2. BASIC CONCEPTS OF PRODUCTION DISEASES
BLOOD COMPONENTS-
Blood glucose Energy metabolism
Urea, Albumin, Hb Protein metabolism
Ca, P, Mg Major mineral metabolism
Na, K Electrolyte metabolism
Cu, Co, Iodine Trace elements
3. TYPES OF METABOLIC PROFILE TESTS
Compton Mini metabolic Individual preventive
examination
Hb Only to assess energy and
protein intake
Blood glucose
PCV Cholesterol
BUN SGOT
Glucose Blood glucose
Serum Inorganic Ca, P, Mg Serum urea Nitrogen
K & Na Albumin
Total serum protein
A : G
•Between 4-10 weeks after
calving
•Done at the interval of 4- 6
weeks.
4. SUPPLEMENTARY INFORMATION FOR MPT ( metabolic profile test)
• Individual
– Age
– Date of calving
– Milk yield and mastitis status
– Amount and type of concentrate and fodder fed/day
– Body condition
– Consistency of feces
• Whole herd
– Average daily forage intake.
– Analysis of forage and grains
– Total herd production & number of cows in milk & milk quality data.
– Individual daily yield of 6 cows during 3 consecutive peaks.
– Presence of clinical signs if any
5. INTERPRETATION OF METABOLIC PROFILE TEST
• The nutritional status of the animal in terms of energy , protein and mineral status
is being interpreted based on the data available on various blood components
1. ENERGY STATUS – GLUCOSE
• Influenced by chemical nature of carbohydrate, physical form of feed & roughage
content of ration.
• Stress, excitement, low environment temperature and corticosteroids increase the
glucose level
• Low blood glucose produces ketosis and is responsible for poor conception rate
2. PROTEIN STATUS - Urea, albumin, total protein, PCV & Hb reflect the protein status
• Globulin and total protein increase with age.
• Albumin, urea decrease with increasing age.
• Urea and Hb with PCV: Increase during summer.
• Hb and PCV inversely related to current milk yield.
• Low urea reflects low protein status
• Albumin and Hb decrease reflects long standing low protein status
• Albumin concentration related to conception rate.
6. 3. MINERAL STATUS-
• P: Tend to fall following long term insufficient dietary intake, hyperphosphatemia
occur while grazing on higher fertilized pasture.
• Ca: Vary within narrow limits. Abnormally low levels in late pregnancy indicate a
dangerous situation.
• Mg: Deprivation of feed and fall in environmental temperature produces clinical
hypomagnesaemia. Supplementation of Mg salt is protective.
• Na, K, Cu & selenium: Assessed by sampling pregnant animals receiving no
supplemental concentrates
• Physiological
• Season, milk yield & stage of lactation produce significant fluctuations.
8. INCIDENCE OF MILK FEVER
• 5-10 yrs age group most commonly affected
• High prevalence during 3 rd – 7th calving
• Jerseys breed is the most susceptible than other breeds.
• High susceptibility when animals are fed with high protein diet before and after
calving
• Complete milking in first 48 hrs- precipitating factor
• Majority cases occur within 72 hours postpartum
• Acid - diet decreases the incidences
• Alkaline diet increases the incidence
FACTORS PRECIPITATING OCCURRENCE OF MILK FEVER
• Failure of mobilization of Ca to circulation from body reserves
• Depletion of reserves by development of negative Ca balance in late pregnancy
• Increased estrogen levels – interfere with Ca mobilization from bone
• Hypomagnesaemia – decrease Ca mobilization from bone
• Coliform mastitis – toxin decreases serum Ca and P levels
9. PATHOGENESIS OF MILK FEVER
• Hyperaesthesia instead of hypersensitivity, tetany of head and limbs instead of
convulsions
• Decrease of muscle tone – vulnerability increases for prolapse of uterus or vagina
Hypothermia , depression of consciousness
• Ca:Mg is 6:1 - If serum Mg decreases these sign continues during second stage of
milk fever
• Phosphorus decrease, prolong the duration of recumbency
Clinical signs of milk fever varies with the stage of the disease
• I Stage - prodromal stage
• II Stage - Sternal recumbency
• III Stage - Lateral recumbency
10. STAGE I OF MILK FEVER-
• Excitement and tetany
• Hypersensitiveness
• Muscular tremor of head and limbs
• Disinclined to eat and move
• Grinding of teeth
• Protruding tongue
• Stiff hind limb
• Animals ataxic and falls easily
• STAGE II OF MILK FEVER
• Sternal recumbency with lateral kink
