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Ruminal Acidosis In Goats

Sheep Diseases

Sheep Diseases

Ruminal acidosis is a dietary condition resulting from various degrees of over-eating on starchy foods, such as cereals and concentrate rations. Therefore, it often occurs under intensive sheep finishing systems (Piercy and Kemp, 1990). The degree of ruminal acidosis can vary from cases of indigestion with a mild watery scour to cases of sudden death or a very severe and distressing illness resulting in death (Braun et al., 1992). In more severe cases, the outlook is often poor and it may lead to complications, such as pregnancy toxaemia. Ruminal Acidosis is often caused by sudden changes of diet, such as the introduction of concentrates in late pregnancy, altering the composition of micro-organisms in the rumen . In North America ruminal acidosis is frequently seen in feedlot lambs and lactating or pregnant ewes that have experienced rapid changes in their ration (Wolf, 2007), but it is unlikely to be seen in extensive grass-fed systems. In Mediterranean countries concentrate-based diets lead to cases of sub-acute acidosis (Blanco et al., 2015) The rumen becomes more acidic than it should because concentrate-based diets increase volatile fatty acids production in the rumen, increasing the fraction of propionate and lactate which lowers the rumen pH (Enemark, 2008). An acidic rumen leads to inflammation or rumenitis (Patra et al., 1993; Piercy and Kemp, 1990). This in turn causes diarrhoea, dehydration and sometimes death. The energy metabolism in the liver of the animal may also be altered due to a limited availability of carbohydrate substrate (Huber et al., 1984). Clinical signs of mild sub-acute cases are diarrhoea, but with continued appetite. In more severe cases animals are depressed, they stop eating and are often found standing or lying with ears down and grind Continue reading >>

Grain Overload, Acidosis, Or Grain Poisoning In Stock

Grain Overload, Acidosis, Or Grain Poisoning In Stock

What is grain overload? Grain overload (acidosis, grain poisoning) occurs when cattle, sheep or goats eat large amounts of grain. The grain releases carbohydrate into the animal's rumen and this rapidly ferments rather than being digested normally. Bacteria in the rumen produce lactic acid, resulting in acidosis, slowing of the gut, dehydration and often death. What causes grain overload? Wheat and barley are the most common causes of grain overload, but it occasionally occurs with oats and lupins. Crushing or cracking of grain by a hammermill increases the likelihood of grain overload, because these processes result in quicker release of carbohydrates. Cases are often seen when: stock are suddenly grain fed without being gradually introduced to the grain or pellets there is a sudden change in feeding regimen or in the grains being fed stock graze newly harvested paddocks (where there may be spilled grain or unharvested areas) stock get unplanned access to grain or pellets, such as around silos. Which classes of stock are affected? Cattle sheep and goats of any age can be affected if they eat more grain than they can digest normally. Signs of grain overload: depressed appearance lying down diarrhoea dehydration and thirst bloating (of the left side of the abdomen) staggery or tender gait and 'sawhorse' stance deaths. What are the treatments for grain overload? Consult a veterinarian for a treatment plan, as treatment will vary according to the severity of the disease. Treatments include intravenous fluids, drenching with bicarbonate solution or milk of magnesia, intraruminal antibiotic injections, thiamine or steroid injections, and surgery for very valuable animals. Following grain overload, the rumen lining takes up to six weeks to repair, so recovering animals will s Continue reading >>

