猪副嗜血杆菌病和猪附红细胞体病混合感染的诊治

近几年来，猪的附细胞体病流行很广，且母猪呈隐性感染趋势，侵害猪全身系统的猪副嗜血杆菌病的传播也很严重，而且，一旦发病多呈混合感染，使临床诊断及治疗越来越困难。现就临床诊治过程中遇到的一例猪副嗜血杆菌病和猪附红细胞体病混合感染的诊疗过程介绍如下：     

猪咳喘综合症的临床诊断及防治技术浅探

前言：猪咳喘综合症是指猪发病后，表现为以咳嗽、喘气、呼吸困难、体温升高或正常，生长受阻等为主要临床症状的一类疾病。该类疾病多发于规模化养猪场，其病因常因患畜感染了猪蓝耳病、猪伪狂犬病、猪喘气病、猪传染性胸膜肺炎、猪传染性萎缩性鼻炎、猪链球菌病、猪巴氏杆菌病、猪流行性感冒等病原微生物所致：近年来，由于集约化养猪生产模式增多，     

猪呼吸道症候群的鉴别诊断

一、概述 猪呼吸道症是一组较大的症候群．临床上常见10种病。其中．病毒性传染病3种．分别是非洲猪瘟、猪流行性感冒（以下简称猪流感）、猪繁殖与呼吸道综合征：细菌性传染病4种．分别是猪气喘病、猪李氏杆菌病、猪传染性胸膜肺炎、猪肺疫；寄生虫病2种．分别是猪弓形虫病和猪肺线虫病：猪中毒病1种即猪山芋黑斑病中毒。共同临床特征：呼吸困难．个别病患猪呈腹式呼吸或呈犬坐势呼吸。     

当前中小型养猪场和散养户存在的问题

笔者在近几年的临床诊疗实践中发现，一些小型养殖场、养殖户对猪病的预防和控制工作虽然也采取了一系列相应的措施，但猪病仍然多发，而且难以治愈，损失惨重，有的甚至停产转行。归纳起来主要存在以下几方面的问题：     

猪巴尔通氏体病的诊断和治疗

近几年来，在本市周围的几个农场中，发生了猪附红细胞体病，这种传染病已为人们所熟知。然而也有时检查出其病原为猪巴尔通氏体，其临床、病原与前者极其相似，易被人们所忽视。我们在诊断猪附红细胞体病时，对猪巴尔通氏体病作了一些研究，现将情况报告如下：     

浅析猪夏秋季节高热性疫病

夏秋季节对养猪业来讲可以从每年5月至11月初，在长达半年的时间里，因诸多原因导致这段时间内猪病常见多发。据粗略统计，夏秋季节猪病发生率约占全年的70％左右。这段时间内猪病的显著特点是在临床上以高热为主要特征，体温大多升高到41℃以上，呈稽留热或反复高热。其中常见多发的高热性疾病有：猪瘟、猪丹毒、猪肺疫、仔猪副伤寒、猪败血性链球菌病、猪流行性感冒、猪传染性胸膜肺炎、猪弓形体病、猪附红细胞体病等。     

育肥猪青霉素过敏一例

育肥猪青霉素过敏一例猪青霉素过敏并不多见，临床上一般不作皮试。笔者曾见猪对青霉素过敏一例，报道如下：墨河乡狄胡村胜利组一头５０公斤左右的育肥猪有病。病初情况：精神不振、不食、体温４１．５℃，鼻孔流鼻液。初诊为流感。用青霉素治疗，３０分钟后，表现哮喘。...     