• No tetany but unable to get up
• Muzzle – dry
• Skin and extremities – cold
• Temperature – Subnormal (97-101ºF)
• Pupil – dilated – no reflex
• Eyes – disparity in the size of pupils staring and dry – pupillary light reflex decrease or
absent
• Relaxation of anus and loss of anal reflex-dung in rectum
• Circulatory system - decrease heart sound – veins cannot be raised
• Weak pulse, ruminal stasis, forced expiratory grunt
11. STAGE III OF MILK FEVER
• Lateral recumbency
• Coma
• Limbs – flaccid, unable to get up
• Pulse – impalpable
• Heart sounds – inaudible 120/min
• Unable to raise the vein
• Bloat if without treatment – animal dies within a period of 12 – 24 hrs
• Milk fever with hypomagnesaemia and hyperphosphatemia
• Tetany and hypersensitiveness beyond 1st stage
• Excitement and fibrillary and twitching of the eyelids
• Tetanic convulsion by touch or sound
• Trismus
• Heat and respiratory rate-accelerated
• Heart sound – increased
• Death occurs due to respiratory failure
• Reproductive tract
• Dilated cervix, normal presentation of fetus, uterine prolapse, dystocia, retained
placenta
12. DIAGNOSIS OF MILK FEVER
• Estimation of serum levels of Ca, Mg, P
• Ketosis (concurrent) – animal rise after Ca therapy but continue to have signs of
ketosis
• Ischemic muscle necrosis (Degenerative myopathy)
– Post mortem – pale muscle surrounded by normal color
– SGOT increase
• History of access to plant rich in oxalates
TREATMENT AND CONTROL MEASURES FOR HYPOCALCAEMIC ANIMALS
• Treatment
• Treatment during I stage – ideal
• Longer the interval between recumbency and treatment, greater the incidence of
downer cow due to ischemic muscle necrosis
• To be placed in sternal recumbency until the treatment ends to avoid aspiration
pneumonia.
• Calborogluconate 500 ml to 1 liter – 3 g/10 lb, 50% i/v, 50% s/c
• Do not milk for 6 hours.
13. Dose of Calcium
• 1 gm Ca / 45kg (100 lb)
• 25 % calcium borogluconate = 10.4 gm /500ml
• Cattle – 400-500ml i/v , 100-200 gm s/c
• Goat- 15-20 gm i/v, 5-10 g s/c
Response to Calcium therapy
• Belching
• Muscle tremor – flanks→ whole body
• Pulse rate decreases and amplitude improves
• Heart sound intensity is increased
• Sweating of muzzle
• Defecation – firm stool with mucous
• Urination does not follow until cow rises
• Wait for 5-8 hrs until it stands. If not repeat the dose
• If it doesn’t stand after 24 hrs – use hip lifters
14. Unfavourable Response to Calcium therapy
• Cardiac irregularities
• Heart rate increased
• Shallow respiration.
Prevention
• Dietary management during the transition period
• Feed low Ca (<20 g Ca /day) and normal level of P for 2 weeks prior to parturition
• Avoid drastic change in the diet (3 or 4 days time for change)
• Negative (DCAD diet) Dietary cation- anion difference programme
• Parentral vitamin D and analogs
• Vitamin D2 20-30 million units / day for 3-7 days antepartum
• 1,25 (OH2)D3 – 10,000 IU i/m / 24 hrs prior to parturition. If no delivery repeat at 24
hrs interval 270 mg until delivery
• Calcium gel oral dosing before calving, at calving and 12 and 24 h after calving
• CaCl2 40-50 g
15. ACUTE PARTURIENT HYPOCALCEMIA IN GOATS
• Etiology
• A depression of ionised calcium in tissue fluid is the basic biochemical defect in
acute parturient hypocalcaemia.
• Epidemiology
• Occurrence of acute parturient hypocalcaemia in goats is apparently rare.
• There is fall in serum calcium and phosphorus levels in all goats at kidding due to
onset of lactation
• In heavy milking goats, an absolute deficiency of calcium at any stage of lactation
will precipitate the disease.
• Milking goats get affected mostly during 4-6 years of age
• Cases occur before and after kidding, some even 3 weeks after parturition.
• Pathogenesis: Similar to dairy cows
• Clinical signs - Similar to dairy cows
16. Dignosis- Based on clinical signs
• Rapid response to calcium therapy
• Serum calcium 2 to 6 mg/dl
Treatment: 25% Calcium Borogluconate 80-100ml slow I/V
ACUTE PARTURIENT HYPOCALCEMIA IN BITCHES –
Synonym: Eclampsia, Peurperal tetany
Definition - It is a metabolic disease occurring commonly in young bitches within 2-10
days of whelping and clinically characterized by restlessness, excitement, panting
and tonic-clonic convulsions.
