猪副嗜血杆菌病的防治策略

猪副嗜血杆菌病是由猪副嗜血杆菌引起的一种猪的传染病.该病主要危害1～28周龄的哺乳仔猪、保育仔猪和生长猪,病理变化包括多发性浆膜炎、多发性关节炎、肺炎、胸膜炎、心包炎、脑炎,因此该病又称为猪的多发性浆膜炎和关节炎.猪副嗜血杆菌在环境中普遍存在,与其他病毒、细菌共同作用致病性更强.猪感染此病后病程复杂、死亡率高、治疗困难、损害严重.     

副猪嗜血杆菌病及其防治

副猪嗜血杆菌病又称革拉泽氏病,是由副猪嗜血杆菌引起的以多发性浆膜炎和关节炎为特征的内源性继发感染性疾病。该病主要危害1～28周龄的哺乳仔猪、保育仔猪和生长猪,主要的病理变化包括多发性浆膜炎、多发性关节炎、肺炎、     

副猪嗜血杆菌病的防制

副猪嗜血杆菌病又称猪格拉泽氏病、多发性纤维素性浆膜炎和关节炎。是由副猪嗜血杆菌引起哺乳阶段、保育猪阶段猪群高发的一种典型的应激性疾病。主要症状为多发性浆膜炎、多发性关节炎、肺炎、胸膜炎、心包炎和脑炎等，呈呼吸困难、颤抖和共济失调，常常与其他疾病混合感染，     

副猪嗜血杆菌的研究进展

副猪嗜血杆菌(Haemophilus parasuis,HPs)引起猪的多发性浆膜炎与关节炎,以纤维素性多发性浆膜炎、关节炎和脑膜炎为特征[1]。1910年,德国K.Glasser首次报道猪的纤维素性浆膜炎和多发性关节炎是由一种革兰阴性小杆菌引起的。1922年,S.     

副猪嗜血杆菌病的流行特点与防治

副猪嗜血杆菌可引起猪多发性浆膜炎、关节炎,常与猪繁殖与呼吸综合征、猪圆环病毒病等一起并发或继发,引起仔猪在断奶前后出现严重的呼吸道疾病和关节肿胀。1主要特性副猪嗜血杆菌病又称多发性纤维素性浆膜炎和关节炎,也称格拉泽氏病,简称副猪。副猪嗜血杆菌     

浅析母猪副猪嗜血杆菌病的防治

副猪嗜血杆菌病又称多发性纤维素性浆膜炎,或称格拉泽氏病,是由副猪嗜血杆菌引起的传染病。临床上以体温升高、关节肿胀、呼吸困难、多发性浆膜炎、关节炎和高死亡率为特征,严重危害仔猪和青年猪的健康。副猪嗜血杆菌的感染可呈多种临床类型,以纤维素性多发性浆膜炎、多发性关节炎和脑膜炎为其临床特征。通常发病年龄从2周龄至4月龄,多见于5-8周龄的仔猪,发病率可达10%-15%,病死率可达50%。     

副猪嗜血杆菌病的防治措施

<正>副猪嗜血杆菌病又称革拉泽氏病,本病是"猪高热病"的凶手之一,近年来,已造成很多规模化猪场严重的经济损失。该病主要危害2～28周龄的哺乳仔猪、保育猪和生长猪;主要病理变化包括多发性浆膜炎、多发性关节炎、肺炎、胸膜炎、心包     

副猪嗜血杆菌病的诊断与防治

副猪嗜血杆菌病又称＂革拉泽氏病＂,该病主要危害1～28周龄的哺乳仔猪、保育仔猪和生长猪,病理变化表现多发性浆膜炎、多发性关节炎、肺炎、胸膜炎、心包炎、脑炎,因此又称为猪的多发性浆膜炎和关节炎。副猪嗜血杆菌在环境中普遍存在,经常与病毒、细菌等病原微生物混合感染。猪感染后病程复杂、死亡率高、难以治疗,是目前危害养猪业的典型细菌性疾病之一。我们在实践中遇到一猪场突发该病，现将诊疗情况报告如下：     

