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1.
林密  孙继国  柴静 《猪业科学》2003,20(12):57-59
本实验测定了环丙沙星、氧氟沙星、单诺沙星、红霉素、罗红霉素、泰勒菌素、泰妙菌素、四环素等8种药物对羊肺炎支原体两个标准株Y98和Y-goat的体外抑菌浓度以及红霉素与氧氟沙星、泰勒菌素对Y-goat和四环素与氧氟沙星、泰勒菌素对Y98的联合药敏作用。对羊肺炎支原体两个标准株对抗菌药物的敏感性进行了分析。  相似文献   
2.
测定了环丙沙星、氧氟沙星、单诺沙星、红霉素、罗红霉素、泰乐菌素、泰妙菌素、四环素等8种药物对羊肺炎支原体两个标准株Y-98和Y-goat的体外抑菌浓度以及红霉素与氧氟沙星、泰乐菌素对Y-goat和四环素与氧氟沙星、泰乐菌素对Y-98的联合药敏作用.结果表明,这8种抗菌药物对Y-goat和Y-98的MIC(μg/mL)分别为:环丙沙星0.223、0.002 23,氧氟沙星0.281、0.014 0,单诺沙星0.136、0.014 0,红霉素0.021 8、无效,罗红霉素0.032 7、无效,泰乐菌素0.042 2、0.039 0,泰妙菌素0.021 7、0.052 0,四环素0.195、0.052 0.红霉素与氧氟沙星的联合药敏指数为1,是相加作用;红霉素与泰乐菌素对Y-goat的联合药敏指数为1.5,是无关作用;四环素与氧氟沙星、泰乐菌素对Y-98的联合药敏试验指数均为0.375,是协同作用.  相似文献   
3.
AIM: To observe the therapeutic effect of Jiedu-Qingfei mixture on Mycoplasma pneumoniae (MP)-infected rat lung tissues and to explore its mechanism. METHODS: SD rats (n=40) were randomly divided into 4 groups:blank control group, model group, Jiedu-Qingfei group and positive control group, with 10 rats in each group. The rats in experimental groups were slowly dripped with 1×109 CFU/L MP solution into their nostrils for 4 d. One rat in each group was sacrificed for MP nucleic acid detection at the second day after inoculation, and the other rats were given gavage therapy. The rats in blank control group and model group were intragastrically given the same volume of normal saline, the rats in Jiedu-Qingfei group were given 8 mL/kg Jiedu-Qingfei mixture daily for 4 weeks, and the rats in psoitive control group were given dexmethasone sodium phosphate (0.5 mg·kg-1·d-1). After the experiment, the rats were killed. The serum and bronchoalveolar lavage fluid (BALF) were collected for detecting the levels of interleukin-12 (IL-12), IL-13 and TNF-α by ELISA. The right lung tissues were used for pathological observation and HE staining, while the left lung tissues were used to detect the expression of NF-κB p50, I-κBα and p38 mitogen-activated protein kinase (p38 MAPK) at mRNA and protein levels. RESULTS: The results of MP nucleic acid detection showed that all the rats except blank control group were MP nucleic acid positive, indicating that the rat model of MP infection was successfully established. On the 1st day of the treatment, the pathological scores of the lung tissues in model group and Jiedu-Qingfei group were significantly higher than those in blank control group (P<0.05). After treatment, the pathological scores of the lung tissues in mo-del group were significantly higher than those in blank control group and Jiedu-Qingfei group. The levels of IL-12 in the serum and BALF in model group were significantly lower than those in blank control group after MP infection (P<0.05), while those after treatment with Jiedu-Qingfei mixture were significantly higher than those in model group (P<0.05). The levels of IL-13 and TNF-α in the serum and BALF of MP-infected rats were increased significantly, while those after treatment with Jiedu-Qingfei mixture were significantly lower than those in model group (P<0.05). The mRNA expression levels of NF-κB p50 and p38 MAPK in model group were increased significantly (P<0.01). After treatment, the mRNA expression levels of NF-κB p50 and p38 MAPK were decreased significantly compared with model group (P<0.01). The mRNA expression level of I-κBα in model group was significantly lower than that in control group. After treatment, the mRNA expression of I-κBα in Jiedu-Qingfei group was significantly higher than that in model group (P<0.05). The protein levels of NF-κB p50 and p38 MAPK in the lung tissues of model group were significantly higher than those of blank control group. After treatment, the protein expression of NF-κB p50 and p38 MAPK was decreased significantly. The protein level of I-κBα in model group was significantly lower than that in blank control group, and after treatment with Jiedu-Qingfei mixture, the protein expression level of I-κBα was increased significantly (P<0.05). CONCLUSION: Jiedu-Qingfei mixture may attenuate lung tissue inflammation caused by MP through NF-κB and p38 MAPK pathways.  相似文献   
4.
