Nutrient Imbalances
To maintain the health, vigour and productive ability of animals, a farmer needs to manage those factors which can challenge the health of the animal. There are four factors which need to be managed correctly to reduce the chance that diseases will occur.
- Poor nutrition.
A well-fed animal has a much better chance of fighting off disease and can convert nutrients over maintenance requirements into products.
- Stress.
Any stress placed on an animal will make it more susceptible to disease (e.g., Pasteurella). Stress includes factors such as parturition, fatigue from walking or being transported long distances, poor housing, excessive cold (especially when combined with dampness), excessive heat, high humidity, and dehydration.
- Lack of tolerance.
Animals in some areas are more tolerant to certain diseases because they have built up resistance to those factors through being exposed to them for many generations. For example, goats are browsers, and thus less susceptible to picking up internal parasites from grazing infected pastures. Thus, if you then put a goat onto pastures, he will pick up internal parasites more easily.
- Lack of immunity.
It is important to maintain an animal’s immunity levels. There are two ways, one is allowing the newborn to receive colostrum in the first few days after birth, and the other is through vaccination.
In general, long-term stress causes an increase in the production of cortisol by the adrenal cortex around the kidneys. Persistently elevated levels of cortisol in the blood cause the cells to develop a resistance to the function. of insulin (which is to allow the entry of glucose into cells). Thus, glucose cannot enter cells and cannot be utilised by the cells to function normally, since glucose is the basic energy source for life. Elevated cortisol levels due to stress also cause a reduction in levels of FSH, LH, and growth hormone thus directly impairing reproduction and growth. Also, cortisol induces protein catabolism (breakdown) thus inducing muscle weakness.
Horses
In both humans and horses, metabolic syndrome, Cushing’s illness, insulin resistance, glucose intolerance, and “glycemic indices” of feeds and meals have received considerable attention in recent years. These words have been applied to adult horses with a higher prevalence of laminitis and developing orthopaedic illnesses (growing horses). The words are derived from human medical literature, where they have extremely specific clinical and scientific definitions that do not always correspond directly with equine conditions.
Insulin resistance (IR) is a reduced sensitivity of the body’s cells to insulin’s facilitation of glucose uptake, resulting in higher-than-normal insulin release in response to a carbohydrate meal. Blood glucose concentrations may be normal (compensated) or elevated (hyperglycaemia, uncompensated glucose intolerance). This has been well-defined in horses and appears to coincide closely with what is seen in humans.
Cushing’s disease is classically due to tumours in the pituitary gland. These tumours cause unregulated secretion of adrenocorticotrophic hormone (ACTH) that stimulates increased cortisol release from the adrenal gland, mimicking a stress response. The higher-than-normal blood concentrations of cortisol contribute to the classic clinical signs of hyperglycaemia, IR, excessive thirst (polydipsia) and urination (polyuria) and hair loss. In horses, the syndrome is associated not only with IR, polyuria, and polydipsia but also with reproductive failure in mares and laminitis. Instead of hair loss, horses that have pituitary tumours tend to retain their long, shaggy, winter coats throughout the year. Though tumours are usually present, they tend to be in a different location in the horse’s pituitary gland than in other species. Therefore, it has been proposed that this syndrome in horses should be called “pituitary dysfunction.”
Metabolic syndrome (MS) is characterised by compensated or uncompensated insulin resistance and hypertension in humans that do not have pituitary tumours and is often, but not always, associated with obesity. Hypertension has not been documented in horses “diagnosed” as having MS, but they are prone to laminitis, which involves hypertensive changes in the blood supply to the hoof and is frequently obese. There is disagreement as to whether non-obese IR horses are truly comparable to humans with MS.
Colic in Horses
Horse suffering from colic.
Colic is a painful, sometimes fatal, condition that strikes fear in the heart of any horse owner. Many cases of colic are mild and can be resolved with veterinary intervention.
The two main classifications for colic are non-strangulating and strangulating, describing whether blood flow to the intestinal tissue is restricted (strangulating) or not (non-strangulating).
The term ‘colic’ is used to describe abdominal pain in horses. It is not one specific condition but rather a symptom associated with numerous abnormalities that affect the horse’s digestive organs. Horses evolved as hindgut fermenters, grazing for most of the day while constantly moving. However, modern management practices are not always aligned with the natural lifestyle of horses.