猪脾多发牲出血牲梗死的探{=寸与质量卫生评价

猪脾多发性出血性梗死是生猪宰后检验时比较常见的一种病变。这里介绍一种非传染性、麻电引起的猪脾多发性出血性梗死,以供同行商榷。     

猪副嗜血杆菌病的防治

猪副嗜血杆菌病又称革拉泽氏病,是由猪副嗜血杆菌引起的一种细菌性多发性浆膜炎。于1910年首次报道猪副嗜血杆菌感染,又称格拉塞尔氏病,我国于2003年发现猪有此病感染。该病主要危害1—28周龄的哺乳仔猪、保育仔猪和生长猪,主要的病理变化包括多发性浆膜炎、多发性关节炎、肺炎、胸膜炎、心包炎、脑炎,发病率为15％～90％,死亡率有时可高达90％。近年来,猪副嗜血杆菌经常与其它病原混合感染,临床防治非常困难,应以预防为主,采取综合措施,控制该病的发生和发展。     

2型猪链球菌病

猪链球菌能引起猪脑膜炎、心内膜炎、关节炎、肺炎和败血症等,并可以感染人,是一种重要的人畜共患病病原。该菌有35个血清型,其中2型流行最广、致病性最强。本文就2型猪链球菌病的病原、流行病学、致病机理、检测技术及免疫预防等各方面情况作一综述。     

Intracellular invasion and persistence: survival strategies of Streptococcus suis and Mycobacterium avium ssp. paratuberculosis

Streptococcus (S.) suis and Mycobacterium avium ssp. paratuberculosis (MAP) differ substantially in their host specificity and tissue tropism. S. suis is a facultative pathogen in swine, which mainly colonises the upper respiratory tract and can cause meningitis, septicemia, arthritis and pneumonia. In contrast, MAP is an obligatory pathogen causing paratuberculosis in ruminants, and shows high tropism for the intestinal tract. Both pathogens are able to invade and persist in host cells. In S. suis, the significance of invasion for pathogenesis is a matter of controversial discussions. In vitro it has been shown that S. suis is internalized by epithelial cells and survives intracellularly for at least 24 h. However, at present there is no evidence that S. suis invades epithelial cells also in vivo. In MAP, on the other hand, persistence in macrophages is generally considered a crucial step in pathogenesis, but it remains to be elucidated, how it contributes to pathophysiology of the disease. The two pathogens exemplify how intracellular invasion and persistence might play different roles in pathogenesis. In S. suis, intracellular life may represent only a transient retreat phase, whereas in MAP it is the predominant in vivo niche of the pathogen.     

Optimization of Establishment Conditions of Mouse Model of Mycoplasma suis

In order to explore the infection characteristics of Mycoplasma suis(M.suis), and optimize the establishment of infection model of M.suis,this research designed the infection test with different mice (A test), different pathogen forms (B test), frozen pathogens (C test), and studied on mice model of blood reinfection (D test). On the basis of a comprehensive assessment of each test in the blood of mice infection, the first infection time, the clinical symptoms and the average duration of infection, to analyze whether the different treatments and different pathogenic mice forms, cryopreservation of pathogen and the mouse model of blood infection had influence on the establishment of mouse model. PCR detection, electron microscope observation and specific gene fragment sequencing were used to determine whether the pathogen of mice infected with the model was consistent with that of M.suis. The results showed that the infection effect of the spleen group was the best in the A test. In the B test, the infection effect of the M.suis positive blood samples group was the best. In the C test, the infection effect of the non-frozen positive blood group was better than that of the cryopreserved group. In the D test, the positive model of pig blood samples and mice model positive blood group had no significant difference. The results of PCR detection, electron microscope observation and specific gene fragment sequencing showed that the pathogen of mouse model was identical with that of M.suis. The results showed that the infection condition of the mice infected with the mouse model was influenced by the different treatment of the mice, the different forms of pathogens and the cryopreservation of the pathogen,and the model of Kunming mice without spleen infected with M.suis positive blood samples was the best.     

