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REASONS AND
TREATMENT OF
PROLONG CALVING IN
CATTLE
MUHAMMAD ALI
PARTURITION
PARTURITION IS INDUCED BY THE FETUS. IT IS INITIATED BY RISING CORTISOL LEVELS
IN THE FETUS THAT PROVOKE A CASCADE OF ENDOCRINE ACTIVITY IN THE DAM.
FETAL CORTISOL INCREASES AS A RESULT OF INCREASED ADRENOCORTICOTROPIC
HORMONE (ACTH) PRODUCTION BY THE MATURING FETAL PITUITARY CAUSED BY
FETAL STRESSORS SUCH AS HYPOXIA AND HYPERCAPNIA.
GESTATION LENGTH IS UNIQUE TO EACH FETUS, BUT APPROXIMATE GESTATION
LENGTHS CAN BE ASCRIBED TO EACH SPECIES
FACTORS
IN CATTLE, GESTATION LENGTH IS INFLUENCED BY FACTORS SUCH AS..
 THE BREED OF THE COW AND BULL.
 CALF GENDER
 SINGLE VS MULTIPLE BIRTH
ENVIRONMENTAL FACTORS:
NUTRITION, AMBIENT TEMPERATURE, AND THE SEASON OF THE YEAR, HAVE A
SMALLER INFLUENCE.
CALVES BORN IN SPRING AND SUMMER WERE CARRIED SHORTER TIMES AND WEIGHED
LESS THAN THOSE BORN IN FALL AND WINTER.
CAUSES
• IN MANY CASES, PROLONGED GESTATION IS INCORRECTLY DIAGNOSED
BECAUSE OF HUMAN ERROR.
• MISCALCULATION OF THE PROSPECTIVE CALVING DATE, FAILURE TO
RECORD A SUBSEQUENT SERVICE, FAULTY PREGNANCY DIAGNOSIS, AND
INCORRECT IDENTIFICATION OF ANIMALS MAY LEAD TO A DIAGNOSIS OF
PROLONGED GESTATION IN AN ANIMAL THAT HAS A NORMAL
PREGNANCY.
• THE LIFE OF THE DAM MAY BE AT RISK IF PROLONGED GESTATION IS
ALLOWED TO CONTINUE, AND TERMINATION OF THE ABNORMAL
PREGNANCY IS RECOMMENDED.
PROLONGED GESTATION ASSOCIATED WITH
FETAL DEFORMITY
• PROLONGED GESTATION ASSOCIATED WITH FETAL
DEFORMITY CASES USUALLY OCCUR AS THE RESULT OF
SOME COMPROMISE OF THE HYPOTHALAMIC-PITUITARY-
ADRENAL AXIS OF THE FETUS, WHICH IS NO LONGER ABLE
TO INITIATE PARTURITION. THE AFFECTED FETUS MAY
EITHER DIE AND BE ABORTED OR LIVE ON INDEFINITELY IN
THE UTERUS. GENETIC, INFECTIOUS, AND UNKNOWN
CAUSES HAVE BEEN ASSOCIATED WITH THIS PROBLEM.
GENETIC ABNORMALITIES
PROLONGED GESTATION ASSOCIATED WITH FETAL ADRENAL FUNCTION
IT IS A GENETICALLY DETERMINED PROLONGED GESTATION CAUSED BY AN
AUTOSOMAL RECESSIVE GENE OF THE FETUS IN HOLSTEIN-FRIESIAN COWS. THE
FETAL ADRENAL GLANDS FAIL TO PRODUCE CORTICOSTEROIDS AT TERM, IN
RESPONSE TO FETAL ACTH. AS A RESULT, THE FETUS CONTINUES TO GROW UNTIL
IT OUTGROWS ITS BLOOD SUPPLY. INDUCTION WITH DEXAMETHASONE DOES NOT
INDUCE NORMAL LABOR AND PARTURITION BECAUSE OF INSUFFICIENT
PREPARATION OF THE BIRTH CANAL. A CESAREAN SECTION WILL SAVE THE DAM,
BUT THE FETUS INVARIABLY DIES DUE TO ADRENAL INSUFFICIENCY.
