METABOLIC AND DIGESTIVE DISEASES OF DAIRY CATTLE
Lactic Acidosis
Fat Cow Syndrome
Ketosis
Bloat
Displaced Abomasum
Milk Fever
Grass Tetany
Diarrhea
LACTIC ACIDOSIS
Consumption of large quantities of concentrates over a short period by unadapted cattle can cause lactic acidosis (founder,
laminitis, acute indigestion). Grains are high in starch (a readily available carbohydrate)and during the fermentation of starch by
microorganisms to propionate, glucose can accumulate and in doing so promotes the rapid growth of lactic acid producing
bacteria. As the production of lactic acid increases, the ability of other microorganisms to use the lactic acid is exceeded and
concentration of lactic acid increases and the pH of the rumen decreases. As the pH of the rumen decreases (acidity increases)
many of the normal bacteria and protozoa are inhibited or killed releasing endotoxins.
Lactic acid is also absorbed from the rumen and causes a drop in blood pH. This condition, called lactic
acidosis, may cause the cows to stop ruminating and go off feed. Death can occur but in most cases cows
recover spontaneously after a few days. The high acidity in the rumen can also damage the papillae that
line the rumen wall and which serve as sites for absorption of VFA's. Damage to the papillae reduces VFA
absorption, reduces milk production and reduces feed efficiency. Damage to the papillae also allows for
increased absorption of lactic acid and the endotoxins into the blood stream. Frequently the increase in
blood lactic acid causes severe damage to the capillaries in the corium regions of the limbs resulting in the
typical syndrome of foot problems known as laminitis, often with permanent damage. The increase in lactic
acid is also related to the decrease in the amount of sulphur containing amino acids in the hoof. The
subsequent reduction in disulphide linkages in the keratin of the hoof causes a loss of structural integrity in
the hoof and increases the susceptibility of the hoof to injury.
Some concentrates have a much higher tendency to cause lactic acidosis. Wheat is much worse than corn,
with barley being intermediate. Cattle should be adapted to high concentrate rations over 3 to 4 weeks to
avoid digestive upsets.
Treatment for lactic acidosis is difficult, although the controlled feeding of buffers may provide some relief
from the high acid conditions. Removal of the concentrates from the diet will also help. Damage to the
mucosal lining of the rumen and intestines will result in decreased absorptive ability which may remain for
an extended period of time and therefore, reduced performance.
FAT-COW SYNDROME
Fat cow syndrome is the name given to a combination of metabolic, digestive, infectious, and reproductive conditions affecting
the overly fat cow near the time of calving. Cows having this condition have a greatly increased susceptibility to stress and
disease, especially around calving. Cows having low milk production and/or long dry periods and fed too much concentrates may
become over fat and susceptible to fat cow syndrome. Cows suffering from fat cow syndrome have increased incidences of
dystocia (difficult calving), ketosis, retained placenta, deaths, milk fever, mastitis, metritis (uterine infection), displaced
abomasum, and "downer" cow syndrome. These cows also show extensive liver and kidney damage.
The prognosis for cows afflicted with the syndrome is poor, therefore, the best approach is to avoid the
condition. The extent of fat-cow syndromes can be minimized by the careful allocation of grains during
lactation based on body condition, body weight, and milk production.
KETOSIS
Ketosis in dairy cows occurs within the first 6 to 7 weeks after calving with most cases occurring 2 to 4 weeks after calving.
Ketosis is named for the most prevalent metabolic characteristic, i.e. increased plasma concentrations of the ketone bodies,
acetone, acetoacetate and beta-hydroxybutyrate. The increased concentration of ketone bodies results from a negative energy
balance caused by an increased requirement for nutrients in the synthesis and secretion of milk. The removal of glucose from
the blood stream for milk lactose synthesis indirectly stimulates fatty acid mobilization from adipose tissue and subsequent fatty
acid oxidation in the liver. Ketones arise from incomplete oxidation of fatty acids in the liver due to the low concentration of
glucose in the blood.
Ketosis can be grouped into two types: primary and secondary.
