3 SARA, Ruminal Drinkers and Ruminal Alkalosis

Transcript

Greetings to all,

In lesson two we have discussed rumen lactic acidosis. In that Etiopathogenesis, Clinical signs, Diagnosis, and Treatment and control you have discussed. I hope that would have been very useful to you. In this lesson, that is lesson three we are going to discuss three topics one is Subacute ruminal acidosis, Ruminal drinkers, and Ruminal alkalosis.

Let us first discuss the,

Subacute ruminal acidosis: is a management problem so here the acidosis is going to be there in a continuous way in the herd. So the animals which are continuously taking excessive carbohydrate source and low number/less amount of fiber diet, it is going to happen in the herd problem, it is going to be a herd problem, so what will happen in this situation, excessive carbohydrate is taken animal will adopt for that carbohydrate source and it will maintain the pH from 5-6, but it is not going to happen as alike clinical sign like that of acute carbohydrate engorgement, the animal will have signs like diarrhea, laminitis, and it is having some reduction in the milk yield, low milk fat like that. So here is what will happen, that will lead to cellulose digestion bacteria/fiber digestion bacteria will be low, other cellulose bacteria will be low and the sugar starch digestion bacteria will be dominating and there will be lactate replacing that is producing bacterias also more.

So let us discuss Pathogenesis; so continuous ingestion of the carbohydrate source, the less amount of roughages intake, will lead to the subacute ruminal acidosis by reducing the rumen pH, by the way of producing multiple fatty acids and also lactate content, so it will affect the lactate and the high level of volatile fatty acid leading to low pH, that will affect the cellulolytic bacterial activity and fiber digestion is impacted. So that will lead to production loss in the case of cattle.

Clinical signs like diarrhea intermittently semi-solid nature, mold waterous in nature and some of the animals may have a distended abdomen, loss of bodily conditions and some animals going to show some laminitis, hoof problems. So, the animal had some laminitis problems in the herd. So collectively we have to examine the herd, we should inquire about the history, if excessive carbureted sources are given continuously, that should be addressed.

In some cases, it may also lead to Haemoptysis and epistaxis associated with venal caval thrombosis and pulmonary hemorrhage. In this case, there is fiber is to be there to have more production of the acetic acid, if the acetic acid production is less in case of carbohydrate intake, that will lead to milk fat depression that’s one of the important things, so the owner may report that milk fat depression is there in a herd and the diarrhea is there and the animal is having laminitis, you have to think about subacute ruminal acidosis.

The Clinical signs: you can see the picture, you will be able to see there some other hoof abnormalities, so it may be a

• Ridges development in the hoof or overgrown hoof,
• Sole ulcerations,
• Sole hemorrhages,
• The white line in the hooves and
• there will be misshapen hooves.

So these are the things that are there in the herd, we need to think about some common problems, it’s maybe because of excessive carbide administration or it may be due to some mineral deficiencies.

The Treatment; we have to go for

• Antacid treatment, so Magnesium hydroxide 500 gram for 450 kg body weight, you can give orally,
• the buffering diet: diet should be modified in a way it should have a buffering,
• so, the animal should be provided adequate palatable hay, by the way, it is improving the mastication, so more amount of saliva is secreted, so that will go for a buffering in the rumen,
• you have to fit the feeding of concentrate in different quantities at different times morning and evening how to split and give, by this way you can reduce a load of volatile fatty acid and lactate levels in the rumen, and
• Another thing is feeding the roughages first, then you have to go for a concentrate that will help the animal to elevate from this condition.