PROLONG GESTATION WITH CRANIO FACIAL
DEFECTS IN THE FETUS
• IT IS THOUGHT TO BE CAUSED BY A RECESSIVE GENE.
• AFFECTED FETUSES CEASE TO GROW AT 7 MO GESTATION.
• THERE IS NO SPONTANEOUS PARTURITION IN AFFECTED CATTLE BECAUSE OF
THE NONFUNCTIONAL OR ABSENT PITUITARY GLAND IN THE FETUS. CALVES ARE
USUALLY DEAD WHEN DELIVERED.
PROLONG GESTATION ASSOCIATED WITH MULTIPLE SKELETON ABNORMALITIES
AFFECTED CALVES SHOW EVIDENCE OF PITUITARY APLASIA OR HYPOPLASIA.
ARTHROGRYPOSIS(CURVING OF JOINTS), TORTICOLLIS.
INFECTIOUS CAUSES
BOVINE VIRAL DIARRHEA:
ALTHOUGH BOVINE VIRAL DIARRHEA VIRUS CAN CAUSE ABORTION IN CATTLE, IT CAN
ALSO PRODUCE CONGENITAL DEFECTS IN THE FETUS. THESE INCLUDE CEREBELLAR
HYPOPLASIA, ANENCEPHALY(ABSENCE OF A MAJOR PORTION OF THE BRAIN), AND
HYDROCEPHALY. AFFECTED CALVES MAY BE BORN WITH SEVERE DEFECTS OF THE CNS,
BUT PROLONGED GESTATION OCCASIONALLY OCCURS IF PITUITARY FUNCTION IS
COMPROMISED.
BLUE TONGUE VIRUS:
TRANSMITTED BY INSECTS, INFECTION CAN OCCASIONALLY CAUSE PROLONGED
GESTATION. THE FETUSES OF COWS EXPOSED TO THE VIRUS AT 60–120 DAYS OF
PREGNANCY DEVELOPED HYDRANENCEPHALY (BRAIN'S CEREBRAL HEMISPHERES ARE
ABSENT), WHEREAS FETUSES EXPOSED LATER IN PREGNANCY DEVELOPED LESS SEVERE
CNS DEFECTS.
PROLONGED GESTATION
ASSOCIATED WITH FETAL DEATH
IN CASES OF FETAL MUMMIFICATION, FETAL DEATH IS OFTEN NOT IMMEDIATELY
APPARENT. IN SUCH CASES, THE CORPUS LUTEUM PERSISTS IN THE OVARY, AND
THERE IS NO VAGINAL DISCHARGE AND NO SIGNS OF ESTRUS. THE ABNORMAL
PREGNANCY IN SUCH ANIMALS CONTINUES INDEFINITELY. AFFECTED ANIMALS ARE
NORMALLY IDENTIFIED WHEN OWNERS NOTICE THAT EXTERNAL SIGNS OF LATE
PREGNANCY, INCLUDING ABDOMINAL ENLARGEMENT, ARE LESS OBVIOUS THAN IN
OTHER MEMBERS OF A GROUP. CLINICAL EXAMINATION REVEALS THAT THE FETUS
IS DEAD, ALTHOUGH THE DAM IS PREGNANT. RECTAL EXAMINATION REVEALS AN
IRREGULARLY SHAPED, CONTRACTED UTERUS WITH A FETAL MASS BUT NO FETAL
FLUID WITHIN IT. THERE IS NO FREMITUS IN THE UTERINE ARTERY.
DIAGNOSIS
WHEN A NUMBER OF CASES OF PROLONGED GESTATION ARE SEEN IN A HERD, A
FULL INVESTIGATION SHOULD BE CONDUCTED IN AN ATTEMPT TO IDENTIFY THE
CAUSE AND POSSIBLY A PREVENTIVE PROGRAM.
TESTS FOR EVIDENCE OF PATHOGENIC VIRUSES OR SEROLOGIC EVIDENCE OF
EXPOSURE TO THEM MAY LEAD TO CLEAR EVIDENCE OF VIRUS INVOLVEMENT
IN SOME CASES, THE CAUSE OF PROLONGED GESTATION REMAINS UNKNOWN.