Rumen Acidosis In Small Ruminants And Its Therapeutic Management

Rumen Acidosis In Small Ruminants And Its Therapeutic Management

Rumen Acidosis in Small Ruminants and Its Therapeutic Management Department of Veterinay Medicine, Veterinary Science and Animal Husbandry, G.B. Pant University of Agricultural and Technology, Uttarakhand, India Forty two small ruminants, 26 (61.90%) sheep and 16 (38.10%) goats were treated for rumen acidosis. 19 (45.24%), 12 (28.57%), 6 (14.29%) and 5 (11.90%) animals had eaten apple, cooked rice (wazwan left over) turnip and chapatti respectively and manifested clinical form of ruminal acidosis with, 2.86%; (n=18) as mild (Rumen fluid pH=6.32 0.09316), 38.09%;(n=16)moderate (Rumen fluid pH=5.71 0.074) and 19.05%; (n=8) (Rumen fluid pH=4.54 0.159) as severe ruminal acidosis and accordingly they were classified as group I, II and III, respectively. In group I rumen motility was reduced (1.670.162) and subsequently it was almost absent in group III(0.130.125). Rectal temperature recorded to be 102.580.166, 101.260.188and 100.831.061in group I, II and III respectively. There was a significant increase heart and respiratory tares before treatment in all the groups. A significant increase in blood glucose and Hb, PCV and TEC was also observed in mild, moderate and severe acidotic animals. Therapeutic measures consisted of neutralization of acidity by oral and / or parenteral use of isotonic (1.3%) and hypertonic (5%) sodium bicarbonate with adequate fluid therapy. Oral and parenteral use of isotonic (1.3%) sodium bicarbonate was given to moderate rumen acidosis. Administration of oral sodium bicarbonate, bolus Rumentas was given to groups I and II and a course of antihistaminic drug was also given to all the groups of animals. Moreover, animals of group II and III were also offered intravenous injection of high dose vitamin B1 along with fluids. Gastric lavage and cud tran Continue reading >>

Grain Overload In Ruminants

Grain Overload In Ruminants

Grain overload is an acute disease of ruminants that is characterized by rumen hypomotility to atony, dehydration, acidemia, diarrhea, depression, incoordination, collapse, and in severe cases, death. Etiology and Pathogenesis: The disease is most common in cattle that accidentally gain access to large quantities of readily digestible carbohydrates, particularly grain. Grain overload also is common in feedlot cattle when they are introduced to heavy grain diets too quickly. Wheat, barley, and corn are the most readily digestible grains; oats are less digestible. Less common causes include engorgement with apples, grapes, bread, batter’s dough, sugar beets, potatoes, mangels, or sour wet brewer’s grain that was incompletely fermented in the brewery. The amount of feed required to produce acute illness depends on the kind of grain, previous experience of the animal with that grain, the nutritional status and condition of the animal, and the nature of the ruminal microflora. Adult cattle accustomed to heavy grain diets may consume 30–45 lb (15–20 kg) of grain and develop only moderate illness, whereas others may become acutely ill and die after eating 20 lb (10 kg) of grain. Ingestion of toxic amounts of highly fermentable carbohydrates is followed within 2–6 hr by a change in the microbial population in the rumen. The number of gram-positive bacteria (such as Streptococcus bovis) increases markedly, which results in the production of large quantities of lactic acid. The rumen pH falls to ≤5, which destroys protozoa, cellulolytic organisms, and lactate-utilizing organisms, and impairs rumen motility. The low pH allows the lactobacilli to utilize the carbohydrate and to produce excessive quantities of lactic acid. The superimposition of lactic acid and its salts Continue reading >>

Avoiding And Treating Grain Overload

Avoiding And Treating Grain Overload

Grain overload, also known as Lactic Acidosis or Acute Carbohydrate Engorgement, is a condition experienced by ruminants such as cattle, sheep and goats. Wild ruminants such as elk and deer appear to be more susceptible to this condition than traditional livestock species. Acidosis usually occurs when animals have consumed large quantities of cereal grains or other sources of readily fermentable starch, or have had their diet suddenly switched from a high roughage diet to a high concentrate diet. It will usually manifest itself in the herd in one of two ways an acute case will usually be terminal, while milder cases can be turned around. There is also the possibility that some of the affected animals will be more susceptible to secondary infections. Acidosis is caused by an increase in lactic acid-producing bacteria in the rumen and the rapid production of lactic acid in both the d- and l- forms (these are the same chemical formula but have different rotational movement). It commonly occurs when there is a sudden change in diet, or when animals gain access to grain in large quantities. However, animals that are maintained on a high energy ration may normally be in a marginal state of acidosis due to the formation of lactic acid by the rumen bacterial flora. Therefore, ingredient changes, poor mixing of grains in the ration, or faulty feeding can produce acute acidosis in your deer. Treatment must begin as soon as it is realized that an animal has eaten more than a normal amount (as little as half again as much) of grain or other sources of readily fermentable starch. The longer the treatment is delayed, the more difficult it is to reverse the progressive chain of events that will end in death in 2 to 4 days. The underlying problem is the rapid fermentation of starch in Continue reading >>