Typical practices such as stall confinement and low forage intake have become key contributors to the increased risk of colic. The most common types of colic are related to impaction, in which undigested feed or foreign bodies such as parasites block the movement of digesta through the intestines and cecum.
More serious cases involving a “twisted gut” can block blood flow to the area, causing tissue death. This needs to be rectified by surgery to avoid further complications.
Top 11 causes of colic in horses:
- Stall confinement.
- High grain or low forage diets.
- Inadequate deworming practices.
- Sand ingestion.
- Abrupt feeding changes.
- Dehydration.
- Mouldy feed or hay.
- Stress.
- Long-term use of NSAIDs (non-steroidal anti-inflammatories).
- Dental problems.
- Previous history of colic.
Pigs
Calcium deficiency is more likely to occur in pigs than a deficiency of phosphorus because swine are often fed rations made up largely of grains or grain byproducts, together with some protein-rich concentrates, and these feeds are usually good sources of phosphorus but low in calcium. Vitamin D is closely related to the metabolism of calcium and phosphorus and is therefore considered for deficiency diseases involving these two minerals.
When pigs are housed during the winter and early spring because of bad weather, rickets of young animals occur before the bones stop growing in length. However, if the pigs are fed improperly and aren’t given free access to direct sunlight, it can happen at any time of the year.
Similar to other young animals, swine exhibit the same rickets symptoms. Affected pigs frequently have poor appetites, an unsightly appearance overall, soft, brittle bones, and are typically lame, especially in the later stages of the illness.
By making dietary corrections, rickets can be easily avoided or treated in their early stages. Young pigs with access to direct sunlight accumulate significant amounts of vitamin D. However, it is risky to solely rely on vitamin D reserves during prolonged periods of confinement unless the pigs are fed in outdoor lots with access to direct sunlight. Rickets will manifest when the body’s reserves of this vitamin are substantially depleted.
Calcium Deficiency in Brood Sows
Breeding pigs, especially pregnant or nursing sows, exhibit severe symptoms if their diet is calcium deficient. This deficiency is most prevalent in pigs kept in floored pens without access to pasture and fed a diet primarily made up of cereal grains without a balanced mineral composition.
Young pig suffering from rickets.
Calcium insufficiency symptoms in pigs:
- Rough scaly skins, dirty in appearance.
- The pigs occasionally appeared “off their feet” with their legs bending inward and manifested what appeared to be rickets’ hallmark symptoms.
- The sows often refused their feed towards parturition, indicating nutritive disturbances.
- They had great difficulty in farrowing and could not stand on their feet for two or three days afterwards.
- No signs of milk could be seen before or after farrowing, and their udder was very flabby, especially in comparison with the normal sows.
- Very few pigs survived at weaning time and even the few left-made very poor live weight gains. It should be observed, however, that the sows themselves when they farrowed appeared to be in good condition.
Right feed formulation in the right combination with the right ingredients will go a long way in the first two weeks.
Phosphorus Deficiency
As previously mentioned, calcium is more likely to be deficient in typical pig rations than phosphorus, which is the opposite of the situation with cattle. However, phosphorus deficiency may occur when pigs are grazed on pasture or on cultivated root crops with little to no grain and no protein- or phosphorus-rich mineral supplement.
The following symptoms were seen in pigs fed diets deficient in phosphorus:
- A loss of appetite.
- Poor utilisation of feed and storage of energy.
- A failure to make normal growth and to develop bone.
- Muscle normally.
- A lowering of inorganic phosphorus in the blood.
- A marked increase in thirst and a corresponding excretion of urine.
Vitamin A Deficiency
Pigs raised in dry lots without access to green feed, well-cured forage, or other sources of carotene or vitamin A are most likely to suffer from vitamin A deficiency. Night blindness is one of the first symptoms of the deficiency. Pigs with severe vitamin A deficiency would convulse or fall over on one side when excited, roll their eyes, struggle a little or lie with their legs extended, squeal in pain and show signs of laboured breathing. The animals were partially or blind, and their eyes discharged water.