Primary ketosis is primarily an energy imbalance with high levels of ketones that is not associated with
another underlying problem.
Secondary ketosis is an energy imbalance with a slight elevation of ketones caused by an underlying
disease problem such as a displaced abomasum, hardware disease, uterine infections, or other ailments
that affect feed intake.
The most common characteristics of primary ketosis include:
Most often seen in high producing dairy cattle and rarely seen in beef cattle
Occurs in well conditioned or fat, high producing dairy cattle during the first 6 to 7 weeks of lactation during the time of high
levels of milk production
Occurs primarily in housed animals and rarely in pasture cattle
Repeats often in the same cow year after year and sometimes is seen in the cow's daughters (inherited). Successful treatment
of cows with ketosis has allowed for cows to produce more progeny which may have a predisposition to produce large quantities
of milk and to develop ketosis.
Cows with primary ketosis may exhibit nervous symptoms (25% of cases) such as biting the manager or
drinking cup, licking on various things, head tilting and leaning into the stanchion, having an excited
appearance or appearance of a cow with rabies, bellowing, and charging. The cow will exhibit a selective
appetite; first refusing to eat silage, then grain, and lastly hay. The manure will often become scanty, firm,
and covered with mucus. Milk production will decrease over 2 to 4 days, the cow will become gaunt in
appearance and often appear sleepy, and a ketone odour will be detectable in milk, urine, and breath.
Ketosis can be prevented by several means:
Avoiding over fattening cows during lactation and the dry period. Cows should be in good condition (3.5 to 3.75 using a 5 point
scale) but not over fat.
Avoiding digestive upsets by increasing grain intakes gradually during the last 10 days of the dry period (maximum intake of 5
kg at calving) and during the first weeks of lactation.
Feeding or drenching propylene glycol to susceptible cows during lactation. Propylene glycol serves as an energy source and
glucose precursor and will reduce the levels of ketones in the blood.
Feeding diets adequate in protein but not high in protein
Limiting the intake of silages high in butyric acid, and by
Providing the opportunity of the cows to exercise.
Treatment of primary ketosis is usually by intravenous infusions of dextrose solutions, and the drenching
of propylene glycol or sodium propionate (a glucose precursor). These treatments serve to increase blood
glucose and decrease blood ketone concentrations. Treatment of secondary ketosis is more difficult
because of the influences of the diseases causing the ketosis.
BLOAT
Bloat is characterized by the buildup of gas within the rumen and is a major cause of death in cattle that are grazing winter
wheat, legumes such as alfalfa, white clover (ladino), red clovers and alsike clover, or other succulent forages. Bloat caused by
excessive intakes of grain is not a major problem in the dairy industry, but is more of a problem in beef feedlots. Causes of
death from bloat are primarily mechanical. Over distension of the rumen puts pressure on the diaphragm, which reduces the size
of the thoracic cavity. Mechanical pressure on the posterior vena cava can also alter the normal circulation of blood, reducing
oxygen transfer to tissues.
Young wheat and legumes contain considerable quantities of pectin, a carbohydrate found in all plants.
Pectin methylesterase, an enzyme needed for plant growth, converts pectin to pectic acid and carbon
dioxide. The enzyme is required for plants to increase in size and is most active during rapid growth.
Legumes and small grains contain higher levels of the enzyme than grasses and leaves contain more than
the stems. The pectic acid released when bound with water forms a stable gel which traps bubbles of
carbon dioxide to form a viscid froth. The feeding of succulent legume tops or small grains reduces the
buoyancy of rumen contents, allowing the feed particles to gravitate to the lower regions of the rumen for
more rapid digestion.
Normally gas produced by rumen fermentation rises to the top of the rumen and is belched out (eructation).
During bloat formation, gas bubbles produced by small grains, legumes, and ground feed cling to feed
particles or become trapped within the froth, thereby preventing the formation of large bubbles which can
rise and be belched. Belching mechanisms are triggered by free gas and can be inhibited by froth or by
liquid. Raising the level of the rumen fluid can mechanically prevent belching. Factors such as saponins,
saliva, pectin, and the level of water soluble protein also contribute to bloat.