猪病毒性疾病该如何选择抗病毒药物？（上）

目前猪群中发生的疾病主要表现为病原的多重感染，在其感染的病原中除有细菌或寄生虫之外，80％是病毒感染。因此，在猪病防控中重点是要防控好病毒病。兽医临床上防控猪的病毒病，常采用的措施有：一是要加强科学饲养，管理好猪群；     

一起猪链球菌病的诊治报告

猪链球菌病是由溶血性链球菌感染的一种传染病，根据临床症状主要分为猪败血型链球菌病和猪淋巴脓肿型链球菌病。猪败血型链球菌病一般由C群兽疫链球菌引发，主要症状为：突然发病，体温升高到4l℃一42℃，呼吸迫促，间有咳嗽，     

猪败血性链球菌病的诊治

猪链球菌病是由链球菌所引起的。自然条件下，以架子猪和仔猪发病较多。一年四季均可发生，但以5～11月份发生最多，多经呼吸道(鼻、咽粘膜)或伤口感染，呈散发或地方性流行。临床上分为猪败血性链球菌病、猪链球菌性脑膜炎和猪淋巴结脓肿三个类型。2004年9月11日我县一饲养户的猪发生该病，情况如下：     

某规模化猪场猪伪狂犬病的诊断

试验采用流行病学调查、临床观察和实验室检查对华北地区某疑似伪狂犬病发病猪场进行了诊断。猪场发病情况主要为母猪流产,新生仔猪死亡率较高,肥猪死亡率低。发病或死亡仔猪扁桃体充血出血、溃疡,肺脏出血、水肿,心肌色淡、心包积液,脑膜充血;表现为坏死性扁桃体炎、出血性淋巴结炎、出血性间质性肺炎、间质性心肌炎和非化脓性脑炎。发病猪扁桃体、肺脏、脑组织匀浆上清液接种家兔后出现奇痒等典型症状并很快死亡。发病猪脑组织可检出猪伪狂犬病毒gD基因特异性目的片段。猪场伪狂犬病野毒感染抗体阳性率为63%（63/100）。本试验结果表明,确诊该猪场发生了伪狂犬病。     

Localisation of swine hepatitis E virus in experimentally infected pigs

The distribution of intravenously inoculated swine hepatitis E virus (HEV) was assessed by in situ hybridisation for a period of 50 days. Evidence of apparent clinical disease was found in only one pig in the HEV infected group. The only gross lesion observed was mildly enlarged mesenteric lymph nodes at 50 days post infection (dpi). Histopathologically, mild lymphoplasmacytic infiltration and focal hepatocellular necrotic lesions were found in HEV-infected pigs. Swine HEV nucleic acids were detected by RT-PCR in the faeces at 3 dpi in 100% of the 18 pigs infected with the virus. Thereafter, the number of positives declined.The most consistent and intense signal was found in the liver of infected animals using in situ hybridisation. The positive cells were hepatocytes, Kupffer cells, bile epithelial cells and interstitial lymphocytes. Swine HEV RNA was localised in the cytoplasm of the hepatocytes, with a slightly granular pattern of staining, but hybridisation signals were not observed in degenerative or vacuolated hepatocytes. HEV was much less frequently detected in extrahepatic tissues such as lymph nodes, tonsil, spleen and small and large intestine. It was concluded that swine HEV had replicated primarily in the hepatocytes and infection resulted in subclinical infection with minimal histopathological changes in the liver.     

Paramyxovirus infection in pigs with interstitial pneumonia and encephalitis in the United States.

In the last few years, newly recognized paramyxoviruses have been associated with severe disease in several animal species, including swine, as well as in human beings. Recently, a paramyxovirus was isolated from a swine herd in the northcentral United States that experienced an epizootic of respiratory and central nervous system disease. Affected pigs had interstitial pneumonia with necrotizing bronchiolitis and encephalitis characterized by lymphocytic perivasculitis and diffuse gliosis. Germ-free pigs inoculated with this isolate developed mild clinical illness and similar but less severe histopathologic lesions in lungs and brain.     