Nutritional Deficiencies and Excesses Affecting Pig Welfare
The majority of nutritional problems in pigs are brought on by clinical disease-related deficiencies, though they can also be brought on by dietary excesses of specific nutrients.
The issues related to poor nutrition have significantly decreased with the current understanding of the nutritional needs of pigs and the components of the various dietary ingredients. However, there are still some instances of dietary deficiencies, which can be divided into four categories: energy, protein, vitamins, and minerals.
Poor growth is a hallmark of vitamin deficiency, but it can also be attributed to a variety of other factors. Today, it’s common to have mineral deficiencies, especially in areas where it’s challenging to meet lactation demands in genotypes that are currently undergoing rapid growth.
Symptoms of metabolic and nutrient deficiencies and excesses in pigs.
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Nutrient |
Deficiency Symptoms |
Excess Symptoms |
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Calcium (Ca) |
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Copper (Cu) |
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Iodine (I) |
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Iron (Fe) |
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Magnesium (Mg) |
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Manganese (Mn) |
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Phosphorus (P) |
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Potassium (K) |
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Amino Acids |
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Biotin (vit B7) |
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Choline |
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Cyanocobalamin (vit B12) |
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Energy |
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Fat and Fatty Acids (Linoleic) |
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Folic Acids |
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Nicotinamide (Niacin; vit B3) |
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Pantothenic Acid (vit B5) |
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Protein |
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Poultry
The complex business of raising poultry necessitates close attention to the health and welfare of the flock. Successful and long-term production needs to maintain the health and welfare of poultry in farming operations.
Common metabolic diseases of poultry.
Understanding the common health conditions that can affect poultry and putting the right management techniques (such as balanced nutrition, preventive measures, and prompt treatment) in place can aid in their effective prevention and treatment.
Visceral Gout (Urolithiasis)
A common condition seen in older layer flocks is visceral gout, which is characterised by the buildup of uric acid crystals in organs like the kidney, heart, lungs, and gut. It frequently results in kidney failure and can increase flock mortality.
Low phosphorus diets, lack of water, excessive calcium intake before sexual maturity, and high levels of vitamin D3 are some of the factors that contribute to kidney damage. Gout-related deaths in poultry are typically recurrent, and affected birds may not exhibit any symptoms before passing away or appear frail.
Fatty Liver Syndrome
An imbalance in energy and protein intake leads to excessive fat accumulation in the liver, which is the cause of fatty liver syndrome. In caged laying hens and sporadically in breeder turkey hens, this condition is frequently seen. The sedentary lifestyle and high-calorie diet of caged hens increase their susceptibility to this syndrome.
Clinical signs of fatty liver syndrome in chickens.
Cloacal Prolapse
When the cloaca (vent) of laying hens becomes permanently everted and inflamed, as a result of trauma from pecking, cannibalism, or large egg size, it is known as cloacal prolapse. The strain of the bird, the quality of the beak trimming, the nutrition, the availability of space, the intensity of the light, and the size of the egg can all have an impact on the severity and frequency of this condition.
Osteomalacia (Softening of Bones)
Usually, caged birds exhibit calcium depletion in the long and medullary bones, which primarily implies that there is decreased activity or exercise as a predisposing factor. Birds may appear healthy at the time of their initial paralysis and will have an egg with a shell in the oviduct. Due to the birds’ inability to access food or water, they either starve to death or become dehydrated.
If pullets are fed a high calcium diet (minimum of 3.5% calcium) at least two weeks before the first oviposition, a high incidence of cage layer fatigue can be avoided. Bone fractures are more likely to occur in older caged layers, especially during transportation.
Rickets is the term for young birds with soft bones. This disorder is typically brought on by intestinal malabsorption linked to enteric diseases, low vitamin D3 levels, or abnormal calcium-to-phosphorus ratios in the diet. The birds have long bones, extremely pliable beaks, and are frequently recumbent. However, they are bright and alert.
Vitamin E (Alpha-Tocopherol) Deficiency
The term “crazy chick disease” or “cherry brain” are other names for this condition. The root of this illness is a deficiency in vitamin E. Wide variety of birds can be affected by this deficiency, but young chicks and turkey poults are typically the ones to get the diagnosis. Vitamin E, a naturally occurring antioxidant, is crucial for maintaining brain tissue and promoting embryonic development, particularly in growing birds. Selenium is necessary for vitamin E’s metabolism.
