2 Pathogenesis and Clinical Findings

Transcript

Welcome to lesson-2, so before the previous lesson, you have seen that is How, What is Hypermagnesaemic in dairy cattle, What are the risk factors that predispose the cattle to go for Hypermagnesaemic and the Role of Magnesium, that is a How the Magnesium level is maintained, Magnesium Homeostasis, and the various Risk factor involved with and the Etiology for Hypermagnesaemic.

In today’s class, we will see about the Pathogenesis and the Clinical signs of Hypermagnesaemic here that is various stages of Paracute form and a Subacute and Chronic form of Lactation Tetany in cattle. So I have already explained about the Pathogenesis or Homeostasis of Hypermagnesaemic, normally the source of Magnesium is through diet only and it reaches the rumen and the normal sodium-potassium ratio is 5:1, there will be active absorption of the Magnesium through the rumen wall. Even the source of sodium and potassium is through saliva also, so the saliva that reaches the rumen, that maintains the normal sodium-potassium ratio of 5:1 and absorbed magnesium majorly it goes for a skeletal tissue, as well as body tissue and the excess, is excreted in the urine and feces.

Then whenever there are various risk factors as we have seen, the sodium-potassium ratio is get altered is reduced ratio of 3:1, and the absorption of magnesium decreases, so naturally like Hypermagnesaemic here there will not be any mobilization of Magnesium from the bone reserve except in calves, so the only the Homeostasis is maintained by reabsorption of Magnesium or reduced excretion whenever there is demand for magnesium at a serum level. So the reduced magnesium in the serum in spite of the reabsorption of magnesium from the urine causes a severe deficiency and neurological signs.

The major effect of magnesium even though exits an effect on various enzymatic activities, the acute deficiency of magnesium, mainly causes neurological signs. The reason behind this there is acute whenever there are serum magnesium decreases, equally the magnesium level of CSF also decreases, hence there will be the central nervous system signs are more predominant than the peripheral nerve, and as we as I already mentioned Magnesium is mainly required for the release of neurotransmitters that is esterase choline and for the transmission of impulses at the motor end plate. So whenever there is a deficiency it causes muscle irritation and all the neurological signs. The reason for the Clinical signs are: as we already discussed there are various Risk factors that are causing a reduced Magnesium level in the serum, like inclement weather, and then feeding or grazing on lush green pasture, as well as the cereal crop grasses like wheat pasture or barley or a rice cereal crop grasses, and then excess fertilization of the feedstuff, that is a pasture land causes increased potassium content of grasses and predisposed to go for Hypermagnesaemic as well as the excess urea feeding also increases the increased Ammonium content of rumen that impair the Magnesium absorption and finally the reduced dry matter intake, reduces the volatile fatty acid current of rumen decreases the magnesium level. And the stress and other factors that predispose the animal to go for Hypermagnesaemic and finally we are getting Clinical signs. So there are major 3 forms of Hypermagnesaemic here encountered Acute form, Subacute form, and Chronic form.

Acute Hypermagnesaemic Tetany: So this is a more challenging one to treat and here there is an acute reduction of Magnesium in Lactating dairy cattle that may cause sudden death. So what happens the animal will normally be on grazing land it suddenly stops grazing and the animal will have a disinclination to move and it has a tremor in the body and even slight external stimuli, the animal becomes a hyperaesthetic to external stimuli and there will be a violent behavioral activity, frenzy behavior, you can appreciate. So this is the classical portion of Hypermagnesaemic, so the animals are immediately after showing hyper setting signs and then trimmers of muscles, the twitching of ears, there will be mild tetany, and the animal falls, and it attains there will be an extension of all the limbs and then the deviation of head and neck towards the laterally and it attains opposite onus posture and the animal will have stiffening of limbs and there will be twitching of muscles and then frothing at the mouth and the animal will show tonic-clonic convulsions.

So in this you can see, this is actually a young cattle that is a fed with a green fodder immediately after that within few hours, the animal showed some frenzy behavior and it is a highly hyperaesthetic to external stimuli and there will be sprinkler ears and the animal behaves violently. So here you can see the animal is uncontrollable and it is moving here and there and there are excitatory behavioral signs, we can appreciate in the animal, it is also Hypermagnesaemic here. So other than neurological signs, usually after the animal show tonic-clonic convulsion, the animal will die finally due to respiratory arrest. And sometimes the episodes of signs will occur 3 to 4 times and if the animal is untreated, then it will die.

So apart from neurological signs, the animal will have an increase in temperature and respiration and the heart rate- the intensity of the cardiac sound will be more pronounced, so even with some distance you can hear the loud cardiac sound otherwise known as thumbs and then usually the death occurs in animal within few hours of manifesting the neurological signs.

Subacute Hypermagnesaemic Tetany: this is the duration of the onset of clinical signs or 3 to 4 days, so slow onset of signs so the animal is hyperaesthetic and there will be tremors of muscles and the ears pricked up, and the animal will have apprehension, and it may have some frenzy behavior and stamping of feet and the appetite may be sluggish and milky less, this adult dairy cow that is a high yielder cow presented with excitatory signs, and it has a frenzy behavior and it’s a pricked up ear and it’s a responding to the hyperesthesia that is excessive responsibilities to external stimuli. In the Sub-acute form, the major clinical signs are tremors and tetany of limbs, but whenever the animal is exposed to external stimuli or sudden excitement, the animal will go for tonic-clonic convulsion and it may die also.

Chronic Lactation Tetany: this is the common form we can see because it’s a hidden cause for most of the downer cows. What happens is the animal will have only unthriftiness and then reduced appetite, and reduced milk yield, and can currently because of reduced hypo magnesium level, magnesium is important to source for a secretion of parathyroid gland hormone that is Parathormone that we have already seen in a Hypocalcemia class, so what happens is the chronic deficiency of magnesium may predispose the animal for hypercalcemia so hyper magnesium and hypercalcemia occurs concurrently and most of the time in making the animal downer cow, so it is an important cause for downer cow along with hypercalcemia, most of the time the animal will not respond to calcium treatment unless you include magnesium there will not be any response. So Tetany signs are common in this stage.

In this lesson, we have seen what is a Hypermagnesaemic is a Pathogenesis of Hypermagnesaemia and various stages of clinical manifestation like Acute form, Subacute form, and Chronic form, mainly Neurological signs and concurrent occurrence of Hypocalcemia in cattle.