Nutritional Problems (new)

Nutritional Problems (new)

Animal salt lick

(c) M. Saleem

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Energy and Protein Deficiency


Animals require energy and proteins for different body functions. Energy is required for maintenance (to maintain the body, respiration and digestion), production (growth, milk and workforce) and reproduction (pregnancy). An animal derives energy from dietary carbohydrates. Proteins are required for formation of body tissue. Proteins can be derived from feed and are formed by intestinal flora.

Adequate suppy of both energy and protein is essential for the general health of any animal. The requirement of both energy and protein by any animal depends on the bodyweight of the animal and the the degree of production expected from the animal. Prolonged deficiency of both proteins and energy would result in loss of condition and in ability to be productive. 

Malnutrition if prolonged eventually leads to death. Malnutrition caused by lack of energy and proteins may occur anywhere in the world but is more prevalent in the tropics. Animal feeds vary in their levels of energy and proteins. Straws such as rice straw and wheat straw are poor sources of both proteins and energy whereas concentrates like dairy meal may be rich in both. 

In the tropics, good quality pastures may provide adequate protein and energy for maintenance and production. However in situations of drought or overgrazing, animals are liable to receive inadequate energy or proteins from pastures. 


Signs of Energy and Protein Deficiency

Energy Deficiency 

Deficiency of energy is the most common nutrient deficiency which limits the performance of grazing animals. Feed may be inadequate due to overgrazing, drought, poor quality or digestibility or expense. Sometime forage may contain an excess of water, limiting energy intake. 

Energy deficiencies result in: 

  • Retarded growth in young animals and a delay in the onset of puberty.
  • A shortened lactation in milking animals and decline in milk production.
  • In mature animals, a marked loss of bodyweight, especially during late pregnancy and early lactation.
  • Prolonged periods of anoestrus, lasting several months, which have marked effect on the reproductive performance of a breeding herd.
  • Calves and lambs may be born weak and undersized.


Protein Deficiency 

Protein deficiencies usually accompany energy deficiencies. They are not usually as severe and take the form of: 

  • Reduced appetite in young animals.
  • Lowered feed intake.
  • Lack of muscle development.
  • A prolonged time to reach maturity.
  • In mature animals there is loss of weight and decreased milk production.



Prevention - Control - Treatment

Treatment and prevention of malnutrition is beyond the reach of most farmers. Diseases that worsen the effects of malnutrition can be alleviated by appropriate treatment e.g. deworming. Severely malnourished animals usually do not survive even when food again become available, so if a drought is expected or feed sources otherwise too few, it is wisest to sell/slaughter the weaker animals before the condition goes down too much. 

Malnourished animals should not be forced to be productive e.g. by putting them to work. This will only worsen the condition.


Vitamin Deficiency


In ruminant diseases, only fat soluble vitamins A, D and K have real importance. 


Vitamin A

This is available in most green plants, and if the animals graze on well managed pastures and forage, deficiencies will not occur. However, cattle fed on poor quality roughage, such as poor quality hay and straw, require supplemention. 

Clinical Signs of Vitamin A Deficiency 

  • Decreased appetite leading to reduced growth.
  • Impaired night vision.
  • Increased still births in pregnant animals due to affected reproductive function, especially in cases where dry cows are offered poor diets.
  • Fainting fits in calves: the calf collapses as if in a deep sleep then gets up and walks away quite normally.
  • In latter stages of deficiency, bone growth is affected and this may cause pressure on nerves to the eye, which may lead to total blindness.

Diganosis of Vitamin A Deficiency 

This can be done by investigating the history of animals and their diets, and by analysis of blood and liver samples in a laboratory. 


Vitamin D

There is little vitamin D in plants. Animals obtain most of it from the sun. Vitamin D is necessary for the absorption of calcium and phosphorous from the intestines and the deposition of the minerals in bone as well as in the maintenance of normal blood levels. Vitamin D deficiency in young calves is likely to occur when they are housed in dim lights and offered poor quality diets. 

Clinical Signs of Vitamin D Deficiency 

  • Reduced Growth Rates.
  • The legs may be bent and there is abnormal swelling, with stiffness and lameness occurring in a number of animals.
  • The teeth may be out of line and the jaw bone deformed.


Treatment is by injecting vitamin D and by correcting the ration, including oral supplementation with vitamin D. 



Vitamin K

This is available in plenty in leafy forages. Primary deficiency does not occur. Deficiency can be induced by dicoumarol poisoning such as warfarin rat poison and mouldy clover hay, which inhibit the action of vitamin K. Vitamin K is involved in blood-clotting mechanisms. 

Clinical Signs of Vitamin K Deficiency 

  • Failure of blood clotting, including excessive bleeding from cuts.
  • Appearance of large red hemorrhagic areas in the membranes of the mouth, eyes and nose.
  • Abdominal pain and lameness.

Treatment and Prevention 

  • Identify and remove the source of poison.
  • Give Vitamin K by mouth or through injection.


B Vitamins

This group of vitamins is formed by micro-organisms in the rumen and any excess is absorbed by the cow. They are also present in ample quantities in milk and therefore primary dietary deficiency is never seen.


