This document discusses production diseases of cattle. It begins by defining production diseases as those induced by management practices, with metabolic diseases being typical examples. It then discusses several specific production diseases of cattle in detail, including milk fever/parturient paresis, ketosis/acetonemia, and fatty liver syndrome, covering the etiology, epidemiology, clinical signs, diagnosis, and treatment of each disease.

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Dr. Nireeksha Jain

3. ETIOLOGY,
EPIDEMIOLOGY,
SYMPTOMS,
DIAGNOSIS,
TREATMENT OF
PRODUCTION
DISEASES OF CATTLE,
HORSE, PIG, POULTRY
(PART-1)
14
3
LECTURE
TOPICS

4. UPSC PYQ’s
1) Discuss the modern concepts of Diagnosis and treatment of
PRODUCTION DISEASES of dairy livestock ? (2014)

5. PRODUCTION DISEASES
The term ‘ PRODUCTION DISEASES’ refers traditionally to
those diseases induced by management practices,
metabolic diseases are typical examples.
• The effects are independent of other diseases, & at times
are long-lasting.
• Production Diseases are often multifactorial & appear at
the same stage of lactation.

6. PRODUCTION DISEASES OF
CATTLE
1) MILK- FEVER / PARTURIENT PARESIS :
Parturient paresis is an acute to per-acute non-febrile disease, occuring in
dairy cows/ buffaloes, around time of parturition. The disease is clinically
manifested by weakness, recumbency and circulatory collapse.
Etiology
• Sudden loss of calcium into milk during onset of lactation at parturition or
near the parturition, resulting in low levels of ionized calcium in tissue
fluids causes onset of hypocalcaemia.
• The plasma calcium in milk fever is reduced to a level of 2-7 mg/dl.
Commonly, the phosphorus level is also decreased, and cows are
hypoglycaemic.

7. • Feeding of calcium rich diet (more than 100 g of calcium daily)
during the dry period increases the chances of the disease.
• Alkaline diet with an excess concentration of sodium (Na) and
potassium (K) increase incidence of hypocalcaemia.
• Since most of the leguminous fodder and grasses are alkaline
and rich in potassium, the chances of milk fever are more when
legume rich diet is fed during pre-partum period.
EPIDEMIOLOGY
• Mature high producing cows and buffaloes in the age group
of 5-10 years and at their 3rd to 7 lactation are relatively more
susceptible.
• Cows of Jersey breed are thought to be more prone to milk
fever, frequently found in high-yielding dairy cows.
• Composition of diet during dry and pre-partum periods, and
environmental factors influence occurrence of milk fever.
• More common in late winters, spring.
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8. SYMPTOMS
• Three discernible stages of milk fever are reported in cows.
• In the first stage, the animal remains standing but is disinclined to move and
becomes anorectic. Rumen stasis, agalactia and a brief stage of excitement and
tetany with hypersensitivity, shaking of head, protrusion of tongue, grinding of
teeth and tremors of head and limbs are the common signs. The rectal
temperature is normal or slightly above normal.
• In the second stage, cows and buffaloes are unable to stand and suffer from
prolonged recumbency with lateral kink in the neck or head tucked into their
flanks. The muzzle and eyes are dry, extremities are cold and temperature is
subnormal. There are signs of bloat, rumen stasis and constipation. Inability of
animals to urinate is reflected by distended bladder.

9. 9
SYMPTOMS
• The third stage is marked by lateral recumbency, and the animals are
almost in comatose condition. Severe bloat, low temperature, increased
heart rate with almost inaudible heart sounds and impalpable pulse are
seen during this stage.
• Clinical outcome in milk fever may be complicated by concurrent
hypomagnesaemia or hypophosphataemia.

10. DIAGNOSIS
• The disease needs to be differentiated from hypophosphatemia,
hypomagnesaemia, downer cow syndrome, carbohydrate
engorgement, mastitis, toxic metritis and other systemic toxaemias.
• The diagnosis of milk fever is confirmed by marked decrease in
calcium and phosphorus concentrations in serum, and a
favourable response to the treatment with calcium borogluconate.

