Ketosis (Acetonaemia) in Cattle
Ketosis in Cattle
The Condition
Ketosis, or acetonaemia,
is a metabolic disorder. Hypoglycaemia is the major factor involved in the
onset and development of clinical signs of ketosis. There is a gradual loss of
body condition over several days or even weeks. There is also a moderate
decline in milk yield over two to four days before the onset of obvious
clinical signs. The disease is most commonly seen in high-yielding dairy cows
in early lactation. Secondary ketosis as a result of another disease can be
seen at any stage of lactation. Beef cows can also suffer from ketosis during
pregnancy.
Introduction
Ketosis is a common
disease of adult cattle. It typically occurs in dairy cows in early lactation
and is most consistently characterized by partial anorexia and depression. Rarely,
it occurs in cattle in late gestation, at which time it resembles pregnancy
toxemia of ewes. In addition to inappetence, signs of nervous dysfunction,
including pica, abnormal licking, incoordination and abnormal gait, bellowing,
and aggression are occasionally seen. The condition is worldwide in
distribution, but is most common where dairy cows are bred and managed for high
production.
Ketosis in dairy cows
The clinical signs
include a refusal to eat grain and concentrate feeds and a more sudden drop in
milk output. There is a sweet smell of acetone in the breath and milk. Some
cows may exhibit nervous signs, which include excessive salivation, abnormal
chewing movements, licking of walls, gates or metal bars, malcoordination with
apparent blindness and a degree of aggression. The nervous signs often only
last for a few hours. The affected cows have fatty infiltration and
degeneration of the liver. To satisfy the requirements of milk production, the
cow can draw on two sources of nutrients, food intake and body reserves. During
early lactation, the energy intake is insufficient to meet the energy output in
milk and the animal is in a negative energy balance.
In conventional farming,
this is considered to be a normal metabolic situation in high-yielding dairy
cows. These cows will have slightly raised blood ketone levels and may even
excrete ketones in urine and milk. Cows in early lactation are therefore in a
vulnerable situation, and any stress that causes a reduction in feed intake may
lead to the onset of clinical 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. However, the liver cannot deal with the
acetyl-CoA, which results from the oxidization of these fatty acids, because of
a lack of energy. The excess acetyl-CoA is converted into the ketone bodies,
acetoacetate and b -hydroxybutyrate and, to a small extent, acetone. Tissues
other than the liver can use ketone bodies, but if their production exceeds the
rate at which they are used by muscle and other tissues, they accumulate, and
ketosis is the result. Ketone bodies are excreted in milk and urine.
The reduction of
propionic acid production is usually the result of underfeeding or a reduced
feed intake caused by inappetance. The inappetance may be caused by a
deterioration of forage quality, sudden changes in diet or excessive fatness at
calving. Other risk factors are parity, ketosis in the previous lactation,
305-day milk yield in the previous lactation and the average milk protein
percentage in the previous lactation. Butyrate is a precursor of acetyl-CoA and
is therefore ketogenic. In the UK,
the butyric acid content of silage is of considerable importance in the
aetiology of the disease, because wet conditions predispose to butyric
fermentation of the silage. Silage intake containing high levels of butyric
acid is also less palatable to cattle.
Secondary ketosis
Secondary ketosis is
common and is the result of diseases causing a reduction in appetite in early
lactation, such as displaced abomasum,
mastitis, metritis, etc. In areas of cobalt deficiency,
ketosis is commonly diagnosed in grazing cattle. Cobalt is required for
rumen microbial synthesis of vitamin B12 and is also essential for adequate
utilization of propionic acid.
Etiology and Pathogenesis
The pathogenesis of
bovine ketosis is incompletely understood, but it requires the combination of
intense adipose mobilization and a high glucose demand. Both of these
conditions are present in early lactation, at which time negative energy
balance leads to adipose mobilization and milk synthesis creates a high glucose
demand. Adipose mobilization is accompanied by high blood serum concentrations
of nonesterified fatty acids (NEFA). During periods of intense gluconeogenesis,
a large portion of serum NEFA is directed to ketone body synthesis in the
liver. Thus, the clinicopathologic characterization of ketosis includes high
serum concentrations of NEFA and ketone bodies and low concentrations of
glucose.
In contrast to many other species, cattle with
hyperketonemia do not have concurrent acidemia. The serum ketone bodies are
acetone, acetoacetate, and β-hydroxybutyrate (BHB). There is speculation that
the pathogenesis of ketosis cases occurring in the immediate postpartum period
is slightly different than that of cases occurring closer to the time of peak
milk production.
Cases of ketosis in very
early lactation are usually associated with fatty liver. Both fatty liver and
ketosis are probably part of a spectrum of conditions associated with intense
fat mobilization in cattle. Ketosis cases occurring closer to peak milk
production, which usually occurs at 4-6 wk postpartum, may be more closely
associated with underfed cattle experiencing a metabolic shortage of
gluconeogenic precursors than with excessive fat mobilization. The exact
pathogenesis of the clinical signs is not known. They do not appear to be
associated directly with serum concentrations of either glucose or ketone
bodies. There is speculation that they may be due to metabolites of the ketone
bodies.
