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1.
采用功率密度408.39 mW,能量密度244.60 J/cm~2的He-Ne激光照射交巢穴,治疗新生羔羊腹泻病,具有显效快、疗程短、方法简便、减少劳动强度及降低治疗费用等特点,是一种新的理疗方法。 相似文献
2.
我国养猪业发展迅速,整体水平在不断提高,但是与养殖业较为发达的国家相比仍有一些差距。以每年每头母猪断奶的仔猪数(PSY)为例,目前国外养猪发达国家PSY普遍已超30头,而我国却仍在25头左右,仍有较大的提升空间。仔猪护理工作在生猪生产过程中尤为重要,一旦护理措施不当就会造成仔猪死亡,从而降低PSY,直接影响到养猪企业的经济效益。规模猪场仔猪死亡的主要原因就是由于仔猪护理不当所引起的,仔猪护理问题一直是养猪业的一个难题。文内以2020年4—5月上海某规模猪场某栋产房新生仔猪(共477头,其中压死8头,瘦弱致死12头,腹泻致死亡的32头)为例,介绍规模猪场的仔猪护理及注意事项,以期为仔猪护理工作提供借鉴。 相似文献
3.
Mechanisms of Tritrichomonas foetus Pathogenicity in Cats with Insights from Venereal Trichomonosis 下载免费PDF全文
M.K. Tolbert J.L. Gookin 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2016,30(2):516-526
Almost 20 years has passed since trichomonosis was first recognized as a potential cause of diarrhea in domestic cats. Despite progress in confirming disease causation, developing means for diagnosis, and identifying approaches to treatment of the infection, we still know very little about how this parasite causes diarrhea. With increasing recognition of resistance of trichomonosis to treatment with 5‐nitroimidazole drugs, new treatment strategies based on an understanding of disease pathogenesis are needed. In this review, lessons learned from the pathogenesis of venereal trichomonosis in people and cattle are applied to clinical observations of trichomonosis in cats in effort to generate insight into areas where further research may be beneficial. 相似文献
4.
Clinicopathological Phenotype of Autosomal Recessive Cholesterol Deficiency in Holstein Cattle 下载免费PDF全文
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[目的]研究中兽药复方“痢克”对试验性小鼠腹泻的治疗作用。[方法]观察痢克对小鼠小肠墨水推进率的影响,研究蓖麻油与番泻叶引起小鼠腹泻模型的止泻作用并描记兔离体肠管蠕动波,观察药物对蠕动波的影响。[结果]结果表明,中药复方“痢克”能明显抑制小鼠小肠墨水推进长度;对蓖麻油引起的小肠腹泻能明显减少湿粪次数,对番泻叶引起的大肠性腹泻作用较弱。兔离体肠管描记显示,它能明显降低由硝酸毛果芸香碱引起的兔肠管蠕动增强。[结论]“痢克”能够抑制小鼠小肠推进和有效抑制肠蠕动,具有较好的抗腹泻作用。 相似文献
7.
Gookin JL Nordone SK Argenzio RA 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2002,16(1):12-21
Cryptosporidium is a clinically and economically important infection whose pathogenic effect begins with colonization of the intestinal epithelium. Despite intensive efforts, a consistently effective therapy for the infection has yet to be identified. Morbidity and mortality results from ongoing loss of absorptive epithelium, which leads to villous atrophy and malabsorption and release of inflammatory mediators that stimulate electrolyte secretion and diarrhea. With further clarification of the mechanisms underlying enterocyte malfunction in Cryptosporidium infection, it should be possible to design rational nutritional and pharmacologic therapies to enhance nutrient and water absorption, promote the clearance of infected enterocytes, and restore normal villus architecture and mucosal barrier function. 相似文献
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Arroyo LG Weese JS Staempfli HR 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2004,18(5):734-738
Despite empirical clinical association of infection with Clostridium difficile with colitis in horses, a causal link has not been confirmed. The objective of this study was to develop a model of C. difficile-associated diarrhea in foals with normal transfer of passive immunity. Nine 1-day-old pony foals were inoculated intragastrically with spores or vegetative cells of C. difficile. Five foals were challenged with spores, with 2 receiving 10(5) colony-forming units (CFUs) and concurrently 3 receiving 10(7) CFUs once daily for 3 days. Clindamycin was administered orally to disrupt gastrointestinal flora. A further 4 foals were challenged by orogastric administration of 10(10) CFUs of vegetative cells once daily for 3 days or until diarrhea developed. This group did not receive clindamycin. Spore and vegetative cell preparations were negative for toxins of C. difficile and common enteropathogens. Clinical signs varied from mild abdominal discomfort and pasty feces to colic and watery diarrhea in 8 of 9 foals. Four of 5 foals challenged with spores developed mild diarrhea, whereas all foals challenged with vegetative cells developed moderate to severe diarrhea. C. difficile was isolated from feces of all foals between 24 and 72 hours after inoculation and toxins A or B or both were detected in the feces of all foals by an enzyme-linked immunosorbent assay. We concluded that spores and vegetative cells of C. difficile are capable of colonizing the gastrointestinal tract, producing toxins, and inducing clinical signs similar to those encountered in naturally occurring cases. This study fulfilled Koch's postulates for C. difficile-associated diarrhea in foals and provides a model for consistent reproduction of the disease for future studies. 相似文献
10.
Ewaschuk JB Naylor JM Palmer R Whiting SJ Zello GA 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2004,18(5):744-747
The origin of D-lactate, the most important acid contributing to metabolic acidosis in the diarrheic calf, is unknown. We hypothesized that because D-lactate is produced only by microbes, gastrointestinal fermentation is the source. The objective of this study was to determine whether D-lactate production occurs in the rumen, colon, or both, and to measure D- and L-lactate concentrations in urine. Fecal, rumen, blood, and urine samples were obtained from 16 diarrheic and 11 healthy calves. Serum electrolyte concentrations were measured in both groups, and blood gas analyses were performed for diarrheic calves. All samples were analyzed for D- and L-lactate by high performance liquid chromatography (HPLC). Diarrheic calves were generally hyperkalemic with high serum anion gap, depressed serum bicarbonate, and low blood pH. L-lactate was markedly higher in rumen contents (22.7 mmol/ L [median]) and feces (8.6 mmol/L) of diarrheic calves than healthy calves (0.5 mmol/L and 5.1 mmol/L, respectively), but not different in serum or urine. Rumen, fecal, serum, and urine D-lactate concentrations were all significantly higher (P < .05) in diarrheic calves (17.0, 25.4, 13.9, and 19.2 mmol/L, respectively) than in healthy calves (0.5, 9.1, 1.4, and 0.5 mmol/L, respectively). Higher D-lactate concentrations in the rumen and feces of diarrheic calves suggests these sites as the source of D-lactate in blood and urine. 相似文献