11. TREATMENT AND
PREVENTION
• Animals respond favourably to early treatment with intravenous
administration of calcium boro-gluconate salt.
• The usual dose for cows and buffaloes is 1 g calcium per 45 kg
body weight, which is calculated to 400-800 ml of 25% solution
depending upon their body weight.
• Rapid intravenous administration of total dose of calcium may
be detrimental due to cardio-toxic effect of calcium.
• In large-heavy body weight half of the total dose may be given by
subcutaneous route after initial intravenous infusion.
• Oral administration of calcium solution avoids cardio-toxicity in
mild cases of milk fever.
• Vitamin D (20-30 million unit) given in the feed for 5-7 days
before parturition.

12. ACETONEMIA /
KETOSIS
Ketosis, also known as acetonaemia or ketonaemia is a multifactorial
disorder that commonly occurs in dairy cows and buffaloes immediately after
calving or in early lactation. The disease is characterized by partial anorexia
and depression.
Etiology
• Ketosis occurs due to negative energy balance associated with intense
adipose mobilization and a high glucose demand.
• High yielding dairy cows and buffaloes are more likely to suffer,
particularly in the early stage of lactation and immediately after parturition.
• Factors that decrease energy supply to animals or stimulate energy
supply via fat or that increase demand for glucose enhance ketone body
production.

13. EPIDEMIOLOGY
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• Dairy cows in early lactation (the first 6 weeks after parturition)
are at risk of ketosis, with most cases occurring in the first 2
weeks of lactation ( due to negative energy balance)
• Occurs mostly in milking animals.
• Incidence higher in third lactation or following that.
• Secondary ketosis may occur in any type of animal where
breakdown of fats are induced out of starvation due to conditions
like fever, mastitis, abomasal displacement.

14. CLINICAL
FINDINGS
1. In dairy cows and buffaloes, ketosis can occur in two clinical forms, viz.
wasting and nervous.
2. The wasting form is more commonly seen and is characterized by decrease
in appetite, and milk yield. The animal is often lethargic and abdomen appears
empty.
3. The body weight is rapidly reduced and skin elasticity is lost due to
disappearance of subcutaneous fat giving a woody appearance to the affected
animals.
4. A characteristic acetone smell is detectable on the breath and often in milk.
Few cases of wasting-form may show nervous signs including transient bouts
of staggering and partial blindness.
5. Signs in nervous form may develop suddenly, which include walking in
circle, straddling or crossing of legs, head pushing into the stanchion, apparent
blindness, aimless movements and wandering.

15. CLINICAL FINDINGS
6. Depraved appetite, vigorous licking and chewing of the inanimate
objects are also seen.
7. There may be hyperesthesia, incoordination and moderate tremor and
tetany.
8. Many cows and buffaloes, which are in negative energy balance
during early pregnancy suffer from sub clinical ketosis, which is
characterized by ketonuria and sharp fall in milk yield. Such cases can be
identified on repeated urine examination between 5 and 12 days post-
partum.

16. Diagnosis
 The diagnosis of ketosis is established on the basis of case history
indicating presence of risk factors, and the biochemical tests to
detect the presence of hypoglycaemia, and ketone bodies in blood,
milk and urine.
 In many countries commercial kits for cow-side test are available to
detect ketone bodies in urine or milk. The majority of these tests are
based on detection of acetoacetate or acetone.
 Ketone body concentration in urine is affected not only by ketone
level in blood, but also by the amount of urine excreted.
 A milk strip test to detect presence of B-hydroxybutyrate (BHBA) is
recently commercialized. The sensitivity and specificity of this test
are reported to be 73.96% and 69-96%, respectively.