• Predisposing factors
• Atony of smooth muscle and skeletal muscle
• In appropriate calcium supplementation
• Heavy litter size
• Lactation in young bitches
• Toy breeds
• Neuromuscular tetany
• Concurrent hypoglycemia is the cause of signs of tonoclonic convulsions.
17. • Dignosis
• History of late pregnancy and early lactation
• Clinical signs are always observed in nursing bitches
• Characterstic symptoms
• Low serum calcium level - less than 7 mg/dl
• Low blood glucose - less than 80 mg/dl
• Treatment
• Remove the sucking puppies
• 25% calcium borogluconate 1ml/kg b.wt slow I/V
• 20% dextrose 30-50ml slow I/V
• To control Fits - Diazepam 0.5 mg /kg b.wt slow I/V
18. • LACTATION TETANY IN MARES
• Synonyms: Eclampsia, Transit tetany.
• Mortality rate is high i.e.> 60%
• Occurs in lactating mares- at about 10th day of foaling or 1-2 days after weaning
• Mares grazing on lush pasture - heavy flow of milk - more susceptible
• Hard physical work , housing wild ponies and prolonged transport are precipitating
factors
CLINICAL SIGNS OBSERVED IN LACTATION TETANY-
Severe cases -sweat profusely, difficulty in moving because of tetany and in-
coordination, stiff gait, tail is slightly raised, rapid violent respiration, wide
dilatation of nostrils, distinct thumping sound from chest(due to spasm of
diaphragm), muscular fibrillation-massseter trismus, no prolapse of membrane
nictitans.
19. • Temperature normal or increased slightly.
• Pulse rate-normal early, later elevated and irregular.
• Attempts to eat and drink, but unable to swallow.
• Urination and defecation kept in abeyance.
• Peristalsis is reduced.
• Recumbency with in 24 hrs-convulsions- die after 48 hrs of illness
• . Serum Ca: - > 8mg% - excitability ; 5-8 mg% -spasm ; <5 mg % - recumbency and
stupor
• DIFFERENTIAL DIAGNOSIS AND TREATMENT OF LACTATION TETANY
• Differential diagnosis
• Tetanus -prolapse of membrane nictitans, no relationship to recent foaling or
weaning or physical exertion.
• Laminitis - anxiety, muscle tremor, pain in the foot.
• Treatment
• Inj. Calcium solutions- complete recovery.
• Main sign of recovery-voiding large volumes of urine.
20. DOWNER COW SYNDROME
• Downer - unable to rise after 24 hrs and after 2 Calcium treatments.
• Usually occurs as a complication following hypocalcaemic parturient paresis.
• Characterised clinically by,
– Prolonged recumbency even after 2 successive Ca therapy
– Down at least for 24 hrs without any apparent reason
– Traumatic injury to limb muscles and nerves
– Ischemic necrosis of limb muscles
– Myocarditis
– Fatty infiltration and degeneration of liver
Creeper cow –
• Alert & can support on fore quarters but unable to use hind quarters after therapy
for Milk fever.
• May occur due to hypokalemia.
21.
22. Etiology –
• Traumatic injuries of muscles especially medial thigh muscle. Rupture of gastrocnemius
tissues around hip joint muscle, Obturator muscles & tendon.
• Traumatic injuries to nerves of the limbs viz., sciatic, obturator, radial and peroneus.
• Prolonged recumbency after an over long delay (> 4 hrs) in the treatment of milk fever
may result in ischemic necrosis.
• Serum electrolyte imbalance or deficit
• Persistent hypophosphatemia.
• Insufficient amount of Ca (ischemic necrosis) as treatment for milk fever
• Hypokalemia with hypophosphatemia is a typical manifestation in creeper cow (alert,
bright, crawl about but couldn’t raise).
• Toxemia in per acute or acute mastitis, acute diffuse peritonitis, uterine rupture,
aspiration pneumonia, traumatic reticulitis / pericarditis.
• Managemental causes: malnutrition, over fat, slippery floors, epidural anaesthesia.
23. • Preoteinuria indicate extensive muscle damage
• Some animals make no effort to rise
• Many make frequent effort to rise but unable to get up ( creeper) - frog like
attitude on non slippery surface (bare ground or damp bedding)
• Some cases are able to stand with assistance (lifting on tail head or hip slings)
• In some cases, hind legs are extended on each side and reach up to elbow joint
(due to dislocation of hip joint or traumatic injuries surrounding hip with or without
rupture of ligaments)
• Diagnosis
• A thorough clinical and laboratory examination is required
• Arrived at after eliminating all known causes of recumbency in a cow which had
milk fever and failed to rise with in 24 hrs following 2 successive course of
treatment
24. TREATMENT FOR DOWNER COW SYNDROME
• Treatment is not specific but symptomatic
• Inj. Magnesium salts, Po4, corticosteroids.
