Metabolic
Diseases
Prof. Dr
Hamed Attia
How Can You succeed
in treatment A Case
1- Diagnosis
2-Correct
Treatment(25%).
‫الصحيح‬ ‫العالج‬
‫النجاح‬ ‫عوامل‬
1-Method of diagnosis
1-Correct Diagnosis
(75%).
‫الجيد‬ ‫التشخيص‬
.1-Case history
2-Clinical
examination
3-Laboratory
examination
1-Correct Diagnosis
 Animal
Housing
Feed and
water supply
1- Correct Case History
{َّ‫ن‬ِ‫إ‬ َ‫و‬ََِّّ‫ه‬ِ‫ن‬‫و‬ُ‫ُط‬‫ب‬َّ‫ِي‬‫ف‬َّ‫ا‬‫ِّم‬‫م‬َّ‫م‬ُ‫ك‬‫ِي‬‫ق‬ْ‫س‬ُّ‫ن‬ًَّ‫ة‬َ‫ْر‬‫ب‬ِ‫ع‬َ‫ل‬َِّ‫ام‬َ‫ع‬ْ‫ن‬َ‫ِيَّاأل‬‫ف‬َّْ‫م‬ُ‫ك‬َ‫ل‬‫ن‬ِ‫م‬َََّّ‫ين‬ِ‫ب‬ ِ‫ار‬‫ِلش‬‫ل‬َّ‫ا‬ً‫غ‬ِ‫ئ‬‫آ‬َ‫ًاَّس‬‫ص‬ِ‫ل‬‫ا‬َ‫اَّخ‬ً‫ن‬َ‫ب‬‫َّل‬ٍ‫دَم‬ َ‫ٍَّو‬‫ث‬ ْ‫ر‬َ‫ف‬َِّ‫ْن‬‫ي‬َ‫ب‬}
milking machine.milking machine.
َّ‫ًا‬‫ص‬ِ‫ل‬‫ا‬َ‫اَّخ‬ً‫ن‬َ‫ب‬‫ل‬‫ا‬ً‫غ‬ِ‫ئ‬‫آ‬َ‫س‬َََّّ‫ين‬ِ‫ب‬ ِ‫ار‬‫ِلش‬‫ل‬
Metabolic Disorders
2- Udder œdema
1- Hypocalcemia (Milk Fever)
2- Ketosis (Acetonemia)
1- Fatty Liver Syndrome
3- Retained Placenta
1-Energy-Related
Disorders
2-Minerals & Vitamins-Related
Disorders
What is milk fever?
Definition:
a metabolic disorder which
results from a temporary loss of
the calcium in the blood stream.
Hypocalcemia
Normal Blood Ca
Lethargy (dullness and listless behavior)
unsteady gait
Unable to stand
Coma and death
9 - 11
8 - 9
7
6
4
Signs
Blood Ca
(mg/100 ml)
Sub-clinical
hypocalcemia
Clinical
hypocalcemia
(Milk Fever)
calcium
Physiological function of calcium:
Formation of bone and milk.
Essential in the clotting of blood
Maintenance of neuromuscular
excitability.
Essential for muscle contraction.
A-Sub-clinical hypocalcaemia
 It occurs in the late
stages of pregnancy
 With History of:
 Decrease of ruminal
wall (signs of
indigestion).
(passage of small
semisolid feces).
 .
After parturation
With History of:
 Retained placenta
 , uterine prolapse
 Decrease of
ruminal wall.
(passage of small
semisolid feces).
B-Clinical hypocalcaemia
Etiology:
 Excessive loss of Ca in the colostrum .
 Impairment of absorption of Ca from the
intestine at parturition.
 Deficiency of vitamin D .
 Increase Ca feeding during the dry period
 Pre-partum diet high in phosphorus .
 Dietary anion cation balance : Diets high in
(Na, K)
 4) Acidosis and diarrhea reduce calcium
absorption.
Clinical findings
There are three stages of the disease:
The first stage:
 Hypersensitivity, musclar tremors .
 Stiffness in gait, difficult to stand or move .
 Shaking of the head, protrusion of the tongue
and grinding of the teeth.
 Normal or slightly elevated temperature due to
hyper-excitability.
 Anorexia, rumen stasis, absence of defecation
Second stage
(Sternal recumbancy)
 The cow is unable to rise.
 Depression of consciousness.
 Lying on sternum and the head turned into the flank.
