Comparison by plaque assay of bovine rotavirus and a bovine enterovirus-like agent

Enterovirus-like particles from feces of calves are a frequent source of contamination of bovine rotavirus isolates. A study of plaque formation using BSC-1 cells indicated differences in behaviour of the viruses which could be used for differentiation the purification. The enterovirus-like particles produced well-defined plaques earlier and reached their optimal size much more rapidly than did the rotavirus. Furthermore, plaques produced by bovine enterovirus-like particles were significantly larger than those of bovine rotavirus. The viral cytopathic effects on the cells within the plaques were also characteristic for each virus.     

Pathologic changes caused by transplacental infection with an adenovirus-like agent in pigs

Five hysterectomy-derived colostrum-deprived pigs housed in individual cages with positive ventilation developed severe skin cyanosis and edema of the subcutaneous tissues in the submandibular, thoracic, and abdominal regions. The 5 pigs were killed 7 to 10 days after birth. Eosinophilic intranuclear inclusion bodies were found in endothelial cells of capillary and small blood vessels throughout the body. Ultrastructurally, nuclei of these affected endothelial cells contained small crystalline arrays of virus particles, which were considered to belong to the adenovirus-like group from their size and structure. The present results indicated that the porcine adenovirus-like agent might also have the ability to produce transplacental infection.     

The pathogenesis of an enteric infection in pigs,experimentally induced by the coronavirus-like agent,CV 777

Sixteen 2–3-days-old caesarean-derived, colostrum-deprived piglets were each dosed oro-nasally with 2 ml of a bacteria-free filtrate containing 10⁴ pig-infectious-doses of CV 777. The piglets were killed at intervals of 12 to 120 h after infection. The coronvirus-like agent caused a local infection of the intestinal tract which resulted in villous atrophy, malabsorption and diarrhea. The pathogenesis of this infection was similar to that of transmissible gastroenteritis (TGE), a known coronaviral infection of pigs. However, where were some differences. By immunofluorescent staining, CV 777 antigens were not only detected in the epithelial cells covering the small intestinal villi, but also in the cells of the colonic surface epithelium. Occasional fluorescence was also seen in the small intestinal crypt epithelium, but the regenerative capacity of the crypts was not affected. The progress of intestinal epithelial cell infection by CV 777 was much slower than that in TGE, resulting in a longer incubation period and in less drastic epithelial cell destruction. The infection of regenerating cells occurred to a much higher degree during the late stage of a CV 777 infection than has been observed in TGE.     

Gastric and enteric phytobezoars caused by ingestion of persimmon in equids

CASE DESCRIPTION-13 equids (10 horses, 2 donkeys, and 1 pony) were examined for signs of colic (n = 7), weight loss (6), anorexia (3), and diarrhea (2). Ten equids were evaluated in the fall (September to November). Seven equids had a history of persimmon ingestion. CLINICAL FINDINGS-A diagnosis of phytobezoar caused by persimmon ingestion was made for all equids. Eight equids had gastric persimmon phytobezoars; 5 had enteric persimmon phytobezoars. Gastroscopy or gastroduodenoscopy revealed evidence of persimmon ingestion in 8 of 10 equids in which these procedures were performed. TREATMENT AND OUTCOME-2 of 13 equids were euthanatized prior to treatment. Supportive care was instituted in 11 of 13 equids, including IV administration of fluids (n = 8) and treatment with antimicrobials (5), NSAIDs (5), and gastric acid suppressants (4). Persimmon phytobezoar-specific treatments included dietary modification to a pelleted feed (n = 8); oral or nasogastric administration of cola or diet cola (4), cellulase (2), or mineral oil (2); surgery (4); and intrapersimmon phytobezoar injections with acetylcysteine (1). Medical treatment in 5 of 7 equids resulted in resolution of gastric persimmon phytobezoars. Seven of 8 equids with gastric persimmon phytobezoars and 1 of 5 equids with enteric persimmon phytobezoars survived > 1 year after hospital discharge. CLINICAL RELEVANCE-Historical knowledge of persimmon ingestion in equids with gastrointestinal disease warrants gastroduodenoscopy for evaluation of the presence of persimmon phytobezoars. In equids with gastric persimmon phytobezoars, medical management (including administration of cola or diet cola and dietary modification to a pelleted feed) may allow for persimmon phytobezoar dissolution.     