TREATMENT
IN A CASE OF SUSPECTED PROLONGED GESTATION, THE DAM'S BREEDING RECORDS, IF
AVAILABLE, SHOULD BE CHECKED TO ENSURE THAT PARTURITION TRULY IS OVERDUE.
TREATMENT OF A CASE IN WHICH GESTATION IS NOT GENUINELY PROLONGED MAY
RESULT IN THE DELIVERY OF A PREMATURE FETUS THAT IS UNLIKELY TO SURVIVE.
RECTAL EXAMINATION OF THE UTERUS AND ITS CONTENTS IS AN IMPORTANT
DIAGNOSTIC AID. FETAL PARTS MAY BE PALPABLE, AND IN SOME CASES IT IS
POSSIBLE TO DETECT AN ABNORMAL CRANIUM.
AN ULTRA SONOGRAPHIC SCAN MAY CONFIRM THE PRESENCE OF FETAL
ABNORMALITIES, INCLUDING A THIN-WALLED, FLUID-FILLED CRANIUM.
• IN TRUE PROLONGED GESTATION, THE FETUS IS UNLIKELY TO BE OF ANY ECONOMIC VALUE.
TREATMENT SHOULD BE AIMED AT FETAL DELIVERY WITH MINIMAL DAMAGE TO THE DAM.
• ADMINISTERED BOTH PROSTAGLANDIN F2A AND THE CORTICOSTEROID DEXAMETHASONE BY
THE IM INJECTION.
• LUTEOLYSIS IS INDUCED BY THE PROSTAGLANDIN, AND THE MATERNAL HORMONE CASCADE
THAT PRECEDES PARTURITION IS INITIATED BY THE CORTICOSTEROID.
• IN CATTLE'S, 500 MCG CLOPROSTENOL (SYNTHETIC ANALOGUE OF PROSTOGLANDIN F2Α.)
AND 20 MG DEXAMETHASONE ARE GIVEN.
• A SINGLE DOSE OF THESE TWO DRUGS IS NORMALLY EFFECTIVE. PARTURITION SHOULD BEGIN
IN 24–72 HR.
• INDUCED PARTURITION SHOULD BE MONITORED CAREFULLY.
• ASSISTANCE MAY BE REQUIRED IF THERE IS EVIDENCE OF UTERINE INERTIA OR
DAMAGE TO THE ABDOMINAL WALL, EITHER OF WHICH MIGHT MAKE EXPULSIVE
EFFORTS INEFFECTIVE
• IF THE FETUS IS LARGE AND DYSTOCIA OCCUR THEN TRACTION IS APPLIED IF NOT
POSSIBLE THEN GO FOR CAESARIAN SECTION.
• AFTER FETAL DELIVERY, UTERINE INVOLUTION MAY BE ENCOURAGED BY
ADMINISTRATION OF OXYTOCIN. RETENTION OF FETAL MEMBRANES IS MANAGED IN
THE USUAL WAY.
• FLUID THERAPY, ANTIBIOTICS, AND TREATMENT WITH NSAIDS SUCH AS FLUNIXIN
MEGLUMINE MAY AID RECOVERY AND PROVIDE ANALGESIA.
THANK YOU.!

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Reasons and treatment of prolong calving in cattle

  • 1. REASONS AND TREATMENT OF PROLONG CALVING IN CATTLE MUHAMMAD ALI
  • 2. PARTURITION PARTURITION IS INDUCED BY THE FETUS. IT IS INITIATED BY RISING CORTISOL LEVELS IN THE FETUS THAT PROVOKE A CASCADE OF ENDOCRINE ACTIVITY IN THE DAM. FETAL CORTISOL INCREASES AS A RESULT OF INCREASED ADRENOCORTICOTROPIC HORMONE (ACTH) PRODUCTION BY THE MATURING FETAL PITUITARY CAUSED BY FETAL STRESSORS SUCH AS HYPOXIA AND HYPERCAPNIA. GESTATION LENGTH IS UNIQUE TO EACH FETUS, BUT APPROXIMATE GESTATION LENGTHS CAN BE ASCRIBED TO EACH SPECIES
  • 3. FACTORS IN CATTLE, GESTATION LENGTH IS INFLUENCED BY FACTORS SUCH AS..  THE BREED OF THE COW AND BULL.  CALF GENDER  SINGLE VS MULTIPLE BIRTH ENVIRONMENTAL FACTORS: NUTRITION, AMBIENT TEMPERATURE, AND THE SEASON OF THE YEAR, HAVE A SMALLER INFLUENCE. CALVES BORN IN SPRING AND SUMMER WERE CARRIED SHORTER TIMES AND WEIGHED LESS THAN THOSE BORN IN FALL AND WINTER.