Identification Of Differentially Expressed Proteins In Liver In Response To Subacute Ruminal Acidosis (sara) Induced By High-concentrate Diet

Identification Of Differentially Expressed Proteins In Liver In Response To Subacute Ruminal Acidosis (sara) Induced By High-concentrate Diet

Identification of Differentially Expressed Proteins in Liver in Response to Subacute Ruminal Acidosis (SARA) Induced by High-concentrate Diet Jiang, Ni, Zhang, Zhang, and Shen: Identification of Differentially Expressed Proteins in Liver in Response to Subacute Ruminal Acidosis (SARA) Induced by High-concentrate Diet DOI: Identification of Differentially Expressed Proteins in Liver in Response to Subacute Ruminal Acidosis (SARA) Induced by High-concentrate Diet Tel: +86-2584396763, E-mail: [email protected] College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China Received November 16, 2013 Revised January 20, 2014 Accepted March 04, 2014 Copyright 2014 by Asian-Australasian Journal of Animal Sciences This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The aim of this study was to evaluate protein expression patterns of liver in response to subacute ruminal acidosis (SARA) induced by high-concentrate diet. Sixteen healthy mid-lactating goats were randomly divided into 2 groups and fed either a high-forage (HF) diet or a high-concentrate (HC) diet. The HC diet was expected to induce SARA. After ensuring the occurrence of SARA, liver samples were collected. Proteome analysis with differential in gel electrophoresis technology revealed that, 15 proteins were significantly modulated in liver in a comparison between HF and HC-fed goats. These proteins were found mainly associated with metabolism and energy transfer after identified by matrix-assisted laser desorption ionization/time of flight. The results indicated that glucose, lipid and Continue reading >>

Physiological, Biochemical And Histopathological Effects Of Fermentative Acidosis In Ruminant Production: A Minimal Review | Xu | Spanish Journal Of Agricultural Research

Physiological, Biochemical And Histopathological Effects Of Fermentative Acidosis In Ruminant Production: A Minimal Review | Xu | Spanish Journal Of Agricultural Research

Physiological, biochemical and histopathological effects of fermentative acidosis in ruminant production: a minimal review Rumen acidosis is increasingly recognized as a significant disorder in ruminants that increases the morbidity and mortality of animals, especially for dairy cattle and sheep. Acidosis is not just D-lactate which disturbs the acid-base status and the severity of acidosis is related to many factors and not only due to the level of lactic acid production, resulting in difficulties in diagnosing acidosis. Therefore, an understanding of the physiological, biochemical, and histopathological effects of rumen acidosis is fundamental for developing effective methods of prevention and treatment of fermentative acidosis. The present review evaluates the physiology, biochemistry, and pathophysiology of fermentative acidosis as well as gives a conclusion and look-forward. The information will benefit the health and welfare of ruminants and contribute to modern systems of ruminant production. acid accumulation; diagnosis; influence; livestock Ahrens F.A., 1967. Histamine, lactic acid, and hyper tonicity as factors in the development of rumenitis in cattle. Am J Vet Res 28, 1335-1342. PMid:6053540 Allen M.S., 2000. Effects of diet on short-term regulation of feed intake by lactating dairy cattle. J Dairy Sci 83, 1598-1624. Andersen P.H., 2000. Bovine endotoxicosis: aspects of relevance to ruminal acidosis. PhD thesis. The Royal Veterinary and Agricultural University, Copenhagen. Aschenbach J.R., Oswald R., Gabel G., 2000. Transport, catabolism and release of histamine in the ruminal epithelium of sheep. Pflugers Arch 440, 171-178. PMid:10864012 Aslan V., Thamsborg S.M., Jrgensen R.J., Basse A., 1995. Induced acute ruminal acidosis in goats treated with yeast (Sac Continue reading >>