Pathogenesis of feline enteric coronavirus infection

Fifty-one specific pathogen-free (SPF) cats 10 weeks to 13 years of age were infected with a cat-to-cat fecal-oral passed strain of feline enteric coronavirus (FECV). Clinical signs ranged from unapparent to a mild and self-limiting diarrhea. Twenty-nine of these cats were FECV na?ve before infection and followed sequentially for fecal virus shedding and antibody responses over a period of 8-48 months. Fecal shedding, as determined by real-time polymerase chain reaction (RT-PCR) from rectal swabs, appeared within a week and was significantly higher in kittens than older cats. FECV shedding remained at high levels for 2-10 months before eventually evolving into one of three excretion patterns. Eleven cats shed the virus persistently at varying levels over an observation period of 9-24 months. Eleven cats appeared to have periods of virus shedding interlaced with periods of non-shedding (intermittent or recurrent shedders), and seven cats ceased shedding after 5-19 months (average 12 months). There was no change in the patterns of virus shedding among cats that were excreting FECV at the time of a secondary challenge exposure. Four cats, which had ceased shedding, re-manifested a primary type infection when secondarily infected. Cats with higher feline coronavirus (FCoV) antibody titers were significantly more likely to shed virus, while cats with lower titers were significantly less likely to be shedding. Twenty-two kittens born to experimentally infected project queens began shedding virus spontaneously, but never before 9-10 weeks of age. Natural kittenhood infections appeared to be low grade and abortive. However, a characteristic primary type infection occurred following experimental infection with FECV at 12-15 weeks of age. Pregnancy, parturition and lactation had no influence on fecal shedding by queens. Methylprednisolone acetate treatment did not induce non-shedders to shed and shedders to increase shedding.     

采用PCR方法对我国蜱伯氏疏螺旋体感染的流行病学调查

通过调查我国已有的4种蜱伯氏疏螺旋体的感染情况,以进一步阐明莱姆病在中国的分布与流行状况。本研究通过筛选扩增伯氏疏螺旋体外膜蛋白A(OspA)基因片段的通用引物,获得1对特异性引物,优化反应条件后建立用于检测蜱体内伯氏疏螺旋体的PCR方法,其扩增片段大小为307 bp。该方法可检测出10 pg的阿氏疏螺旋体(Ba)、1 pg的伽氏疏螺旋体(Bg)和0.01 pg的狭义伯氏疏螺旋体(Bb)的3种不同基因型的伯氏疏螺旋体的OspA基因组DNA,表明其敏感性较好,适用于蜱感染伯氏疏螺旋体状况的调查。本研究从我国7个省采集到的667只蜱,进行伯氏疏螺旋体感染的流行病学调查,分类鉴定表明这些蜱分属革蜱属、血蜱属、牛蜱属和扇头蜱属。PCR检测所获数据表明它们的感染率分别为4%(10/264)、6%(11/137)、31.4%(59/185)和31%     

Proliferative enteropathy: a global enteric disease of pigs caused by Lawsonia intracellularis

Proliferative enteropathy (PE; ileitis) is a common intestinal disease affecting susceptible pigs raised under various management systems around the world. Major developments in the understanding of PE and its causative agent, Lawsonia intracellularis, have occurred that have led to advances in the detection of this disease and methods to control and prevent it. Diagnostic tools that have improved overall detection and early onset of PE in pigs include various serological and molecular-based assays. Histological tests such as immunohistochemistry continue to be the gold standard in confirming Lawsonia-specific lesions in pigs post mortem. Despite extreme difficulties in isolating L. intracellularis, innovations in the cultivation and the development of pure culture challenge models, have opened doors to better characterization of the pathogenesis of PE through in vivo and in vitro L. intracellularis-host interactions. Advancements in molecular research such as the genetic sequencing of the entire Lawsonia genome have provided ways to identify various immunogens, metabolic pathways and methods for understanding the epidemiology of this organism. The determinations of immunological responsiveness in pigs to virulent and attenuated isolates of L. intracellularis and identification of various immunogens have led to progress in vaccine development.     

