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Mastitis is an infection (inflammation) of the udder caused by microorganisms (bacteria) entering the quarter through the teat end. When the bacteria load becomes too high due to dirty environment or damaged teats (allowing invasion), infection may occur. Most of the mastitis cases (about 95%) are subclinical (show no signs) but result in lower milk production and higher cell count (an indicator of milk spoilage). When stress occurs, subclinical mastitis flares up and become clinical.

Causes of Mastitis

Bacteria are by far the most common causes of mastitis. Chief pathogens include

– Streptococcus agalactiae

– Staphylococcus aureus


  1. agalactiae is the most common cause of subclinical mastitis but rarely cause acute mastitis. The organism lives inside the cow’s udder and survives only for a short time outside the mammary gland. It spreads primarily during milking via the milking machine, and contaminated hands and materials (cloths).
  2. aureus lives inside and outside the udder on the teat skin. The microorganism can cause both clinical and sub-clinical mastitis and spreads the same way as S. agalactiae.

Infections caused by coliform bacteria are less common than other types, but can cause very severe cases of clinical mastitis. Coliform bacteria are abundant in wet bedding materials, manure and polluted water. Coliform mastitis occurs more frequently in herds which are relatively free of other types of mastitis infections, are housed in unsanitary conditions or milked while the udders are wet.

Detection of Mastitis

  • Clinical signs: Mild signs include flakes or clots in the milk and may have slight swelling of infected quarter. Severe signs include secretion of abnormal milk: hot, swollen quarter or udder; cow may have a fever, loss of appetite, dehydration and death may occur.
  • Strip cup: The strip cup is an important in the milking parlor for determining the presence of clinical mastitis. The test is rapid and can easily be adapted as a part of milking routine. Few streams of the foremilk are squirted onto the strip cup and are visually examined for milk abnormalities. The strip cup test should be conducted on every cow at every milking and milk from any cow found to have abnormal milk should be withhold from the supply.
  • California mastitis test: The California Mastitis Test (CMT) estimates the number somatic cells present in the milk.

Prevention of Mastitis

The goal of every mastitis control program is to prevent bacteria from entering a normal and healthy mammary gland. This means that each step involved in proper milking procedures must occur at each milking every day for each cow in the herd.

This can be achieved through several ways:

  • Proper milking hygiene: Bacteria are transmitted from infected to uninfected through hands of the milker. Thus the milers’ hands should be washed thoroughly with disinfected soaps before milking and clinically infected cows should be milked last.
  • Teats should be cleaned and dried before milking.
  • Milking machine: The machine should function properly by ensuring proper vacuum levels (minimal fluctuation) through proper maintenance of vacuum regulator.
  • Dipping the teats. Teat dipping reduces the rate of new infection substantially.
  • Ensure use of suitable disinfectant.
  • .
  • Dry cow therapy: Effective use of infused antibiotic into each quarter can reduce considerably the occurrence of mastitis in dry cows. This treatment is also very effective in clearing chronic and subclinical mastitis that are difficult to treat during lactation.
  • Culling of chronic cases: This clears the reservoirs.
  • Nutrition: Deficiencies of selenium and vitamin E in feed have been associated with increased cases if mastitis.

Cost of Mastitis

The greatest amount of money lost with mastitis is reduction in milk yield. Increased cost is also in from treatment, discarded milk and with chronic mastitis, premature culling. Acute cases of mastitis can result in loss of the animal through death.

Milk Fever

Milk fever is a common metabolic disorder in dairy cattle that generally affects older, high producing cows. It may also be referred to as parturient paresis or hypocalcaemia.

At the beginning of lactation high yielding cows experience a sudden rise in demand for calcium to replace the large amount lost through milk. This may result in great decrease in blood calcium if the cow is not able to replenish the calcium fast enough, causing a disease called milk fever.

The majority of milk fever cases occur within 48 to 72 hours of calving when demand for calcium for milk production exceeds the body’s ability to mobilize calcium reserves. Fever is a misnomer as body temperature is usually below normal.

Low blood calcium interferes with muscle function throughout the body causing general weakness, loss of appetite and eventually heart failure.

Signs of Milk Fever

At first, cow experiences muscle tremors, lack of appetite, and unsteadiness.

Eventually, cow is unable to rise, body temperature falls, and constipation occurs.

Cows go down to a sitting position often with a kink in her neck. Death can occur if the cow is not treated promptly.

Causes of Milk Fever

The onset of milk production drains on the animal’s blood calcium levels. If the cow is unable to replace this calcium quickly enough due to loss of its ability to mobilize reserves of calcium in bone and absorb calcium from the gastrointestinal tract, milk fever occurs. Older cows are more susceptible as they produce more milk and are unable to replenish calcium quickly.

Prevention of Milk Fever

Management of the diet can be a valuable aid in preventing milk fever. The key to prevention of milk fever is management of a close-up dry cow which should be kept on a low calcium diet. This stimulates their calcium regulatory system to keep the blood levels normal by mobilizing the body stores from the bone.