Articular cartilage blood vessels in swine osteochondrosis

Perfusion studies in swine with early lesions of osteochondrosis demonstrated that lamellar areas of chondrocyte necrosis within reserve zones of growth areas occurred only in regions of nonperfused articular cartilage. Articular cartilage with a similar anatomical location was perfused in some animals. Occasionally, nonperfused articular cartilage showed vascular alterations within cartilage canals without evidence of significant perivascular or lamellar necrosis. By light microscopy, some vessels within or adjacent to nonperfused articular cartilage had normal morphology; however, ultrastructural abnormalities were found in some vessels of all cartilage canals adjacent to necrotic cartilage lamella. Minimal alterations were in the few cartilage canal vessels that appeared normal by light microscopy, and the surrounding chondrocytes showed only minimal alterations. Early cartilage canal alterations were seen in the endothelium of cartilage canal capillaries, and ultrastructural changes in these vessels were similar to those described with experimentally induced, direct vascular injury. Vascular injury was followed by leakage of plasma and cells into the interstitial space of the cartilage canal. Necrosis of the vessel wall and interstitial tissue caused the cartilage canals to appear empty or to be filled with fibrin-like material. Although the vascular changes could be considered as part of the normal process of cartilage maturation and cartilage canal chondrification, observations suggest that in domestic swine the attendant cartilage necrosis and chondrolysis is exuberant. It is suggested that alterations in cartilage canal vessels play a major role in the pathogenesis of articular cartilage lesions that are found in osteochondrosis of swine.     

“猪高热病”的防治

我国不同地区曾出现了以高热、不食、呼吸困难、皮肤病变等为主要症状,剖检以淋巴结肿大、瘀血、出血,心脏水肿、冠状动脉瓣出血,肺水肿、间质性肺炎、肾瘀血、出血、苍白、脾肿大坏死等为主要病变的"猪高热病",给养猪业造成了较大的损失。研究表明,本病有的是由高致病性猪蓝耳病单一病因引起,有的是以猪蓝耳病为主,混合或继发感染猪瘟、猪圆环病毒病、猪链球病菌、猪附红细胞体病等混合病因引起。致病的复杂性增加了诊断和防控的难度。为进一步做好防治工作,降低发病率和死亡率,减少经济损失,本人结合实际工作,提出以科学免疫、严格卫生消毒、加强饲养管理等预防措施为主,并及时正确诊断治疗的综合防治措施。     

New pig disease in Hungary: postweaning multisystemic wasting syndrome caused by circovirus (short communication)

Postweaning multisystemic wasting syndrome (PMWS), a new disease in Hungary, was recognized in a swine herd located in Southeast Hungary, during the early winter of 1999. The first clinical signs of paleness, anaemia, and leanness appeared immediately after weaning, at the age of 40-50 days. Pustules were frequently observed on the skin of the trunk, and signs of necrotic dermatitis were also visible. A syndrome of poor growth and wasting was characteristic of the affected pigs. A porcine circovirus (PCV), the suspected causative agent, was detected by polymerase chain reaction (PCR). Sequencing data and restriction endonuclease (RE) analysis of the PCR products suggested that the virus belonged to the PCV-II group where all the causative agents of PMWS are also grouped.     

Ochratoxicosis in Iowa swine

Ochratoxicosis was diagnosed in 2 Iowa swine herds. In both cases, clinical signs consisted of increased urination and water consumption. Pale tan kidneys were found in affected pigs at necropsy. Histologic examination of renal tissue from an affected pig revealed diffuse tubular nephrosis and interstitial fibrosis. In both cases, ochratoxin A was detected by thin-layer chromatography in extracts of whole corn and ground complete feed. Ochratoxicosis was reproduced in swine with feed obtained in one of the cases.     

Experimental swine vesicular disease, pathology and immunofluorescence studies.