AIM: To investigate whether Mycoplasma pneumoniae (Mp)-induced interleukin-1β (IL-1β) production in RAW264.7 cells is through the activation of NLRP3 inflammasome via reactive oxygen species (ROS). ME-THODS: RAW264.7 cells were randomly divided into 3 groups. In normal group, RAW264.7 cells were treated without Mp. In model group, RAW264.7 cells were treated with 1∶ 10 multiplicity of infection (MOI) of Mp. In NAC group, RAW264.7 cells were pretreated with N- acetylcysteine (NAC) at a concentration of 5 mmol/L for 30 min before infection with Mp. The RAW264.7cells were infected with Mp (1∶ 10 MOI) for 4, 8, 16 and 24 h in model group and NAC group, respectively. The intracellular ROS level was analyzed by flow cytometry. The mRNA expressions of NLRP3, ASC and caspase-1 were detected by real-time PCR. The protein levels of NLRP3, ASC and caspase-1 p20 were determined by Western blot. The levels of pro-inflammatory cytokine IL-1β in the supernatant were measured by ELISA. RESULTS: Compared with normal group, the production of ROS were significantly increased at 4, 8, 16 and 24 h after infection, the mRNA expression of NLRP3, ASC and caspase-1 were increased at 8, 16 and 24 h after infection, the protein levels of NLRP3, ASC and caspase-1 p20 were increased at 16 and 24 h after infection, and the releases of IL-1β were increased at 24 h after infection in model group (P<0.01). Compared with the model group, the level of ROS in NAC group decreased, so as the expression of NLRP3, ASC and caspase-1 at mRNA and protein levels and the releases of IL-1β in the supernatant at the corresponding time points. CONCLUSION: Mp may stimulate the ROS production to activate NLRP3 inflammasome in RAW264.7 cells.  相似文献   
5.
为了阐明引起石河子地区某规模化奶牛场犊牛呼吸道症状的主要细菌性病原体及其生物学特性,本研究采集2~6月龄犊牛鼻拭子与肛拭子各39份,通过细菌分离培养、形态学观察、生化分析、PCR扩增16S rRNA基因和溶血酵素(khe)基因、药敏试验和小鼠致病性试验等方法对分离菌株的生物学特性进行分析。结果显示,分离菌株中有3株在MIAC平板上形成紫红色带有沉淀环的菌落(鼻拭子1株,肛拭子2株),且镜检为革兰氏阴性短杆菌,疑为肺炎克雷伯菌。全自动微生物分析系统显示,分离株与肺炎克雷伯菌相似性均为96%;PCR扩增16S rRNA基因测序结果显示,分离株与GenBank数据库中肺炎克雷伯菌核苷酸相似性在96.5%~99.8%之间,肺炎克雷伯菌特异性基因khe阳性且相似性达99%以上;药敏结果显示,分离菌株对青霉素类、头孢菌素类、一代和二代氨基糖苷类、四环素类、一代大环内酯类、磺胺类、多烯类、林可酰胺类抗菌药呈现出不同程度的耐药;对三代氨基糖苷类、二代大环内酯类、氯霉素类、多肽类、喹诺酮类抗菌药敏感,且呈现不同程度的多重耐药性;致病性试验结果表明,分离菌株均可不同程度导致小鼠死亡且以鼻拭子分离株致病性较强。本研究成功分离鉴定石河子地区规模化奶牛场引起犊牛呼吸道症状的肺炎克雷伯菌3株,并阐明分离菌的部分生物学特性,为新疆地区牛源肺炎克雷伯菌病的检测、诊断及临床治疗提供技术支撑。  相似文献   
6.
猪臭鼻克雷伯氏菌的分离与鉴定   总被引:2,自引:0,他引:2  
从呼吸系统症状明显、高热、耳朵等薄皮处发绀的病猪血与病死猪的心血、肝、脾中分离到1株细菌,经形态学观察、生化试验鉴定为臭鼻克雷伯氏菌;经人工感染小白鼠试验,表明具有较强的毒性。选用药敏试验筛选的敏感药物——头孢曲松钠治愈了病猪,控制了疫情。  相似文献   
7.