Polyserositis in pigs caused by infection with Mycoplasma

A bovine adenovirus was isolated from a yearling heifer with systemic adenovirus infection. The virus was characterized as a subgroup 2 bovine adenovirus but could not be typed with reference antisera to the 10 known bovine adenovirus serotypes. A serological survey of cattle in the northern half of the North Island showed the prevalence of precipitating antibodies to bovine adenoviruses to be 43.3%.     

Bovine abortion caused by infection with Leptospira pomona

Abstract

Extract

A gram-negative pleomorphic facultative aerobic organism, indistinguishable morphologically and culturally from that isolated from suppurative epididymitis in rams and described by Dodd &; Hartley (1955) Dodd, D. C. and Hartley, W. J. 1955. N.Z. vet. J., 3: 105–105. [Taylor &; Francis Online] , [Google Scholar], has, over the last five years, been isolated at this laboratory on more than ten occasions from polytenosynovitis and pyaemia in lambs, and on one occasion from mastitis in a ewe. It still remains to characterize and classify this organism, but Roberts has made a detailed comparison of it with his Histophilus ovis (Roberts, 1956 Roberts, D. S. 1956. Aust. vet. J., 32: 330–330.  [Google Scholar]) and considers that the two are indistinguishable (Roberts, 1958, pers. comm.).     

肉鸡自然感染和实验性感染鹦鹉热衣原体的病理学观察

肉鸡鹦鹉热衣原体病是由鹦鹉热衣原体引起的一种接触性人兽共患传染病。在自然条件下，肉鸡可感染本病，肉雏鸡表现沉郁、呼吸困难，甩鼻、采食量下降，常常呈恶病质状态，最终衰竭死亡，耐过鸡只生长受阻，给肉鸡生产造成了巨大的损失。禽源鹦鹉热衣原体株对人有致病性，人感染后主要表现为非特异性流感样症状，可导致肺炎、心内膜炎和脑炎等多种病症，严重威胁着人类的健康。     

微生态制剂促康生Ⅱ号治疗大肠杆菌抗药性菌株引起的仔猪黄痢

笔者用微生态制剂-促康生Ⅱ号对仔猪黄、白痢进行预防试验,尤其对氯霉素、土霉素、链霉素和恩诺沙星治疗无效的发病仔猪,再用促康生Ⅱ号进行治疗,取得极为满意的效果,有关这方面情况尚未见报道. 1 材料与方法 1.1 药物氯霉素注射液、链霉素注射液、恩诺沙星注射液均符合国际或部标.土霉素碱符合国标.促康生Ⅱ号为深褐色液体,含有多种有益微生物的活菌制剂,由南京农业大学微生态制剂组提供.     

Yersinia ruckeri,the causative agent of enteric redmouth disease in fish

Enteric redmouth disease (ERM) is a serious septicemic bacterial disease of salmonid fish species. It is caused by Yersinia ruckeri, a Gram-negative rod-shaped enterobacterium. It has a wide host range, broad geographical distribution, and causes significant economic losses in the fish aquaculture industry. The disease gets its name from the subcutaneous hemorrhages, it can cause at the corners of the mouth and in gums and tongue. Other clinical signs include exophthalmia, darkening of the skin, splenomegaly and inflammation of the lower intestine with accumulation of thick yellow fluid. The bacterium enters the fish via the secondary gill lamellae and from there it spreads to the blood and internal organs. Y. ruckeri can be detected by conventional biochemical, serological and molecular methods. Its genome is 3.7 Mb with 3406–3530 coding sequences. Several important virulence factors of Y. ruckeri have been discovered, including haemolyin YhlA and metalloprotease Yrp1. Both non-specific and specific immune responses of fish during the course of Y. ruckeri infection have been well characterized. Several methods of vaccination have been developed for controlling both biotype 1 and biotype 2 Y. ruckeri strains in fish. This review summarizes the current state of knowledge regarding enteric redmouth disease and Y. ruckeri: diagnosis, genome, virulence factors, interaction with the host immune responses, and the development of vaccines against this pathogen.