 Reflexes are absent with protrusion of the tongue .
 Absence of papillary light reflexes and anal reflex.
 Bloat, rumen stasis and constipation.
 Subnormal temperature (36-38˚C)
 Deep and irregular breathing.
Sternal recumbancy
SternalSternal
recumbancyrecumbancy
Third stage
(Lateral recumbency stage)
Lateral recumbency.
bloat.
Subnormal temperature (35 –
36.5˚C)
Coma death.
Treatment
 (A) Hygienic treatment:
 1) Ample space should be provided with soft clean
bedding under sternum.
 2) Clean water supply.
 3) Easy digested food. Using stomach tube to avoid
aspiration pneumonia.
 4) Rotate the affected
animal from side to side
to avoid tympany and
hypostatic congestion.
(B)-Medical treatment
 1)Source of Calcium A-
Small cow(300- 400 Kg):
R/500 ml (375 ml IV very
slowly and
125 ml SC after 30 min. at
different sites.
 Large cow( More than
500 Kg B .w.)
 1 Liter:
 ½ Liter at morning
 ½ Liter at evening
Examples of Ca preparation R/Ca boro-gluconate (20% or 25%)
 Or
R/ Cal. D. Mg (Ca & Dextrose & Mg)
R/Calcium amino-plex (Ca & amino acids).
NB:
 I/v Ca solution should be slowly to prevent
cardiac arrest.
 Continue for 3-5 days days or till complete recovery
(2) Compounds which increasing calcium
level in blood:
R/ AD3E&C (10 ml / daily IM).
& R/ACTH 400-500 IU I/M
3) Anti-inflammatory (Non Steroidal)
R/Declo-phenac Na 2.5% 4 ml/100 Kg B W.
(4) Supportive treatment:
R/Dextrose 25% or 40% 2 liter IV.
Downer Cow Syndrome
1-ALERT DOWNERS
Calving paralysis
Fractures
Hypocalcemia
Hypomagnesemia
Hypophosphatemia
Simple indigestion
II-Downer with depression
Impaction
Severe hypocalcemia
Severe hypomagn.
Severe .Toxic mastitis
Dehydration
Toxic metritis
Uterine torsion
1-Hypophosphatemia
Post Parturient Hemoglobinuria
(Red Water)
1-Definition
 It is a metabolic hemolytic disease of cattle and
buffaloes characterized clinically by
hemoglobinuria and anemia and biochemically by
intravascular hemolysis and hypophosphatemia
2-Incidence and occurrence
(1) It is usually occur 2-4 weeks after
parturition in cows and in mid-term of
gestation in buffaloes.
(2) Animals are susceptible between fifth
and tenth calving.
(3)It is usually occurs at the end of
barseem season (April-May)
3-Causes
 (1) Diets low in phosphorus or unsupplemented
with ph.
 (2) Feeding of cruciferous plants such as
Barseem, grass, turnips, (contain thiocyanites as
toxins) and carbage (contains thiouracil as
toxins).
Clinical findings
 (1) Colour of urine may vary from
light brown in mild cases to deep
red or coffe coloured in severe
cases.
 (2) In-appetence, pica, dull,
depression and weakness develop
suddenly.
 (3) Severe depression of milk yield
(although in some less cases, the
cow continues to eat and milk
normally for 24 hours after
discoloration of the urine. Milk
may be
 (4) Dehydration develops quickly.
 (5) MM are pale and anemic or
icteric in sever cases
 (6) the cardiac impulse and
jugular pulse are much
augmented with tachycardia.
 (7) Cessation of rumination and
constipation
 (8) The feces are usually dry and
firm.
 (9) Dyspnea due to anemic
anoxia.
 (10) The course of the acute
disease extends from 3-5 days, the
cow becomes weak and stagger
and finally recumbent (Downer).
Complications
 (1) Gangrene and sloughing of the tips of the
tail or teat or ear or the digits.
 (2) Ketosis commonly occurs.
 (3) Death may occur within a few hours or
days, in non-fatal cases, convalescence
requires about 3 weeks and recovering animals
often show pica.
Main Line of Treatment
Hyagenic Medical Supportive T
To Success in Treatment
Correct
Diagnosis
Drug Used Dose&
Route of adm.