Sheep & Goats Amaferm

Sheep & Goats Amaferm

Sheep are ruminants, and ruminants must have roughage in their diet to keep the rumen functioning properly. Roughage is defined as any feed ingredient that has a high concentration of fiber that breaks down slowly. The best roughage is long coarse fiber. Long coarse fiber is plant material that is from 3/8 inch to 1-1/2 inches in length or longer. The rumen works best when the roughage effect takes place. The coarse materials rub against the walls of the rumen, stimulating the muscles to contract and relax agitating the materials in the rumen. The resulting slurry of materials is more easily digested by the microorganisms that inhabit the rumen. Think of the rumen as a fermentation vat. Once the microorganisms have done their initial work, the animal regurgitates and re-chews the coarse materials before the microorganisms can metabolize them to benefit the ruminant. Forage digestion is greatest when the rumen pH is between 6 to 6.8. At a pH above this, not enough VFA are being produced to provide energy to the animal, and at a pH below 6, the forage digesting bacteria become less effective. When saliva mixes with the cud, buffers in the saliva help keep rumen acidity down. Rumen microorganisms work best in a neutral to slightly-acidic environment. When sheep are fed sugars, starches, and other rapidly digested feeds (grain-based feeds), the rumen becomes more acidic. Introducing long fiber into the rumen helps minimize this acidic effect by the longer chewing time that is necessary to break down and digest the fibrous materials. The longer fibrous material has to be re-chewed, and therefore remains in the rumen longer adding to this buffering effect. This nutritional balance is critical to the good health of the ruminant consuming forage. When this balance gets out of Continue reading >>

Ruminal Lactic Acidosis In Sheep And Goats.

Ruminal Lactic Acidosis In Sheep And Goats.

Abstract The clinical findings in 37 sheep and goats with acute ruminal lactic acidosis included a disturbed general condition characterised by anorexia, apathy, teeth grinding and muscle twitching, ruminal stasis, and the excretion of soupy or watery faeces. The ruminal fluid of affected animals was milky, had a sour odour and a low pH. There was a predominance of Gram-positive bacteria in smears of ruminal fluid. In comparison with 10 control animals, the rumen fluid of 23 sheep with ruminal lactic acidosis had higher lactic acid and lower volatile fatty acid concentrations. In addition, the affected animals often had haemoconcentration and metabolic acidosis. Treatment included single or repeated transfer of ruminal fluid from healthy cows and, depending on the severity, the administration of antacids, yeast and chlortetracycline, and the intravenous infusion of isotonic sodium chloride and 5 per cent sodium bicarbonate solutions. Of the 37 treated sheep and goats, four died within 24 hours, and three others were euthanased after one, two and three days because their condition rapidly deteriorated. Thirty animals were discharged one to nine days after treatment. Twenty-nine of them (78.4 per cent) recovered completely but one was euthanased later. Continue reading >>

Battling Bloat

Battling Bloat

Baking soda isn’t a magical cure-all for goats. Anyone with a hobby goat will invariably be told to feed it baking soda (sodium bicarbonate) at some point. It’s promoted as a cure for everything from bloat to urinary stones. Most of the time, this advice is misplaced. Let’s discuss what the function of baking soda is and what it does and doesn’t do. Sodium bicarbonate (NaHCO3) is a biochemical that buffers the rumen. What this simply means is that it keeps the rumen pH stable. This is important because the microbes that digest hay thrive in a pH of 6.0-6.8 while grain-digesting microbes thrive at a pH of 5.5-6.0 so we need to keep rumen pH within a narrow window for rumen health. Also, pH directly affects the ability to absorb certain nutrients. So, yes, sodium bicarbonate is very beneficial. But what most people don’t realize is that the ruminant animal produces its own sodium bicarbonate in the saliva without being fed baking soda. During the act of cud chewing, copious amounts of bicarbonate are transferred into the rumen. Goats fed long-stem forages (grazing pastures or receiving hay) will produce more saliva (and thus bicarbonate) than goats fed grains or finely ground hay that don’t require cud chewing. Since goats rarely have an issue with rumen pH being too high, we will focus on the issues occuring when it drops too low. This condition is called acidosis. When rumen pH drops, a vicious cycle begins. As the pH drops, the grain-digesting microbes thrive while the fiber-digesting microbes do poorly. One of the by-products of grain digestion is lactic acid. So the more grain these microbes digest, the more acid is produced and the lower pH goes. Eventually, the pH drops so low the microbes die and the rumen stops contracting. Rumen contractions normally Continue reading >>

