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Author: Prakash Babu Bommala Publisher: ISBN: Category : Electronic dissertations Languages : en Pages : 80
Book Description
Ingestion of endophyte-infected tall fescue (E+) may result in fescue toxicosis, which is associated with a significant reduction in feed intake. It is possible that the reduction in caloric intake could contribute to some of the symptoms associated with this condition. The following study evaluated this possibility. Time-related changes in core body temperature (Tc), activity, feed intake and body weight were determined in rats fed diets containing either endophyte-infected seed (E+), uninfected fescue seed (E- ), or uninfected fescue seed at the level consumed on the previous day by rats fed the E+ diet (PFE+; pair-fed). These diets were fed for seven days at thermoneutrality (i.e., 21°C), followed by three days of exposure to thermoneutral (TN; 21°C) or heat stress environments (HS; 31°C). Cumulative effects of both E+ diet and HS on feed intake and body weight gain were observed. Average daily Tc of E+ and PFE+ rats tended to decrease during the preheat period by reducing the daily minimum Tc, with greater reduction in the PFE+ group. During HS, the average daily Tc of E+ group increased with a shift in diurnal Tc values to a higher level indicative of hyperthermia. In contrast, the daily Tc and circadian rhythm of the PFE+ group was similar to TN groups, suggesting that reduced feed intake might explain the hypothermia experienced during at thermoneutrality, but not the hyperthermia experienced by the E+ group during heat stress. Prolactin levels were decreased in E+ fed rats irrespective of ambient temperature. There was no effect of E+ treatment on serum parameters at TN. During HS, E+ treatment lowered cholesterol and amylase levels relative to E- levels. The PFE+ treatment lowered cholesterol in both environments, and reduced amylase, ALP, and albumin relative to E- treated animals in the HS environment. The above results suggest that decreased feed intake partially contributes to the hypothermia at thermoneutrality in E+ and PFE+ groups, but only explains some of the E+ effects during short-term heat stress.
Author: Prakash Babu Bommala Publisher: ISBN: Category : Electronic dissertations Languages : en Pages : 80
Book Description
Ingestion of endophyte-infected tall fescue (E+) may result in fescue toxicosis, which is associated with a significant reduction in feed intake. It is possible that the reduction in caloric intake could contribute to some of the symptoms associated with this condition. The following study evaluated this possibility. Time-related changes in core body temperature (Tc), activity, feed intake and body weight were determined in rats fed diets containing either endophyte-infected seed (E+), uninfected fescue seed (E- ), or uninfected fescue seed at the level consumed on the previous day by rats fed the E+ diet (PFE+; pair-fed). These diets were fed for seven days at thermoneutrality (i.e., 21°C), followed by three days of exposure to thermoneutral (TN; 21°C) or heat stress environments (HS; 31°C). Cumulative effects of both E+ diet and HS on feed intake and body weight gain were observed. Average daily Tc of E+ and PFE+ rats tended to decrease during the preheat period by reducing the daily minimum Tc, with greater reduction in the PFE+ group. During HS, the average daily Tc of E+ group increased with a shift in diurnal Tc values to a higher level indicative of hyperthermia. In contrast, the daily Tc and circadian rhythm of the PFE+ group was similar to TN groups, suggesting that reduced feed intake might explain the hypothermia experienced during at thermoneutrality, but not the hyperthermia experienced by the E+ group during heat stress. Prolactin levels were decreased in E+ fed rats irrespective of ambient temperature. There was no effect of E+ treatment on serum parameters at TN. During HS, E+ treatment lowered cholesterol and amylase levels relative to E- levels. The PFE+ treatment lowered cholesterol in both environments, and reduced amylase, ALP, and albumin relative to E- treated animals in the HS environment. The above results suggest that decreased feed intake partially contributes to the hypothermia at thermoneutrality in E+ and PFE+ groups, but only explains some of the E+ effects during short-term heat stress.