Duration
‫النجاح‬ ‫عوامل‬
‫حالة‬ ‫عالج‬ ‫قى‬
Medical
Source of ph Hematincs Saline
1-Source of ph
I/V&I/M S/C Orally
2-Hematinics
A-Blood transfusion
(In sever cases) Iron & VitB12.
(1) Sources of phosphorus
 A) IV slowly administration of 60
of sodium acid phosphate in 300
ml of distilled water on the first
day .
 Followed by further SC injections
of similar doses at 12-hours
intervals till recovery.
 Similar daily doses (60 g) by
mouth
NB:
Treatment should be continued till 3-5 days
after disappearance of red urine (complete recoverty)
B) patent phosphorus preparation as:
R/ Tonophosphan (Ph 10%)
R/ 50ml( 25 ml IV daily&25 ml I/M till
recovery).
C) Oral dosing with bone meal (120 g)
twice daily or dicalcium phosphate daily
for 5 days till recovery.
Or:
Superphos Sachets 3
One sachet daily (oral route)
(2) Hematinic preparation:
 (A) in sever cases:
 Blood transfusion 3-4 L of whole blood to a 450
kg cow is indicated in severe cases.
 Additional transfusion is necessary if cow is still
weak and mucous membranes are pale.
 (B) In less sever cases:
 iron, copper, cobalt, vitamin B12 ) .4) R/Antoplex
15 ml I/M
1-General symtoms
 1-Stiff leg.
Stiffness in gaite and arched
back.
 2-Poor growth rates.
Animals do not grow as well as
pasture conditions indicate.
 3-Coat and condition.
Rough, coarse coat and are in
poor condition.
 4-Not eating barseem
Partial loss of appetite
Chronic ph def
Delayed onset of puberty , Delayed
postpartum estrus, Repeat breeding.
& Increase incidence of cystic follicles .
5-Reproductive abnormalities
‫الجاموس‬ ‫فى‬ ‫تحدث‬ ‫الظاهرة‬ ‫هذه‬
‫شهرمارس‬ ‫فى‬-‫عام‬ ‫كل‬ ‫من‬ ‫ومايو‬ ‫ابريل‬
Main Line of Treatment
 1-Ph source
 R/Phospho-nor tonic 20- 30 Ml I/V or I/M
‫اسبوع‬ ‫لمدة‬ ‫يوميا‬ ‫الحقن‬
 2-Steroidal anti-inflammatory
 R/Dexamethasone 10Ml I/V
 (daily for 4 days).
 3-Treatment of ketosis:
 R/Dextrose 25% 2 Liter I/V
 R/Propylene Glycol ¼ Liter Orally
 (Or Glycreine or Treacle)
3-Hypomagnesemia
(Grass tetany-Grass stager-
Lactating tetany)
 It is a highly fatal metabolic neuretic disease in
adult ruminant and nutritional deficiency disease in
calves (milk tetany or calf tetany).
 It is characterized biochemically by
hypomagnesemia and clinically by hyperaesthesia,
tetany and convulsions, and finally death .
1-Definition
 (1) Lactation tetany: More common in mare than cow
which give profuse amount of milk with ingestion of
excessive green grass.
 (2) Grass tetany : It occurs in animals maintained on
green grass or newly grown grass which are deficient in
Mg.
 (3) Milk tetany (Whole milk tetany): It occurs in calf
fed on milk diet.MM
Classification according
to the causes:
 Decrease in Mg level :
 (1) Feeding on diet or food deficient in magnesium.
 (2) Reduced food intake (decrease dietary Mg
contents) or decrease in the amount of absorbed Mg.
2-Main causes
 The disease may be acute, subacute and chronic:
 [1] Acute lactation tetany:
 (1) The animal may be grazing and suddenly cease to
graze and appear uncomfortable with twitching of the
muscles and ears.
 (2) Severe hyperaesthesia so that any slight
disturbances such as sudden noise or touch leads to
attacks of continuos bellowing and frenzied
galloping.
 (3) Staggering gait then fall down on the ground with
obvious tetany of the limbs which is rapidly followed
by clonic spasm and convulsions lasting for about a
minute.
Clinical findings
 (4) During the convulsive
episodes there is opithotonus
(Back head), nystagmus
(rotation of eye ball),
champing of the jaws,
frothing at the mouth,
pricking of the ears,
retardation of the eye lids.

Clinical findings
 Between episodes the animal lies
quite but a sudden noise or
touch stimulate another attack.