Bloat can kill quickly, sometimes in only a few hours. Bloat can be prevented by:
Including roughage in the diet: Roughage stimulates rumen motility and reduces the amount of legumes or small grains
consumed in a given time,
Maintaining adequate particle size for the grain, which serves to stimulate rumen motility but also to reduce the rate at which
the grain is digested,
Maintaining adequate levels of effective fiber in the diets (21% acid detergent fiber),
Feeding large quantities of minerals or salts to provide a prophylactic effect: This is usually expensive and difficult to
administer to large groups of animals,
Feeding a surface tension reducing agent of an anti-frothing agent: Poloxalene is commonly used as a treatment but can also
be used as a preventive. Poloxalene is available in various forms such as bloat guard block, granules, and molasses liquid mix.
Detergents have also been used but care should be exercised because some detergents can be irritating to the digestive system.
Beef producers occasionally use one pound of tide per 25 kg bag of salt provided free choice to grazing cattle to limit bloat,
Feeding ionophores such as bovatec and rumensin will reduce the incidence of bloat: Neither ionophore has been approved for
use in dairy cows but bovatec mixed with salt and offered free choice or in a supplement fed at fixed rates is approved for use in
grazing dairy heifers on pasture. Rumensin has been approved for bloat control in beef animals and non-lactating dairy animals
over 200 kg as a slow-release osmotic pump which is deposited into the rumen using a balling gun, and
Limiting the time allowed for animals to graze bloat causing pastures: Cows are not likely to bloat if they are grazed for 1 to 2
hours on lush pasture after the dew has dried. A common practice of feeding long hay to appetite prior to turning the cattle on
pasture has proven to limit bloat.
Treatment of bloat involves the release of the trapped gas or foam by passing a tube into the rumen. A
trocar or knife inserted into the paralumbar fossa on the left flank can be used as a last resort. Treatments
including the drenching of anti- foaming agents such as poloxalene, fats, oils, detergents, or silicones are
preferred if bloat is detected early enough.
DISPLACED ABOMASUM
Displaced abomasums usually occur within a month after parturition, primarily in older and larger dairy cows. Usually the
abomasum is displaced under and to the left of the rumen, however, in 20% of the cases the abomasum is displaced to the right
of normal position. The incidence of displaced abomasum is much higher in cows fed high-concentrate, low-forage diets and in
those fed finely chopped forage. Theories for the occurrence range from over fat cows to decreased forage or effective fiber
intake. Over fat cows are believed to show a reduced appetite after calving. This reduced appetite limits intake of forage and in
turn reduces the muscle tone of the rumen. Movement of the abomasum is then possible. Low fiber diets will also reduce rumen
muscle tone but also reduce rumen fill.
Although the severity of the displacement varies among cows, typical symptoms include reduced appetite
and feed intake, lower milk production, loss of body weight, and mild secondary ketosis.
Prevention can be achieved by avoiding excessive intakes of concentrates during the dry period, feeding
adequate long hay prior to and after parturition, and limiting body condition.
MILK FEVER
Milk fever (parturient paresis) is a common disease of high producing dairy cows and occurs primarily during the first 3 days
after calving, but may occur 1 to 2 days before calving, and sometimes as late as 7 days after calving. On rare occasions a milk
fever disease occurs during mid-lactation or even in non-lactating cows. The disease usually occurs in older cows and seldom
occurs in first and second calf cows. Cows which have milk fever after one calving are more likely to have milk fever in
subsequent lactations. Some breed differences may also exist.
The illness is due to low levels of blood calcium with signs of milk fever appearing when calcium levels
drop to about 50 to 70 percent of normal (10 to 12 mg/100 ml blood serum is normal). Blood calcium levels
drop below normal because calcium secreted in milk exceeds that replenished by blood (from bone and the
digestive tract). Two litres of colostrum milk contains as much calcium as 40 to 50 litres of blood. During
peak milk production, dietary sources of calcium provides only 70 percent of the cow's needs and the rest
comes from calcium in bone (resorption). The rate of absorbtion of calcium from the intestine depends on
the amount of calcium, phosphorus, and vitamin D in the diet. Resorption of calcium from bone depends on
the capacity of parathyroid glands to produce parathyroid hormone, which speeds removal of calcium from
bone to maintain blood calcium levels (see discussion of vitamin D in vitamin module for more information).