When the demand for calcium increases at calving, calcium can be mobilized much more rapidly thus preventing milk fever. Lucerne, a feed high in calcium and potassium, should not be a major ingredient in close-up dry cows’ diets. In early lactation, high yielding cows should receive as much calcium as possible. High risk cows can be injected with Vitamin D3 2-8 days prior to calving.

Diets providing less than 15gcalcium/cow/day and fed for at least 10 days before calving will reduce the incidence of milk fever.


Ketosis, or acetonaemia, is a metabolic disorder in cattle associated with an inadequate supply of the nutrients necessary for the normal carbohydrate and fat metabolism that is seen mainly in times of high milk production in early lactation.

During early lactation, the energy intake is insufficient to meet the energy output in milk and the animal is in a negative energy balance. Hypoglycemia (low blood sugar) is the major factor involved in the onset and development of clinical signs of ketosis. Ketosis affects high producing cows during the first 6-8 weeks of lactation when cows are in negative energy balance.

Ketosis occurs when energy intake fails to meet the requirements for high glucose production, necessary for mainte-nance and milk lactose production.

The excessive ketone bodies in the bloodstream come from the breakdown of fat when the animal is forced to draw on its bodily reserves for energy.

Although the metabolism of body fat provides energy for cows, the nervous system is dependent on glucose, and the ketones produced as a result of excessive fat metabolism can have toxic effects. The excess ketone bodies are eliminated in the urine, milk and breathe of the animal.

Predisposing factors

Cows of any age may be affected but the disease appears more common in later lactations peaking at about the 4th lactation. Over conditioning at calving has been associated with increased incidence of ketosis

A reduction in the production of propionic acid, the main precursor of glucose in ruminants, will result in hypoglycaemia. Hypoglycaemia leads to a mobilization of free fatty acids and glycerol from the fat stores. The reduction of propionic acid production is usually the result of underfeeding or a reduced feed intake caused by in-appetence. The in-appetence may be caused by poor feed quality, sudden changes in diet or excessive fatness at calving.

Clinical signs of Ketosis

In many cases of ketosis, the disease is sub-clinical, with the cow’s performance and health compromised, but without obvious clinical signs. The clinical signs of ketosis include lack of appetite (refusal to eat even concentrates) and a sudden drop in milk output. There is a sweet smell of acetone in the urine, breath and milk.

Cows will have raised blood ketone levels and may excrete ketones in urine and milk. There is a gradual loss of body condition over several days or even weeks. 

Prevention of Ketosis

Ketosis causes financial loss through lost production and treatment. It may be prevented by management strategies that maintain a good appetite and supply adequate feed to meet this appetite during the late dry period and immediately after calving. These strategies include;

  • Avoid sudden changes in feed type to newly calved animals
  • Ensure cows in body condition 4.0 or less prior to calving.
  • Ensure that any health problems that may cause reduced feed intake are treated as early as possible.


Acidosis is a syndrome related to a fermentative disorder of the rumen resulting in overproduction of acid resulting in lowering of rumen pH below pH 5.5. The problem is related to feeding management, where the ration has high levels digestible carbohydrates and low effective fiber.

Acidosis commonly occurs when switching from a high fiber to high concentrate diet (that is rich in fermentable carbohydrates (starches and sugars)). Large amounts of starch and sugar stimulate bacteria that make lactic acid. In a normal, healthy rumen, lactic acid production equals lactic acid use.

Large amounts of starch and sugar stimulate bacteria that make lactic acid. In this instance, bacteria that normally use lactic acid cannot keep up with production.

Lactic acid is about ten times a stronger acid than the other rumen acids and causes the rumen pH to decrease. As the rumen pH drops below 6.0, bacteria that digest fiber begin to die depressing fiber digestion. 

Causes of Acidiosis

  1. Diets very high in readily fermentable carbohydrates and low in roughage
  2. Very fast switch from high forage to high concentrate.
  • Excessive particle size reduction by feeding finely chopped forage

Signs of Acidiosis

  • Low milk fat test (one of the end products of fiber digestion (acetate) is a precursor of milk fat synthesis).
  • Diarrhea (Accumulation of acid causes an influx of water from the tissues into the gut resulting in diarrhea. The feces are foamy with gas bubbles. There is an appearance of mucin/fibrin casts in feces).

Sore hooves-laminitis

Endo-toxins resulting from high acid production in the rumen also affect blood capillaries in the hoof, causing them to constrict resulting in laminitis.

High levels of acid in the rumen also cause ulcers in the rumen resulting in infiltration of bacteria into the blood causing liver abscesses, which are seen at post mortem.

Prevention Sore hooves-laminitis

  • Good management practices are needed to prevent the predisposing situations from occurring. The root problem must be found and corrected.
  • Buffers can also be used to prevent drop in rumen pH when high concentrate diets are fed. Ensuring presence of effective fiber in the diet promotes production of saliva which is a buffer.