 (5) The temperature rises (40 to
40.5ºC) after severe muscle
exertions.
 (6) Death usually occurs (from
respiratory failure) within a half
to one hour .
 the mortality rate is high.
 (1)It is common in pregnant
buffaloes, there is slight
inappetence, wildness of the
facial expression and
exaggerated limb movements.
 (2) Stagger gait or stiffness of
the limbs
 (3) Loss of appetite which
accompanies by rumen stasis
and decrease in milk yield.
[2] Subacute lactation tetany:
Hypomagnesmia
1-Hygienic treatment:
Complete rest of the affected animal
in quite place.
2-Medical treatment:
 (A) Source of magnesium:
 By IV (200-300 ml of 5%) solution
of Mg sulfate. (It causes rapid rise
in serum Mg within 3-6 h) followed
by SC injection of 200-300 ml of
20% solution of Mg sulfate.
5-Treatment
 (B) A magnesium-rich enema: 60 g of Mg Cl in
250 to 500 ml of warm water results in rapid
absorption of Mg.
 (C) Oral Mg oxide:
 60 g for 5 to 6 days as an alternate form of
therapy.
 (D) Tranquilizer and narcotics :
 R/Complene 3-4 ml I/M
 3-Supportive treatment:
 R/Dextrose 25% 1-2 L I/V daily for 3-4 D
 R/Tri B (B1,B6,B12) ampoules
one pox daily I/M for 4-5 days
 Definition :
 It is a nutritional disease in
calves 2-4 months of age or
older which are fed only a milk
diet (Milk is low in magnesium
and gives adequate Mg for the
requirement of growing calf up
to 50 Kg).
2-Milk tetany
tetanyCalf
 (1) The animal suddenly cease
to graze and twitching of the
muscles of the jaws and ears.
 (2) Hyperthesia: bellowing,
general spasms and convulsion
with great fear.
 (3) Stagger gait and fall down
on the ground with tetany and
or paresis of the limbs and
convulsions.
 (4) Anxious or wild expression
Clinical findings
 (5) Retraction of the eye lids
(nystagmus), pricking of the
ears and opisthotonus.
 Between the episodes, the
animal lies quietly for some
interval, but any slight noise or
touch give rises to another
attack.
 (6) Grinding of the teeth and
frothing from the mouth.
 As in hypomagnesemia
 Divide the on 10
Treatment
3-Ketosis
 Most animals suffering from any diseasesd
condition and stop eating :
 ِِSuch as in : FMD - Lumpy Skin Disease-
Diarrhea -Pnemonia :
 are usually suffering from ketosis and
hypoglycemia and should be injected by dextrose
25% (I/V) and given glycerine, molases and or
treachle.
‫جدا‬ ‫مهمة‬ ‫ملحوظة‬
Treatment Options Indication
Dextrose
Propylene glycol
Dexamethasone
Make Glucose
Decreased Production
(less glucose demand)
Increased Appetite
Fatty Liver Disease
Of Cattle
It usually develops before and
during parturition.
Endocrine changes associated
with parturition and
lactogenesis contribute to the
development of fatty liver.
Cows that are over conditioned at
calving are most likely to develop fatty
liver .
cows that develop fatty liver at calving
are most susceptible to ketosis.
Etiology
“fatty liver syndrome,” is a multifactorial
syndrome of peri-parturient dairy cows.
It occurs most frequently in production
situations that commingle dry cows and
lactating cows in a single group.
These cattle are likely to become
over-conditioned late in lactation
or during their dry period.
Mortality can be as high as 25%
Metritis, retained Placenta,
Mastitis, Milk fever, and
displaced abomasum diseases
that can be present with fatty
liver syndrome.
Clinical Findings :
low milk production .
increased clinical mastitis poor
reproductive performance.
Diagnosis
Liver biopsy .
Blood glucose concentrations are
low .
 blood NEFA and β-hydroxybutyrate
concentrations are high
Prevention and Treatment
Reducing the severity and duration of
negative energy balance .
Avoiding:
1- Overconditioned cattle .
2-Rapid diet changes .
3-Unpalatable feeds.
Environmental stress
Important Notes
Cows within a herd should enter the dry
period with an average body condition
score of 3-3.5.
)body condition score of ≥4.0) should not
be feed restricted because this will
promote fat mobilization and increase
blood NEFA and liver triglyceride.
The critical time for the
prevention of fatty liver is 1
week before to 1 week after
calving.
