Detection of Ureaplasma diversum in the upper airways of Australian feedlot cattle

Bovine respiratory disease (BRD) exerts a major impact on the beef cattle industry nationally and worldwide, with a range of aetiological factors impacting its pathogenesis. Previous research has focussed on an increasing number of bacteria and viruses that have been shown to play a role in eliciting disease. Recently, additional agents have been emerging as potential contributors to BRD, including the opportunistic pathogen Ureaplasma diversum. To determine if U. diversum was present in Australian feedlot cattle and if that presence was linked to BRD, nasal swabs were collected from a cohort of 34 hospital pen animals and compared to 216 apparently healthy animals sampled contemporaneously at feedlot induction and again after 14 days on feed at an Australian feedlot. All samples were subjected to a de novo polymerase chain reaction (PCR) assay targeting U. diversum in combination with other BRD agents. U. diversum was detected at a low prevalence in cattle at induction (Day 0: 6.9%, Day 14: 9.7%), but in a significantly greater proportion of cattle sampled from the hospital pen (58.8%). When considering the presence of other BRD-associated agents, co-detection of U. diversum and Mycoplasma bovis was most common in hospital pen animals receiving treatment for BRD. These findings suggest that U. diversum may be an opportunistic pathogen involved in the aetiology of BRD in Australian feedlot cattle, in combination with other agents, with further studies are warranted to identify if a causal relationship exists.     

小檗碱对炎症性肠病肠道屏障的影响及其信号通路

小檗碱是传统中药黄连等植物的主要活性成分,具有抗菌消炎、调节机体免疫等作用,可改善由炎症性肠病(IBD)导致的肠道屏障损伤。小檗碱通过抑制Toll样受体(TLRs)/核转录因子κB(NF⁃κB)、Janus活化激酶(JAK)/信号转导与转录激活子(STAT)信号通路和激活胰岛素样生长因子1(IGF⁃1)/胰岛素样生长因子结合蛋白(IGFBPs)信号通路,缓解IBD引起的肠道机械屏障、化学屏障、免疫屏障和微生物屏障功能损伤。本文就小檗碱的来源及理化性质、IBD的病理特征、小檗碱对IBD肠道屏障的修复作用及其信号通路进行综述,以期为畜牧生产中保护动物肠道健康提供参考。     

双歧杆菌及其产品缓解肠炎症状的研究进展

双歧杆菌具有调节肠道菌群、缓解功能性胃肠道疾病的功能,是目前广为使用的用于改善人体肠道的益生菌之一。炎症性肠病（inflammatory bowel disease,IBD）是一种慢性复发性炎症性疾病,该疾病伴随着肠黏膜溃疡、细胞死亡,并且容易复发。近年来,相关报道在肠炎治疗方面提到了双歧杆菌的益生作用。本文概述双歧杆菌、双歧杆菌产品、双歧杆菌代谢物对IBD的缓解效果,为双歧杆菌在医药方面的应用提供新的研究方向。     

兔病毒性出血症母源抗体动态与抗病毒感染的关系和对策

兔病毒性出血症疫苗免疫母兔所产６、１５、３０、４５、６０、日龄共１２６只兔的母源抗体随日龄增长而下降，至３０￣４５日龄，４８￣８５％的兔为阴性，其平均值为２＾３。强毒攻击耐过母兔所产的未吃初乳、已吃初乳、１５、３０、４５、６０、９０及１１４日龄以上兔１８６只的母源抗体也随日龄增长而消失，但消失时间长，其平均值至１１４ｄ后才降至２＾３。已吃初乳仔兔抗体平均值比未吃初乳高，未吃初乳兔的抗体与母兔基本持     

Autologous Platelet Concentrates as an Adjunctive Treatment for Chronic Laminitis in a Mare with Pituitary Pars Intermedia Dysfunction

The aim of this article was to describe a case of a 7-year-old mare with chronic laminitis secondary to pituitary pars intermedia dysfunction that was successfully treated with autologous platelet concentrates (APC) obtained by the tube method, 4 months before being treated with oral pergolide. After the diagnosis of pituitary pars intermedia dysfunction, the patient was treated with three intralesional injections of APC at 10-day intervals. APC presented a mean concentration of 430 ± 22 × 10⁶ platelets and 8.6 ± 1.3 leukocytes/mL. The treatment with APC produced growth of the hooves at a rate of 5 mm/wk and substantially reduced the foot pain (lameness) after two APC applications. The mare could be ridden 2 weeks after the third APC treatment. The treatment with oral pergolide 4 months later improved the clinical picture of the patient, albeit hirsutism remained. APC could be useful as adjunctive treatment of chronic laminitis in horses. However, additional clinical studies are necessary to determine the safety and effectiveness of APC in chronic laminitis.     