Sub-acute Ruminal Acidosis (sara) In Dairy Cows

Sub-acute Ruminal Acidosis (sara) In Dairy Cows

414 T. Mutsvangwa - Research Associate/University of Guelph; T. Wright - Acting Dairy Cattle Nutritionist/OMAFRA Table of Contents Introduction Sub-acute ruminal acidosis (SARA), also known as chronic or sub-clinical acidosis, is a well-recognized digestive disorder that is an increasing health problem in most dairy herds. Results from field studies indicate a high prevalence of SARA in high-producing dairy herds as producers respond to the demands for increased milk production with higher grain, lower fibre diets that maximize energy intake during early lactation. Dairy herds experiencing SARA will have a decreased efficiency of milk production, impaired cow health and high rates of involuntary culling. The economic cost associated with SARA can be staggering. It is estimated that SARA costs the North American dairy industry between $500 million and $1 billion (U.S.) annually, with the costs per affected cow estimated at $1.12 (U.S.) per day. The challenge for dairy farmers and dairy nutritionists is to implement feeding management and husbandry practices that prevent or reduce the incidence of SARA, even in high-producing dairy herds where higher levels of concentrate are fed to maximize energy intake. What is SARA? SARA is a disorder of ruminal fermentation that is characterized by extended periods of depressed ruminal pH below 5.5-5.6. Ruminal fluid pH is a measure of the acidity or alkalinity of ruminal contents. A lower pH means higher acidity. For optimum ruminal fermentation and fibre digestion, ruminal pH should lie between 6.0 and 6.4, although, even in healthy cows, ruminal pH will fluctuate below this level for short periods during the day. This drop in ruminal pH is a result of the breakdown of dietary carbohydrates (e.g. starch), particularly from cereal g Continue reading >>

Pregnancy Toxaemia And

Pregnancy Toxaemia And

Contents Industry Background Management Nutrition Animal Health Breeding Fibre Production Fibre Marketing Meat Production and Marketing Pasture and Weed Control Economic Analysis Tanning Skins ketosis in goats The diseases pregnancy toxaemia and ketosis can cause severe problems in goats. While the diseases are clinically different and occur during different stages of pregnancy and lactation, the basis of the disorder is essentially the same: a decrease in blood sugar levels and an increase in ketones. In ruminants, glucose is synthesised mainly from propionic acid (a volatile fatty acid produced in the rumen) and from amino acids. The amount of glucose that is absorbed directly depends on how much dietary carbohydrate escapes rumen fermentation and is digested in the small intestine. This form of glucose uptake varies with different feeds as well as their treatment. Ruminants can use products from rumen fermentation, such as volatile fatty acids, for most of their energy requirements. However, the nervous system, kidneys, mammary gland and foetus have a direct requirement for glucose. During periods of peak glucose requirement (late pregnancy and early lactation) problems may arise due to a glucose deficiency. The incidence of pregnancy toxaemia and ketosis varies with the two main types of goats. In dairy goats with a genetic potential for high milk production, ketosis may be a potential problem; in non-milch goats (Angora, Cashmere and meat) pregnancy toxaemia is more common. PREGNANCY TOXAEMIA Main causes The most important cause of pregnancy toxaemia is a decline in the plane of nutrition during the last six to eight weeks of pregnancy. This places the pregnant female in a difficult situation because the developing foetus imposes an unremitting drain on available m Continue reading >>

Induction Of Subacute Ruminal Acidosis Affects The Ruminal Microbiome And Epithelium

Induction Of Subacute Ruminal Acidosis Affects The Ruminal Microbiome And Epithelium