Bloat is the abnormal accumulation of gas in the rumen. There are three categories of bloat:

  • Frothy bloat which occurs when diets that lead to the formation of a stable froth or foam in the rumen are fed.
  • Free gas bloat caused by diets that lead to excessive gas production
  • Free gas bloat caused by failure to eructate rumen gases leading to accumulation (e.g. esophageal obstruction).
  • When bloat occurs, gases cannot escape and they continue to build up causing severe distention of the abdomen, compression of the heart and lungs, and eventually death. 

Predisposing factors

Bloat is a risk when animals are grazing young, lush pasture, particularly if the pasture has high legume content (clover or lucerne). Ruminant animals produce large volumes of gas during the normal process of digestion which is either belched or passes through the gastrointestinal tract. If anything interferes with the gas escape from the rumen, bloat occurs.

Natural foaming agents in legumes and some rapidly growing grasses cause a stable foam to form in the rumen. Gas is trapped in small bubbles in this foam in the rumen and the animal cannot belch up the gas. Pressure builds up in the rumen causing an obvious swelling on the left side of the body.

Signs of Bloat

  1. Animal stops grazing and is reluctant to walk
  2. The left side of abdomen is distended
  3. The animal strains to urinate and defecat
  4. Rapid breathing — mouth may be open with tongue protruding
  5. Staggering

                                                       Staggering; a sign of bloat in a cow


Prevention of Bloat

  • Pasture management: Legumes should be introduced into the diet gradually over several days. Avoid cows gorging on new pastures by feeding them on other feeds before letting them out to graze. Silage, hay or more mature pasture can be used to reduce the cow’s appetite.

Initially, cows should only be allowed access to the pasture for short periods (one hour or so) and monitored closely during grazing and immediately after removal.

Cutting and wilting the pasture for 2 – 3 hours prior to feeding reduces the risk of bloat.

Preventative medication: Detergents and anti-foaming agents can be drenched prior to grazing.


A sharp knife can be used to puncture the rumen on the left side of the animal (at the farm level as an emergency).

Puncturing the rumen with the standard trocar and cannula is a quickest way to release the gas which cannot be expelled with a stomach tube. The trocar is used to puncture while the canula is left in place to release the gas.

                                                         Trocar and cannular



Internal parasites


Worms are internal parasites found mostly in the digestive system of animals. Eggs from the adult worm are passed with the animal’s faeces onto the ground where they hatch into larvae and are passed into the animals when they feed on contaminated pasture. While within the animal, the larvae develop into adults, lay eggs and the cycle is repeated. Some worms will pass through another animal (an intermediate host) before getting to the final (definitive) host.

Worms cause several types of damage to the host:

  1. They suck the blood of animals and this may lead to death from anaemia (shortage of blood in the body).
  2. They consume nutrients causing deficiencies and leading to poor health, growth and production. This is the major negative effect of worms on farm animals.
  3. Some worms may block the intestines and small passages in the body interfering with movement of food and flow of digestive enzymes.
  4. They cause damage to the cells lining the gut and interfere with production of enzymes and absorption of nutrients.
  5. Irritation to cells of the gut may cause diarrhoea and loss of body fluids leading to dehydration, abdominal pain (colic) and loss of appetite.

Worms are generally classified into round and flat worms.

Symptoms of worm infestation:

Symptoms of worm infestation may not be obvious and can easily be ignored or mistaken for other illnesses. They are likely to be most severe during the dry season when animals are not well fed.

 Table showing Classification of worms


   Type of worms                  Common worms                                              Where found


Flat worms                     Liver flukes Bile ducts (liver)                         Bile ducts (liver)

Tapeworms Muscles                                         muscles

Lungworms Lungs                                             lungs

Round worms                 Barberpole worm Stomach                              stomach

Brown stomach worm

Small stomach worm or stomach hair worm

Thread-necked intestinal worm Intestines        intestines

Small intestinal worms

Hook worms

Nodular worms


Non-specific signs include:

  • Lower than expected weight gain and/or weight loss
  • decreased milk production
  • lacks of appetite
  • Poor body condition.

Specific signs include:

  • The animal appears pale around the eyes (anaemia)
  • has a dry, dull coat
  • Animal may appear to be swollen around the jaws owing to accumulation of body fluid (referred to as ‘bottle jaw’)
  • In some cases, adult worms or tapeworm segments may be seen in the faeces
  • Diarrhea (may be bloody), loss of weight, and death may occur.

Treating worms

If worm infestation is suspected all animals should treated with broad-spectrum dewormers (antihelmintics). For advice on which type of dewormer to use and the method of administration, one should consult a veterinarian.

There are several types of dewormers containing different preparations of antihelmintics that can be used to control different types of worms. It is advisable to use the correct type of antihelmitic and this is possible through identification of the type of worm by taking a sample of the fecal material to a laboratory.

While in doubt, ask the veterinarian for advice on when to deworm, and which type of dewormer to use.

Control of worms

Deworming – routine deworming (every 3 months) is recommended especially at the start of the rains. 

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