Glucose or Propylene glycol
daily during the final week
prepartum.
Late Stage of pregnancy
or after parturation
Complete loss of appetite
Abduction of elbow
Abnormal heart sounds
أمراض التمثيل الغذائى فى حيوانات المزرعة

أمراض التمثيل الغذائى فى حيوانات المزرعة

  • 2.
  • 3.
    How Can Yousucceed in treatment A Case
  • 4.
  • 5.
    1-Method of diagnosis 1-CorrectDiagnosis (75%). ‫الجيد‬ ‫التشخيص‬
  • 6.
  • 7.
     Animal Housing Feed and watersupply 1- Correct Case History
  • 8.
    {َّ‫ن‬ِ‫إ‬ َ‫و‬ََِّّ‫ه‬ِ‫ن‬‫و‬ُ‫ُط‬‫ب‬َّ‫ِي‬‫ف‬َّ‫ا‬‫ِّم‬‫م‬َّ‫م‬ُ‫ك‬‫ِي‬‫ق‬ْ‫س‬ُّ‫ن‬ًَّ‫ة‬َ‫ْر‬‫ب‬ِ‫ع‬َ‫ل‬َِّ‫ام‬َ‫ع‬ْ‫ن‬َ‫ِيَّاأل‬‫ف‬َّْ‫م‬ُ‫ك‬َ‫ل‬‫ن‬ِ‫م‬َََّّ‫ين‬ِ‫ب‬ ِ‫ار‬‫ِلش‬‫ل‬َّ‫ا‬ً‫غ‬ِ‫ئ‬‫آ‬َ‫ًاَّس‬‫ص‬ِ‫ل‬‫ا‬َ‫اَّخ‬ً‫ن‬َ‫ب‬‫َّل‬ٍ‫دَم‬َ‫ٍَّو‬‫ث‬ ْ‫ر‬َ‫ف‬َِّ‫ْن‬‫ي‬َ‫ب‬} milking machine.milking machine. َّ‫ًا‬‫ص‬ِ‫ل‬‫ا‬َ‫اَّخ‬ً‫ن‬َ‫ب‬‫ل‬‫ا‬ً‫غ‬ِ‫ئ‬‫آ‬َ‫س‬َََّّ‫ين‬ِ‫ب‬ ِ‫ار‬‫ِلش‬‫ل‬
  • 9.
    Metabolic Disorders 2- Udderœdema 1- Hypocalcemia (Milk Fever) 2- Ketosis (Acetonemia) 1- Fatty Liver Syndrome 3- Retained Placenta 1-Energy-Related Disorders 2-Minerals & Vitamins-Related Disorders
  • 10.
    What is milkfever? Definition: a metabolic disorder which results from a temporary loss of the calcium in the blood stream.
  • 11.
    Hypocalcemia Normal Blood Ca Lethargy(dullness and listless behavior) unsteady gait Unable to stand Coma and death 9 - 11 8 - 9 7 6 4 Signs Blood Ca (mg/100 ml) Sub-clinical hypocalcemia Clinical hypocalcemia (Milk Fever)
  • 12.
    calcium Physiological function ofcalcium: Formation of bone and milk. Essential in the clotting of blood Maintenance of neuromuscular excitability. Essential for muscle contraction.
  • 13.
    A-Sub-clinical hypocalcaemia  Itoccurs in the late stages of pregnancy  With History of:  Decrease of ruminal wall (signs of indigestion). (passage of small semisolid feces).  .
  • 14.
    After parturation With Historyof:  Retained placenta  , uterine prolapse  Decrease of ruminal wall. (passage of small semisolid feces).
  • 15.
    B-Clinical hypocalcaemia Etiology:  Excessiveloss of Ca in the colostrum .  Impairment of absorption of Ca from the intestine at parturition.  Deficiency of vitamin D .  Increase Ca feeding during the dry period  Pre-partum diet high in phosphorus .  Dietary anion cation balance : Diets high in (Na, K)  4) Acidosis and diarrhea reduce calcium absorption.
  • 16.
    Clinical findings There arethree stages of the disease: The first stage:  Hypersensitivity, musclar tremors .  Stiffness in gait, difficult to stand or move .  Shaking of the head, protrusion of the tongue and grinding of the teeth.  Normal or slightly elevated temperature due to hyper-excitability.  Anorexia, rumen stasis, absence of defecation
  • 17.