Vitamin C 

This is produced in tissues of all farm livestock (cattle, sheep and goats) and dietary supply is unnecessary.

Mineral Imbalance


Minerals are essential for all animals and influence the efficiency of livestock production. Five percent of the bodyweight of an animal consists of minerals. 

Causes of Mineral Imbalance

Farming practices can determine the presence or absence of specific mineral nutrients in animal feed. Heavy applications of nitrogen fertilizer can reduce the copper, cobalt, molybdenum, and manganese content of the pasture. Lime may reduce plant copper, cobalt, zinc and manganese levels but increase the molybdenum content.

Cattle sometimes deteriorate in spite of an abundant feed supply. Mineral imbalances (deficiencies or excesses) in soils and pastures may be responsible for low production and reproductive problems among grazing animals in the tropics. Mineral deficiencies in grazing animals are associated with specific regions and are directly related to soil characteristics. Plants grown on tropical soils have been shown to be highly deficient in a number of major and trace minerals needed by grazing animals. Thus, it is necessary to provide these elements as dietary supplements to promote effecient and profitable livestock production in warm climatic regions. 

In tropical regions marked leaching and weathering of soils under conditions of heavy rainfall and high temperatures make the deficient in plant minerals. 

Increasing crop yields remove minerals from the soil at a faster rate so deficiencies are frequently found on the most progressive farms. 

Even though a diet may contain adequate amounts of particular nutrients, other factors decrease the absorpotion of that nutrient, thus reducing the value of the dietary suppy. Excess phosphate reduces calcium absorption. Excess calcium reduces the absorption of iodine. Many other examples exist of antagonisms between elements. 


Signs of Mineral Imbalance

  • Wasting diseases.
  • Loss of hair, depigmented hair and skin disorders.
  • Non-infectious abortion.
  • Diarrhea.
  • Loss of appetite or depraved appetite.
  • Bone abnormalities.
  • Tetany.
  • Low fertility.


Mineral Requirements

At least 15 mineral elements have been identified as nutritionally essential for ruminants. There are 7 major minerals - Calcium, Phosphorus, Potassium, Sodium, Magesium and Sulphur and 8 trace minerals - Cobolt, Copper, Iodine, Iron, Manganese, Molybdenum, Selenium and Zinc. 

Mineral requirements depend on the level of productivity. For example, the minimum zinc requirements for spermatogenesis and testicular development in male sheep are higher than for growth. Manganese requirements are similarly lower for growth than for fertility in sheep. 

Improved management practices that lead to improved milk production and growth rates for ruminants will necessitate more attention to mineral nutrition. Levels of mineral deficiencies that are small under low levels of production become more severe with increased levels of production, and previously unsuspected nutritional deficiency signs usually occur as production levels increase. 

Specific mineral imbalances are associated with specific soil types. 

Important differences in mineral metabolism are the result of breed and adaptation. It is not unusual for cattle introduced into an area to show deficiency signs while the indigenous breeds which are slow-growing and late-maturing do not exhibit the deficiencies to the same degree. The cattle which are new to the region and have not adapted may sweat profusely and lose saliva and mucous from the mouth, thus losing significant quantities of minerals, particularly in the arid tropics. 

Since tropical plant foods contain less minerals during the dry season, it is logical to assume that grazing livestock would most likely suffer mineral inadequacies during this time. However it has been found that mineral deficiencies are more common during the wet season. During the wet season livestock gain weight rapidly and there is thus a greatly increased requirement for these elements by the grazing animal. During the dry season, inadequate protein and energy results in animals losing weight which lowers mineral requirements. 

Incidence of Mineral Deficiencies and Toxicities

The mineral elements most likely to be lacking under tropical conditions are Calcium, Phosphorus, Sodium, Copper, Cobalt, Iodine, Selenium and Zinc. In some regions, under specific conditions, Magnesium, Potassium, Iron and Manganese may be deficient and excesses of Fluorine, Molybdenum and Selenium and extremely detrimental.


Diagnosis of Mineral Deficiencies and Imbalance

Mineral nutrition disorders range from severe mineral deficiencies or toxicities characterized by well-marked clinical signs and obvious signs of disease to mild and temporary conditions difficult to diagnose and expressed as a vague ill health or unsatisfactory growth and production. The mild conditions assume great importance because they occur over large areas and affect a large number of animals in addition to the fact that they can be confused with the effects of energy and/or protein deficiencies and various types of parasite infestation. 

  • Clinical signs of mineral deficiencies, pathological and biochemical examinations, along with mineral analyses of soil, water, plant and animal tissues and fluids have all been used, with varying degrees of success to establish mineral deficiencies and excesses, but the most reliable method of confirming mineral deficiencies is in the response from specific mineral supplementation.
  • Blood mineral data must always be viewed with caution. Bone and liver tissue are much more reliable.
  • Common salt, because it tastes good, is a valuable 'carrier' for other minerals. Mineral supplements should be available 'free choice' and offered in rain-proof boxes. Consumption is often 10% less when provided in block versus loose form.
  • Properly forumulated supplements are of benefit to livestock only if they are available at all times ina fresh, dry form and presented in suitably constructed feeder boxes, accessible by all members of the herd or flock.
  • A 'complete' mineral mixture should contain salt, a Fluorine-Phosphate source, Calcium, Cobalt, Copper, Iodine, Manganese, and Zinc, Selenium, Magnesium, Potassium, Sulphur, Iron or additional elements can be incorporated into a mineral supplement as new information suggests a need.
  • Information printed on the tag attached to the bag of mineral supplement is sometimes incorrect or expressed in a way that makes it difficult for the farmer to know what is being purchased and if it is adequate for the purpose intended. Seek expert advice in case of doubt.



