5. DISEASES OF CATTLE
(cntd…)
PPH ( POST- PARTURIENT
HAEMOGLOBINURIA /
HYPOPHOSPHATEMIA)
The post-parturient haemoglobinuria (PPH) is an acute
disease of high yielding buffaloes and cows. The
disease occurs immediately after parturition and
characterized by rapid intravascular haemolysis,
anaemia, haemoglobinuria, weakness, marked
decrease in milk production and death in untreated
cases.
6. ETIOLOGY
The disease is usually associated with dietary phosphorus
deficiency. and occasionally due to feeding of cruciferous
plants. It may also be related to copper and selenium
content in the diet.
EPIDEMIOLOGY
• High yielding cows and buffaloes in their third lactation are
most commonly affected, particularly after 2-5 week of calving.
• Exposure to extremely cold weather and ingestion of cold
water may precipitate haemoglobinuria.
• The disease is more commonly recorded in buffaloes reared
in rural areas.
7. CLINICAL SIGNS / SYMPTOMS
1. There is sudden onset of haemoglobinuria (red or
coffee coloured urine), inappetance, weakness and
severe reduction in milk yield.
2. Animal becomes dehydrated.
3. Faeces are dry and scantly.
4. Dyspnoea and moderate rise in temperature may be
present in cows but seldom seen in buffaloes.
5. The jaundice is seen in late state and animal becomes
progressively weak and recumbent.
6. Respiratory distress/ shortness of breath.
8. 8
DIAGNOSIS
Clinical signs of dark urine and anaemia are suggestive of
PPH.
Clinical signs
Estimation of Phosphorus level in blood.
The serum inorganic phosphorus concentration in PPH is
markedly reduced (0.5-3.0 mg/dl) as compared to normal level
(4.0-7.0 mg/dl).
The disease needs to be differentiated from leptospirosis, water or
salt poisoning, chronic copper intoxication etc.
9. Treatment and
prevention
1. Transfusion of large quantity of whole blood (4-5 litre for a 450 kg
cow or buffalo) is highly effective treatment.
2. Intravenous copper glycinate (1.5 mg/kg body weight,) or oral
copper sulphate .
3. Intravenous sodium acid phosphate solution can check
haemolysis.
4. Correction of mineral imbalance and adequate provision of
phosphorus in the diet are recommended to prevent occurrence of
the disease.
5. Ascorbic acid (7.5 g in 500 ml normal saline intravenously)
along with mineral mixture is effective in treatment of PPH in
buffaloes.
10. PRODUCTION DISEASES IN
HORSES
AZOTURIA IN HORSES / MONDAY-MORNING SICKNESS
Paralytic myoglobinuria is a disease of horse, occurring during
exercise after a period of inactivity on full ration. The disease is
characterized by myoglobinuria and muscle degeneration.
ETIOLOGY
Horses taken off the track work because of minor injuries or illness
are often maintained on full working rations and become affected
when taken back to work ,major parts of grains remain stored in
muscles as glycogen. On Monday, during exercise the problem
starts with the onset of the disease. So, the disease is most
commonly known as "Monday morning disease."
11. EPIDEMIOLOGY
• The disease is mostly confined to equidae family.
• Healthy horse is very much susceptible to the
disease.
• Occurring particularly in race horses fed heavily on
grain.
• In most instances there is a history of a period of
complete inactivity for 2 or more days immediately
preceding the onset of the disease.
13. CLINICAL
SIGNS
▪ Signs develop within 15 minutes to one hour after the beginning of
exercise, which need not be vigorous.
▪ Perhaps even only simple walking may cause the condition.
The condition is mainly seen in animals in good condition when first
worked or put into training.
(a) One limb or all the four may be affected but the common finding is
involvement of both hind legs. There is sudden cramp of the muscles of
the hindquarters. Muscles of hind limbs (quadri-ceps, femoris and
gluteus muscles) are stiff, hard and board like. There is lameness;
soreness over the rump, crouching and great restriction of movement of
hind limbs.
(b) Severe pain and distress are accompanied by stiffness of the gait,
struggling, restlessness and repeated attempts to rise.
14. CLINICAL SIGNS
14
c ) Profuse sweating
d) Respirations are rapid, pulse small and hard.
e) Temp. may rise to 40.5 deg.c in later stages. (severe cases)
f) Urine is coffee colored/ deep red brown due to presence of
myoglobin.
g) Appetite, water-intake are often normal.
16. DIAGNOSIS
▪ Severe cases present no major difficulty in diagnosis.
▪ The disease is diagnosed by history, clinical findings and clinical
pathology.
▪ The disease is differentiated with following diseases :
▪ (a) Similar lameness may occur in laminitis in which there is a history
of engorgement with grain, no discolouration of urine, sensitive
lamina of hoof is inflammed due to histamine release.
▪ (b) Reddish discolouration of the urine is more common in
haemoglobinurea over paralytic myoglobinurea .
▪ (c) Illiac thrombosis: Can be detected on rectal palpation.
17. TREATMENT
1. All possible cares should be taken so that animal is able to stand.
2. Further exercise should be avoided and slinging may be advisable
in some cases.
3. Rest must be absolute until the horse gains complete muscular
control.
4. Narcosis with chloral hydrate or (tranquilisers) may be
necessary if pain is severe or the horse makes repeated efforts to
rise. Tranquilisers may be better than chloral hydras.
5. Corticosteroids in fairly large doses are to be administered
intravenously. Thiamine hydrochloride (Vit B) is the most specific
drug because thiamine helps in lactate metabolism @ Dose. 0.5-1
g 1/m followed by 100-200 thrice daily orally.
6. The injection of Vitamin E and selenium is also recommended.
18. LACTATION TETANY IN MARES
Lactation tetany of mares (eclampsia, transit tetany) Hypocalcaemia
in mares causes lactation tetany, which is characterized by
abnormal behaviour, incoordination and tetany.