    Second stage (Sternal recumbancy) The cow is unable to rise.  Depression of consciousness.  Lying on sternum and the head turned into the flank.  Reflexes are absent with protrusion of the tongue .  Absence of papillary light reflexes and anal reflex.  Bloat, rumen stasis and constipation.  Subnormal temperature (36-38˚C)  Deep and irregular breathing.
  • 18.
  • 20.
    Third stage (Lateral recumbencystage) Lateral recumbency. bloat. Subnormal temperature (35 – 36.5˚C) Coma death.
  • 21.
    Treatment  (A) Hygienictreatment:  1) Ample space should be provided with soft clean bedding under sternum.  2) Clean water supply.  3) Easy digested food. Using stomach tube to avoid aspiration pneumonia.
  • 22.
     4) Rotatethe affected animal from side to side to avoid tympany and hypostatic congestion.
  • 23.
    (B)-Medical treatment  1)Sourceof Calcium A- Small cow(300- 400 Kg): R/500 ml (375 ml IV very slowly and 125 ml SC after 30 min. at different sites.
  • 24.
     Large cow(More than 500 Kg B .w.)  1 Liter:  ½ Liter at morning  ½ Liter at evening
  • 25.
    Examples of Capreparation R/Ca boro-gluconate (20% or 25%)  Or R/ Cal. D. Mg (Ca & Dextrose & Mg) R/Calcium amino-plex (Ca & amino acids). NB:  I/v Ca solution should be slowly to prevent cardiac arrest.  Continue for 3-5 days days or till complete recovery
  • 26.
    (2) Compounds whichincreasing calcium level in blood: R/ AD3E&C (10 ml / daily IM). & R/ACTH 400-500 IU I/M 3) Anti-inflammatory (Non Steroidal) R/Declo-phenac Na 2.5% 4 ml/100 Kg B W. (4) Supportive treatment: R/Dextrose 25% or 40% 2 liter IV.
  • 27.
  • 28.
  • 29.
    II-Downer with depression Impaction Severehypocalcemia Severe hypomagn. Severe .Toxic mastitis Dehydration Toxic metritis Uterine torsion
  • 30.
  • 31.
    1-Definition  It isa metabolic hemolytic disease of cattle and buffaloes characterized clinically by hemoglobinuria and anemia and biochemically by intravascular hemolysis and hypophosphatemia
  • 32.
    2-Incidence and occurrence (1)It is usually occur 2-4 weeks after parturition in cows and in mid-term of gestation in buffaloes. (2) Animals are susceptible between fifth and tenth calving. (3)It is usually occurs at the end of barseem season (April-May)
  • 33.
    3-Causes  (1) Dietslow in phosphorus or unsupplemented with ph.  (2) Feeding of cruciferous plants such as Barseem, grass, turnips, (contain thiocyanites as toxins) and carbage (contains thiouracil as toxins).
  • 34.
    Clinical findings  (1)Colour of urine may vary from light brown in mild cases to deep red or coffe coloured in severe cases.  (2) In-appetence, pica, dull, depression and weakness develop suddenly.  (3) Severe depression of milk yield (although in some less cases, the cow continues to eat and milk normally for 24 hours after discoloration of the urine. Milk may be
  • 35.
     (4) Dehydrationdevelops quickly.  (5) MM are pale and anemic or icteric in sever cases  (6) the cardiac impulse and jugular pulse are much augmented with tachycardia.  (7) Cessation of rumination and constipation  (8) The feces are usually dry and firm.  (9) Dyspnea due to anemic anoxia.  (10) The course of the acute disease extends from 3-5 days, the cow becomes weak and stagger and finally recumbent (Downer).
  • 36.
    Complications  (1) Gangreneand sloughing of the tips of the tail or teat or ear or the digits.  (2) Ketosis commonly occurs.  (3) Death may occur within a few hours or days, in non-fatal cases, convalescence requires about 3 weeks and recovering animals often show pica.
  • 37.
    Main Line ofTreatment Hyagenic Medical Supportive T
  • 38.
    To Success inTreatment Correct Diagnosis Drug Used Dose& Route of adm. Duration ‫النجاح‬ ‫عوامل‬ ‫حالة‬ ‫عالج‬ ‫قى‬
  • 39.
    Medical Source of phHematincs Saline
  • 40.
  • 41.
  • 42.