• Vitamin E and Se
• Solutions containing K, P, Ca, Mg
• Fluid therapy- oral and parental
• Turn the cow from side to side
• Physiotherapy to avoid muscle damage
• Non slippery ground surface
• Antibiotic for septic conditions
• Anti inflammatory
• Lifting devices.
25. BOVINE KETOSIS
• Nutritional or metabolic disease in high yielding cows in early lactation results in
negative energy balance.
• Failure to provide sufficient glucose on heavier demands of glucose and glycogen, than
can be met by their digestive and metabolic activity.
Dysfunction of adrenal gland & Relative hypothyroidism------ Stress of parturition, lactation
(cattle) and stress of late pregnancy (in ewes) and stress of malnutrition leads to
decreased ACTH activity.
• Composition of ration - ensilage (high in butyric acid) are more ketogenic than hay.
• High protein diets produces more butyric acid.
• Animals in 4 -10 weeks post-partum, peak milk yield and decreased dry mater intake
are prone for ketosis.
• Starvation decrease propionic acid (relative) resulting in excessive utilization of fat.
• Hepatic insufficiency - primary or secondary . Hypoglycemia results in mobilization of
fat & its deposition in liver - perpetuation of hepatic insufficiency.
26. • OVINE KETOSIS
• A disease of intensive farming system and relatively rare in grazing units.
• Ketosis in goats - identical with ovine ketosis
• Etiology
• Increased plasma cortisol due to environmental and nutritional stress, failure by
liver to metabolize the cortisol.
• Decline in plane of nutrition during last 2 months of pregnancy.
• Exposure to inclement weather , cold
• Worm load Eg. Haemonchus contortus.
• Epidemiology
• Highly fatal, mostly during last month of pregnancy
• Ewes carrying more than 1 lamb are more susceptible
• Precipitating factor - fall in plane of nutrition and short periods of starvation up to
48 hours (by management), cold inclement weather.
27. EPIDEMIOLOGY OF KETOSIS
• Ketosis is of two types - Primary (Estate acetonemia) and secondary
• Primary (estate acetonemia)
– Excessive feeding of ensilage
– Inadequate exercise
– Over fatness at calving time
– Inadequate energy intake during early lactation
– Specific dietary deficiency of cobalt (essential for metabolising propionic acid),
phosphorous and vitamin B12
• Secondary ketosis is caused by
– Reduction in appetite
– Abomasal displacement
– Traumatic reticulitis
– Metritis
– Mastitis
– Fluorosis
28. Ketosis in cows is mostly sporadic
• Most common during 1st month of lactation
• Less common during 2nd month of lactation
• Occasionally during late pregnancy
• Higher frequency in 20 - 30 days of calving
CLINICAL FINDINGS IN KETOSIS - Bovine ketosis
• Wasting form-
• Gradual but moderate decrease in appetite and decreased milk yield over 2-4 days
• First refuse grains, ensilage but continue to eat hay.
• Woody appearance (due to loss of cutaneous elasticity and s/c fat)
• Normal temperature, pulse and respiratory rate
• Ketone odour from mouth and milk
• Staggering and partial blindness may occur transiently.
• Spontaneous recovery in about a month, but milk yield never return to normal
level; sharp drop in SNF content of milk in wasting form.
29. Nervous form
• Suddenly appear Bizarre, delirium, walking in circles, straddling or crossing of legs, head
pushing or leaning onto stanchion, apparent blindness, aimless movements, wandering,
vigorous licking of the skin and inanimate objects
• Chewing movements with salivation
• Hyperaesthetic- bellowing on pinching or stroking
• Moderate tremor and tetany
• Nervous sign usually occur in short episodes which last for 1 or 2 hrs and may recur at
intervals of about 8 to 12 hrs
• Affected cows may injure themselves during the nervous episodes
• Ovine and Caprine ketosis
• Similar to nervous form of ketosis in cows
• Separate from flock and apparent blindness (alert but disinclined to move).
• Grinding of teeth
• Later stages - more severe nervous signs, tremors of muscles of head, twitching of lips,
champing of jaws and salivation
• Clonic contraction of cervical muscles, dorsal flexion or lateral deviation of head,
circling, convulsions spread to the whole body.
• Recurrent attack and drowsiness between convulsions
• Star gazing, incordination, falling when attempting to walk
• Smell of ketone in breath.
