鸡滑液囊支原体感染的防治

鸡滑液囊支原体感染(MS)又称滑液支原体感染、滑液囊霉形体感染、滑膜囊霉形体感染、传染性滑液囊炎、传染性滑膜炎,是鸡和火鸡的一种急慢性传染病,关节肿大,滑液囊和腱鞘发炎症状     

鸡滑液囊支原体感染

鸡滑液囊支原体感染（MS）又称滑液支原体感染、滑液囊霉形体感染、滑膜囊霉形体感染、传染性滑液囊炎、传染性滑膜炎．是鸡和火鸡的一种急慢性传染病，关节肿大，滑液囊和腱鞘发炎症状明显。该病病程长，笼养鸡不易被发现，经常给养鸡生产造成难于弥补的损失。     

一起鸡滑液囊支原体感染的诊治

鸡滑液囊支原体感染(MS)又称滑液支原体感染、滑液囊霉形体感染、滑膜囊霉形体感染、传染性滑液囊炎、传染性滑膜炎,是鸡和火鸡的一种急慢性传染病。临床上,有些病例表现为严重的关节病症,而另外一些病例则表现为严重的呼吸道症状,也有二者兼而有之的。,临床表现为关节肿大、跛行,滑液囊和腱鞘发炎症状明显,其它内脏也有病变。该病病程绵延长,笼养鸡最初感染不易被发现,经常给养鸡生产造成难于弥补的损失,该病分布于全世界,近几年笔者发现该病在中国的部分地区发病率有增多趋势。     

鸡传染性滑液囊支原体的诊治

鸡传染性滑液囊支原体又称传染性滑膜炎，是由滑膜支原体所引起的鸡和火鸡的一种急性或慢性传染病。以侵害关节滑液，腱鞘膜和气囊为主，其特征为关节、腱鞘和脚掌肿胀，气囊有干酷物。本病主要发生于雏鸡，特别是肉雏鸡多见，发病率一般为5％-15％，死亡率约为1％-10％。     

鸡滑液囊支原体病的诊疗

鸡滑液囊支原体病又称传染性滑膜炎,是由滑膜支原体所引起的鸡的一种急性或慢性传染病.该病以侵害关节滑液,腱鞘膜和气囊为主,其特征为关节、腱鞘和脚掌肿胀,气囊有干酪物.2009年7月,东平县大羊乡一肉鸡养殖场相继出现了鸡滑液囊支原体疾病,该鸡场鸡群感染该病后,死亡肉鸡120余只,死亡率为3%左右.     

鸡的传染性滑膜囊炎的诊治

鸡传染性滑膜囊炎又名鸡滑液囊支原体病或称滑液囊霉形体病,是由鸡滑液支原体引起鸡和火鸡的一种急性或慢性传染病。主要侵害关节滑膜和腔鞘膜,引起关节肿大、滑膜囊炎、胶鞘炎和亚临床上呼吸道感染,2008年6月上旬,陕西某大型鸡场发生了一种育成鸡以站立、行走不稳、关节肿大、病程长、死亡率低为特征的传染病。经诊断为由滑液囊支原体引起的鸡传染性滑膜炎,现报告如下。     

鸡传染性滑膜炎的诊断与防治

鸡传染性滑膜炎又称滑液囊支原体、滑液囊霉形体,是鸡和火鸡等禽类的一种急慢性传染病。该病在世界很多国家均已发现,近些年在我国出现了发病率上升的趋势,且发病后较难根治,严重影响养殖场户的经济效益。该病的主要特征是关节肿大,滑液囊和腱鞘炎症状明显。     

鸡滑液囊支原体病的诊治

滑液囊支原体病又称传染性滑膜炎,病原是滑液囊支原体,是鸡和火鸡的一种急性到慢性的疾病,主要涉及关节的滑液囊和腱鞘,引起渗出性滑膜炎,腱鞘炎.本病在临床上时有发生,危害养鸡业的健康发展.     