Porcine eperythrozoonosis: from Eperythrozoon suis to Mycoplasma suis

Mycoplasma suis (formerly known as Eperythrozoon suis ) is the most prevalent agent causing haemolytic anaemia in swine. The disease is also known as porcine eperythrozoonosis. M.suis is a small, pleomorphic bacteria parasitizing porcine erythrocytes. To date, no in vitro cultivation system for M.suis has been established and, therefore, our knowledge about the characteristics of M.suis and the pathogenesis of porcine eperythrozoonosis is rather limited. M.suis can cause acute disease, but the major significance of M.suis infections lies in the fact that M.suis can establish chronic and persistent infections leading to a higher susceptibility to other infections, especially of the respiratory and digestive tracts. The present article summarizes the current knowledge of the pathogen, the clinical signs and pathogenesis, diagnostic as well as therapy and prophylaxis.     

Characterization of porcine dendritic cell response to Streptococcus suis

ABSTRACT: Streptococcus suis is a major swine pathogen and important zoonotic agent causing mainly septicemia and meningitis. However, the mechanisms involved in host innate and adaptive immune responses toward S. suis as well as the mechanisms used by S. suis to subvert these responses are unknown. Here, and for the first time, the ability of S. suis to interact with bone marrow-derived swine dendritic cells (DCs) was evaluated. In addition, the role of S. suis capsular polysaccharide in modulation of DC functions was also assessed. Well encapsulated S. suis was relatively resistant to phagocytosis, but it increased the relative expression of Toll-like receptors 2 and 6 and triggered the release of several cytokines by DCs, including IL-1β, IL-6, IL-8, IL-12p40 and TNF-α. The capsular polysaccharide was shown to interfere with DC phagocytosis; however, once internalized, S. suis was readily destroyed by DCs independently of the presence of the capsular polysaccharide. Cell wall components were mainly responsible for DC activation, since the capsular polysaccharide-negative mutant induced higher cytokine levels than the wild-type strain. The capsular polysaccharide also interfered with the expression of the co-stimulatory molecules CD80/86 and MHC-II on DCs. To conclude, our results show for the first time that S. suis interacts with swine origin DCs and suggest that these cells might play a role in the development of host innate and adaptive immunity during an infection with S. suis serotype 2.     

IgA1 protease contributes to the virulence of Streptococcus suis

Streptococcus suis (S. suis) is a major swine pathogen and emerging zoonotic agent. However, the current understanding of the S. suis pathogenesis of infection remains limited. In the present study, the contribution to the pathogenesis of S. suis was evaluated on IgA1 protease (or iga gene), which has been regarded as a virulence factor of gram-negative pathogenic bacteria and of certain gram-positive pathogenic bacteria. In contrast to the wild type (WT) strain of S. suis serotype 2, the isogenic iga mutant (Δiga) constructed by allelic replacement showed significantly decreased lethality to pigs. The present study suggests that IgA1 protease might contribute to S. suis pathogenesis.     

Detection of Streptococcus suis by in situ hybridization, indirect immunofluorescence, and peroxidase-antiperoxidase assays in formalin-fixed, paraffin-embedded tissue sections from pigs.