Lack of appetite is usually one of the earliest signs of milk fever. Little or no feces are passed, although
the anal opening is very relaxed. Initially the cow may be excited and then progresses to extreme
depression associated with loss of ability to stand or even maintain a normal lying position on the sternum.
These changes may take place in a few minutes or in hours. During the early development stages a cow
may show lack of coordination (usually rear legs first), lean into a stanchion, stagger, and finally fall down.
There may be some evidence of bloating because the cow is unable to belch gases building up in the rumen.
The increased pressure associated with the bloating may cause the uterus to prolapse. Many cows tend to
have a far away look in their eyes, cold ears, drying noses, and in winter, moisture accumulated on the
hairs of the back. In an attempt to lie on the abdomen, the cow's head is often held to the side.
Temperature of the cow may increase slightly depending on the level of excitability, but is usually
decreased, therefore, the term "milk fever" is a misnomer. Prolonged deficiency of calcium can lead to
coma and eventually death.
Milk fever may be associated with a number of complications:
Unable to calve because muscle activity is lacking and the cow is unable to force the calf through the birth canal.
Uterine prolapse often because of bloat or sliding back into the gutter of tie stalls.
Mastitis, because of injury to teats or mammary gland as coordination and muscle strength diminishes during the development
of milk fever. Milk fever cows are also less able than normal cows to protect themselves against bacterial infections.
Metritis and retained placenta result from lack of muscle tone to expel the placental membranes after calving, and because of
the inability to fight infections.
Muscle injuries of hind legs and hip joint dislocations resulting from slipping on concrete during the early development of milk
fever, and also during recovery of milk fever.
Aspiration pneumonia in which rumen ingesta is regurgitated and aspirated into the lungs to cause a severe and usually fatal
pneumonia.
Treatment for milk fever is generally inexpensive providing it is given early during the development of milk
fever. Treatment usually consists of intravenous, intraperitoneal and/or subcutaneous infusions of a
calcium gluconate (borogluconate) solution (generally 250 to 500 ml of solution containing 8 to 12 grams of
calcium; some solutions may contain magnesium, phosphorus and/or potassium). Calcium solutions can kill
cows if given too rapidly or in too great a quantity. Dosages are based on cow size and tolerance to
calcium solution. Approximately 75 percent of cows with milk fever respond to one treatment and recover:
The almost instantaneous (within 30 minutes) recovery can be quite dramatic. The remaining cows may
show a recovery, but then relapse, or show a slow recovery lasting 2 to 4 days.
Milk fever can be prevented in a large percentage of cases. Incomplete milking for the first three or four
milkings to reduce the drain of calcium from the blood, may serve to reduce the incidence of milk fever.
Injections of massive doses of vitamin D or vitamin D metabolites can reduce the incidence of milk fever is
given during the last 3 to 7 days before calving. The 3 to 7 days is required to stimulate the resorption
mechanisms of bone and absorptive capacity of the intestinal tissues. Injections given less than 3 days
have limited value and injections given greater than 7 days before calving may increase the susceptibility
of the cow to milk fever. Rations low in calcium and high in phosphorus (ie. providing 80 to 100 grams of
calcium and 30 to 40 grams of phosphorus per head per day) will reduce the incidence of milk fever when
fed for several weeks prior to calving. More recent literature would suggest that the cation (sodium,
potassium) to anion (sulphur, chlorine) balance may be more important in preventing milk fever than
calcium and phosphorus concentrations. Legume hays such as alfalfa usually provide more calcium than
required and may increase the susceptibility to milk fever.
GRASS TETANY
Occasionally large numbers of lactating dairy cows die from grass tetany which is caused by low magnesium in blood and
extracellular fluid. Most grass tetany occurs during cool seasons when cows are grazing lush-fast growing pastures high in
potassium and low in magnesium usually resulting from high application of nitrogen and potassium fertilizers. The potassium
reduces the availability of magnesium to cause a decrease in blood magnesium concentrations much like calcium depletion during
milk fever. However, cows suffer from "grass tetany" even though body reserves of magnesium are not severely depleted.