公鸡感染滑液囊支原体的诊治

滑液囊支原体病是由滑液囊支原体所引起的鸡和火鸡的一种急性或慢性传染病。该病以侵害关节滑液、腱鞘膜和气囊为主，其特征为关节、腱鞘和脚垫肿胀，气囊有干酪物。本病主要发生于雏鸡，常发生于4-12周龄。病鸡和带茵鸡是主要的传染源，其持续排茵时间可达40天左右。本病既可经种蛋垂直传播。也可经呼吸道水平传播，在同一鸡舍内传播很快，但在鸡舍间不易传播。     

蛋鸡滑液囊支原体病的治疗

鸡滑液囊支原体病又称鸡传染性滑膜炎,是由鸡滑液囊支原体(MS)引起的鸡和火鸡的一种急性或慢性传染病。主要发生于30~90日龄鸡群,该病可经种蛋垂直传播,也可经呼吸道和排泄物、空气中的气溶胶传播。2000年以来,我国各地报道规模化肉鸡养殖场发病率较高。近几年来,随着蛋鸡产业的快速发展。     

Virulence of Mycoplasma synoviae strains in experimentally infected broiler chickens

Seven field isolates of German origin and the type strain WVU 1853 of Mycoplasma synoviae (MS) were experimentally investigated for their virulence in mycoplasma-free broiler chickens. Two groups of birds were inoculated at 6 days of age with each isolate, one group into the thoracic air sac and the other group intravenously and all surviving birds were examined at necropsy 17 days post inoculation (pi). Groups of negative control birds received sterile Frey's broth medium by intravenous and intra-air sac inoculation, respectively. Variation in virulence was evaluated on the basis of significant differences in incidence, severity and extend of MS-induced airsacculitis and synovitis as well as isolation rates of MS especially from parenchymous organs. All the strains tested were pathogenic but varied in their virulence for broiler chickens. Based on differences of the virulence, the isolates were classified to the categories: (1.) highly virulent, (2.) virulent, (3.) moderately virulent and (4.) slightly virulent. (1) Strains WVU 1853 and 246-91 induced a systemic disease associated with multiple synovitis and bilateral airsacculitis (2) Strains 93-92 and 151-77 induced bilateral airsacculitis similar to WVU 1853 and 246-91 but rarely a systemic disease after exposure by intra-thoracic airsac inoculation. (3) In comparison, strains 27-79, 76-93 and 513-83 caused less frequently airsacculitis and even if, then only at the side of intra-airsac exposure. (4) Strain 91-93 has been found to differ significantly from all the other isolates in its capacity to produce disease independently from the inoculation route. After intravenous inoculation, findings gave no indications for strains with selective tropism to the epithelial membranes of the lower respiratory tract or to those of the joints, tendon sheaths and bursae. However, the presented data of the experiments suggest that the MS strains tested differ in their potential capacity to invade systemically and produce acute septicaemia.     

DNA probes for Mycoplasma gallisepticum and Mycoplasma synoviae: application in experimentally infected chickens

DNA probes specific for Mycoplasma gallisepticum and M. synoviae were selected from genomic libraries prepared in the pUC13 vector. The probes hybridized with the DNA of a wide spectrum of strains within each homologous species, but did not react with the heterologous species or with DNA from any other avian mycoplasma or bacteria tested. Experimental infection and contact exposure of chickens to M. gallisepticum served as models to test the effectiveness of the DNA probe in diagnosis as compared with serological and culture detection methods carried out in parallel. A correlation was generally found between the level of M. gallisepticum in tracheal swabs and the effectiveness of the probe, although a predictably reactive level of mycoplasmas was not always detected. Treatment of clinical specimens with acetylcysteine to disrupt mucus improved the detection rate. Dot-blot hybridization with probe pMG4 enabled positive identification of M. gallisepticum at an early stage of infection, prior to the development of a serological response in the infected chicken. Results are obtainable within 4 days of sampling, much more rapidly than culture, and also in clinical specimens from which mycoplasma isolation is impossible, such as carcasses. The results indicate that the use of DNA probes for the early and rapid detection of M. gallisepticum infection is feasible; a development which can replace laborious culture techniques and less effective serological methods, and thus reduce the time required for diagnosis.     

Monitoring Mycoplasma gallisepticum and Mycoplasma synoviae infection in breeder chickens after treatment with enrofloxacin.