AIM:To study the variety of cytokines in severe bacterial pneumonia of Sprague Dawleg (SD) rats. METHODS:A total of 60 SD rats were randomly divided into three groups: model Ⅰ group (n=24), model Ⅱ group (n=24), and control group (n=12). Rats in the model Ⅰ group and the model Ⅱ group were intratracheally instilled with suspension of klebsiella pneumoniae at different doses. Rats in the control group were intratracheally injected with 1 mL saline. On the 2nd, 4th and 6th day after intratracheal instillation, 1/3 rats in each group were killed to determine the concentration of IFN-γ, IL-6 and TNF-α in blood. RESULTS:The levels of IL-6 and TNF-α in model groups were higher than those in control group, while the level of IFN-γ was lower. The change of cytokines was more significant in the model Ⅱ group (severe pneumonia) than those in the model Ⅰ group. CONCLUSION:The cytokines we studied may play an important role in the pathogenesis of severe pneumonia. The change of cytokines is more significant in severe pneumonia than those in common pneumonia.  相似文献   
8.
克雷伯氏菌胞外多糖的制备与组成分析   总被引:1,自引:0,他引:1  
利用不同血清型的克雷伯氏菌Klebsiella菌株液体发酵,制备胞外多糖,并采用气相色谱和化学分析方法分析胞外多糖的化学组成。结果表明,菌株K26产胞外多糖的能力最高,培养48h和72h的产量分别为3.11mg/ml和3.89mg/ml;各实验菌株的胞外多糖的单糖组成包括甘露糖、葡萄糖和半乳糖。  相似文献   
9.
肺炎克雷伯氏菌强毒株的分离鉴定及16-23SrRNAITS序列分析   总被引:1,自引:1,他引:0  
为确诊疑似仔猪肺炎克雷伯氏菌(K.pneumonia)感染,并研究其病原的致病性、耐药性、16-23SrRNA ITS系统进化特征,本研究从云南因肺炎、腹泻而大量死亡的仔猪中分离到1株革兰氏阴性短粗杆菌,命名为KP14013,对其进行生化鉴定、16SrRNA鉴定,研究其对小白鼠和仔猪的致病性,并对其16-23SrRNA ITS基因进行测序和遗传进化分析。结果显示,KP14013分离株生化特征与肺炎克雷伯氏菌相符,其16SrRNA与GenBank中23株肺炎克雷伯氏菌代表株之间的同源性均为99%,将KP14013鉴定为肺炎克雷伯氏菌。KP14013对小白鼠半数致死量(LD50)为3×101.8 CFU,腹腔注射3×108 CFU可使仔猪100%致死。16-23SrRNA ITS系统进化关系结果表明,KP14013与GenBank中收录的15株肺炎克雷伯氏菌形成进化树的一个分支,属于同一个亚群,它们之间的核苷酸同源性为98.4%~99.2%。本研究证实了肺炎克雷伯氏菌是该起仔猪腹泻大量死亡的病原;KP14013分离株为毒力极强菌株,具有多重耐药性,其16-23SrRNA ITS与GenBank中收录的肺炎克雷伯氏菌代表株之间核苷酸存在差异,可用于肺炎克雷伯氏菌菌株间的鉴别。  相似文献   
10.
为筛选出联合抗生素对肺炎克雷伯氏菌具有协同抗菌作用的天然产物。采用药敏纸片法测定肺炎克雷伯氏菌对8种抗生素的耐药性,采用微量肉汤稀释法测定抗生素和3种天然产物的最小抑菌浓度,应用棋盘法分别测定花青素和咖啡酸与抗生素联用对肺炎克雷伯氏菌的抗菌活性,并通过生长曲线评估咖啡酸与抗生素联用的协同抑菌作用。结果表明,肺炎克雷伯氏菌对8种抗生素均耐药,抗生素的MIC值为16->512 μg/mL。花青素和咖啡酸具有较好的抗菌活性,MIC值分别为25 μg/mL和1875 μg/mL,肉桂醛无抗菌作用,MIC>250 μg/mL。花青素与头孢他啶和克林霉素联用对肺炎克雷伯氏菌具有协同抗菌作用,2种抗生素的MIC值降低了4倍,咖啡酸与8种抗生素存在协同作用,抗生素的MIC值降低了8~>4096倍。抗生素与咖啡酸联用的协同抗菌效果优于其与花青素的组合,且咖啡酸与磺胺甲恶唑和氯霉素联合使用能持续抑菌至少24 h。本研究首次报道了咖啡酸与抗生素联用对多重耐药肺炎克雷伯氏菌具有显著协同抗菌作用,表明联合疗法是消减细菌耐药性的一种有效策略。  相似文献   
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