MAIN METABOLIC DISEASES OF CATTLE
Traditionally these are thought of as diseases of livestock caused by productivity
practices when the body reserves cannot meet the metabolic needs. They are common
in intensive or high production systems. The major disorders commonly affecting the
fresh calved cow are usually the result of nutrition and feed management problems.
Metabolic disorders are completely interrelated and tend to occur together.
In cattle, the obvious metabolic diseases are milk fever (Calcium deficit), Grass
staggers (Magnesium) and Ketosis or Acetonaemia (Energy). The latter is closely
related in both cause and effect to Fatty Liver syndrome and it itself necessitates
inclusion as an important metabolic disorder. It would also be very remiss to exclude
probably our biggest challenge in the management and hence metabolism of dairy
cows that of SARA or Sub-Acute Rumen Acidosis which is also closely interrelated
with both Ketosis and Fatty Liver.
All these can produce an acute, temporary, but potentially fatal deficiency. Correcting
the diet for cows during the period from late pregnancy to peak lactation is crucial in
preventing these diseases. Management of the dry cow, crucially the transition period,
and also following on into the fresh cow period plays an important role in the control
of metabolic disorders.
. Milk Fever
Milk fever is probably the most common metabolic disorder of cattle that usually
occurs around calving time commonly between 12 hours before and 72 hours after.
About 75% of milk fever cases occur within 24 hours after calving and less than 5%
beyond 48 hours. The name milk fever is misleading since the cow does not have a
fever. Incidence of milk fever is related to age. It is most common in older high
producing cows from third calving onwards and it rarely occurs in first-calf heifers.
As milk yields nationally have increased over the last 30 years so has milk fever
incidence from 3% to 9%. Cows having milk fever once are apt to repeat. Channel
Island breeds tend to be more susceptible.
Symptoms are probably quite familiar. They represent a sluggish depressed
metabolism and appear as a wobbly or recumbent cow with cold ears, dry muzzle,
low temperature, reduced rumination, constipated dry faeces and flaccid weak
muscles, frequently unable to rise. When down the cow commonly has a swan-neck sbend appearance. It is probably the most common cause of sudden death in dairy
cows. It also causes calving difficulties with “cows not getting on with it” and
consequently still births .Commonly Retained Placenta is an inevitable consequence
and increased incidence of this should ring alarm bells for investigation of
hypocalcaemia. Similarly via effect on muscle function you may also see more uterine
torsions and/or uterine prolapses. Not so commonly linked but equally important is a
similar role in the cause of displaced abomasums (DAs).
Treatment is via Calcium Borogluconate given intravenously and/or
subcutaneously;commonly with additional Magnesium or Phosphorus as these
minerals are closely interlinked. Use of oral calcium salts via pastes, drenches or
boluses allow levels to be maintained for longer and reduce likelihood of relapses.
Cause and PreventionMilk fever is caused by extra Calcium demand from the blood into the milk at calving
coupled with the inability of the cow to change her metabolism rapidly enough to
keep blood Calcium level up.
The dairy cow gets Calcium from two sources; mobilization from bone and absorption
from the digestive tract. This is controlled by the parathyroid hormone which helps
mobilization from bone and also stimulates the release of a form of vitamin D that in
turn increases Calcium absorption in the small intestine. The inability of the cow to
mobilize Calcium and respond quickly enough is likely to be caused by imbalances
involving Calcium, Phosphorus, and Magnesium ;overload of Potassium; and
disturbance of the cation-anion balance. This is influenced by age;mineral levels in
dry period;nature of ration in terms of fibre content and influence on speed of gut
passage.Thus dry summers with reduced grass growth will have low milk fever
incidence whereas long wet spells with lots of the green stuff, possibly high in Potash,
with cows quite loose and less time for mineral absorbtion in the gut will have high
incidence
Prevention
The traditional way of preventing milk fever is to limit Calcium intake during the dry
period. This will allow the dry cow to adapt to deficiency and make her better able to
respond to demand in early lactation. In cows fed limited amount of Calcium and
Phosphorus during the dry period, bone and small intestine respond better to
stimulation from parathyroid hormone and active vitamin D.
Magnesium is an important co-factor in the absorbtion and mobilization of calcium
and thus magnesium supplementation can also be important. This is commonly given
as Magnesium chloride flakes via the water trough(50-60 gms/cow/day).
