Lecture 11 : Animal Diseases

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By- Dr. Nireeksha Jain

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Dr. Nireeksha Jain

3. INTRODUCTION !
Myself Dr. Nireeksha Jain
-BVSc from SKUAST-J
-MVSc from SKUAST-J in Animal
Genetics and Breeding & Research.
- Upsc cse experience of 4 years.
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4. ANIMAL DISEASES
DEFICIENCY
DISEASES OF
DOMESTIC
ANIMALS AND
BIRDS (part-1)
11
4
LECTURE

5. 5
UPSC PYQ’s :
1. What are the clinical manifestations of Vitamin B complex
deficiency diseases in poultry ? (2018)
2. Describe the clinical manifestations of Vitamin deficiency in
poultry? (2017)
3. Identify the deficiency disease in a layer flock with the
problem of leathery eggs and treatment ,control of same?
(2016)

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DEFICIENCY DISEASES OF ANIMALS
Animals may suffer from diseases caused by deficiencies of
energy and proteins, mineral nutrients and vitamins, which
generally occur either due to deficiency in the diet or
abnormal absorption, utilization or requirement of the
nutrients. Type of soil, plants and vegetation, farming and
feeding practices, and physiological status of animal are
important predisposing factors. Climatic conditions and
genetic variables also influence occurrence of deficiency
diseases. Usually deficiencies under natural conditions are
complicated by other factors and their diagnosis may not be
simple.

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A) ENERGY & PROTEIN DEFICIENCIES –
 Deficiencies of protein and energy are the most common
nutrient deficiencies, which adversely affect production and
performance of farm animals.
 The two deficiencies often occur concurrently due to
inadequate quantity or poor quality of feed.
 Underfed livestock receiving insufficient quantity or quality of
feed are more likely to suffer from protein and energy
deficiencies.
 The feed may be of poor quality or may be in short supply
due to overgrazing, drought, flood or general scarcity.
 Feed of low digestibility and excess water content may
also be responsible for deficiencies of protein and energy.

8. Clinical findings
1. In young animals- retarded growth and delayed onset
of puberty.
2. Mature lactating animals- decline in milk yield, a short
lactation, reduced body weight, and poor reproductive
performance including prolonged anoestrus.
3. Long duration of energy and protein deficiency during
late lactation causes undersized, weak neonates with
high neonatal mortality.
4. The increased intake of poor quality roughage may
cause abomasal impaction.

9. PREVENTION
Prevention
• Preventive measures include provision of adequate nutrients to
meet requirement according to age, stage of lactation and
physiological conditions of animals.
• Available guidelines can be followed to estimate the requirements.
• Other factors such as environmental temperature and body
condition scoring of cattle and sheep should also be considered to
calculate dietary requirements for animals.

10. B) Cobalt deficiency
The deficiency of cobalt (Co) is more commonly seen in ruminants
fed on diets deficient in this essential micronutrient. Cobalt is
stored only in limited amounts and needs to be supplied in diet
continuously for synthesis of vitamin B₁₂ in the rumen. Diet deficient
in cobalt may reduce the vitamin B2 synthesis by over 90%.

11. B) Cobalt deficiency
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Clinical findings:
1. Cattle and sheep are affected alike and present similar clinical
signs. Cobalt deficiency in ruminants impairs oxidation of
propionate.
2. Animals on cobalt deficient diets exhibit gradual decline in appetite,
loss of body weight, anaemia emaciation, and weakness.
3. Cattle show signs of pica and reduced milk yield.
4. Wool production in sheep is retarded both quantitatively and
qualitatively. Severe lacrymation, usually matting the wool of face.
5. Stillbirths, increased neonatal mortality and birth to weak lambs.

12. TREATMENT
1. Oral dosing with cobalt and vitamin B or intramuscular
administration of vitamin B12 are effective therapies,
2. Monthly dose of 300 mg cobalt can prevent mortality in lambs.
Vitamin B can be given in 100 to 300 ug doses in lambs and
sheep at weekly interval.
3. Supplementation of cobalt in diet @ 0.06 to 0.07 mg/kg dry
matter can prevent cobalt deficiency in cattle and sheep.
4. Top dressing of pastures using copper sulphate 400 to 600
g/ha annually in cobalt deficient areas is recommended.
5. Controlled cobalt releasing boluses, or cobalt-heavy pellets
are available for oral administration in ruminants
6. Addition of cobalt with anthelminthics is also an effective
preventive measure.
7. Administration of vitamin B12 @ 2 mg per animal at
bimonthly also reduce the risk of cobalt and vitamin B12
deficiencies.