ETIOLOGY
It is very obscure disease, so actual etiology not well established but
some suggestions say that if the disease occurs within 2 weeks after
parturition, it may be due to hypoglycemia, and if late in lactation
period, them may be hypocalcemia. The condition also occurs in
horses after prolonged physical exertion or transport.
19. LACTATION TETANY IN
MARES
EPIDEMIOLOGY
The disease was more common when the draught horse breeding was
widely practised.
CLINICAL SIGNS
1. Increased excitability in mild cases.
2. Severely affected animals show profuse sweating.
3. Rapid laboured respiration.
4. Dilatation of nostrils accompanied with synchronous diaphragmatic
flutter.
5. Signs of tetany such as stiff gait, muscle tremors, inability to chew,
recumbency, convulsions and cardiac arrhythmias.
20. TREATMENT
1. In severe cases, the serum calcium is below 8 mg/dl.
Untreated lactating mares may sometime die within 24-
48 hours.
2. Slow intravenous administration of calcium
borogluconate (300-500 ml of 25% calcium
borogluconate solution) is effective in the treatment.
3. Voiding of large volume of urine is one of the early signs
of favourable response.
21. PRODUCTION DISEASES OF PIG
21
PORCINE STRESS SYNDROME
(Synonym: Malignant Hyperthermia)
It is a hypermetabolic problem in pigs affecting skeletal
muscles causing changes like rigidity of muscles,
accompanied by high rise of temperature, difficulty in
respiration, irregularity in beat followed by high mortality.
22. ETIOLOGY
22
This is related to inherited defect due to autosomal recessive gene. This
is called as sensitivity gene (HAL Gene). This gene is found in blood
groups of pigs having same chromosome.
EPIDEMIOLOGY
The lean and heavy muscled pigs are mostly susceptible.
Several factors have been incriminated for the precipitation of the
problem.
• Breed risk factor. Some animals are susceptible to halothene.
Halothene-positive a include, Landrace, Yorkshire, Duroc, Pietrain and
Poland
• Transport risk factor. Transportation for a long time having high
environmental temperature make the animals susceptible.
23. SYMPTOMS
23
Malignant hyperthermia which is observed in halotheme susceptible
animals are characterised by high rise of temperature with change in the
muscles.
Initially there is stiffness of muscles followed by rigor mortis. Along with
hyperthermia, tachycardia and tachyarrhythmia ensues resulting to death.
Excess post mortem glycolysis may produce huge lactic acid which in turn
lowers the pH.
As a result, the pale soft exudative pork develops.
There is atropy of the muscle and development of distinct spiral ridge.
24. Diagnosis
24
• This is based on history, clinical signs and laboratory analysis.
Genetic analysis-DNA analysis has been considered as a sensitive
test.
• This disease is required to be differentiated from(a) Mulberry
heart disease(b) Heat stroke(c) Viral encephalomyelitis.(d)
Septicaemic conditions (e) Hypocalcaemic tetany.
25. TREATMENT
25
The treatment for acute condition is not generally
undertaken.
(i) Specific treatment- At first attempt should be made to
eliminate the effect of stressor or anaesthetic. Dantrolene is
the drug of choice. It may be given @ 4-5 mg/kg body weight
through intravenous route.
26. TREATMENT
26
(ii) Supportive treatment-
(a) Fluid therapy has to be resorted.
(b) Sodium bicarbonate has to be administered to minimize acidosis.
(c) Cooling to be done to reduce temperature. Ice cool rectal enema
can be given.
(d) Atropine sulphate to reduce cardiac arrhythmia.
(e) Vitamin E and Vitamin-C can be supplemented to protect cell
membrane integrity.
27. HYPOGLYCEMIA / BABY-PIG
DISEASE / 3-day PIG DISEASE
27
Hypoglycaemia is one of the important
disease in new born pigs which occur due to
abrupt fall blood glucose level (less than 50
mg/dl). There is death of sizeable percentage
of piglets during first few days of life due to
acute hypoglycaemia.
28. ETIOLOGY
28
Any factors causing interference of food intake may predispose the
disease. Sows if not provided with high energy palatable ration during
gestation period may produce susceptible baby pigs. Agalactic and
dysgalatic condition of the sows will produce hypoglycaemic piglets.
EPIDEMIOLOGY
This condition may occur in calves and foals where hypoglycaemia is due
to secondary causes, septicaemia or hypothermia. Piglets in their initial
period of seven days used to suffer.
30. CLINICAL SIGNS
30
The disease is characterized by erection of hair.
Subnormal body temperature, anorexia, dullness and
excessive shivering. Torticollis, convulsion and ataxia may
be evident.
There is rigidity of head and neck muscles.
Finally coma supervenes and piglets die.
Death usually occurs within 24 to 36 hours following onset of
clinical manifestations.
31. DIAGNOSIS
31
• Characteristic clinical signs, history and estimation of
blood glucose level help to arrive at a precise diagnosis.
• The other diseases which lower the blood glucose level
should be ruled out from the diagnosis arena.
32. TREATMENT
32
• Affected piglets should be supplemented with glucose.
• 10 to 25 ml of 5% glucose should be given through
intraperitoneal route.
• This injection may be repeated at 4 to 6 hours interval till the
condition improves and piglets can suckle their mother.
• Attempt should be made to provide a warm environment
33. CONTROL
33
• Sows should be provided with rich carbohydrate diets
especially lactose diet.
• Sows fallen sick during gestation period should be treated
promptly.
• Sows should be put in warm farrowing pen during and
following farrowing.
• Sow should be selected from breeding stock in such a way
that they have higher lactational ability and very much
docile in nature.