Supplementation of the dry cow diets with anionic salts altering the dietary cation
anion balance (DCAB) is another effective method of preventing milk fever. Anionic
salts reduce the incidence of milk fever by increasing the mobilization of Calcium
from bones. They are helpful when there is a high incidence of milk fever or when it
is difficult to control Calcium consumption during the dry period. Anionic salts are
effective in rations with high Calcium levels (150 g per day). They should not be fed
when Calcium intake is low. Therefore it is very important to analyze feed ingredients
especially forages, as book values on mineral content can be misleading.
Urine pH is affected by changes in the cow’s acid-base status and therefore, checking
urine pH can help producers monitor the effectiveness of a ration containing anionic
salts. This method relies heavily on attention to detail and daily monitoring and rapid
response. Some people resort to an easier partial DCAB system using higher than
standard levels of magnesium salts e.g.250 gms in the water and/or on the feed.
Hypomagnesaemia or Grass Staggers
Grass staggers is a disease affecting cattle and sheep not receiving adequate available
Magnesium. The low availablity of Magnesium in forage may be from either low
Magnesium concentrations or to factors in the forage that reduce its availability to the
animal .Older, lactating cow are most susceptible. Cows cannot store Magnesium and
hence any reduction in food supply coupled with extra demand will result in disease.
It has also been shown that reduced energy intake will interfere with Magnesium
absorbtion.
It has been classified into three main types based on diet and season .The spring type
affects lactating cows a few days after they are put out on grass. The winter type
affects cattle fed winter rations in confinement. The out-winter type affects cattle in
late winter that have been maintained thoughout the winter on sparse pasture plus
some supplemental hay.
It is an essential metabolite involved in many enzyme reactions and nerve and muscle
function and so deficiency leads to nervous symptoms of hyperexcitability, muscle
twitching ,spasms progressing to convulsions and death. Sub clinically it may present
as a herd picture of nervy cows reluctant to enter the parlour and giving less milk.
Also commonly associated is an increased incidence of milk fever.
Treatment involves intravenous injection of calcium borogluconate with additional
magnesium sulphate also given subcutaneously- NEVER give magnesium
intravenously.
Control is via adequate supplementation in feed ;via water troughs-but care with
levels as it is very unpalatable; mineral licks; pasture dressing with calcined
magnesite (magnesium oxide);sometimes oral boluses. Also important prevention
measures are provision of long fibre e.g.straw or big bale silage. adequate energy
levels, correct use of fertilizers high sodium and low potassium. Providing adequate
shelter and avoiding sudden dietary changes.
Ketosis/Acetonaemia
A metabolic disorder, that results from inadequate nutrient intake (especially energy)
by the dairy cow in early lactation. When blood glucose level is too low, the cow
mobilizes body reserves, especially fat. Part of the mobilized body fat will be
converted to ketones in the liver (e.g. acetone), which results in elevated ketone levels
in the blood.
Commonly occurs ten days to 6 weeks after calving in high producing cows. Peak
incidence is about 3 weeks. Many high producing dairy cows go through a subclinical primary ketosis in early lactation when milk production exceeds nutrient
uptake and body reserve has to be used. Under feeding, inappetence.Fat cows/Fatty
liver syndrome, Cobalt deficiency, Butyric silage can all predispose to Ketosis.
Other problems such as retained placenta, tyre-wire disease, displaced abomasum can
act as predisposing factors to secondary ketosis.
Symptoms
Loss of appetite especially to concentrates.
A sweet pear-drop smell on the breath and subtly on the milk is discernible by some.
Rumen inactivity appears later but faeces appears firm and “waxy”.
Weight loss
Lower milk yield
Nervous form sometimes seen with circling, head pressing ,licking walls and
abnormal chewing as main symptoms.
Diagnosis
Simple cow-side tests are available to check the ketone levels in the milk and urine as
well as a blood test which measures BHB and is commonly used in blood profiles as
a monitoring tool.
Treatment
All treatments of ketosis aim to increase blood glucose level and thus reduce tissue
mobilization
- Intravenous glucose injection: The most rapid and direct way of supplying blood
glucose. However, relapses occur when glucose infusion is used as the sole treatment.
Thus it should be followed by one of the longer acting treatments.
- Hormonal treatment:. Glucocorticoids (cortisone) cause the cow's body to produce
glucose from protein tissues. However, prolonged use of this hormone is not
recommended.
- Oral sugar precursors: Sodium propionate and propylene glycol are two oral sugar
precursors that can be used by the cow to produce sugar in the liver. They can be fed
or drenched at a rate of 250-450 g per day usually following glucose or hormonal
treatment.
Prevention
- Avoid over-conditioned cows in late lactation and dry period.