Symptoms of grass tetany include hyper-irritability, increased nervousness, restlessness, muscle twitching
and tetany, grinding of teeth and excessive salivation. Experimentally induced magnesium deficiency in
calves produced anorexia, hyperemia, increased excitability, and calcification of soft tissues.
Treatment of grass tetany involves the replenishment of magnesium through feeding of magnesium sources
and intravenous infusions of magnesium. Full recovery can be expected.
Prevention is accomplished by providing adequate amounts of magnesium to lactating especially when
conditions are conducive to the development of grass tetany.
DIARRHEA
Diarrhea (scours) is not one specific disease, rather it is the chief symptom produced by a variety of bacteria, viruses, protozoa,
environmental stresses, and feeding errors. Calves are most susceptible to serious scours at birth primarily because of the
sterile and non-functional state of it's digestive system. Failure to consume proper amounts of colostrum is a contributing factor
to scours.
Diarrhea can be caused by large variety of bacteria such as Escherichia coli and Salmonella typhimurium. E.
coli is normally found in the lower intestine of all animals and does not create problems, but occasionally
increase the severity of inflammation caused by other organisms and may even become invasive itself. The
diarrhea caused by E. coli are most severe when calves are less than 10 days old and is called "white
scours" or colibacillosis type scours. Salmonella infections can cause scours in calves older than 2 weeks
of age and are contracted from adult animals not showing the symptoms.
Viruses, both non-specific and specific (Bovine virus diarrhea, BVD), can cause scours by eroding the
microfine surfaces of the intestine, thereby preventing the absorption of nutrients. Calves infected with
BVD soon after birth may recover without signs, may die suddenly, or may become chronically infected.
Enterotoxemia caused by Clostridium perfringens can cause diarrhea, however, in many cases death may
be the only sign.
Scours resulting from feeding can be caused by feeding inadequately formulated milk replacers or
insufficient milk, abrupt dietary changes, and excesses of protein or fat.
Diarrheas occur as a result of an alteration of movement of fluid and nutrients through the intestinal wall.
The alteration can be from an increase in secretion, a decrease in absorbtion, or both. The result is an
accumulation of fluids and nutrients in the gut which provides an excellent place for bacteria to multiply.
The electrolytes, water, sugars, and amino acids which are needed for the calf are passed in wet feces. A
calf can easily lose 10 percent of it's total weight in one day, and by the time 20 percent is lost the calf is
dead. With diarrhea, body tissues and fluids produce excess acid, blood flow and blood pressure is
decreased, kidney function is reduced, and the body loses the ability to excrete the excess acid.
Electrolyte shifts also result in an imbalance in salts. The accumulated acids and salts are extremely toxic
to the heart. Dehydration is the most noticeable consequence of diarrhea, and it causes sunken eyes,
roughened hair, inelastic and doughy skin, and legs cool to the touch. The calf will eventually lose interest
in feeding, begin to get up more slowly, and finally be unable to rise at all.
Treatment of calf scours should be aimed first at replacing lost fluids, second at restoring normal acidbase balance, and third at furnishing nutrients to body tissues. Most cases of diarrhea are self-limiting,
therefore, the main objective is to keep the calf alive until disease runs it's course. Antibiotics may be
helpful for fighting bacterial infections, yet could kill beneficial bacteria during viral infections. Milk or milk
replacer feeding is often discontinued from the onset of symptoms until at least 24 hours after diarrhea
ceases. Replacement fluids at near body temperature should be given in the place of milk or milk replacer.
Electrolytes solutions are commercially available for this purpose.
Provision of adequate quantities of colostrum and a clean, dry environment will aid in the prevention of
scours in calves. Keep purchased animals separate from the main herd for 3 to 4 weeks to ensure that
diseases are not spread inadvertently. Vaccines and bacterins can also provide a first line defense against
organisms that may cause diarrhea.