Calcium and Phosphorus

In cattle the most common mineral deficiency is lack of Phosphorus. In most livestock grazing areas of tropical countries, soils and plants are low in Phosphorus. 

These elements have a vital function in almost all tissues in the body and must be available to livestock in the proper quantaties and ratio. 

  • 99% of the Calcium and 80% of the Phosphorus in the entire body are found in the bones and teeth.
  • Calcium is essential for skeletal formation, normal blood clotting, neuromuscular excitability, enzyme activation and permeability of membranes.
  • Phosphorus is essential for proper functioning of rumen micro-organisms, especially those which digest plant cellulose, utilization of energy from feeds, buffering of blood and other fluids, many enzyme systems and protein metabolism.-

A dietary Calcium: Phosphorus ration between 1:1 and 2:1 is assumed to be ideal for growth and bone formation as this is approximately the ratio of the two minerals in bone. If there are excessive amounts of Calcium and Phosphorus in the diet, the availability of certain trace elements may be decreased. 

Deficiency signs of borderline Calcium and Phosphorus deficiencies are not easily distinguishable from other deficiencies. 

An inadequate intake of Calcium may cause:

  • Weakened bones.
  • Slow growth.
  • Low milk production.
  • Convulsions in severe deficiencies.

Signs of Phosphorus deficiency are not easily recognized except in severe cases, when the following can be seen:

  • Fragile bones.
  • General weakness.
  • Emaciation.
  • Stiffness.
  • Reduced milk production, and
  • Chewing of wood, rocks, bones and other objects (Note that abnormal chewing of objects may also occur with other dietary deficiencies).

Severe Phosphorus deficiency results in sub-normal growth and reproduction and a depraved appetite or "pica", as illustrated by bone chewing, which may lead to botulism. 

Cattle suffering extreme Phosphorus shortage may go for two to three years without producing a calf, or even coming into heat. In Phosphorus deficient areas, if a calf is produced, cows may not come into regular heat until the body phosphorus levels are restored. 

Due to limitations of serum Calcium and Phosphorus as an indicator of status, an analysis of the ration and bone composition and breaking strength are the best ways of assessing a deficiency of Calcium and Phosphorus.

Prevention and Control 

  • Calcium and Phosphorus deficiencies can be prevented or overcome by direct treatment of the animals through supplementation, in the diet or water supply, or indirectly by appropriate fertilizer treatment of the soils on which the pasture to be consumed are grown.
  • In intensively farmed areas Phosphate applications designed primarily to increase pasture yields also increase Phosphorus concentrations.
  • The easiest and cheapest procedure is to provide a phosphatic mineral supplement in troughs or boxes protected from the rain. Good sources of mineral Phosphate are Dicalcium Phosphate or Superphosphate.



Magnesium is abundant in most common feedstuffs. It is widely distributed among plant and animal tissues with some 70% of body Magnesium present in the skeleton. Magnesium is important for neuromuscular activity. 

The dietary Magnesium requirements of livestock depends on the species and breed, age, and rate of growth or production. The general requirements for maintenance are 3 mg/kg bodyweight for maintenance and 120 mg/kg milk. 

Hypomagnesemic Tetany, when violent convulsive episodes occur, is caused by a reduction in the concentration of Magnesium in the cerebro-spinal fluid, leading to hyperexcitability, muscular spasms, convulsions, respiratory distress, collapse and death. The disorder occurs after a decrease in plasm Magnesium concentration when absorption of dietary Magnesium is unable to meet the requirements fro maintenance. 

The condition is not common in the tropics, being a disease of colder climates, associated with cold, wet, windy weather, little sunshine and no access to shelter or to supplementary feed. Failure to eat during bad weather may be a factor and cold weather stress may increase urinary excretion of Magnesium. 

The condition is also associated with lush pastures heavily fertilized with potash and nitrogen which interfere with the absorption of dietary Magnesium. 

In the most acute form, affected cows, which may appear to be grazing normally, suddenly throw up their heads, bellow, gallop in a blind frenzy, fall and exhibit severe convulsions. Death may occur within half an hour. Animals may be found dead but an indication that teh animal has had convulsions before death may be deduced from the marks on the ground. 


Slow intravenous in jection of Magnesium salts or a combination or a solution containing both Magnesium and Calcium is generally effective, but treatment must be given quickly to prevent death. 

Prevention and Control 

  • Magnesium fertilizers, such as calcined magnesite, can significantly increase pasture concentrations.
  • Foliar dusting of pastures at regular intervals is another method of delivering Magnesium to pastures.
  • Daily oral supplements of 60g for cattle or 10g for sheep may be given during the danger period.
  • For calves and cows being fed concentrates, provision of 50g Magnesium Oxide in 300-400g of concentrate mixture is adequate. Incorporating it into mineral mixes, drenches, molasses-based free choice supplements or sprinkling the mineral onto feed such as grains, chopped roots or silage, are satisfactory means of supplementation.