Overconditioning causes depressed appetite at freshening and may increase
fatty liver problems. Body condition score should be 2.5-3 at calving. A well
managed transition period and fresh cow period and well balanced rations are
the key to successful prevention.
- Monitoring of milk quality results particularly milk proteins via Herd
Companion can be an excellent early warning system.
Fatty Liver Syndrome
The syndrome occurs in high producing dairy cattle where overfeeding in the dry
period results in overfat cows at calving. The depressed appetite and intake around
calving and consequent negative energy balance leads to rapid weight loss via
excessive fat mobilization from body reserves and high levels of fatty acids in the
blood in the form of non-esterified fatty acids (NEFA). When fatty acids increase in
the blood, the liver increases its uptake of free fatty acids. Free fatty acids in the liver
are converted to triglycerides. Liver in ruminant animal has a very limited capacity of
utilizing fat. Therefore, fat deposition and accumulation occurs in the liver (fatty
liver).It is usually associated with an overconditioned dairy cow within a few days of
calving. Although commonly thought to develop after calving it is thought that fat is
often deposited from around day 17 pre partum to day 1 post partum and so
management of the dry cow and actually more correctly the late lactation cow is
paramount here.
Symptoms
Symptoms are similar to those of ketosis and include depression of appetite and
overall depression. It is associated with reduced production, reduced performance
and poor immune reponse.
The syndrome is usually associated with other metabolic disorders such as milk fever
(Unresponsive or relapsing milk fever is a common first sign)., ketosis, mastitis,
retained placenta and Displaced Abomasums(DAs)–Cows mobilizing fat were 7.5X
more likely to get one and fat cows (BCS>3.5) were 5 times more.
.
Treatment
Cows with fatty liver syndrome do not respond very well to treatments. Treatments
similar to those used for ketosis can be tried (e.g. intravenous glucose). In many cases,
the most economic treatment is to cull extremely fat cows before they calve.
Prevention
The best way to prevent fatty liver syndrome is to avoid excessive fatty acid
mobilization. Proper nutrition and feed management practices are critical to minimize
negative energy balance, especially in early lactation. The cow's body condition in
late lactation and during the dry period should be monitored to ensure that the cow is
not over-conditioned ideally BCS 2.5-3. During the dry period the cow should not
lose or gain more than 0.5 body condition. Dry period nutrition particularly
management of the Far-Off dry cow is key. Monitoring via condition scoring of cows
from late lactation onwards and via blood tests e.g. NEFA levels are very useful tools.
.
Rumen Acidosis
Subclinical acidosis (SARA) occurs in high yielding dairy cows on diets high in
rapidly digested carbohydrates which lead to rumen pH(normally 6.5 to 7) dropping
to below 6.This leads to poor rumen function, reduced dry matter intake, pain,
indigestion, loose faeces and low milk fat levels. Undigested fibre in faeces and
smearing of faeces over flanks, rump and perineum are tell-tale signs. A chronic state
can lead to sub-clinical laminitis causing increased lameness via solar ulceration and
white line disease.
During normal digestion in cattle feed is broken down in the rumen into fatty acids
which reduce the Ph. But for the rumen to function normally its pH must stay above 6.
Diets high in fibre are crucial to encourage rumination ,chewing and the production of
saliva which is the natural source of bicarbonate, in order to buffer the fall in rumen
Ph.
Risk factors for SARA are:
Diets high in soluble starches and sugars and low in fibre
Infrequent feeding of concentrates
Restriction of forage due to shortage, palatability or feed access problems.
Poor transition feed management.
Reducing SARA can lead to reduced lameness incidence, and hence improved
productivity, fertility and welfare .Digestion will improve and thus Dry Matter Intake
(DMI) will increase and so milk yield ;less condition loss and so less effect on fertility
also..You will also see a decreased incidence of LDAs.
Prevention involves
Replacing soluble sugars and starches with more fibrous feeds and fats and reducing
the rate at which starches are broken down..
Inclusion of Buffers can be useful to help in the management of this condition.
Offer high quality forages to provide adequate long fibre and minimum NDF of 35%.
Increasing forage: concentrate ratios and spreading concentrates load over day via
frequent feeding i.e. TMR rather than parlour fed concs.
Careful management of the cows diet pre and post partum.. particularly introduction
of the lactating ration in the transition period. This allows rumen microbes to
acclimatize to the type of nutrient to be fed post calving.
Monitoring of milk fat levels via e.g. Herd Companion can act as a very effective
early warning system.