Ascites Syndrome and Right Ventricular Failure in Broilers
A live bird frequently exhibits no symptoms. The muscles of the heart, gizzard, legs, and breast can be seen at necropsy to have white to yellow areas. Feed restriction can be used to reduce the ascites caused by genetics, but this can also slow down the growth rate and performance of the birds. It is important to address the underlying cause of ascites and improve the living conditions for the broiler chickens to prevent this condition and improve the overall health of the flock.
Sheep
The following six main metabolic diseases in ewes occur during times of increased nutritional demand, i.e., in late pregnancy and early lactation:
- Pregnancy toxaemia (twin lamb disease).
- Hypocalcaemia (milk fever).
- Hypomagnesaemia (grass staggers).
- Johne’s disease.
- Abomasal bloat.
- Lambing sickness.
If these diseases are not treated quickly, they can lead to death, so careful management during these periods is essential to minimise production losses. The key to controlling metabolic diseases is managing ewe body condition score (BCS) and nutrition.
Pregnancy Toxaemia (Twin Lamb Disease)
Twin lamb disease is seen in late pregnancy due to a negative energy balance where feed levels do not meet the high nutritional demand (70% of foetal growth occurs in the last 8 weeks of pregnancy). Although often seen in thinner twin-bearing older ewes, it can also occur in overfat ewes.
Signs:
- Affected ewes appear disorientated and separate themselves from the rest of the flock.
- They are lethargic with no appetite and can go blind.
- Death can occur.
Treatment:
- The ewe should be isolated and offered palatable feeds and water.
- Treatment with propylene glycol and/or intravenous.
- Glucose injection can be successful where ewes are still able to walk when treatment starts.
- Glucocorticoid injection will raise blood glucose; this may however also induce lambing in late pregnancy.
- Affected ewes need to be checked regularly for signs of lambing or abortion as they may be too weak to expel the lambs unaided.
Lambing Sickness and Hypocalcaemia (Milk Fever)
Hypocalcaemia or milk fever is a lack of calcium in the bloodstream and usually occurs in the late stages of pregnancy (the last 6 weeks) and early stages of lactation (first three months) when the demand for calcium is at its highest.
Due to a deficiency in calcium in their diet, ewes may already be predisposed to a calcium deficiency. For instance, ewes grazing oxalate-containing plants that bind calcium in the intestines and prevent absorption or eating grain diets without added calcium or poor-quality pastures are at risk. Milk fever is more likely to affect older ewes.
The imbalance between energy supply and demand brought on by inadequate nutrition is what leads to lambing sickness. 70% of lamb growth takes place during the final two months of pregnancy. Even if they had no nutritional issues earlier in their pregnancy, it more frequently affects ewes who are expecting twins. Even though ewes with lambing sickness may appear to be in good health, their nutritional levels will have dropped for a variety of reasons, such as nutrient-deficient pastures.
Ewes with twins or triplets are usually affected with milk fever and lambing sickness.
Certain dietary and environmental factors can place extra stress on ewes and trigger the onset of lambing sickness and milk fever. These factors in late-pregnant ewes include:
- Mustering for shearing or crutching.
- Holding off feed for long periods such as in the yards for shearing or crutching, or while trucking.
- Severe cold, rain or wind cause ewes to seek shelter rather than graze and the extra muscular contractions required for shivering and maintenance of body heat exhaust low energy reserves.
- The sudden change of diet, for example onto lush pastures, resulting in dietary upsets or being held in eaten-out holding paddocks.
Signs:
- The ewe is weak and unable to stand.
- The rumen stops working and fluid is often expelled from the nose.
- Without treatment, the ewe can fall into a coma and die within 24 hours.
Treatment:
- Slow intravenous administration of 20 – 40 ml of a 40% calcium boro-gluconate solution given over 30 – 60 seconds. This is available at farm merchants but vet advice on treatment should be sought before attempting. Eructation (belching) is seen 1 – 2 minutes after the injection and the ewe will often quickly stand and walk away within 5 minutes.