Potassium is essential for life and is required for a variety of body functions. Excitement and stress tends to increase urinary loss of Potassium and diseases with fever or diarrhea further increase Potassium loss. 

Potassium deficiency results in non-specific signs such as: 

  • Slow growth.
  • Reduced feed and water intake.
  • Lowered feed efficiency.
  • Muscular weakness.
  • Nervous disorders.
  • Stiffness and emaciation.

Prevention and Control 
Young plants generally contain adequate amounts of Potassium but during an extend dry season deficiencies may occur. Supplemental Potassium salts may be added when grazing dry range pastures and when urea is substituted for plant proteins. 


Sodium and Chlorine (Salt)

Sodium and Chlorine are essential for proper water metabolism, nutrient uptake and transmission of nerve impulses. 

The need for Sodium and Chlorine by livestock has been demonstrated for thousands of years by a natural craving for common salt. Sodium is the critical nutrient in salt. Giving livestock salt in the diet at a level of 0.5% is adequate for all farm species. 


  • The intial sign of Sodium and Chlorine deficiency is a craving for salt. Deficient animals will like wood, soil and sweat from other animals and drinking water.
  • A prolonged deficiency causes loss of appetite, decreased growth, unhealthy appearance, reduced milk production and loss of weight.
  • Livestock depreived of salt may be so anxious to get it that they may injure themselves in attempting to reach salt.

Sodium deficiency is most likely to occur: 

  • During lactation, due to secretion of Sodium in milk.
  • In rapidly growing animals.
  • Under tropical or hot semi-arid conditions when large losses of water and Sodium occur in sweat and where pastures are low in Sodium.
  • In animals grazing pasture heavily fertilized with Potassium, which depresses plant Sodium levels.

Even after prolonged severe deficiency salt levels secreted in milk remains high. Thus, lactating animals suffer most from lack of salt in the diet. 

Tropical plant feeds normally do not contain sufficient quantities of Sodium to meet the requirement of grazing livestock throughout the year. This inadequacy is easily overcome by providing salt mixes, usually containing added Iodine and Cobalt. Most animals can tolerate large quantities of dietary salt when an adequate supply of water is available. However when animals are deprived of salt for a period of time, re-introduce it slowly and with care. Sudden re-introduction can result in severe diarrhoea and in some cases,, violent nervous symptoms due to swelling of the brain. 


Cobalt - "Nakurtis"

Cobalt is required by micro-organisms in the animal's stomach in order to make Vitamin B12. Vitamin B12 is necessary for proper energy utilization. 

Primary Cobalt deficiency occurs on soils which are deficient in Cobalt. Land which is extremely deficient in cobalt is unsuitable for raising ruminants and where it is somewhat deficient low growth and production may make rearing sheep and cattle unprofitable. 

A wasting disease of ruminants, known locally as 'Nakuruitis' because it occurs near the township of Nakuru, is caused by cobalt deficiency. Cattle in poor conditions, dosed with cobalt pellets over a seven month period, gained almost 200 lb more than those that were not given cobalt. 

The deficiency occurs only in grazing animals and primary cobalt deficiency occurs only where soils are deficient in cobalt. Heavy liming may reduce the amount of cobalt in the soil. 

Most severe deficiencies occur when animals graze on lush pastures because they have a lower cobalt content than more slowly growing plants. 

Symptoms of Deficiency 

  • Animals on Cobalt deficient pastures gradually lose appetite, and failure of growth or loss of weight is followed by extreme loss of appetite, rapid muscular wasting, depraved appetite, severe anaemia and death.
  • If the deficiency is mild or marginal the above signs may not occur and only the young most susceptable animals may exhibit signs of weaness, indistinguishable from those caused by parasitism or low feed intake.
  • Mild forms of Cobalt deficiency in grazing ruminants are difficult to diagnose as the only signs may be a state of weakness and no anaemia. As a result the only sure way of establishing that a Cobalt deficiency is present is by observing and measuring the response to the oral administration of Cobalt or Vitamin B12 injections in terms of increased appetite and weight gain.

Affected animals respond to oral dosing with Cobalt or intramuscular injections of Vitamin B12. 

Prevention and Control 
This is best done by top-dressing affected pastures with Cobalt salts. At the same time cobalt should be included in the supplemented mineral mixture at a rate of 0.1 mg Cobalt daily for sheep and 0.3 to 1.0 mg Cobalt daily for cattle. 

In extensive range grazing the use of heavy Cobalt pellets of Cobalt Oxide is the preferred method. The pellet is in teh form of a bolus - 5g for sheep and 20g for cattle - which, when given by mouth, lodges in the reticulum and gives off Cobalt in very small but adequate amounts. 



Copper and Molybdenum

Copper is essential in haemoglobin production, the functioning of enzyme systems, as a component of various body pigments and is involved in the central nervous system, bone metabolism and heart function. 