Author: Raja Sekhar Settivari Publisher: ISBN: Category : Electronic dissertations Languages : en Pages :
Book Description
Fescue toxicosis results from intake of toxins in fescue containing an endophytic fungus, Neotyphodium coenophialum. Time-related changes in rats associated with intake of an endophyte-infected fescue diet (E+) were evaluated under thermoneutral (TN), and both short- and long-term heat stress (HS) conditions. Short-term E+ intake decreased feed intake and growth rate under both conditions, whereas rats exhibited signs of adaptation during long-term exposure with better recovery occurring under TN conditions. Rats fed an E+ diet did not change core temperature during TN, but under HS conditions they exhibited a short-term increase in core temperature above control level. However, there was adaptive return of this temperature to TN level with long-term exposure. Short-term E+ intake at TN decreased serum glucose, urea nitrogen, alkaline phosphatase, and cholesterol; whereas long-term E+ intake under these conditions resulted in complete adaptation. In contrast, short-term E+ intake at HS did not affect serum biochemistry, while long-term intake decreased all the above mentioned serum parameters. Serum prolactin level was decreased during both short- or long-term TN and HS conditions. The E+ diet decreased hepatic antioxidant gene expression, with even greater reduction as a result of HS. Long-term E+ intake and HS increased expression of cytochrome P450 and detoxification pathways, respectively. Genes associated with immune response increased with long-term E+ at TN, but decreased with E+ diet at HS. Similarly, genes coding for chaperone and DNA repair decreased with long-term E+ at TN, but increased with E+ and HS. Recovery observed in E+ rats at TN could be attributed to increased gene expression for detoxification and immune response, whereas decreased antioxidant and immune response associated genes could contribute to distress associated with E+ at HS. Fescue toxicosis results from intake of toxins in fescue containing an endophytic fungus, Neotyphodium coenophialum. Time-related changes in rats associated with intake of an endophyte-infected fescue diet (E+) were evaluated under thermoneutral (TN), and both short- and long-term heat stress (HS) conditions. Short-term E+ intake decreased feed intake and growth rate under both conditions, whereas rats exhibited signs of adaptation during long-term exposure with better recovery occurring under TN conditions. Rats fed an E+ diet did not change core temperature during TN, but under HS conditions they exhibited a short-term increase in core temperature above control level. However, there was adaptive return of this temperature to TN level with long-term exposure. Short-term E+ intake at TN decreased serum glucose, urea nitrogen, alkaline phosphatase, and cholesterol; whereas long-term E+ intake under these conditions resulted in complete adaptation. In contrast, short-term E+ intake at HS did not affect serum biochemistry, while long-term intake decreased all the above mentioned serum parameters. Serum prolactin level was decreased during both short- or long-term TN and HS conditions. The E+ diet decreased hepatic antioxidant gene expression, with even greater reduction as a result of HS. Long-term E+ intake and HS increased expression of cytochrome P450 and detoxification pathways, respectively. Genes associated with immune response increased with long-term E+ at TN, but decreased with E+ diet at HS. Similarly, genes coding for chaperone and DNA repair decreased with long-term E+ at TN, but increased with E+ and HS. Recovery observed in E+ rats at TN could be attributed to increased gene expression for detoxification and immune response, whereas decreased antioxidant and immune response associated genes could contribute to distress associated with E+ at HS.
Author: Deepan Kirubaharan Kishore Publisher: ISBN: Category : Electronic dissertations Languages : en Pages : 188
Book Description
Tall fescue is widely used as pasture grass in the United States, and is the most important cool season grass for grazing animals. Certain fungi also grow on these grasses which produce toxins, resulting in reduced feed intake (FI), body weight (BW) and a compromised thermoregulatory system when consumed by animals . Our first study showed that sensitizing rats helped them adapt to the toxin by maintaining a lower core body temperature on subsequent exposure. The short-term study showed an increased proinflammatory response to stimulation with bacterial toxins. In the long-term study, the proinflammatory response was less severe with adaptation. However, cell mediated immunity was compromised, which makes animals susceptible to invading pathogens. This research identified adaptive responses to fescue toxicosis that highlighted shifts in immune function.