17. Treatment and
prevention
 Ketosis can be effectively treated by re-establishing normoglycaemia
and reducing ketone body production.
 Administration of 500 ml of 50% glucose intravenously is a
common treatment, which provides rapid recovery.
 Care should be taken to avoid peri-vascular leakage of the glucose
solution as it may cause severe swelling and irritation.
 Glucocorticoids such as dexamethasone or isoflupredone
acetate- 5 and 20 mg intramuscularly provide more sustained
response.
 Propylene glycol administered orally @ 225 g twice daily for 2
days followed by 110 g for 2 days gives good results, especially in
less severe cases.
 Use of insulin (200-300 IU) intramuscularly and vitamin B,, is also
recommended for treatment of ketosis.

18. FAT COW SYNDROME / FATTY LIVER
Fatty liver or fat cow syndrome (hepatic lipidosis, pregnancy toxaemia in
cattle).
Fatty liver or hepatic lipidosis is a major metabolic disease of dairy cows. It is
caused by decrease in energy intake and negative energy balance during
parturition associated with excessive mobilization of body fat to liver.

19. ETIOLOGY
 A decrease in energy intake due to shortage of feed or inability of cows
to consume adequate amount of feed during late pregnancy or lactation.
 Sudden demand of energy during immediate post-partum period in over-
conditioned cows and deprivation of feed in high yielding pregnant cows
precipitate fatty liver disease.
 The disease conditions that predispose fatty liver include metritis,
mastitis, ketosis, acidosis, retained placenta, milk-fever and left-side
abomasal displacement.
 Overfeeding of cows during dry period predisposes fatty liver.
 Genetic factors are also proposed to influence mobilization of body lipid
reserves.

20. EPIDEMIOLOGY
 The disease occurs sporadically depending on feed and
management practice. It has been found to be frequent in loose
housing where cattle on all stages of lactations are fed and
managed in one group
 Cows with long dry period due to low production. or infertility are
predisposed to become excessive fat and thus it may be a herd
infertility problem.
 Any such above conditions may be responsible for mobilization of
excessive quantity of fat from body reservoirs to liver due to
inappetence because of a sudden demand for energy in the
immediate post partum period.
 In lactating dairy cows the disease is evident.

21. CLINICAL SIGNS
1. Fatty liver cows do not show any characteristic signs
2. Affected animals are generally obese and palpation over flank
indicates excessive subcutaneous fat.
3. There is drop in milk yield and reduced feed intake.
4. The rumen movements may be absent in anorectic animals.
5. The temperature, pulse and respiration rates are within normal
range.
6. Ketonuria, hypoglycaemia, hyperammonaemia and endocrine
changes may accompany fatty liver.
7. The severely affected cows gradually become weak and
recumbent, and die within 7-10 days.
8. Most cases of fatty liver recover albeit in several days.

22. DIAGNOSIS
1. Clinical diagnosis of fatty liver is difficult.
2. The biopsy of liver is the reliable method to detect severity of the
condition.
3. Disease conditions associated with the clinical signs similar to fatty
liver disease should be differentiated.
4. Left side abomasal displacement is characterized by pings over
the abdomen, ketosis and inappetance.
5. Metritis and retained placenta may be accompanied by fever,
inappetance, ruminal atony and foul smelling discharge from vagina.
6. Changes in activities of liver specific enzymes, lipid profile, glucose
and NEFA concentrations in blood are used as laboratory diagnostic
tools.

23. Treatment and prevention
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1. Severe cases of fatty liver do not respond very well to the
treatment and prognosis for such cases, particularly with
nervous signs, is poor.
2. Animals should be provided plenty of good quality feed and
water. Intravenous administration of 5% glucose and balanced
salt solution along with intra-ruminal administration of rumen
fluid (5-10 litres) from normal cows are effective.
3. Glucagons @ 10 mg/day intravenously or 15 mg/day
subcutaneously for 14 days is effective in reducing liver
triglyceride.
4. Glucocorticoides, propylene glycol and insulin are also
useful in treatment of fatty liver.
5. Propylene glycol can be given orally @ 500-1000 ml day
during the last week of gestation.

24. THANKS!
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