• Course: become recumbent in 3-4 days and then coma for 3-4 days
30. Field test (Rothera’s reaction) : Milk and urine can be tested.
It measures only Aceto acetic acid.
ß hydroxybutyric acid – no reaction
Acetone - very little reaction
Primary ketosis - strong colour
Secondary ketosis - moderate reaction
31. Metabolite Level when diseased Normal
Primary hypoglycemia
Secondary hypoglycemia
20-40mg/dl
>40 mg or above normal 50mg/dl
Ketones - Primary 10-100mg/dl Up to 10 mg / dl
Ketones - Secondary < 50 mg /dl
Urinary ketones
(primary/secondary)
80-130 mg/dl 10-70 mg/dl
Milk ketones Average 40mg/dl 3 mg/dl
Liver glycogen Low
Glucose curve Normal
VFA in blood and rumen Increased
32. • DIAGNOSIS OF KETOSIS
• History with reference to time of calving, duration of pregnancy in
ewes, feeding program
• Biochemical examination reveals hypoglycemia, ketonemia and
ketonuria
• In cases of sub clinical ketosis: Ketonemia with absence of clinical
signs
• Differentiate secondary ketonuria due to
– TRP,
– Bovine pyelonephritis,
– Indigestion,
– Abomasal displacement,
– Metritis and
– Mastitis.
• Nervous form of ketosis should be differentiated from Listeriosis
and Rabies.
• Ovine ketosis: die within 6-7 days
33. • TREATMENT REPLACEMENT THERAPY
• 50 % glucose 500ml I/V, 20 % glucose I/P,
• Propylene glycol or glycerine @ 225 mg / day for 2 days then 110 mg / day for 2
days.
• In sheep, common complication is acidosis. So sodium bicarbonate is to be given
along with replacement therapy.
• Sodium propionate 110 -225 mg/ day, but shows very slow response.
• Lactates: Ca or sodium lactate 1 kg initially, later ½ kg / day for 7 days or
• Sodium acetate 110-500 g/day.
• Ammonium lactate 200g/day for 5 days.
• Anabolic steroids: Effective treatment for pregnancy toxemia of cows. Trenbolone
acetate @ 60mg to 100 mg as single injection.
• Insulin with glucose or glucocorticoids 200 – 300 I.U. Repeat every 24 – 48 hrs.
There is no marked therapeutic advantage.
34. • MISCELLANEOUS TREATMENTS
• Chloral hydrate- Initially, 30 g orally as capsule, later 7 g bid for several days as
drench in molasses or water. It breaks the starch in the rumen and stimulates
production and absorption of glucose. Also, selectively influence rumen
fermentation to produce more of sodium propionate.
• Potassium chlorate can also be given but in some cases it causes severe diarrhea.
• Vitamin B12 and cobalt - for the activation of coenzyme A.
• Monensin sodium enhances the propionate production in the rumen. Dose
25mg/day in grain feed mix.
CONTROL MEASURES FOR KETOSIS
• Ration should contain Co, P and I2.
• Avoid wet ensilage or mouldy hay or dusty hay ( as they have increased levels of
butyrate). Prophylactic feeding of sodium propionate @ 110g daily for 6 weeks.
• Sodium propionate 110 g/ day for 6 weeks
• Propylene glycol @ 350 ml / day for 10 days after serving or 6% of concentrate
ration for 2 months.
• Blood glucose and milk ketone estimation during 6th week of lactation.
35. HYPOMAGNESEMIC TETANY
Characterised by
• Hypomagnesaemia & Hypocalcaemia.
• Clinically clonic-tonic spasms and convulsions, death due to respiratory failure.
• Tetany associated with depression of Mg.
Two types
• Whole milk tetany -due to specific deficiency of Mg in diet.
• Lactation tetany - due to partial dietary deficiency i.e. nutritional / metabolic factors
that decrease availability or increase body loss
Etiology of hypomagnesemic tetany
• Short period of starvation (24-48 hrs).
• High Po4 intake competes with Mg absorption (cereals rich in K, lush green).
• Loss of Mg in milk, urine & digestive secretions.
• During inclement weather (cold, wet, windy weather), hyper activity of thyroid.
• Cows turned out to lush pasture during spring after closed housing in winter.
• Grazing on young green cereal crops may cause wheat pasture poisoning.
• Dry cattle or beef cattle running at pasture in winter time, when nutrition is usually
inadequate.
36. • CLINICAL SIGNS OF HYPOMAGNESEMIC TETANY
• Acute
• Cease to graze, posture of unusual alertness, twitching of muscles and ears.