Author: Sachin Bhusari Publisher: ISBN: Category : Electronic dissertations Languages : en Pages :
Book Description
Fescue toxicosis affects domestic animals grazing fescue pasture infected with the endophytic fungus, Neotyphodium coenophialum. Signs of fescue toxicosis include increased body temperature and respiration rate and decreased milk yield and reproductive performance. Laboratory mice also exhibit symptoms of fescue toxicosis as indicated by reduced growth rate and reproductive performance. Mice were used to study effects of fescue toxicosis on hepatic gene expression. Twenty-seven mice were randomly allocated to a diet containing either 50% endophyte-infected (E+) or endophyte-free (E- ) fescue seed for two wks under thermoneutral conditions. A two-stage ANOVA of microarray data identified thirty-six genes differentially expressed between mice fed E+ and E- diets. The E+ diet resulted in down-regulation of genes involved in sex-steroid pathway and in cholesterol and lipid metabolism. Genes coding for ribosomes and protein synthesis were up-regulated by the E+ diet. Mice were also used to study the effects of chronic heat stress on hepatic gene expression. Twenty-five mice were randomly allocated to either chronic heat stress (cHS; 34 " 1°C) or thermoneutral (TN; 24 " 1°C) conditions for a period of two wks from 47 to 60 d of age. A two-stage ANOVA of 1353 gene oligoarray data identified thirty genes as differentially expressed due to cHS. Genes involved in the anti-oxidant pathway were up-regulated due to cHS. Genes involved in generation of reactive oxygen radicals and a number of mitochondrial expressed genes were down-regulated by cHS. However, cHS did not produce an increase in oxidative stress induced mitochondrial DNA damage. Furthermore, effects of heat stress on changes in gene expression due to fescue toxicosis in mice liver were studied using DNA microarrays. Our goal was to characterize the differences in liver gene expression of mice exposed to chronic heat stress (cHS) and E+ when compared to mice fed E+ at TN. Mice were fed E+ diet under cHS (34 " 1°C; n = 13; E+cHS) or TN conditions (24 " 1°C; n = 14; E+TN) for a period of two wks between 47 to 60 d of age. Forty-one genes were differentially expressed between treatment groups. Genes coding for phase I detoxification and anti-oxidant pathway were up-regulated in E+cHS mouse liver. Key genes involved in de novo lipogenesis and lipid transport were also up-regulated. Finally, genes involved in DNA damage control and unfolded protein responses were down-regulated. In summary, mice fed an E+ diet at TN resulted in change in expression of genes involved in sex-steroid pathway while this pathway was not perturbed in mice exposed to cHS or to E+cHS treatments. Changes in expression of genes involved in lipid and cholesterol metabolism pathway occurred in mice exposed to E+ and to E+cHS treatment. Anti-oxidant gene expression changes occurred in mice exposed to cHS and to E+cHS, but not in E+ treated mice. Interestingly, gene expression changes involved in the detoxification pathway were seen only in mice exposed to combination of E+ and cHS. Biological pathways and gene expression changes identified in mouse liver due to E+, cHS, and E+cHS will help to understand molecular mechanisms by which fescue toxicosis and heat stress affects animals.
Author: Craig A. Roberts Publisher: John Wiley & Sons ISBN: 0891186379 Category : Technology & Engineering Languages : en Pages : 32
Book Description
Fescue toxicosis continues to be one of the most devastating problems in forage–livestock agriculture. Because there is presently no cure, using the most up-to-date management and prevention approaches are crucial. The 2nd edition of this important guide presents an easy-to-understand description of this complex problem, along with recommendations that are practical for real farm use.