Copper is interrelated with other dietary factors including Molybdenum, Sulphur, Zinc, protein Iron and other trace elements. These interactions are important to understand and recognize when considering dietary Copper requirements. 

An excess of Molybdenum in the diet will interfere with the uptake of Copper. Selenium has the efffect of increasing the uptake of Copper in sheep. 

Copper requirements of ruminant animals are powerfully influenced by interactions with other dietary components, especially Molybdenum and Sulphur. Ideal conditions are those in which all the dietary factors affecting Copper absorption and utilization in the animal are at optimal levels. 

With the exception of Phosphorus, deficiency of Copper is the most severe mineral deficiency to grazing livestock in the tropics. Deficiencies in ruminants occur mainly under grazing conditions. Most deficiencies are 'conditioned' deficiencies i.e. normal amounts of Copper are inadequate due to higher than normal amounts of other elemnts such as Molybdenum and Sulphur and other factors whih block the utilization of Copper by the body. 

Clinical signs of Copper deficiency include: 

  • Scours.
  • Pale mucous membranes.
  • Rough and bleached hair.
  • Slow growth and loss of body weight.
  • Bones may break easily and affected cattle may move like a pacing horse rather than like normal cattle.
  • Copper-deficient cattle may die suddenly when exerted.
  • PM lesions may reveal small lesions on the heart.

Determination of the amount of Copper in the diet or the pasture has limited diagnostic value and can be seriously misleading unless other elements with which Copper interacts, particularly Molybdenum and Sulphur are determined as well. 

The main criteria for Copper deficiency is the concentration in the liver. 

Prevention and Control 
Under range conditions, deficiency can be prevented by the provision of Copper containing supplements, by dosing or drenching the animals at intervals with Copper compounds, or by injection of organic complexes of Copper. 

Subcutaneous or intramuscular injection of some safe and slowly absorbed forms of Copper is a satisfactory means of treating animals in Copper deficient areas where the Molybdenum contents of the pasture are moderate. 

The application of Copper containing fertilizers can be an effective means of raising the Copper content of pasture to levels adequate for grazing livestock and increasing pasture yields. 5-7 kg/hectare of Copper Sulphate is usually sufficient for three or four years. 



Other Deficiencies

A deficiency of iodine causes endemic goitre, but this has greatly declined in most countries due to the widespread use of iodised salt. 

Iron and Manganese 
Iron deficiency rarely occurs in adult livestock and supplementation with Iron and Manganese is much less important than for other trace minerals. Most tropical soils are acid, resulting in animal plant feeds having levels generally in excess of requirements. In addition, soil consumption will provide substantial quantities of these minerals to grazing livestock diets, particularly Iron. 

Symptoms due to Selenium deficiency are uncommon in the tropics. Nutritional muscular dystrophy or white muscle disease affects young, rapidly growing calves, lambs and foals, born from dams which have been fed on diets low in Selenium and Vitamin E for long periods, usually during the winter months and in temperate regions. 

When such animals are turned out after winter housing or they begin unaccustomed exercise, they may collapse, be unable to walk, or die suddenly. 

One condition that affects animals even in the tropics is retained afterbirth in mature dairy cows, which may be caused by Selenium/Vitamin E deficiency. 

Zinc deficiency causes a chronic, dry, scaly, cracked skin, non-inflammatory in nature and although well recognized in Europe is uncommon in the tropics. 

Toxic Elements 

The most important of these is Fluorine

In limited amounts Flourine strengthens teeth and bones. In excessive amounts it causes damage. 

Chronic fluorosis is generally seen under three conditions: 

1. Continuous consumption of high Fluorine mineral supplements.
2. Drinking water high in Fluorine and 
3. Grazing on contaminated feeds close to industrial plants which emit toxic levels of fumes and dust. 

Normally plant feeds are not involved in Fluorosis as they have a limited capacity to absorb this element. 

In many parts of Kenya borehole water is excessively high in Fluorine. 

Toxicity of Fluorine in livestock depends on teh amount and duration of ingestion, age of the animal, nutrition, stress factors and individual animal differences. 

  • If animals are young the teeth may become modified in shape, size and colour.
  • The incisors may become pitted, and the molars may show cavaties due to facture or wear.
  • The jaw and long bones develop exostoses and joints may become thickened causing the animal to become stiff and lame.

To prevent flurosis

  • Determine the Fluorine content of water and of supplemental phosphates, whish may contain unacceptably high levels of the element.
  • Observation of animals to detect early signs of fluorosis.
  • If water levels are high, you can use filters or add fresh slaked lime to the water.
  • Watering young stock on fluorine free supplies of water and permitting only adults to drink dangerous supplies and rotating between safe and dangerous water every three months may make it possible to utilize otherwise unsuitable land.


Ketosis in Dairy Cows



Ketosis is a metabolic disease that can affect dairy cows most commonly during the first six weeks of lactation.

Ketosis has no local names in East Africa; in English it is also called Acetonemia or Ketonemia.



The underlying cause is a combination of high energy requirement at the onset of lactation coupled with too low energy in the feed (e.g. poor quality silage, very coarse hay). The volume of feed a cow can eat in a day is limited. If the ingested feed provides less energy than the cow requires the animal runs into a net energy loss that becomes worse over time and the blood sugar level drops. To provide more energy the liver converts body tissue (protein, fat) into extra glucose (sugar). The by-products of this process are ketone bodies, which are toxic and have to be excreted. If the ketone concentration in the blood is too high the cow becomes sick.