    (1) Sources ofphosphorus  A) IV slowly administration of 60 of sodium acid phosphate in 300 ml of distilled water on the first day .  Followed by further SC injections of similar doses at 12-hours intervals till recovery.  Similar daily doses (60 g) by mouth NB: Treatment should be continued till 3-5 days after disappearance of red urine (complete recoverty)
  • 43.
    B) patent phosphoruspreparation as: R/ Tonophosphan (Ph 10%) R/ 50ml( 25 ml IV daily&25 ml I/M till recovery).
  • 44.
    C) Oral dosingwith bone meal (120 g) twice daily or dicalcium phosphate daily for 5 days till recovery. Or: Superphos Sachets 3 One sachet daily (oral route)
  • 45.
    (2) Hematinic preparation: (A) in sever cases:  Blood transfusion 3-4 L of whole blood to a 450 kg cow is indicated in severe cases.  Additional transfusion is necessary if cow is still weak and mucous membranes are pale.  (B) In less sever cases:  iron, copper, cobalt, vitamin B12 ) .4) R/Antoplex 15 ml I/M
  • 46.
    1-General symtoms  1-Stiffleg. Stiffness in gaite and arched back.  2-Poor growth rates. Animals do not grow as well as pasture conditions indicate.  3-Coat and condition. Rough, coarse coat and are in poor condition.  4-Not eating barseem Partial loss of appetite Chronic ph def
  • 47.
    Delayed onset ofpuberty , Delayed postpartum estrus, Repeat breeding. & Increase incidence of cystic follicles . 5-Reproductive abnormalities ‫الجاموس‬ ‫فى‬ ‫تحدث‬ ‫الظاهرة‬ ‫هذه‬ ‫شهرمارس‬ ‫فى‬-‫عام‬ ‫كل‬ ‫من‬ ‫ومايو‬ ‫ابريل‬
  • 49.
    Main Line ofTreatment  1-Ph source  R/Phospho-nor tonic 20- 30 Ml I/V or I/M ‫اسبوع‬ ‫لمدة‬ ‫يوميا‬ ‫الحقن‬  2-Steroidal anti-inflammatory  R/Dexamethasone 10Ml I/V  (daily for 4 days).  3-Treatment of ketosis:  R/Dextrose 25% 2 Liter I/V  R/Propylene Glycol ¼ Liter Orally  (Or Glycreine or Treacle)
  • 50.
  • 51.
     It isa highly fatal metabolic neuretic disease in adult ruminant and nutritional deficiency disease in calves (milk tetany or calf tetany).  It is characterized biochemically by hypomagnesemia and clinically by hyperaesthesia, tetany and convulsions, and finally death . 1-Definition
  • 52.
     (1) Lactationtetany: More common in mare than cow which give profuse amount of milk with ingestion of excessive green grass.  (2) Grass tetany : It occurs in animals maintained on green grass or newly grown grass which are deficient in Mg.  (3) Milk tetany (Whole milk tetany): It occurs in calf fed on milk diet.MM Classification according to the causes:
  • 53.
     Decrease inMg level :  (1) Feeding on diet or food deficient in magnesium.  (2) Reduced food intake (decrease dietary Mg contents) or decrease in the amount of absorbed Mg. 2-Main causes
  • 54.
     The diseasemay be acute, subacute and chronic:  [1] Acute lactation tetany:  (1) The animal may be grazing and suddenly cease to graze and appear uncomfortable with twitching of the muscles and ears.  (2) Severe hyperaesthesia so that any slight disturbances such as sudden noise or touch leads to attacks of continuos bellowing and frenzied galloping.  (3) Staggering gait then fall down on the ground with obvious tetany of the limbs which is rapidly followed by clonic spasm and convulsions lasting for about a minute. Clinical findings
  • 55.
     (4) Duringthe convulsive episodes there is opithotonus (Back head), nystagmus (rotation of eye ball), champing of the jaws, frothing at the mouth, pricking of the ears, retardation of the eye lids.  Clinical findings
  • 56.
     Between episodesthe animal lies quite but a sudden noise or touch stimulate another attack.  (5) The temperature rises (40 to 40.5ºC) after severe muscle exertions.  (6) Death usually occurs (from respiratory failure) within a half to one hour .  the mortality rate is high.
  • 57.