1Department of Animal Sciences, University of Illinois, Urbana, IL, USA 2Department of Animal Science, University of Manitoba, Winnipeg, MB, Canada 3Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada 4Division of Nutritional Sciences, University of Illinois, Urbana, IL, USA Subacute ruminal acidosis (SARA) negatively impacts the dairy industry by decreasing dry matter intake, milk production, profitability, and increasing culling rate and death loss. Six ruminally cannulated, lactating Holstein cows were used in a replicated incomplete Latin square design to determine the effects of SARA induction on the ruminal microbiome and epithelium. Experimental periods were 10 days with days 1–3 for ad libitum intake of control diet, followed by 50% feed restriction on day 4, and ad libitum access on day 5 to the basal diet or the basal diet with an additional 10% of a 50:50 wheat/barley pellet. Based on subsequent ruminal pH, cows were grouped (SARA grouping; SG) as Non-SARA or SARA based on time <5.6 pH (0 and 3.4 h, respectively). Ruminal samples were collected on days 1 and 6 of each period prior to feeding and separated into liquid and solid fractions. Microbial DNA was extracted for bacterial analysis using 16S rRNA gene paired-end sequencing on the MiSeq Illumina platform and quantitative PCR (qPCR). Ruminal epithelium biopsies were taken on days 1 and 6 before feeding. Quantitative RT-PCR was used to determine gene expression in rumen epithelium. Bray–Curtis similarity indicated samples within the liquid fraction separated by day and coincided with an increased relative abundance of genera Prevotella, Ruminococcus, Streptococcus, and Lactobacillus on day 6 (P < 0.06). Although Firmicutes was the predominant phyla in the solid fraction, a Continue reading >>

Grain Overload

Grain Overload

1 This condition which is also called ''acute carbohydrate engorgement'' or ''lactic acidosis'', is life threatening and must be handled as an emergency. Treatment must begin as soon as it is realized that the goat has eaten a more than normal amount (as little as half again as much) of grain or other sources of readily fermentable starch. The longer treatment is delayed, the more difficult it is to reverse the progressive chain of events that will end in death in 2 to 4 days. The underlying problem is the rapid fermentation of starch in the rumen with the resultant production of lactic acid. This acid is picked up by the blood stream in dangerously high amounts that disrupt the normal body chemistry. 2 Clinical Signs The severity of the signs depends largely upon the amount eaten. In the first few hours, a full rumen, restlessness and crying in pain may be all that is seen. There are mild forms which do not progress beyond simple indigestion. However, in severe forms there may be evidence of extreme pain (crying and getting up and down) which will become intermittent and then be predominated by depression. They will often stagger and even appear blind. The appetite will disappear during the first day as will rumen contractions. The fecus may become soft. 3 The temperature will become sub-normal unless the animal is exposed to hot sun. As the acidosis (lactic acid level in the blood and body fluids) increases, circulatory collapse (shock) will begin; this will increase the heart rate. In cattle, animals with a heart rate of less than 100 will much more likely respond to treatment than one with a heart rate of 120-140. It seems likely that a similar prognostic aid would be valid in goats. Respiratory rate becomes fast and breathing is shallow. Diarrhea usually develops Continue reading >>

Acidosis

Acidosis

Acidosis is also known as toxic indigestion. It occurs when a high proportion of concentrate (carbohydrates) is fed in the ration, either acutely or chronically. Signs: Signs may include depression, lack of appetite, bloat, lack of rumination, staggering, diarrhea or lack of manure, muscle twitching, and teeth grinding. Severe rumen acidosis can be accompanied by systemic and often fatal acidosis. Respiratory distress, shock, cardiovascular collapse, coma, seizures and death occur in severe cases. Treatment: Administer 2 to 3 ounces of sodium bicarbonate by mouth, which will help neutralize acid in the rumen. Magnesium hydroxide or magnesium oxide can also be used to neutralize rumen acid. Encourage consumption of long-stemmed grass hay and water. Many animals with acidosis will require IV fluids to survive. Antibiotics will help prevent secondary bacterial overgrowth with undesirable organisms. Thiamin treatment is recommended because polioencephalomalacia is a potential sequela. Anti-inflammatories will help prevent toxicity and founder. Probiotics should be administered to replace the beneficial rumen organisms that have been killed due to low rumen pH. If a goat is showing clinical signs of this disease, a veterinarian should be called to administer proper treatment due to the seriousness of the illness, complicated treatment and number of possible severe complications. Control/Prevention: Control consists of gradual introduction of goats to grain. If goats are being fed a high-concentrate diet, distribute grain over three or more meals per day, at 2 to 3 pounds per meal. Feed whole grains instead of finely-ground grains and dry grain instead of wet. Feed roughage before grain, first thing in the morning. Supplement with bicarbonate of soda or calcium carbonate and Continue reading >>

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