Signs and Symptoms

Ketosis affects the highest yielding dairy cows and begins with very mild signs, which are easily overlooked in the beginning. Affected animals feed less and also give less milk.  The cow appears sleepy and passes firm feces often covered by mucous. If the disease worsens the animal also looses weight rapidly (burning its' energy stores).  Sick cattle may refuse to eat grain, concentrate or dairy flour and try to ingest strange feed (coarse straw, twigs, soil, abnormal objects).  The animal stands with a humpback and some develop a distinct fruity to musty smell in their breath and urine due to the high ketone. Untreated cows can show abnormal behavior (staggering, circling, head pressing, constant licking, bellowing - like Rabies!) and become unable to stand up.



Good observation to detect early symptoms is the most important diagnostic tool. There is also a simple dip test that detects ketone in the cow's urine. It is used by dairy farmers in Europe and North America to test cattle when they suspect ketosis.



In some cattle the reduced milk yield may level out with the low energy in the feed and they do not develop the full symptoms. If better quality feed is provided early, the symptoms will gradually disappear.

Cattle with fully developed ketosis need urgent treatment otherwise they can die from liver failure. In very acute ketosis cases (can't stand up) it is necessary to give a glucose solution intravenously. In addition the veterinarian can inject cortisone and provide oral substances that provide a lot of energy (propylenglykol drench). The most important measure is to check and improve the quality of the basic feed that the cow has been eating.



High yielding dairy cows are very difficult to feed. If you do not always have sufficient amounts of high quality silage or hay on your farm it is better not to breed cattle with too high milk yield (e.g. pure bred Friesian cows). Grade cattle are much hardier and remain healthy and produce a good milk even if feed quality is not always perfect (e.g. during dry season).

It is also important to feed pregnant cattle well, such that they can build up sufficient energy stores in their body to be able to cope with mild ketosis after calving.



Acidosis of the Rumen



Rumen acidosis is a fast killing disease in ruminants that is caused by overeating with grains or ground feed.

In English, acidosis of the rumen is also called lactic acidosis, carbohydrate engorgement or rumen impaction.



When cattle, goats or sheep accidentally gain access to large amounts of grain or concentrate feed and eat too much of it the rumen contents turn acid, which can rapidly kill the animals.

Signs and Symptoms

After eating ground feed first signs appear faster than after ingestion of whole grain.

Visible signs appear more or less in the following order:

  1. Bloat
  2. Pain and kicking against the belly
  3. (Sometimes animals that have eaten a lot of grain start drinking a lot of water)
  4. No more feeding or ruminating at all, no rumen contractions
  5. Staggering or not moving
  6. Lying down and unable to rise, completely dull
  7. Shallow rapid breathing
  8. High temperature up to 41degC (esp. on a hot day)
  9. Diarrhoea, liquid, sour smelling often with undigested grain visible


The larger the amount of grain ingested the more severe the acidosis is going to be. A cow or goat can die already at early stages of the disease. In cattle the time between overeating and death is 1 to 3 days, in goats it can be as short as 3 hours. Cattle may improve and then relapse 2-3 days later. Survivors may also go lame or abort (2 weeks later). - Overeating on grain is especially dangerous in animals that feed on pasture and do not normally receive grains or concentrate feed. In pastured animals 10kg of grain ingested over a short time is enough to kill a cow and 1kg can kill a goat.



The most important is to react promptly when detecting a suddenly severely diseased animal and suspecting overeating with grain. Immediately confirm whether animals on the farm have had uncontrolled access to and eaten large amounts of grain or ground feed.



Animals with milder acidosis and that are still able to stand and walk should be given magnesium hydroxide (400-500gr/cow, 4-5gr/goat) in warm water through the mouth (or by stomach tube). After giving the solution, massage the flank to mix the magnesium hydroxide with the rumen contents. If a vet is quickly available he can administer a 5% sodium bicarbonate solution and electrolytes intravenously. - In animals that show signs of recovery give only good quality hay and no grain at all for 3-4 days.

Severely affected animals may die any moment and should be slaughtered to salvage the meat.

Most animals that relapse after showing temporary improvement also die.



Store grains and concentrate feed safely and out of reach for livestock. When supplementing animals with grain start by giving small amounts of grain in the evening after animals return from grazing and gradually increase the amount over two weeks.



Local names:

Luo: ich-kuot / Embu: nunvita / Gabbra: furfur / Gikuyu: huhita / Kamba: kwimbanywa / Kipsigis: kowiren / Maasai: Embo'ngit, Ediis, empomgit / Maragoli: kuhaata, myika munda/ Meru: mpwna / Samburu: mberini / Somali: bakhakh, dunbudhyo, balao, baalallo, dhibir, dibiyio / Turkana: lotebwo, akitebukin, akiurur / Pokot: lesana /

Other name: Ruminal Tympany



With the onset of long rains, livestock keepers, especially goat, sheep and cattle keepers should become aware of the dangers of bloat to their livestock. Bloat occurs when there is an abrupt nutritional change in the diet and especially when ruminants feed on lush green pastures. It simply means animals have too much gas in their stomach.