• Severe hyperesthesia - even a slight disturbance can precipitate attack, continuous
bellowing, frenzied galloping.
• Falls with tetany of limbs, clonic convulsions, nystagmus, champing of jaws, frothing at
the mouth, pricking of ears, retraction of eyelids
• Temperature - 40 to 40.5ºC.
• Pulse and respiratory rates increased.
• Intensity of heart sounds audible at some distance from cow.
• Death in ½ - 1 hr
• Sub acute
• Gradual onset - 3 to 4 days, Inappetence, Decreased milk yield
• Wildness of facial expression.
• Retraction of head and trismus.
• Sudden movement, noise, restraint and injections can precipitate violent convulsions.
• Treatment is usually effective with marked tendency to relapse.
• Chronic
• Serum Mg decreased
• No clinical signs, but sudden death.
• Paresis / milk fever like syndrome (in lactating cattle) but not responding to Calcium
treatment.
37. Clinical pathology
• In clinical cases- serum Mg level will be from 0.3 to 0.7 mg%. (Normal: 1.7 to 3 mg.)
• Estimation of Ca:Mg ratio in bone. Normal is 70:1
• Decreased levels of CSF Mg (sample can be collected upto 12 hrs after death).
• Low Urine Mg is a good presumptive evidence
Treatment -
• 10% MgSo4 - 100 ml s/c gives only a transient effect and should be followed with
feed supplement
• Narcosis with chloral hydrate
• Tranquilizers
• Morphine to avoid respiratory paralysis
• 50% MgSo4 50-100 ml s/c on one side and Ca borogluconate -150 ml on other side
• Calcium magnesium preparation - 25%: 500 ml i/v followed by concentrated
solution of 50 % MgSo4 200 ml s/c (or) 20 % Mg So4: 200-300 ml i/v
38. NUTRITIONAL HAEMOGLOBINURIA/ POSTPARTURIENT HAEMOGLOBINURIA
• A disease of high producing dairy cows occurring soon after calving & is
characterised by intravascular hemolysis, haemoglobinuria and anemia.
Etiology
• Ration low in P, hay and grass from low P area, draught
• Cu deficiency (incidence reduced when supplemented)
Precipitating factor
• Grazing Brassica sp. plants, rape and turnip and other cruciferous plants, large
quantity of beet pulp, sugar cane top (low in p).
• Exposure to cold weather, cold water - erythrocytes becomes more sensitive to
hemolysis when there is hypophosphatemia & hypocupremia
• Epidemiology
• Prolonged hypophosphatemia is an important predisposing factor
• 'P' deficient soil and drought condition act as precipitating factors
• 50% mortality and 40% morbidity
• Animals in 3-6th Lactation are more prone
39. • Haemoglobinuria and hemolysis does not occur always. Death is mainly due to
anemic anoxia.
• The possible role of Cu and Se deficiency in hypophosphatemia is unclear. In cases
of Cu deficiency, there will be microcytic hypochromic anemia.
• Cu and Se provide protection against effects of orally acquired hemolytic agents of
cruciferous plants.
40. Acute cases
• Rapid onset after 2-4 weeks of calving, course is 3-5 days, red coloured urine,
anorexia, weakness, severe depression of milk yield.
Less acute cases
• Eats and gives milk for 24 hours after red coloured urine.
• Dehydration occurs quickly.
• Haemoglobinuria, inappetence, severe depression of milk yield.
• Temperature – Normal or raised (40ºC).
• Mucous membrane – pallor, later yellow.
• Dyspnoea is obvious.
• Gangrenous necrosis of tail, feet, pastern, ear and teeth (occasionally).
• Milk yield reduced.
• Suffer for 2-3 days and then recumbent followed by death in few hours /days.
If survive
• Weakness and Pica only during convalescence.
• There may be additional sign of 'P' deficiency is recumbency.
• Infertility, Pica, Fall of milk yield.
41. NUTRITIONAL HAEMOGLOBINURIA
• Non-lactating animals of the affected herd in marginal 'P' deficiency area may have
normal range of inorganic P (4-7 mg %).But, lactating animal my have moderately
low levels of 2-3 mg.
• R.B.C decreased – Heinz body seen.
• Urine: Dark red brown to black, moderately turbid, No R.B.C.
• Low Cu in blood & liver.
PM changes
• Jaundiced carcass
• Blood: Dark and thin
• Swelling of spleen
• Liver: Fatty infiltration, swollen
• Dropsy in lower part of the body
• Discolored urine in bladder
42. Differential
• Characteristic clinical signs like hemolytic anemia, haemoglobinuria within 4 weeks
of parturition.
