of the pores of epithelial basement membrane in the intestinal villi and the lymph nodules of ileal Peyer's patches were investigated in the rat small intestine by scanning electron microscopy after the removal of the overlying epithelial cells with OsO(4) maceration. In the duodenum, jejunum and ileum, the pores were mainly distributed at the upper three fourths of the villi, but were scarce around the top of the villi. The diameter of some of the pores in the upper three fourths of the villi was larger than that of those in the lower portion. The protrusion of lymphocytes and the cytoplasmic processes of macrophages were also seen at the orifices of the pores. In ileal Peyer's patches, in contrast, pores were densely distributed in the lower one third of the follicle-associated epithelium (FAE) where M cells were mainly seen. Furthermore, these pores were larger than those found in the upper two thirds. Lymphocytes or cytoplasmic processes of macrophages were frequently seen in the lower one third of FAE. These results suggest that the pores at the basement membrane correspond to the passage of the immunocompetent cells which are in contact with M cells or villous columnar epithelial cells and that the abundance of pores is a sign of aggressive interaction between the particular epithelial cells and the immunocompetent cells at the upper three fourths of intestinal villi and the lower one third of FAE in the rat small intestine.     

Porcine Neonatal Coccidiosis

Coccidia were identified in intestinal sections from 82 piglets comprising 37 consignments from 34 farms, and represented a yearly increasing incidence in the three years 1978 to 1980. Piglets were primarily from medium to large farms with intensive, continuous-farrowing, confinement-rearing programs. Piglets, usually five days to 15 days old, had yellow, fluid diarrhea, became unthrifty and sometimes died. In six piglets from two farms, a green, adherent, fibrinonecrotic membrane was seen throughout most of the jejunum and ileum. Significant gross lesions were not observed in the other 76 piglets. Moderate to severe villous atrophy of jejunum and ileum was seen histologically. Various asexual and sexual stages of coccidia were seen within parasitophorous vacuoles of villar epithelial cells. Multifocal erosions with necrosis of villar tips and occasionally more diffuse mucosal necrosis with fibrinocellular exudate were seen. Isospora suis oocysts were identified in feces from several weaners from one farm. Amprolium and decoquinate mixed in the sow ration at 1 kg/tonne for three weeks prior to and postfarrowing was moderately successful in stopping outbreaks of neonatal diarrhea associated with coccidiosis.     

Scanning electron microscopy of intestine of gnotobiotic piglets infected with porcine rotavirus.

The development of intestinal lesions caused by the porcine rotavirus were studied in six day old gnotobiotic piglets by scanning electron microscopy. The onset of diarrhea followed an incubation period of 17 to 31 hr. The first detectable lesion was observed in the ileum at 12 hr postinfection, a few hours before the onset of diarrhea. At this time enterocytes appeared swollen and began to separate from each other. Seventeen hours after the onset of diarrhea, lesions were quite severe jejunum and ileum. Enterocytes were detaching from the lamina propria leaving denuded areas. Microvilli were sparse on the cell surfaces and there was marked villous atrophy. Regeneration of ileal mucosa was evident at 4.8 days after the onset of diarrhea. Nine days after recovery from diarrhea the intestinal villi had returned to near its normal structure but there remained some evidence of mucosal damage.     

Morphology of the small intestine of weaned piglets and a novel method for morphometric evaluation

The intestinal morphology of 7-week-old pigs was investigated by light (LM) and scanning electron microscopy (SEM). The piglets were fed either a semisynthetic or a cereal-based diet. The shapes of the intestinal villi and crypts of the duodenum, jejunum and ileum were examined. The villi were predominantly tongue-shaped. In the duodenum they were also ridged, branched and folded, and in the jejunum they were also leaf-like and ridged. At places with lymph follicles, the surface of the ileum was rugged with meandering fold-like villi. The crypts of the three segments of the small intestine were mainly coiled and sometimes branched. A novel morphometric evaluation method was introduced using the enlargement factors of each villus and crypt surface. The enlargement factor for the villus surface of the duodenum, jejunum and ileum was 3.13, 3.72 and 2.71, respectively. The factor for the crypt surface of the duodenum, jejunum and ileum was 9.07, 8.94 and 6.53, respectively. Furthermore, the relative proliferation rate and the epithelial renewal index were calculated for the first time. The relative proliferation rate of the duodenum, jejunum and ileum was 32.88, 34.78 and 50.77 proliferations per mm crypt perimeter, respectively. The diets consumed had an influence on the epithelial renewal index being higher for piglets fed the cereal-based diets.     

A comparison of histopathological changes in calves associated with K99- and K99+ strains of enterotoxigenic Escherichia coli.