     (1)It iscommon in pregnant buffaloes, there is slight inappetence, wildness of the facial expression and exaggerated limb movements.  (2) Stagger gait or stiffness of the limbs  (3) Loss of appetite which accompanies by rumen stasis and decrease in milk yield. [2] Subacute lactation tetany: Hypomagnesmia
  • 58.
    1-Hygienic treatment: Complete restof the affected animal in quite place. 2-Medical treatment:  (A) Source of magnesium:  By IV (200-300 ml of 5%) solution of Mg sulfate. (It causes rapid rise in serum Mg within 3-6 h) followed by SC injection of 200-300 ml of 20% solution of Mg sulfate. 5-Treatment
  • 59.
     (B) Amagnesium-rich enema: 60 g of Mg Cl in 250 to 500 ml of warm water results in rapid absorption of Mg.  (C) Oral Mg oxide:  60 g for 5 to 6 days as an alternate form of therapy.
  • 60.
     (D) Tranquilizerand narcotics :  R/Complene 3-4 ml I/M
  • 61.
     3-Supportive treatment: R/Dextrose 25% 1-2 L I/V daily for 3-4 D  R/Tri B (B1,B6,B12) ampoules one pox daily I/M for 4-5 days
  • 62.
     Definition : It is a nutritional disease in calves 2-4 months of age or older which are fed only a milk diet (Milk is low in magnesium and gives adequate Mg for the requirement of growing calf up to 50 Kg). 2-Milk tetany tetanyCalf
  • 63.
     (1) Theanimal suddenly cease to graze and twitching of the muscles of the jaws and ears.  (2) Hyperthesia: bellowing, general spasms and convulsion with great fear.  (3) Stagger gait and fall down on the ground with tetany and or paresis of the limbs and convulsions.  (4) Anxious or wild expression Clinical findings
  • 64.
     (5) Retractionof the eye lids (nystagmus), pricking of the ears and opisthotonus.  Between the episodes, the animal lies quietly for some interval, but any slight noise or touch give rises to another attack.  (6) Grinding of the teeth and frothing from the mouth.
  • 65.
     As inhypomagnesemia  Divide the on 10 Treatment
  • 66.
  • 67.
     Most animalssuffering from any diseasesd condition and stop eating :  ِِSuch as in : FMD - Lumpy Skin Disease- Diarrhea -Pnemonia :  are usually suffering from ketosis and hypoglycemia and should be injected by dextrose 25% (I/V) and given glycerine, molases and or treachle. ‫جدا‬ ‫مهمة‬ ‫ملحوظة‬
  • 68.
    Treatment Options Indication Dextrose Propyleneglycol Dexamethasone Make Glucose Decreased Production (less glucose demand) Increased Appetite
  • 69.
  • 70.
    It usually developsbefore and during parturition. Endocrine changes associated with parturition and lactogenesis contribute to the development of fatty liver.
  • 71.
    Cows that areover conditioned at calving are most likely to develop fatty liver . cows that develop fatty liver at calving are most susceptible to ketosis.
  • 72.
    Etiology “fatty liver syndrome,”is a multifactorial syndrome of peri-parturient dairy cows. It occurs most frequently in production situations that commingle dry cows and lactating cows in a single group.
  • 73.
    These cattle arelikely to become over-conditioned late in lactation or during their dry period. Mortality can be as high as 25%
  • 74.
    Metritis, retained Placenta, Mastitis,Milk fever, and displaced abomasum diseases that can be present with fatty liver syndrome.
  • 75.
    Clinical Findings : lowmilk production . increased clinical mastitis poor reproductive performance.
  • 76.
    Diagnosis Liver biopsy . Bloodglucose concentrations are low .  blood NEFA and β-hydroxybutyrate concentrations are high
  • 80.
    Prevention and Treatment Reducingthe severity and duration of negative energy balance . Avoiding: 1- Overconditioned cattle . 2-Rapid diet changes . 3-Unpalatable feeds. Environmental stress
  • 85.
    Important Notes Cows withina herd should enter the dry period with an average body condition score of 3-3.5. )body condition score of ≥4.0) should not be feed restricted because this will promote fat mobilization and increase blood NEFA and liver triglyceride.
  • 86.
    The critical timefor the prevention of fatty liver is 1 week before to 1 week after calving. Glucose or Propylene glycol daily during the final week prepartum.
  • 87.
    Late Stage ofpregnancy or after parturation Complete loss of appetite Abduction of elbow Abnormal heart sounds