• Deficiency of P
Differential diagnosis
• Parasite – Babesia, Theileria
• High altitudes
• Copper Poisoning
• Plant – Rape
• Bacteria: Anthrax, Leptospira, Bacillary Haemoglobinuria
• Virus – Rinderpest
• Enzootic haematuria
• Myoglobinuria
• Chronic hill haematuria
• Blood transfusion
• Metabolic ketosis
• Pyelonephritis
43. Treatment
• Blood Transfusion (5 to 10 liters) → followed by fluid therapy to prevent
haemoglobinuric nephrosis.
• Acid sodium phosphate 60 gm in 300 ml i/v very slow+ same dose s/c . Further s/c
inj at 12 hours interval for 3 times.
• Orally drench 30 gm Sodium acid Po4 BID.
• Copper glycinate 500mg i/v in copper deficiency cases
• Haematinics during convalescence.
• Bone meal 120 g BID / Dicalcium Po4.– orally for 5 days
• Prevention
• Copper gluconate 120 mg s/c.
• Remove the cruciferous plants.
• Adequate intake of 'P' during early lactation.
44. AZOTURIA
• Synonyms: Paralytic myoglobinuria.
• It is a disease of horses occurring during exercise after a period of inactivity on full
ration. It is characterized by myoglobinuria and muscular degeneration.
• Large stores of glycogen are laid down in muscles during a period of idleness and when
exercise is taken the glycogen is rapidly metabolized into lactic acid.
• Nutritional deficiency of vitamin E and Selenium have also been suggested as a cause.
45. AZOTURIA
• Sporadic cases occur particularly in race horses fed heavily on grains.
• In most instances, history of complete inactivity for 2 or more days immediately
preceding the onset of disease.
• Draft horses on rest because of minor injuries are often maintained on full work
ration and become affected when taken back to work.
• Mycotoxins were also suggested as a predisposing factor, but supporting evidence
was not available.
PATHOGENESIS OF AZOTURIA-
• Gluteal muscles are commonly involved due to their high content of glycogen.
• Myopathic lesion cause pressure on the sciatic nerve and other crural nerve.
46. • Necrotic muscle fibers, hard, painful swelling of the large muscle masses result in
secondary neuropathic degeneration of rectus femoris and vastus muscles leading
to myoglobin liberated from the necrotic muscle fibers followed by dark red brown
urine.
• Death due to decubital septicemia or myohemoglobinuric nephrosis and uremia
and degeneration of myocardium.
CLINICAL SIGNS OF AZOTURIA –
• Signs develop within 15 minutes to 1 hour on work. Signs may disappear in few
hours if the horse is given complete rest immediately, but the condition usually
progress to recumbency.
• First assume a dog sitting posture followed by lateral recumbency.
• Severe pain, restlessness, struggling and repeated attempt to rise.
• Quadriceps femoris and gluteal muscles are hard and board like.
• Urine-dark brown colour.
• Lameness-restriction of hind limbs movement. If exercise is stopped as soon as
lameness occurs the horse may recover in 2-4 days.
47. • TREATMENT FOR AZOTURIA
• Further exercise should be avoided.
• Effort should be made to keep the horse standing.
• Narcosis or chloral hydrate (if pain).
• Corticosteroids I/V.
• Thiamine HCl 0.5 gm I/M- gives favorable results.
• Antihistamines, vitamin E injection.
• Sodium bicarbonate orally or I/V- to keep the urine alkaline to avoid putrificaton of
myoglobin in renal tubules.
• Hot fomentation to affected part.
48. CALF HOOD DISEASES
• These are divided into
– Early postnatal diseases (within 48 hours of birth)
– Delayed postnatal diseases (2-7 days of age)
– Late postnatal diseases (1-4 weeks of age)
• Early postnatal diseases
• Most diseases occurring in this period are non-infectious and metabolic. Eg.
Hypoglycemia and hypothermia due to poor mothering.
• Hypothermia due to exposure to cold and low vigor in neonates due to
malnutrition
• Congenital diseases
– Neonatal rickets
– Goiter
– Croocked calf disease
49. • Delayed postnatal disease
• It is due to failure of passive transfer of colostral immunoglobins.
– Colibacillosis
– Joint ill
– Salmonellosis
– Viral enteric Infections
• Rota virus
• Corona virus
• Late postnatal diseases
• Septicemic disease
• Enteric disease
• Respiratory disease
• Cryptosporidiosis
• White muscle disease
• Ascariasis
50. Diseases of muscles
1. MYASTHENIA (SKELETAL MUSCLE ASTHENIA)
• The common causes of myasthenia in farm animals are
– Ischemia in iliac thrombosis in the horse and after recumbency in cows with
parturient paresis. The end stage of myonecrosis and not reversible.