Enterotoxigenic colibacillosis was experimentally produced in four colostrum-deprived calves given 10(10) Escherichia coli strain 210 (serotype 09+:K30+:K99-:F41-:H-) orally and the histopathological changes compared to those seen in colostrum-fed calves infected in an earlier study with strain B44 (serotype 09+:K30+:K99+:F41+:H-). Escherichia coli strain 210 caused diarrhea, atrophic villi with cuboidal epithelium, and focal accumulations of a few neutrophils in the dome villi above Peyer's patches but neither the clinical nor the histopathological changes were as pronounced as with strain B44. The extent and distribution of adherence to the mucosal surface differed between the two strains. Strain B44 adhered as a continuous layer over most of the absorptive epithelial surface of both the jejunum and ileum. Adherence of strain 210 was restricted to the ileum and the bacteria often adhered focally in "clumps" rather than as a continuous layer, especially on the distal half of the villous surface.     

Morphological features of the gastrointestinal tract of Garganey (Anas querquedula,Linnaeus 1758)—Oesophagus to coprodeum

The present work was aimed to study the gastrointestinal tract in Garganey from the oesophagus to coprodeum by the aid of the gross morphology, scanning electron microscopy and histology. At the level of the thoracic inlet, the oesophagus had a thick part which had numerous tortuous longitudinal folds carried transverse folds on them. Histologically, the thick part had thick epithelium and appeared more folded with more and larger glands. The mucosa of the proventriculus had mucosal folds appeared as a leaf-like with rounded tips. The openings of the proventriculus glands were projected with papillae on the epithelial surface. The gizzard lined with horizontal layer of cuticle which sent vertical parts of cuticle. The duodenal villi were pentagonal in shape with sharply pointed tips, while the jejunal villi were triangular with rounded ends, and the ileal villi were wide and pentagonal in shape with pointed tips. The mucosa of the duodenum, jejunum and ileum was thrown into villi lined by simple columnar epithelium with goblet cells with difference in the form, length, density and number. The apical points of the duodenal and ileal villi appeared pointed, while the jejunal villi had rounded ends. The jejunal villi were longer and numerous than the duodenal villi, but the ileal villi appeared with different length and less numerous. The mucosa of the caecum had numerous mucous glands which surrounded by circular crypts. The rectal mucosa had longitudinal folds and semilunar and circular crypts. The mucosa of the coprodeum had longitudinal folds surrounded by crypts.     

Passive protection against porcine epidemic diarrhea (PED) virus in piglets by colostrum from immunized cows.

The effects of hyperimmune cow colostrum (HCC) on experimentally induced porcine epidemic diarrhea (PED) were investigated in piglets. In experiment 1, four 2-day-old piglets fed HCC containing an antibody titer of 1:512 and another four piglets fed unimmune cow colostrum (UCC) were orally inoculated with 10LD50 of PED virus. The piglets were given colostrum three times a day at 4 hr intervals. Half of the piglets fed HCC showed diarrhea and recovered, and all piglets survived. In contrast, all piglets fed UCC developed diarrhea and three of them died. In experiment 2, 2-day-old piglets fed HCC containing antibody titers of 1:512, 1:128 and 1:32, and UCC were inoculated with PED virus, and survival rates after challenge were 100, 75, 50 and 0 %, respectively. In experiment 3, 1-day-old piglets fed HCC with 1:512 antibody titer or UCC were inoculated and necropsied at 24, 48 and 72 hr after the inoculation for pathological examination. Piglets fed HCC remained healthy and PED virus antigen was not detected in the epithelial cells of the small intestine, and the length of the villi in small intestine was normal. On the other hand, in piglets fed UCC, villous atrophy and PED virus antigen were observed in epithelial cells of the jejunum and ileum from 24 hr. It was concluded that oral administration of HCC to piglets was effective in preventing PED virus infection and reduced their mortality.     

Enterotoxigenic colibacillosis in colostrum-fed calves: pathologic changes.

Enterotoxigenic colibacillosis was experimentally produced in 8 of 9 colostrum-fed calves orally given 10(11) Escherichia coli. The eight calves developed profuse diarrhea accompanied by dehydration and depression. At 12 hours after exposure, all calves were euthanatized for necropsy and for collection of tissues for microscopic examination. Histopathologic changes included stunted villi in the jejunum and ileum, focal degeneration and exfoliation of absorptive epithelial cells at the tips of jejunal and ileal villi, and focal emigration of neutrophils which was especially prominent above the dome area of aggregated lymphatic follicles (Peyer's patches). A layer of E coli adhered to the epithelial surface of the jejunum and ileum. In the duodenum, lesions were minimal or absent and bacteria were not adhering to the mucosa. Histopathologic changes were not observed in other tissues. In two calves examined 24 hours after they were inoculated and in two calves euthanatized 24 to 36 hours after spontaneously developing enteric colibacillosis, lesions were similar to those observed in the calves at 12 hours after exposure.