Monday, November 30, 2015
Thursday, October 08, 2015
Rumen Acidosis - Impaction
Rumen acidosis is a metabolic disease of cattle. Like most
metabolic diseases it is important to remember that for every cow that shows
clinical signs, there will be several more which are affected sub-clinically.
Acidosis is said to occur when the pH of the rumen falls to less than 5.5 (normal is 6.5 to 7.0). In many cases the pH can fall even lower. The fall in pH has two effects. Firstly, the rumen stops moving, becoming atonic. This depresses appetite and production.
Secondly, the change in acidity changes the rumen flora, with acid-producing bacteria taking over. They produce more acid, making the acidosis worse. The increased acid is then absorbed through the rumen wall, causing metabolic acidosis, which in severe cases can lead to shock and death.
Acidosis is said to occur when the pH of the rumen falls to less than 5.5 (normal is 6.5 to 7.0). In many cases the pH can fall even lower. The fall in pH has two effects. Firstly, the rumen stops moving, becoming atonic. This depresses appetite and production.
Secondly, the change in acidity changes the rumen flora, with acid-producing bacteria taking over. They produce more acid, making the acidosis worse. The increased acid is then absorbed through the rumen wall, causing metabolic acidosis, which in severe cases can lead to shock and death.
Cause
The primary cause of acidosis is feeding a high level of
rapidly digestible carbohydrate, such as barley and other cereals. Acute
acidosis, often resulting in death, is most commonly seen in ‘barley beef’
animals where cattle have obtained access to excess feed. In dairy cattle, a
milder form, sub-acute acidosis, is seen as a result of feeding increased
concentrates compared to forage.
Symptoms
Acute acidosis
often results in death, although illness and liver abscesses may be seen before
hand. Cattle may become depressed, go off feed, have an elevated heart rate or
diarrhea.
Sub-acute:
Sub-acute:
- Reduced feed intake
- Poor body condition and weight loss
- Unexplained diarrhoea
- Increase body Temp
- Pulse rate and respiratory rate may rise
- Lethargy
Treatment
Acc. To case :
·
Isotonic
sod. Bicarbonate I\V
·
Sod.
Bicarbonate
·
Anti-histaminic
·
Laxatives
·
Anti-pyretics
·
antibiotic
Prevention
The key to prevention is reducing the amount of readily
fermentable carbohydrate consumed at each meal. This requires both good diet
formulation (proper balance of fiber and nonfiber carbohydrates) and excellent
feed bunk management. Animals consuming well-formulated diets remain at high
risk for this condition if they tend to eat large meals because of excessive
competition for bunk space or following periods of feed deprivation.
Feeding excessive quantities of concentrate and insufficient forage results in a fiber-deficient ration likely to cause subacute ruminal acidosis. The same situation may be seen during the last few days before parturition if the ration is fed in separate components.
Including long-fiber particles in the diet reduces the risk of subacute ruminal acidosis by encouraging saliva production during chewing and by increasing rumination after feeding. However, long-fiber particles should not be easily sorted away from the rest of the diet; this could delay their consumption until later in the day or cause them to be refused completely.
Ruminant diets should also be formulated to provide adequate buffering. This can be accomplished by feedstuff selection and/or by the addition of dietary buffers such as sodium bicarbonate or potassium carbonate. Dietary anion-cation difference is used to quantify the buffering capacity of a diet.
Supplementing the diet with direct-fed microbials that enhance lactate utilizers in the rumen may reduce the risk of subacute ruminal acidosis. Yeasts, propionobacteria, lactobacilli, and enterococci have been used for this purpose. Ionophore (eg, monensin sodium) supplementation may also reduce the risk by selectively inhibiting ruminal lactate producers.
Feeding excessive quantities of concentrate and insufficient forage results in a fiber-deficient ration likely to cause subacute ruminal acidosis. The same situation may be seen during the last few days before parturition if the ration is fed in separate components.
Including long-fiber particles in the diet reduces the risk of subacute ruminal acidosis by encouraging saliva production during chewing and by increasing rumination after feeding. However, long-fiber particles should not be easily sorted away from the rest of the diet; this could delay their consumption until later in the day or cause them to be refused completely.
Ruminant diets should also be formulated to provide adequate buffering. This can be accomplished by feedstuff selection and/or by the addition of dietary buffers such as sodium bicarbonate or potassium carbonate. Dietary anion-cation difference is used to quantify the buffering capacity of a diet.
Supplementing the diet with direct-fed microbials that enhance lactate utilizers in the rumen may reduce the risk of subacute ruminal acidosis. Yeasts, propionobacteria, lactobacilli, and enterococci have been used for this purpose. Ionophore (eg, monensin sodium) supplementation may also reduce the risk by selectively inhibiting ruminal lactate producers.