– Toxins: general toxemia is a cause
• Metabolic effect on muscle fibers include hypokalemia, hypocalcemia and possibly
hypophosphatemia, hypoglycemia in new born pigs and lactic acidemia after
engorgement of grains.
51. 2. Myopathy
• The term myopathy describes the non inflammatory degeneration of skeletal
muscles which is characterized clinically by muscle weakness and pathologically by
hyaline degeneration of the muscle fibers.
• Etiology
• A nutritional deficiency of vitamin E and selenium ( enzootic nutritional muscular
dystrophy) is a common cause in calves, lambs, foals and piglets.
• Exertional or post exercise rhabdomyolysis in horses after unaccustomed exercises
or insufficient training.
• Degenerative myopathy – in new born calves, sheep and goats.
• Toxic agents
• Ischemia
• Neurogenic
• Neoplasms
• Pathogenesis- primary myopathy varies from hyaline degeneration to coagulative
necrosis, affecting particularly the heavy thigh muscles and the muscles of the
diaphragm.
• Myocardial lesions are also commonly associated with the degeneration of skeletal
muscles
52. Myoglobin is excreted in the urine and myoglobinuric necrosis is an important
complication, particularly of acute primary myopathy.
• In Exertional rhabdomyolysis in horses there is enhanced glycolysis with depletion
of muscle glycogen, the accumulation of large amount of lactate in muscle and in
blood and development of hyaline degeneration of myofibers.
• In Secondary myopathy due to ischemia, there may be multiple focal areas of
necrosis which cause muscle weakness and results in an increase of muscle
enzymes in the serum.
• In neurogenic atrophy of muscle, there is flaccid paralysis, a marked decrease in
total muscle mass and degeneration of myofibers with failure to regenerate unless
the nerve supply is atleast partially restored.
53. CLINICAL FINDINGS OF MYOPATHY
• Primary myopathy
• Sudden onset of weakness and pseudoparalysis of the affected muscles, causing
paresis and recumbency and in many cases accompanying respiratory and
circulatory insufficiencies.
• Cardiac irregularity and tachycardia may be evident, and myoglobinuria occurs
in horse and yearling cattle.
• The affected skeletal muscles in acute cases may feel swollen, hard and rubbery
but in most cases it is difficult to detect significant abnormality by palpation.
• Acute cases of primary myopathy may die within 24 hours after the onset of
signs.
• Acute nutritional myopathy
• Muscle stiffness and pain, myoglobinuria, edema of the head and neck,
recumbency and death in a few days.
• Lethargy and stiffness of gait are characteristic of less acute cases.
54. Tying-up
• In Tying – up in horses there is a very sudden onset of muscle soreness 10 -20
minutes following the exercise. There is profuse sweating and the degree of
soreness varies from mild, in which the horse moves with a short, shuffling gait, to
acute, in which there is a great disinclination to move at all. In severe cases horses
are unable to move their hind legs and swelling and rigidity of the croup muscles
develops. Myoglobinuria is common.
Post anaesthetic myositis
• Recovery is prolonged and when initial attempts are made to stand there is lumbar
rigidity, pain and reluctance to bear weight. The limbs may be rigid and the muscle
firm on palpation.
Hyperkalemic periodic paralysis
• Myotonia with prolapse of the third eyelid.
• In secondary myopathy due to ischemia – the affected animal is unable to raise
and the affected hind limbs are commonly directed behind the cow in the foreleg
attitude.
• In neurogenic atrophy there is marked loss of function in the total mass of muscle -
flaccid paralysis, loss of tendon reflexes and failure of regeneration.
55. CLINICAL PATHOLOGY OF MYOPATHY
• Creatinine kinase is a highly specific indication of both myocardial and skeletal muscle
degeneration. CK has a half-life of about 4-6 hours.
• The level of AST is also increased following myopathy but because the enzyme is
present in other tissues such as liver, it is not a reliable indicator of primary muscle
tissue degeneration. Because AST has longer half-life than CK, the level of AST may
remain elevated for several days following acute myopathy.
• TREATMENT FOR MYOPATHY
• Vitamin E and selenium are indicated for the treatment of nutritional muscular
dystrophy.
• Supportive therapy for any case of myopathy, particularly severe cases in which
there is persistent recumbency, consists of:
– Liberal quantities of thick bedding
– Removal from solid floors to softer ground.
– Frequent turning from side to side to minimize secondary myopathy.
– Provision of fluid therapy to prevent myoglobinuric necrosis.
– Palatable nutritious diet.