Streptococcus suis is an important pathogen in pigs and is considered a zoonotic agent. To aid diagnosis of infection caused by S. suis, a species-specific probe targeting 16S ribosomal RNA was designed and used for fluorescent in situ hybridization. Two additional immunohistochemical detection methods, an indirect immunofluorescence assay and a peroxidase-antiperoxidase method, using polyclonal antibodies also were developed. The specificity of the oligonucleotide probe was examined by whole-cell and dot-blot hybridization against reference strains of the 35 serotypes of S. suis and other closely related streptococci and other bacteria commonly isolated from pigs. The probe was specific for S. suis serotypes 1-31. The specificity of the polyclonal antibodies, which has previously been evaluated for use in diagnostic bacteriology for typing of serotype 2, was further evaluated in experimentally infected murine tissue with pure culture of different serotypes of S. suis, related streptococci, and other bacteria commonly found in pigs. The polyclonal antibodies against S. suis serotype 2 cross-reacted with serotypes 1 and 1/2 in these assays. The in situ hybridization and the immunohistochemical methods were used for detection of S. suis in formalin-fixed, paraffin-embedded tissue sections of brain, endocardium, and lung from pigs infected with S. suis. The methods developed were able to detect single cells of S. suis in situ in the respective samples, whereas no signal was observed from control tissue sections that contained organisms other than S. suis. These techniques are suitable for determining the in vivo localization of S. suis for research and diagnostic purposes.     

Characterization of the invasion of porcine endothelial cells by Streptococcus suis serotype 2

Streptococcus suis serotype 2 is an important swine pathogen associated mainly with meningitis. In a previous study, we demonstrated the ability of S. suis serotype 2 to adhere to and invade immortalized porcine brain microvascular endothelial cells (PBMECs) forming the blood-brain barrier. The aim of the current work was to further characterize the mechanism(s) by which S. suis invades porcine endothelial cells. The ability of several S. suis strains to interact with PBMECs was not found to correlate with their geographic origin, virulence, host of origin, or suilysin production. Characterization studies demonstrated that proteinaceous adhesins/invasins, cell wall components, lipoteichoic acid, and serum components (including fibronectin) were involved in interactions between S. suis and PBMECs. In addition to PBMECs, S. suis was able to adhere to and invade 2 porcine aortic endothelial cell lines and primary PBMECs.     

Purification and characterization of the subtilisin-like protease of Streptococcus suis that contributes to its virulence

Streptococcus suis is a major swine pathogen that is responsible for severe infections such as meningitis, endocarditis, and septicemia. S. suis is also recognized as a zoonotic agent and expresses several virulence factors. The recently identified subtilisin-like protease (SspA) of S. suis plays an important role in the pathogenicity of this bacterium in animal models. The objective of the present study was to clone, purify, and characterize the SspA of serotype 2 S. suis P1/7. The SSU0757 gene encoding SspA was amplified and a 4798-bp DNA fragment was obtained. It was cloned into the expression plasmid pBAD/HisB and then inserted into Escherichia coli to overproduce the protein. The recombinant protease was purified by chromatography procedures and showed a molecular weight of 170 kDa by SDS-PAGE. Its activity was optimal at pH 7 and at temperatures ranging from 25°C to 37°C. It had a high specificity for the chromogenic substrate succinyl-Ala-Ala-Pro-Phe-pNa while specific inhibitors of serine proteases inhibited its activity. In addition to degrading gelatin, the protease hydrolyzed the Aα chain of fibrinogen, which prevented fibrin formation by thrombin. The recombinant subtilisin-like protease also showed toxicity towards brain microvascular endothelial cells. Lastly, sera from pigs infected with S. suis reacted with the recombinant SspA, indicating that it is produced during infections. In conclusion, the SspA of S. suis shared similarities with subtilisin-like proteases produced by other pathogenic streptococci and may contribute to the pathogenic process of S. suis infections.     

猪链球菌2型湖南分离株多重耐药性及相关耐药基因研究

基因突变和基因转移是细菌耐药性产生和存在的重要内因,检测与抗生素耐药性相关的基因具有重要的意义.试验选取25份猪链球菌2型湖南分离株对16种抗生素进行药敏试验,检测菌株耐药性;选出了23株有红霉素抗性的菌株,用PCR检测其erm(B)基因.结果显示,猪链球菌湖南分离株对红霉素、四环素、万古霉素和克林霉素具有高耐药性,在23株红霉素抗性菌株中有18株存在erm(B)基因,由erm(B)基因产生的红霉素耐药菌株占到其中的78.3%.因此,erm(B)基因是链球菌2型湖南分离株对红霉素耐药的主要抗性决定基因.