Cow with bloat

(c) W. Ayako, KARI Naivasha



X-ray - dog with bloat
(c) Joel Mills, Wikipedia


How animals get bloat

The rumen of cattle, sheep and goats is like a large container in which a mixture of partly digested feed and liquid is continuously fermenting, producing large quantities of gas. For example, an average cow can produce over a thousand litres of gas in a day. Some of the gas is removed by absorption into the blood stream but most of it is removed by belching during "cudding". If the gas cannot escape, the rumen literally "blows up" and the animal gets bloat. It can happen when:

  • Animals eat too many legumes or too much fresh, lush grass (e.g. olenge grass (Luo))
  • Animal eats too much grain (e.g. finger millet, Acacia pods)
  • Animal eats cassava leaves or peels

Something blocks the passage of food in the stomach or gullet


Types of bloat

There are two types of bloat: Frothy Bloat and Free Gas Bloat.

Animals get Frothy Bloat when the rumen becomes full of froth (foam). Several animals in the herd may get this type of bloat at the same time when they graze on wet, green pasture mixed with legumes in the field. Foaming substances are found in certain plants such as legumes of which lucerne, clover and young green cereal crops are examples.

Frothy Bloat is due to the production of a stable foam, which traps the normal gases of fermentation in the rumen. Pressure increases because belching cannot occur. Initially the distension of the rumen stimulates rumen movements, which makes the frothiness even worse. Later on because of the distension there is loss of muscle tone and loss of the rumen's ability to move spontaneously, compounding the situation.

Saliva has antifoaming properties. More saliva is produced when food is eaten slowly than when it is eaten quickly. Succulent forages are eaten more rapidly and digested more quickly and as a result less anti-foaming saliva is produced. Grazing on immature, lush, succulent, rapidly growing pastures with a high concentration of soluble proteins is most conducive to bloat, as is the stage of growth of the plant, not its degree of wetness.


Causes of Frothy Bloat

  • The primary cause of frothy bloat appears to be a change in the composition of certain pasture plants, the change being one that facilitates the development of a stable foam that in turn prevents belching
  • Frothy Bloat normally happens at the start of wet season when the diet of grazing animals abruptly changes from dry feeds to wet lush pastures that contains some legumes.
  • Animals also get Frothy Bloat when they feed on ripe fruits or other feeds that ferment easily.
  • Some poisonous plants can cause sudden and severe bloat.
  • A sudden change in the type of food can also cause Frothy Bloat.

Frothy bloat can also occur in feedlots with insufficient roughage, or food too finely ground. This leads to a shortage of rumen-stimulating roughage, and prevents the rumen's ability to move spontaneously and hinders belching and release of gas.


Free Gas Bloat is usually due to physical obstruction of the oesophagus, often by a foreign body such as a potato, avocado, apple etc. Grain overload leading to stopping of of normal rhythmic contractions of the rumen wall can also cause this type of bloat as can unusual posture, particularly lying down, as may occur in a cow affected by milk fever. This type of bloat normally only affects one or two animals in the herd at the same time, not several as in the case of Frothy Bloat. As the name suggests, in this type of bloat the gas lies above the food in the rumen and is not mixed with it, as it is in Frothy Bloat.


Signs of Bloat

  • The left side of the abdomen behind the ribs becomes very distended and very tense, like a drum. Later the right side also becomes distended
  • The animal stops eating
  • The animal may grunt and have difficulty in breathing
  • There may be mouth breathing
  • The animal may stamp its feet on the ground
  • Sometimes green froth comes out of the mouth and nose
  • There may be extension of the tongue from the mouth
  • Diarrhoea is common in cases of Frothy Bloat
  • Animals may collapse and die after only an hour or so

There is often frequent urination


Prevention - Control - Treatment

Prevention of bloat

1. Feed the animals with dry grass or hay to fill them up before you turn them out onto new wet lush pasture. For this to be effective the hay or dry grass should form at least one third of the diet.

2. Do not water the animals just before you put them on to wet pasture

3. Do not graze the animals on wet green pasture early in the morning. Wait until the pasture has been dried up by the heat of the morning sun

4. You should gradually increase the grazing hours of the animals on wet green pasture over the first week. Do not put the animals out all day and leave them there.

5. Avoid abrupt changes in the diet of animals and always give newly introduced feeds in small quantities.

6. If possible try to strip graze animals to reduce intake and to maintain grass dominance in the stretch of grass. The pasture ideally should have at least 50% grass.

7. During the risk period the continual administration of anti-foaming agents such as Stop Bloat should be considered.

8. Watch animals closely at all times during the risk period.

9. Keep anti-foaming agents close at hand during the risk period.

10. In feedlot or zero grazing situations rations must contain 10-15% chopped roughage mixed into the complete diet. This should be a cereal, grain straw, grass hay or equivalent. Grains should be rolled or cracked, not finely ground.