Three experimental strains of breeder chickens were accidentally exposed to Mycoplasma gallisepticum (MG) and Mycoplasma synoviae (MS), presumably from a newly introduced group of leghorn-type pullets. The experimental strains subsequently became infected and were diagnosed positive for MG and MS by the serum plate agglutination (SPA) test and confirmed by the hemagglutination inhibition (HI) test and the polymerase chain reaction (PCR) of tracheal swabs. Treatment with 10 mg/kg enrofloxacin via drinking water for 14 days was elected. Before and after initiation of treatment, MG and MS were monitored for changes by SPA, HI, PCR, and culture, with sampling intervals ranging from 1 wk to 7 wk. MG and MS SPA, HI, PCR, and culture were performed at each sampling period, with the exception of weeks 1.0 and 6.5. Week 1.0 included SPA and His for MG and MS. Week 6.5 included PCR and culture for MG and MS. The MG and MS SPA results were positive throughout the 29-wk trial period. MG HI titers declined until the last sampling, whereas the MS HI titers did not decline significantly. PCR for MG yielded only one positive result, which occurred before treatment. MS PCR remained positive throughout the trial period. MG was never isolated from any sample; however, one MS organism was isolated during treatment. The treatment regimen was effective for MG on the basis of PCR results. Treatment with enrofloxacin did not eliminate SPA reactions during the 29-wk trial period. MG HI titers remained in the suspicious range throughout the remainder of the trial period. Four weeks after the treatment ended, MG HIs were reduced by approximately 40%, with MS HIs remaining high throughout the 29-wk period. PCR appeared to be a sensitive and specific test on the basis of correlation with HIs. On the basis of the isolation of MS during treatment and continued subsequent PCR positive reactions, the treatment for MS with enrofloxacin was not as efficacious as for MG.     

Progressive changes in serum proteins and the rheumatoid factor of chickens infected with Mycoplasma synoviae.

Sera from controls and chickens infected with Mycoplasma synoviae were examined for serum protein content by cellulose-acetate electrophoresis, and for rheumatoid factor (RF) by a latex-agglutination test at 8, 18, 28, 38, and 48 days postinoculation (DPI). Mean total serum protein concentration was significantly elevated by 8 DPI and rose to much higher concentrations on each subsequent day of examination. The mean albumin concentration was significantly decreased by 8 DPI, and continued to decline to very low levels at 18 and 28 DPI, after which it began to rise and by 48 DPI did not significantly differ from the controls. The mean alpha-globulin concentrations were significantly elevated on all days of examination. The mean beta- and gamma-globulin concentrations were significantly elevated by 8 DPI and reached maximum levels at 18 DPI but remained elevated throughout the test. The percentage of chickens having RF titers increased on each successive examination day, but only 56% of the chickens had titers at 48 DPI.     

Experimentally induced synovitis of chickens with Mycoplasma synoviae: effects of dexamethasone treatment.

Specific - pathogen - free chickens were inoculated in the right tibiometatarsal joint with a synovitis-derived Mycoplasma synoviae strain before or during dexamethasone treatment. Development of synovitis in chickens inoculated during the drug treatment was apparently delayed in comparison with development of synovitis in non-treated chickens. Severity of clinical synovitis in chickens inoculated before the drug was given was apparently less than that in chickens not treated or in chickens treated with dexamethasone. Histopathologic changes in the early stage of the infection (1 to 2 weeks) were not modified by dexamethasone treatment, although those changes in the succeeding stage (6 to 7 weeks) were greatly lessened. A relationship was observed between the dosage of dexamethasone and the severity of synovitis, as well as the kinds of cells that infiltrated into the joint lesions. Although serum antibody titers in chickens treated with an excessive dose of dexamethasone were markedly lower, clinical, bacteriologic, and histopathologic observations in chickens treated with dexamethasone were similar to those previously found in surgically thymectomized chickens. These results may support the theory that multiple synovitis of chickens caused by M synoviae infection develops mainly because of an immune response, especially by thymus-dependent functions.     

Isolation of Mycoplasma synoviae from infectious synovitis of chickens

This report describes the first isolations of Mycoplasma synoviae from the synovial sheaths and joints of commercial chickens affected with synovitis in Australia. Over 4 years 3 separate outbreaks were investigated in which up to 20% of birds exhibited clinical signs of poor growth and "hot foot" syndrome (swollen inflamed footpads). Once an outbreak occurred, chronic infection of the farm usually ensued. Grossly the hocks and footpads were swollen by a purulent exudate and associated inflammatory changes with histological features of a severe acute synovitis. Seroconversion of the flocks occurred at the time of the development of lesions. M. synoviae specific antibodies were demonstrated by ELISA in the joint fluid of affected birds. It is concluded that the cases described are similar to avian infectious synovitis syndrome caused by M. synoviae previously described overseas.     

Cell-mediated and humoral immune response of chickens to Mycoplasma synoviae.

The leukocyte migration-inhibition test was employed to demonstrate the presence of cell-mediated immunity and to ascertain its relation to immunoglobulin production in Mycoplasma synoviae infection in chickens. With peripheral leukocytes and a preparation of M. synoviae used as antigen, good discrimination was obtained between naturally or experimentally infected birds and uninfected control birds. Only the infected groups showed significant inhibition. Positive migration inhibition values developed in the second week of infection, often before the appearance of hemagglutination-inhibition titers, and continued to accompany the production of immunoglobulins with some degree of correlation for at least 6 or 12 months.