Bloat in Ruminant
Bloat is simply the accumulation of gas in the rumen. This
gas is produced as part of the normal process of digestion, and is normally
lost by eructation. Bloat occurs when this loss of gas is prevented.
There are two sorts of bloat. The least common type is gassy
bloat, which occurs when the gullet is obstructed (often by foreign objects
such as potatoes) or when the animal can’t burp (such as with milk fever or
tetanus).
The second type of bloat is frothy bloat, which happens as
the result of a stable foam developing on top of the rumen liquid, which blocks
the release of the gas. This is by far the most common form of bloat, and
unlike gassy bloat, it is highly seasonal with peaks in the spring and autumn.
This is because the foam is formed by breakdown products from rapidly growing
forages (particularly legumes such as clover and alfalfa). These increase the
viscosity (stickiness) of the rumen fluid and prevent the small bubbles of gas
formed by rumen fermentation from coming together to form free gas that can be
belched off
Clinical Signs
- Distended left abdomen is the most obvious sign
- Usually associated with pain, discomfort, and bellowing.
- Death can occur within 2hrs after the development of bloat
- Gaseous bloat is usually seen in one or two animals. Frothy bloat can affect up to 25% of cases
- In some cases sudden death may be the first sign seen
Diagnosis
- Clinical signs
- History of access to lush pasture
- Passing a stomach tube will distinguish between gassy and frothy bloat. If it’s gassy bloat a stomach tube passed into the rumen will allow the gas build-up to escape through the tube. No such gas is seen in frothy bloat.
Treatment
- Passing a stomach tube is the best treatment for gassy bloat. Once the gas has been released, the cause of the obstruction should be looked for.
- In a few cases a trochar and cannula punched through the side into the rumen will relieve gassy bloat when a stomach tube has not worked. But such cases are rare, and as the trochar provides a tremendous opportunity for introduction of infection, it should only be used as a last resort.
- For frothy bloat, antifoaming agents that disperse the foam should be given by stomach tube. Old-fashioned remedies such as linseed oil and turpentine are effective but newer treatments such as dimethicone or polaxolene are easier to give as the effective dose is much smaller.
- Injection of anti-histaminic drug
- If an outbreak of frothy bloat occurs all cattle on that pasture should be removed immediately and put onto a high fibre diet (hay or straw), and any cows showing bloating signs treated with an anti-foaming agent. The pasture should not be grazed for at least ten days.
Mastitis in cattle
Mastitis is the inflammation of the mammary gland and udder
tissue.
It usually occurs as an immune response to bacterial invasion of the teat canal by variety of bacterial sources present on the farm (commonly through bedding or contaminated teat dips), and can also occur as a result of chemical, mechanical, or thermal injury to the cow's udder.
Mastitis is a multifactoral disease, closely related to the production system and environment that cows are kept in. Mastitis risk factors or disease determinants can be classified into three groups: host, pathogen and environmental determinants.
It usually occurs as an immune response to bacterial invasion of the teat canal by variety of bacterial sources present on the farm (commonly through bedding or contaminated teat dips), and can also occur as a result of chemical, mechanical, or thermal injury to the cow's udder.
Mastitis is a multifactoral disease, closely related to the production system and environment that cows are kept in. Mastitis risk factors or disease determinants can be classified into three groups: host, pathogen and environmental determinants.
Symptoms
Subclinical:
Few symptoms of subclinical mastitis appear, although it is present in most
dairy herds.
Somatic cell counts measure milk quality and can be used as an indicator of mastitis prevalence.
Clinical mastitis: The most obvious symptoms of clinical mastitis in the udder are swelling, heat, hardness, redness or pain.
Milk takes on a watery appearance, flakes, clots or pus is often present.
A reduction in milk yields, increases in body temperature, lack of appetite, and a reduction in mobility due to the pain of a swollen udder are also common signs.
Somatic cell counts measure milk quality and can be used as an indicator of mastitis prevalence.
Clinical mastitis: The most obvious symptoms of clinical mastitis in the udder are swelling, heat, hardness, redness or pain.
Milk takes on a watery appearance, flakes, clots or pus is often present.
A reduction in milk yields, increases in body temperature, lack of appetite, and a reduction in mobility due to the pain of a swollen udder are also common signs.
Treatment
-Antibiotic
-NSAID are widely used for the treatment of acute mastitis. declofene, flunixin meglumine, , and ketoprofen
have been studied as treatments for experimental coliform mastitis or
endotoxin-induced mastitis
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