Treatment of bloat

Depending on the type of bloat, several methods of treatment can be applied:

  • Do not feed the animal for a few hours and make the animal move around (remember it can die within 1 hour if the bloat is severe)
  • For less severe cases of frothy bloat, give 500ml to large animals and 100ml to small animals of any edible vegetable oil, solid cooking oil, butter oil, ghee or milk orally (by mouth). Non-toxic mineral oils can also be used effectively.
  • Severe bloat is an emergency and rapid action is required to save the animal's life. In life-threatening cases where the animal can not breathe, an emergency rumenotomy may be necessary. Puncture carefully the skin and the rumen of the animal on the left flunk to let the gas out. Use a knife or any sharp thing but the best instrument to use is the trochar and cannula. The hole should be made at a hands' width behind the last rib and a hand away from the edge of the backbone. Push hard because the skin is very tough. Gas and froth will come out when you make the hole. It helps to put a tube or cannula through the hole to keep the hole open. There will be an explosive release of gas and rumen contents. Remember that in severe cases if this is not done the animal will die. SO DO IT  (for more information on how to use a trocar please also see Tools for livestock)
  • Pour some vegetable oil into the rumen through the hole to help stop further gas or froth formation. Complications are rare. Call a veterinarian to attend to a punctured abdomen or a difficult case of bloat.
  • Another aid is to tie a stick in the mouth to stimulate the flow of saliva, which is alkaline and helps to denature the foam.
  • Forceful walking may help to coalesce the foam into larger bubbles and stimulate belching.
  • Give bloat medicine such as the following: Stop Bloat, Bloat Guard or Birp once daily for 3 days

In cases of Free Gas Bloat due to a foreign body lodged in the oesophagus, it may have to be dislodged by using a probang or stomach tube, for which the services of a veterinarian will be required.



Common traditional practice

Some of the following practices may have some merit in case of emergencies where no vegetable oil is available:

  • Gabbra: Mix 4 teaspoons of laundry detergent with 1 litre of milk. Drench 1 litre for an adult cow (0.5 litre for sheep and goats)
  • Turkana: Mix 500g Magadi soda with 1 litre of water. Stir well and drench adult cattle with the mixture. For calves, goats and sheep use 0.5 litre. For large camels give 2 litres.
  • Luo: Mix 0.5 litre of paraffin oil with a handful of olulusia (Vernonia amygdalina) leaves and 2 spoons of salt. Drench with half this amount.
  • Kamba: Mix a handful of wood ash with 1 soda bottle (300ml) of water. Sieve and drench adult cattle with this amount. Use half the amount for calves, sheep and goats.

    (Source:ITDG and IIRR 1996)


Review Process

  1. William Ayako, KARI Naivasha. Aug - Dec 2009 
  2. Hugh Cran, Practicing Veterinarian Nakuru. March - Oct 2010 
  3. Review workshop team. Nov 2 - 5 2010
  4. January 2013: Review by Gidi Smolders orgANIMprove
  5. September 2013: Addition of Acidosis, Ketosis by Dr Mario Younan, VSF-G Kenya/Somalia (Oct 2017)
  6. October 2013: Addition of Bloat by Infonet (Oct 2017)


  • For Infonet: Anne Bruntse, Dr Hugh Cran
  • For KAR: Dr Mario Younan KARI/KASAL, William Ayako - Animal scientist, KARI Naivasha
  • For Department of Veterinary Services: Dr Josphat Muema - District Veterinary Officer Isiolo, Dr Charity Nguyo - Kabete Extension Division, Mr Patrick Muthui - Senior Livestock Health Assistant Isiolo, Ms Emmah Njeri Njoroge - Senior Livestock Health Assistant Machakos
  • Pastoralists: Dr Eyra Saitoti Kotonto - Private practioner, Abdi Gollo H.O.D. Segera Ranch
  • Farmers: Benson Chege Kuria and Francis Maina Gilgil and John Mutisya Machakos
  • Language and format: Carol Gachiengo

Information Source Links

  • Barber, J., Wood, D.J. (1976) Livestock management for East Africa: Edwar Arnold (Publishers) Ltd 25 Hill Street London WIX 8LL. ISBN: 071310063X
  • Blood, D.C., Radostits, O.M. and Henderson, J.A. (1983) Veterinary Medicine - A textbook of the Diseases of Cattle, Sheep, Goats and Horses, Sixth Edition - Bailliere Tindall London. ISBN: 0702012866
  • Blowery, R.W. (1986). A Veterinary book for dairy farmers: Farming press limited Wharfedale road, Ipswich, Suffolk IPI 4LG
  • Force, B. (1999). Where the is no Vet. CTA, Wageningen, The Netherlands. ISBN 978-0333-58899-4.
  • Hall, H.T.B. (1995). Diseases and parasites of Livestock in the tropics. Second Edition. Longman Group UK. ISBN 0582775140
  • Hunter, A. (1996). Animal health: General principles. Volume 1 (Tropical Agriculturalist) - Macmillan Education Press. ISBN: 0333612027
  • Hunter, A. (1996). Animal health: Specific Diseases. Volume 2 (Tropical Agrculturalist) - Macmillan Education Press. ISBN: 0-333-57360-9
  • Pagot, J. (1992). Animal Production in the Tropics and Subtropics. MacMillan Education Limited London. ISBN 0-333-53818-8