Epidemiology:
All dairy cows in early
lactation (first 6 wk) are at risk of ketosis. The incidence in lactation is
estimated at 5-16%, but incidence in individual herds varies substantially. Ketosis
occurs in all parities (although it appears to be less commin in primiparous
animals) and does not appear to have a genetic predisposition, other than being
associated with dairy breeds. Cows with excessive adipose stores (body
condition score ≥3.75 out of 5.0) at calving are at increased risk of ketosis,
compared with those with lower body condition scores. Lactating cows with
hyperketonemia (subclinical ketosis—serum BHB concentrations >12 mg/dL) are
at increased risk of developing clinical ketosis, compared with cows with lower
serum BHB concentrations.
Clinical Findings:
In cows maintained in
confinement stalls, reduced feed intake is usually the first sign of ketosis. If
rations are offered in components, cows with ketosis often refuse grain before
forage. In group-fed herds, reduced milk production, lethargy, and an “empty”
appearing abdomen are usually the signs of ketosis noticed first. On physical
examination, cows are afebrile and may be slightly dehydrated. Rumen motility
is variable, being hyperactive in some cases and hypoactive in others. In many
cases there are no other physical abnormalities.
CNS disturbances are
noted in a minority of cases. These include abnormal licking and chewing, with
cows sometimes chewing incessantly on pipes and other objects in their
surroundings. Incoordination and gait abnormalities occasionally are seen, as
are aggression and bellowing. These signs occur in a clear minority of cases,
but because the disease is so common, finding animals with these signs is not
unusual.
Diagnosis:
The clinical diagnosis of
ketosis is based on presence of risk factors (early lactation), clinical signs,
and ketone bodies in urine or milk. When a diagnosis of ketosis is made, a
thorough physical examination should be performed because frequently ketosis
occurs concurrently with other peripartum diseases. Especially common
concurrent diseases include displaced abomasum, retained fetal membranes, and
metritis. Rabies and other CNS diseases are important differential diagnoses.
Trace to mildly positive
results for the presence of ketone bodies in urine do not signify clinical
ketosis. Without clinical signs, such as partial anorexia, these results
indicate subclinical ketosis. Milk tests for acetone and acetoacetate are more
specific than urine tests. Positive milk tests for acetoacetate and/or acetone
usually indicate clinical ketosis. A dipstick designed to detect BHB in milk,
available in Japan and Europe, is more sensitive than milk tests for acetone and
acetoacetate and may be useful for monitoring incidence of subclinical ketosis.
Treatment
Treatment is aimed at
reestablishing normoglycemia and reducing serum ketone body concentrations. Bolus
IV administration of 500 mL of 50% dextrose solution is a common therapy. This
solution is very hyperosmotic and, if administered perivascularly, results in
severe tissue swelling and irritation, so care should be taken to assure that
it is given IV.
Bolus glucose therapy
generally results in rapid recovery, especially in cases occurring near peak
lactation. However, the effect frequently is transient and relapses are common.
Administration of glucocorticoids including dexamethasone or isoflupredone
acetate at 5-20 mg/dose, IM, generally results in a more sustained response.
Glucose and glucocorticoid therapy may be repeated daily as necessary.
Propylene glycol (250-400
g/dose, PO, [~8-14 oz]) acts as a glucose
precursor and may be effective as ketosis therapy, especially in mild cases or
in combination with other therapies. This dose may be administered twice per
day. Overdosing propylene glycol leads to CNS depression.
Ketosis cases occurring
within the first 1-2 wk after calving frequently are more refractory to therapy
than those cases occurring nearer to peak lactation. In these cases, a
long-acting insulin preparation given IM at 150-200 IU/day may be beneficial.
Insulin suppresses both adipose mobilization and ketogenesis, but should be
given in combination with glucose or a glucocorticoid to prevent hypoglycemia.
Use of insulin in this manner is an extra-label, unapproved use. Other
therapies that may be of benefit in refractory ketosis cases are continuous IV
glucose infusion and tube feeding.
Prevention and Control:
Prevention of ketosis is
via nutritional management. Body condition should be managed in late lactation,
when cows frequently become too fat.
The dry period is
generally too late to reduce body condition score. Reducing body condition in
the dry period may even be counterproductive, resulting in excessive adipose
mobilization prepartum.
A critical area in
ketosis prevention is maintaining and promoting feed intake. Cows tend to
reduce feed consumption in the last 3 wk of gestation. Nutritional management
should be aimed at minimizing this reduction. Controversy exists over the optimal dietary
characteristics during this period.
It is likely that optimal
energy and fiber concentrations in rations for cows in the last 3 wk of
gestation vary from farm to farm. Feed intake should be monitored and rations
adjusted to maximize dry matter and energy consumption in late gestation. After
calving, diets should promote rapid and sustained increases in feed and energy
consumption. Rations should be relatively high in nonfiber carbohydrate
concentration, but contain enough fiber to maintain rumen health and feed
intake. Neutral-detergent fiber concentrations should usually be in the range
of 28-30% with nonfiber carbohydrate concentrations in the range of 38-41%.
Dietary particle size
will influence the optimal proportions of carbohydrate fractions. Some feed
additives, including niacin, calcium propionate, sodium propionate, propylene
glycol, and rumen-protected choline, may be beneficial in preventing and
managing ketosis. To be effective, these supplements should be fed in the last
2-3 wk of gestation, as well as during the period of ketosis susceptibility.
posted by مطاعم السعودية @ 11:12 AM
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