13. C) COPPER DEFICIENCY
• Copper (Cu) deficiency may be primary or secondary
(conditional).
• Primary copper deficiency occurs due to its inadequate
dietary intake; whereas secondary copper deficiency
occurs due to its impaired absorption and utilization, even
though dietary copper intake is sufficient.
• The deficiency of copper is clinically marked by
unthriftiness, discolouration of hair, chronic diarrhoea,
neonatal ataxia and anaemia in the later stage.

14. COPPER DEFICIENCY (
CLINICAL SIGNS)
1. The deficiency of copper inhibits activities of metallo-
enzymes in faulty tissue oxidation and associated signs
such as changes in wool of sheep.
2. Impaired tissue oxidation also causes loss of condition and
retarded growth.
3. anaemia in copper deficiency.
4. Impaired collagen formation and significant increase in
osteoporotic activity with osteoporosis, degenerative
diseases of cartilage and other changes in bones and joints
are also seen in copper deficiency.
5. It also affects function of immune cells, heart, nervous
system, and reproductive system.

15. COPPER DEFICIENCY ( CLINICAL
SIGNS
6. Abnormal hair pigmentation is a consistent clinical finding
in copper deficiency in cattle. The change in hair coat colour
are particularly prominent around eyes (be spectacled
appearance), tips of ears and on the flanks.
7. The hair coat is rough and staring.
8. Calves show slow growth with an increased tendency of
bone fracture.
9. Young calves show incoordination, stiff gait and
opisthotonous.
10. Ataxia may occur after exercise with sudden loss in
control of hind limbs resulting in falling or on sitting posture
position.

16. COPPER DEFICIENCY ( CLINICAL
SIGNS
11. Persistent diarrhoea is more common in copper deficiency
associated with molybdenum excess and in peat scour (teart).
12. Falling disease is characterized by head throwing, bellowing,
and falling followed by death.
13. Pine disease or unthriftiness of calves
14. Abnormalities of wool are important clinical findings in primary
copper deficiency in sheep. Wool becomes straight, glossy, and
steely in appearance (steely wool disease).
15. Sway back in sheep is reported from the United Kingdom-
incoordination, erratic movements and spastic paralysis.

17. TREATMENT
1. Copper deficiency can be treated by oral dosing with
copper sulphate given @ 4 g to 2-6 months old calves, 8-10
g for mature cattle and buffaloes at weekly intervals for 3-5
weeks.
2. Copper glycinate can also be given parenterally. In
copper deficient areas, ration should be supplemented with
copper sulphate (5-10 mg copper per kg DM) to provide
minimum dietary requirement .
3. Providing free access to salt-licks, containing 0.25-0.5%
copper sulphate for sheep and 2% for cattle, and top
dressing of pasture with copper sulphate (10 kg/ha) can
also be practised to prevent occurrence of copper

18. Iodine is an important component of thyroid hormones, which play
active role in several physiological process such as control of basal
metabolic rate, oxidation, protein synthesis, immune and muscle functions.
D) IODINE DEFICIENCY

19. CLINICAL
FINDINGS
1. Deficiency of iodine causes decreased production of thyroxin and
stimulation of thyrotrophic hormones by pituitary gland
2. Signs of loss of libido in males, and failure to express oestrous,
abortions and stillbirths in females, and weak new born calves are
important signs of iodine deficiency.
3. Alopecia and palpable thyroid gland are found in different species
4. Defective ossification, lameness and deformity of the hock are also
evident in foals.
5. Characteristic signs in pigs include birth of hairless and weak
piglets
6. Iodine deficiency in adult sheep is marked by thyroid enlargement and
increased length of gestation.
7. Clinical signs in goats are similar to those found in sheep. There is
alopecia of varied severity and goitre in kids
8. In pigs the characteristic findings are birth of hairless, stiffborn or
weak piglets with myoxidine of the skin of neck.