Two day old piglets were inoculated intravenously with 1 ml of swine vesicular disease virus UK-G 27-72 isolate. Using infectivity tests, immunofluorescent staining and gross and histopathological examination, pathogenesis of the infection was studied in tissue specimens collected daily from one through seven days postinoculation. Swine vesicular disease virus had a strong affinity for the epithelia of the tongue, snout, coronary band and lips, the myocardium and the lymphoid elements of the tonsil and the brain stem. The virus had the greatest affinity for the epithelium of the tongue. However, there was no evidence that the tongue was the initial replication site for swine vesicular disease virus. Prickle cells in the stratum spinosum appear to be the primary targets for the virus. The necrotic foci in the stratum spinosum appeared first, followed the next day by reticular degeneration and multilocular intraepidermal vesicular formation. In the digestive tract and most of the other visceral organs the short duration and sudden drop of the virus titres and the negative fluorescence and pathological findings suggest that these are not important sites for the replication of swine vesicular disease virus in this experiment. The virus was recovered from most of the central nervous tissue specimens. Although the piglets had significant central nervous system lesions, signs of impaired central nervous system function were not detected. However, subtle nervous signs could have been obscured by difficulties in locomotion resulting from severe lesions of the feet.     

Porcine epidemic abortion and respiratory syndrome (mystery swine disease). Isolation in Spain of the causative agent and experimental reproduction of the disease.

In March of 1991, a disease that affected pregnant sows and caused a high mortality in unweaned piglets was detected in Spain. Based on the clinical signs observed, mystery swine disease, which had been described recently in Germany, Holland and Belgium, was suspected. From the samples obtained from the affected farm, a filtrable agent (0.22 micron) was isolated on cell culture. It produced cytopathic effects, its replication was intracytoplasmic, it was sensitive to chloroform, and cross-reacted with a Lelystad reference serum. When inoculated into pregnant sows, the agent produced inappetence for 2-4 days, without hyperthermia. One of the sows aborted at 100 days of gestation; the two others had delayed parturitions (days 115 and 116). There was a mixture of healthy piglets, mummified fetuses, stillbirths and weak piglets. Microscopic examination of the lungs of healthy piglets killed at 8 and 12 days of life revealed the presence of interstitial pneumonia. The sera from the three sows at 39 days after infection cross-reacted with the Lelystad virus (titres > or = 1/640), whereas pre-inoculation sera did not recognize it (titres < or = 1/10). This is the first report from Spain of the isolation of an agent (antigenically related to the Lelystad virus), capable of reproducing the disease previously designated as mystery swine disease.     

Isolation of swine infertility and respiratory syndrome virus (isolate ATCC VR-2332) in North America and experimental reproduction of the disease in gnotobiotic pigs.

A recent epizootic of swine infertility and respiratory syndrome (SIRS) in a Minnesota swine herd was investigated. Examination of a sow, neonatal piglets, and stillborn fetuses obtained during the epizootic from the affected herd revealed interstitial pneumonitis, lymphomononuclear encephalitis, and lymphomononuclear myocarditis in the piglets and focal vasculitis in the brain of the sow. Fetuses did not have microscopic lesions. No cause for the infertility and respiratory syndrome was determined. Therefore, attempts were made to experimentally reproduce the disease. Eleven 3-day-old gnotobiotic piglets exposed intranasally to tissue homogenates of piglets from the epizootic became inappetent and febrile by 2-4 days postexposure and had interstitial pneumonitis and encephalitis similar to that seen in the field outbreak. After 2 blind passages in gnotobiotic piglets, tissue homogenates were cultured on continuous cell line CL2621, and a cytopathic virus (ATCC VR-2332), provisionally named SIRS virus, was isolated. Gnotobiotic piglets exposed intranasally to the SIRS virus developed clinical signs and microscopic lesions that were the same as those in piglets exposed to the tissue homogenates, and the virus was reisolated from their lungs. This is the first isolate of SIRS virus in the United States that fulfills Koch's postulates in producing the respiratory form of the disease in gnotobiotic piglets and the first report of isolation and propagation of the virus on a continuous cell line (CL2621). The virus is designated as American Type Culture Collection VR-2332.