Next, let us discuss the Ruminal drinkers: it is seen mostly in the case of calves. calves that are weaned on the first day itself from the form. From the mother, the form condition, so that will lead to this type of condition when it is administered the milk, is administered in the form of bale feeding, that is drinking the milk as such, not suckling the milk, so what will happen drinking the milk will not induces the suckling reflex, so the suckling reflex is very much useful or needed for the closer of the esophageal groove. As we know that young calves may be having more dominant abomasum and an ill-developed rumen reticulum omasum, so in the third, to fourth month only the rumen reticulum abomasum is going to be a normal structure, as in the case of adult animals. So in this case what will happen because of the ill-developed rumen, is the rumen reticular esophageal groove is not properly closed because of suckling reflex is not there, so the milk is directly entering the rumen and there will be putrefaction, the putrefaction will lead to casein clots and graze rumen liquor and animal having abdominal distension and depression, dehydration, it is going to be recumbent and it will also have a clay-like feces and when you are just doing the succussion on the left paralumbar fossa, it will have a fluid splashing sound. So when you are going for any detailed investigation of any dead calves, there will be villainous atrophy, and marker ruminal parakeratosis will be there because it is favoring the growth of a dark color rumen epithelium.

Diagnosis is based on the history of bale feeding and clinical signs, which we have discussed, and another one more test you can adopt in the field condition is the Acetaminophen absorption test which is to be done in a field condition.

• The paracetamol at the dose rate of 20/25 to 30 milligram per kg body weight mixed with the 2 liters of milk, that can be administered to the calves, then you have to wait for some time, you have to take the sequential blood level and you have to estimate the paracetamol level.
• The calf with the ruminal drinkers with the flat Acetaminophen absorption curve will be there so that is indicating that the animal is affected by the rubric drinkers.

The management you have to provide the nipple feeding of milk, in the nipple feeding the nipple pore will be very small. The calf should have more force to suck then only the esophageal groove will be closing, which will make the milk directly enter into the abomasum. The next one is you have to give a milkman’s hand or fingers to suck, so bale feedings to be avoided.

The etiological factor for Ruminal alkalosis is very simple, it is sometimes maybe because of protein putrefaction or NPN (NonProtein Nitrogen) sources excessive administration of urea toxicity. In the urea toxicity, sudden death will be there with the bloating so when you are going for an autopsy you will be able to find out that ammonia generation is more in the groove. But when compared to the other ruminal disorders, ruminal alkalosis is very rare, it is not going to happen in the field condition but confirmation is done only with the rumen fluid collection and examination.

The Clinical signs are there will be a

• Ruminal hypomotility,
• Tympany,
• Vomiting, some animals may have a regurgitation,
• Severe abdominal pain,
• Muscle tremors, the animal will have trembling muscle tremors,
• Muscular weakness,
• Incoordination ataxia,
• Tachypnea, and
• CNS excitation, the animal will develop CNS excitation and die.

In case of urea toxicity, suddenly after injection of the heavy amount of urea, it will be developing hyperammonemia and ammonia is more in the rumen and it will be circulated in the blood and there will be a CNS toxic and sudden death will be there.

Diagnosis:

• We have to collect the rumen liquor and you have to examine the rumen liquor, the pH is more than 7.5, that is indicating that there is a Rumen alkalosis, the reason may be either it may be a protein denaturation or it may be due to urea or NPN (NonProtein Nitrogen) sources excessive injection.
• So one more urea injection is through the urea-treated straws, if it is excessively fed sometimes the urea is more concentrated in the straws which will also affect the condition, rumen dysfunction will lead to alkalosis.
• The strong ammonia odor of the rumen content will be there, so in this picture, we will be able to see the alkaline pH of 9, which we can see in the ruminal alkalosis.

Treatment:

• We have to give Acetic acid or vinegar, so the alkalinization agent is to be utilized as an acidic one. Give acetic acid around the 2-6 liter into the intra-ruminally you have to give bypassing the rumen infusion pump. So, if you want you can also dilute with the water and you can administer.
• Then intravenously normal saline should be administered and other B-complex, Vitamins Supplements to be given.

In this lesson 3, we have discussed the

Subacute Rumen Acidosis, Ruminal drinkers, Ruminal alkalosis in detail.

So, in the next lesson, that is lesson 4, we are going to discuss the Ruminal Tympany.

Thank you!