20. Treatment and prevention
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• Application of tincture of iodine (cattle 4 ml, and pigs and
sheep 2 ml) to inside of flank or parenteral administration of
iodine or drenching pregnant ewes with 280 mg potassium iodide
or 370 mg potassium iodate during fourth or fifth month of
pregnancy are also used for effective prevention of iodine
deficiency.
• Iodine therapy needs to be instituted with precaution as excess
dose may cause toxicity.
• The minimum toxic levels for calves and pigs are 50 ppm and
400 ppm, respectively.

21. E) IRON DEFICIENCY
Iron (Fe) plays an imp. Role in oxygen transport in the body; as a
constituent of Haemoglobin (60 % body iron is found). Deficiency
of iron is not very common in farm animals, except in young
animals. It is characterized by anaemia and associated signs.
Etiology
In animals, iron deficiency is usually primary. Generally, newborn
animals are given sole milk diet, which is a poor source of iron. As
the hepatic iron store in newborn is not enough to maintain normal
haemopoiesis for more than 2-3 weeks, the newborns, particularly
piglets suffer more frequently to iron deficiency.

22. CLINICAL FINDINGS
1. Progressive development of hypochromic-microcytic anaemia is
the characteristic finding in iron deficiency.
2. Piglets at about 3 weeks of age have the highest incidence of iron
deficiency anaemia. Signs of dyspnoea, lethargy, pale skin and
mucosa, oedema of the head and fore quarters and diarrhoea are
seen.
3. Affected animals may die suddenly or may survive in a thin,
unthrifty condition.
4. Iron deficiency also increases severity of Trichuris suis and
Ascaris suum infections in pigs.
5. Iron deficiency in calves, lambs and kids is also associated with
signs of anaemia. Calves also show atrophy of lingual papillae.

23. TREATMENT
1. Treatment includes parenteral administration of organic iron
preparations such as iron dextran, iron sorbitol citric acid
complex or iron gluconate.
2. Weekly intramuscular administration of iron preparation (100-200
mg for piglets, 300 mg iron dextran for lambs and 0.5-1 g
elemental iron for horses) can be used.
3. Vitamin B12 is also used along with iron preparations.
4. Iron deficiency anaemia can be prevented by oral or intramuscular
administration of a commercial grade iron to piglets @ 15 mg daily
until weaning.
5. A diet supplemented with 2 g iron per kg DM to sow is effective
in preventing anaemia in piglets.
6. Calves should be provided iron supplementation in milk replacer
@ 1-2 g per kg DM.

24. F) ZINC DEFICIENCY
Zinc (Zn) is essential for several physiological functions in the
body such as protein Synthesis, carbohydrate and nucleic acid
metabolism, and foetal growth. The deficiency of zinc is
characterized by parakeratosis, loss of hair, reduced feed
intake and deformities of hooves. Parakeratosis is particularly
evident in young growing pigs suffering from zinc deficiency.

25.  Inappetence, poor growth, impaired reproductive performance,
abnormalities of skin and appendages, and decreased efficiency of
feed utilization are common signs of zinc deficiency in different
species of animals.
 Pigs show reduced growth rate and poor body weight gain.
 Cattle show parakeratosis and alopecia involving almost 40% of the
skin area. Stunted growth, signs of stiff gait, swelling of coronets,
hocks and knee joints, alopecia, wrinkling of skin of the legs, scrotum
and neck and head region, and haemorrhages around teeth.
 Zinc deficiency is suggested to precipitate dystocia in cows.
 Sheep show loss of wool, development of thick-wrinkled skin and
reduced fertility.
 Clinical signs of zinc deficiency in goats include reduced hair growth,
testicular size, spermatogenesis and overall growth, alopecia and
parakeratosis.
CLINICAL SIGNS

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Treatment and prevention:
 Supplementation of zinc @ 50 mg/kg DM in diet in form of zinc sulphate
or zinc carbonate can effectively check outbreaks of parakeratosis in
pigs.
 Clinical cure in sheep and goats is achieved by intramuscular
administration of 200 mg of zinc in the form of zinc oxide suspended in
olive oil. Dose of 50 mg zinc cures lambs within 2 months.
 Oral dose of 250 mg zinc sulphate daily for 4 weeks cures zinc
deficiency in goats.
 Restriction of calcium in diet (0.5-0.6%) of growing pigs, and
supplementation of diet with zinc.

27. THANKS!
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