家蚕黑尾病及其防治方法研究

家蚕黑尾病主要是由曲霉菌在蚕尾部寄生引起的一种真菌病 ,从病蚕中分离到病原菌有两种 ,一种孢子表面棘多而长、黄褐色 ,孢子大 ,直径 4～ 6 μm ;一种孢子表面棘短而少、蓝绿色 ,孢子小 ,直径 2～ 3μm。黑尾病在高温多湿条件下多发 ,多发生于 4龄中期至 5龄中期。黑尾病病原菌侵染寄生家蚕的过程是 :病原菌分生孢子附着在蚕尾部背板与节间的三角形节间膜处 ,分生孢子发芽侵入蚕体产生黑色小病斑 ,随病情加重病斑加大 ,甚至在病斑处出现节间断裂 ,直至形成黑尾症状。使用药剂防治黑尾病以 5 %亚迪蚕保最佳     

Longevity of Mycobacterium bovis in brushtail possum (Trichosurus vulpecula) carcasses,and contact rates between possums and carcasses

Abstract

AIM: To determine, for a variety of environmental conditions, how long Mycobacterium bovis might remain viable inside the carcass of a brushtail possum (Trichosurus vulpecula) that died of bovine tuberculosis (Tb), and to measure the rate of contact between free-ranging possums and possum carcasses.

METHODS: Lesions of M. bovis were simulated by inoculating excised spleens weighing 0.5–1 g with 0.2 mL liquid culture containing approximately 5 x 10⁷ cfu M. bovis/mL. Simulated lesions were inserted into possum carcasses (n=48) at the peripheral lymph nodes. Carcasses were placed in the field at two sites (a tussock grassland and a podocarp-broadleaved forest site) and in two seasons (summer and winter) for up to 62 days. Survival rates of M. bovis were estimated by sampling the simulated lesions over time, and culturing the recovered lesion to determine if any viable M. bovis bacteria were present.

The time taken for a free-ranging possum to first encounter a dead possum in its home range was estimated by live-trapping possums and fitting them with proximity loggers (n=13). A ‘contact’ was recorded if these possums came within 40–50 cm of proximity loggers fitted to possum carcasses.

RESULTS: There were strong seasonal and site effects in the survival rate of M. bovis in possum carcasses. In the grassland habitat, no viable bacilli were cultured from any carcass after 3 days in summer, whereas in winter all samples were culture-positive for the first 20 days, and some were still positive after 27 days. The survival rates for forest habitat were intermediate between the results for grassland, and there were no culture-positive carcasses after 9 days in summer or 27 days in winter.

In summer, infected carcasses (n=6) were first encountered by possums a mean 1.9 (range 0.4–6.7) days after placement.

CONCLUSIONS: Possum carcasses were contacted by free-ranging possums within the period that viable M. bovis were shown to survive in a carcass. The risk of such infection is likely to be most significant in winter or in areas with microhabitats where the survival of M. bovis is high. However, the generally low survival rate of M. bovis in possum carcasses and the low frequency of possum-to-carcass contacts indicate this route of transmission alone could not maintain Tb in a possum population.     

Influence of ante‐ and peri‐mortem factors on biochemical and physical characteristics of turkey breast muscle

Summary

The course of post‐mortem breakdown of glycogen and ATP in turkey pectoralis major muscle was markedly influenced by several ante‐ and peri‐mortem variables. Application of a proper stunning procedure was highly effective in preventing peri‐ and post‐mortem muscle stress reactions.

The physiological level of glycogen and ATP was not significantly affected by road transportation covering 260 km. Birds which rested for 24 hrs following transportation had lower glycogen and ATP levels at the moment of slaughter than non‐rested birds.

According to the changes in the rate and extent of post‐mortem biochemical reactions, several meat characteristics such as water‐holding capacity, colour, and tenderness were significantly changed.

Furthermore, the results also indicate that turkey breast muscle is susceptible to a PSE‐like condition as described in pork.     

Hepatitis in dogs. An indexed bibliography of journal articles (1994–2004)

Transmissible spongiform encephalopathies (TSEs) or prion diseases are unique disorders that are not caused by infectious micro-organisms (bacteria or fungi), viruses or parasites, but rather seem to be the result of an infectious protein. TSEs are comprised of fatal neurodegenerative disorders affecting both human and animals. Prion diseases cause sponge-like degeneration of neuronal tissue and include (among others) Creutzfeldt–Jacob disease in humans, bovine spongiform encephalopathy (BSE) in cattle and scrapie in sheep. TSEs are characterized by the formation and accumulation of transmissible (infectious) disease-associated protease-resistant prion protein (PrP^Sc), mainly in tissues of the central nervous system. The exact molecular processes behind the conversion of PrP^C into PrP^Sc are not clearly understood. Correlations between prion protein polymorphisms and disease have been found, however in what way these polymorphisms influence the conversion processes remains an enigma; is stabilization or destabilization of the prion protein the basis for a higher conversion propensity? Apart from the disease-associated polymorphisms of the prion protein, the molecular processes underlying conversion are not understood. There are some notions as to which regions of the prion protein are involved in refolding of PrP^C into PrP^Sc and where the most drastic structural changes take place. Direct interactions between PrP^C molecules and/or PrP^Sc are likely at the basis of conversion, however which specific amino acid domains are involved and to what extent these domains contribute to conversion resistance/sensitivity of the prion protein or the species barrier is still unknown.