- Alternatively, a subcutaneous injection of 60 – 80 ml of 40% calcium boro-gluconate solution may be given in 2 or 3 sites over the thoracic wall behind the shoulder, this takes longer to be effective (it may take up to 4 hours before the ewe responds).
Ewe suffering from milk fever.
Hypomagnesaemia (Grass Staggers)
Hypomagnesaemia or grass staggers occurs in spring and is a deficiency of magnesium caused by increased demand and the forage having insufficient magnesium levels to meet the animal’s requirements. It is often caused by the stress associated with a sudden cold, wet spell of weather and animals on lush or potash-rich grazing.
Hypomagnesaemia occurs in ewes within the month before or after lambing, with the highest incidence occurring after lambing. Affected sheep often have hypocalcaemia and/or hypoglycaemia as well and should be treated for all three conditions.
Signs:
- The first signs are often death, but the ewe may exhibit restlessness, tremors, and unsteady walking.
- Affected ewes will then lie down and have involuntary leg movements and frothing at the mouth.
Treatment:
- Treat with a subcutaneous injection of magnesium sulphate and a slow intravenous injection of a calcium or magnesium and dextrose mixture.
Johne’s Disease
Paratuberculosis was identified by German bacteriologist and vet Heinrich Johne in 1905, hence the common name ‘Johne’s disease’.
Young animals are more susceptible and usually become infected after taking in food or water contaminated with the faeces of infected animals. The bacteria then establish themselves in the intestine.
The disease usually spreads slowly in a herd. Most animals do not show symptoms and it may be years before the disease is eventually diagnosed. Affected animals develop persistent diarrhoea and lose condition. Johne’s disease should not be confused with other ailments that cause a loss of condition, such as worm infestation, coccidiosis, or malnutrition.
Control of Johne’s disease in a flock is based on:
- Culling infected (emaciated) animals.
- Strict hygiene to prevent the spread of the infection, especially via feed and water troughs.
- Buying animals only from farms that have tested negative.
- Testing stud animals.
- Keeping the flock as young as possible.
- Lambing on clean pastures.
Sheep suffering from Johne’s disease.
Abomasal Bloat
Most artificially raised lambs, especially those that are hand-fed warm milk, are prone to abomasal bloat. Lambs that are self-fed cold milk are rarely affected by it. It is thought that an accumulation of bacteria in the lamb’s stomach is what causes abomasal bloat.
Lambs with the condition experience abdominal pain and swollen bellies. Using sodium bicarbonate as a treatment does not always work well. It has been demonstrated that adding yoghurt or probiotics to milk substitutes can lower the incidence of abdominal bloat. Lambs raised artificially need to be vaccinated against enterotoxaemia in particular.
Control of Metabolic Diseases in Sheep
Ewes are scored for their body condition throughout the pregnancy, and their diets are adjusted following their nutritional needs. It is possible to feed the right diets to the ewes in large flocks by dividing them into different groups according to the number of lambs they are carrying. 2 – 3 weeks before lambing, blood samples for the metabolic profile can be useful for turnout pasture management. Consult your veterinarian before adding standard sheep minerals to your diet. Supplementing excessively or when it is not necessary can be harmful.
Common Metabolic Diseases of Cattle
These livestock illnesses are brought on by productivity techniques when the body’s stores of calcium, magnesium, or energy are insufficient to meet metabolic demands. They are crucial in industries like dairy farming where high-yielding animals are needed.
The metabolic conditions ketosis, milk fever, fat cow syndrome, and hypomagnesaemia affect cattle. All of these could result in an immediate, potentially fatal deficiency. Correcting the diet of cows from late pregnancy to the height of lactation is essential for preventing these illnesses. It is crucial to get expert veterinary and dietary advice if these diseases crop up frequently.
For instance, parturient paresis of cows (milk fever) happens when the mass of calcium in the mammary secretion is greater than the cow’s diet or its skeletal reserves can supply. Ketosis also happens when cows are in a negative energy balance. Similar circumstances can be found with magnesium and glucose metabolism, as well as phosphorus and postpartum haemoglobinuria.