Author: Jenny Katherine Bryant Publisher: ISBN: Category : Electronic dissertations Languages : en Pages : 181
Book Description
Fescue toxicosis may result from the intake of ergot alkaloids found in endophyteinfected (E+) tall fescue. The liver if the major organ involved in the pathology of fescue toxicosis, as it is the site where the toxic ergot alkaloids are metabolized. A study performed with rats consuming and E+ diet reported increased expression of Phase I detoxification enzymes and a decreased expression of antioxidants, to suggest an increase of cellular oxidative stress. This study was performed to determine if intake of E+ fescue had the same effect on the expression of detoxification enzymes and antioxidants in cattle. A second objective of this study was to examine changes in the hepatic transcriptome that occur when cattle consume E+ fescue. Missouri- (MO; n=10; 513.6±1.3 Kg BW) and Oklahoma- (OK; n=10; 552.8±12.0 Kg BW) derived Angus steers, maintained at 19-22°C (TN) air temperature for 8 days and then maintained at cycling heat stress for an additional 10 days (26°C night Ta; 36°C day Ta:HS). Cattle were fed diets containing either endophyte-free (E-) or E+ seed (30 [microgram] ergovaline/Kg BW/day) and feed intake (FI) was recorded daily. Blood and liver tissue samples were collected during pretreatment followed by blood samples at Day 4, 11, and 17 and liver tissue samples were collected again on Day 7 and 18. Consumption of E+ fescue resulted in significantly reduced (p!0.05) feed intake in both the TN and HS periods when compared to the E- group. There was also a significantly (p!0.05) lower serum prolactin concentration of E+ steers when compared to E- steers in both the TN and HS periods. These results confirm that E+ steers were experiencing the physiological conditions associated with fescue toxicosis. Real-time PCR was performed to determine expression of selected hepatic Phase I detoxification enzymes and specific antioxidant proteins. Illumina deep sequencing was performed on TN samples from selected fescue-naïve OK steers. Tiling of the sequences to a ~23,500 member reference allowed for the quantification of mRNA transcript abundance in each sample. Real-time PCR demonstrated that cattle consuming E+ fescue did not a significant change in the expression of Phase I detoxification enzymes or antioxidants. Illumina transcriptome analysis confirmed that E+ fescue did not have any significant effect on the expression of selected Phase I genes; however, there were 76 genes whose expression was significantly affected by E+ fescue, including a number of genes involved in !-oxidation of fatty acids, oxidative phosphorylation, Phase II detoxification, antioxidant activity and the stress response. Illumina deep sequencing aided in compiling a list of genes, which should undergo further study to identify the nature of their connection to the clinical signs of fescue toxicosis.
Author: Peter D. Constable Publisher: Elsevier Health Sciences ISBN: 0702070580 Category : Medical Languages : en Pages : 2278
Book Description
Treat the diseases affecting large animals! Veterinary Medicine, 11th Edition provides up-to-date information on the diseases of horses, cattle, sheep, goats, and pigs. Comprehensive coverage includes the principles of clinical examination and making a diagnosis, along with specific therapy recommendations. For easier use, this edition has been divided into two volumes and restructured into a logical, anatomically based approach to disease. From internationally known veterinary experts Peter Constable, Kenneth Hinchcliff, Stanley Done, and Walter Grünberg, this book is the definitive, one-stop reference for farm animal and equine care. Comprehensive coverage includes information essential to any large-animal veterinarian, especially those working with horses, cattle, sheep, goats, or pigs. Coverage of diseases addresses major large-animal diseases of all countries, including foreign animal and emerging diseases. User-friendly format makes it easier to quickly absorb key information. Quick review/synopsis sections make important information on complex diseases easy to find. NEW! Convenient, easy-access format is organized by organ systems, and divides the content into two compact volumes with the same authoritative coverage. Nearly 200 new color photographs and line drawings are included in this edition. NEW full-color design improves navigation, clarifies subject headings, and includes more boxes, tables, and charts for faster reference. New Diseases Primarily Affecting the Reproductive System chapter is added. Updated and expanded chapter on pharmacotherapy lists therapeutic interventions and offers treatment boxes and principles of antibiotic use. Expanded sections on herd health include biosecurity and infection control, and valuable Strength of Evidence boxes. NEW or extensively revised sections include topics such as the Schmallenberg and Bluetongue viral epidemics of ruminants in Europe, Wesselbron disease in cattle, hypokalemia in adult cattle, equine multinodular pulmonary fibrosis, Hendra virus infection, porcine reproductive and respiratory syndrome, torque teno virus, and numerous recently identified congenital and inherited disorders of large animals. Additional content is provided on lameness in cattle and the diseases of cervids.
Author: Prakash Babu Bommala
Author: Prakash Babu Bommala
Author: Raja Sekhar Settivari
Author: Deepan Kirubaharan Kishore
Author: Sachin Bhusari
Author: Craig Arthur Roberts
Author: Craig A. Roberts
Author: Jenny Katherine Bryant
Author: 
Author: 
Author: Peter D. Constable