Ketosis
Ketosis happens when cows are in a negative energy balance. Magnesium and glucose metabolism and phosphorus and postpartum haemoglobinuria are two examples of situations that are analogous.
Common conditions like displaced abomasum, mastitis, and metritis that cause a decrease in appetite during early lactation can result in secondary ketosis. Because rumen microbes require sufficient cobalt to enable the synthesis of vitamin B12 and to properly utilise propionic acid, ketosis may also be detected in grazing cattle in areas with cobalt deficiency.
Additionally typical of dairy herds with liver fluke or fasciolosis is ketosis.
Ketosis caused by insufficient feed intake.
Restoring the body’s lack of glucose is the primary goal of treatment. There is an immediate need for a quick-acting glucose supplement, and further treatment should be given to ensure a steady supply of glucose for the long term. In ketosis, many long-acting corticosteroids are advantageous because they aid in the breakdown of muscle protein to produce glucose, which immediately restores the blood glucose levels that have fallen.
Maintaining a good transition cow management protocol is essential to preventing the onset of ketosis, with a body condition score being a key element. Cows shouldn’t be overly fat at calving because this lowers feed intake. A BCS of 2.5 – 3 on a scale of 1 – 5 is ideal, with anything higher than 3 being deemed too fat and more likely to enter ketosis. Therefore, it’s crucial to keep an eye on dairy cows’ physical health during the dry season.
Additionally, it should be a goal of the transition cow management protocol to reduce the natural tendency of cows to consume less during the final three weeks of pregnancy. High levels of roughage are also provided, which helps to promote healthy rumen digestion. A high-fibre ration during the dry period can also help to address the issue of decreased voluntary intake at calving. To accurately know what your cows are eating, it’s important to check the quality of the forage being used several times a year.
By providing a highly palatable ration at calving and appropriate accommodations, the overall goal of the transition period is to ease the animal’s transition from gestation to lactation. Early lactation should unquestionably be avoided when making any significant dietary changes. In the early stages of lactation, roughage with a high butyric acid content should be avoided.
Fat Cow Syndrome (Fatty Liver Disease)
Preventing obesity in both heifers and cows before dry-off and calving is the best option because treatment for fatty livers is generally ineffective.
Clinical signs:
The most frequent occurrences of fat cow syndrome involve overweight cows that were overfed in the early stages of pregnancy but suffered from severe nutritional stress in the two months before calving. After calving, the affected cows become lethargic and weak. The pulse is quick and small, and the drops are small and firm. Sternal recumbency follows. A clear nasal discharge is more noticeable than usual. There is rapid and loud breathing. The cows exhibit symptoms for about a week before quietly dying.
Treatment:
If treatment is given on time, it can be effective. Treatment for fat cow syndrome is typically ineffective, especially if the cows are already lying down. It is advised to use anabolic steroids and supportive treatments like intravenous glucose, fluids, and electrolytes, as well as oral propylene glycol, fluids, and electrolytes.
Giving the animal good supportive care and feeding it a balanced diet, such as high-quality hay with little to no grain in the early stages of the drying-off period, are two steps that should be taken to treat the animal.
A vitamin and mineral supplement to fulfil nutritional requirements for protein, energy, calcium, phosphorus, and selenium, and no high-calcium grain mixes until after calving.
Illustration of a normal liver and a fatty liver.
Hypomagnesaemia (Grass Staggers)
Clinical signs:
The prevalence of hypomagnesaemia is highest in adult lactating cows that are grazing on lush grass pastures and calf reared primarily on milk. When the disease’s acute form manifests, affected animals may be grazing normally when it suddenly causes them to stumble, fall, and experience severe paddling convulsions. These convulsion episodes may briefly repeat, and then the patient passes away. It is common to find dead animals in pastures that have no visible signs of illness.
Treatment:
If treatment is given promptly, it can be effective. Hypomagnesemia-related clinical signs necessitate immediate parenteral therapy, with long-term care being of utmost importance.
To stop the spread of tetany and potential fatalities in affected herds, preventative oral magnesium supplementation needs to start right away.
Effective treatment can be achieved if it is administered in time. For cases of hypomagnesaemia, use the same treatment as for milk fever, plus a subcutaneous injection of 200 ml of 50% magnesium sulphate.