  • 4. CAUSES • IN MANY CASES, PROLONGED GESTATION IS INCORRECTLY DIAGNOSED BECAUSE OF HUMAN ERROR. • MISCALCULATION OF THE PROSPECTIVE CALVING DATE, FAILURE TO RECORD A SUBSEQUENT SERVICE, FAULTY PREGNANCY DIAGNOSIS, AND INCORRECT IDENTIFICATION OF ANIMALS MAY LEAD TO A DIAGNOSIS OF PROLONGED GESTATION IN AN ANIMAL THAT HAS A NORMAL PREGNANCY. • THE LIFE OF THE DAM MAY BE AT RISK IF PROLONGED GESTATION IS ALLOWED TO CONTINUE, AND TERMINATION OF THE ABNORMAL PREGNANCY IS RECOMMENDED.
  • 5. PROLONGED GESTATION ASSOCIATED WITH FETAL DEFORMITY • PROLONGED GESTATION ASSOCIATED WITH FETAL DEFORMITY CASES USUALLY OCCUR AS THE RESULT OF SOME COMPROMISE OF THE HYPOTHALAMIC-PITUITARY- ADRENAL AXIS OF THE FETUS, WHICH IS NO LONGER ABLE TO INITIATE PARTURITION. THE AFFECTED FETUS MAY EITHER DIE AND BE ABORTED OR LIVE ON INDEFINITELY IN THE UTERUS. GENETIC, INFECTIOUS, AND UNKNOWN CAUSES HAVE BEEN ASSOCIATED WITH THIS PROBLEM.
  • 6. GENETIC ABNORMALITIES PROLONGED GESTATION ASSOCIATED WITH FETAL ADRENAL FUNCTION IT IS A GENETICALLY DETERMINED PROLONGED GESTATION CAUSED BY AN AUTOSOMAL RECESSIVE GENE OF THE FETUS IN HOLSTEIN-FRIESIAN COWS. THE FETAL ADRENAL GLANDS FAIL TO PRODUCE CORTICOSTEROIDS AT TERM, IN RESPONSE TO FETAL ACTH. AS A RESULT, THE FETUS CONTINUES TO GROW UNTIL IT OUTGROWS ITS BLOOD SUPPLY. INDUCTION WITH DEXAMETHASONE DOES NOT INDUCE NORMAL LABOR AND PARTURITION BECAUSE OF INSUFFICIENT PREPARATION OF THE BIRTH CANAL. A CESAREAN SECTION WILL SAVE THE DAM, BUT THE FETUS INVARIABLY DIES DUE TO ADRENAL INSUFFICIENCY.
  • 7. PROLONG GESTATION WITH CRANIO FACIAL DEFECTS IN THE FETUS • IT IS THOUGHT TO BE CAUSED BY A RECESSIVE GENE. • AFFECTED FETUSES CEASE TO GROW AT 7 MO GESTATION. • THERE IS NO SPONTANEOUS PARTURITION IN AFFECTED CATTLE BECAUSE OF THE NONFUNCTIONAL OR ABSENT PITUITARY GLAND IN THE FETUS. CALVES ARE USUALLY DEAD WHEN DELIVERED. PROLONG GESTATION ASSOCIATED WITH MULTIPLE SKELETON ABNORMALITIES AFFECTED CALVES SHOW EVIDENCE OF PITUITARY APLASIA OR HYPOPLASIA. ARTHROGRYPOSIS(CURVING OF JOINTS), TORTICOLLIS.
  • 8. INFECTIOUS CAUSES BOVINE VIRAL DIARRHEA: ALTHOUGH BOVINE VIRAL DIARRHEA VIRUS CAN CAUSE ABORTION IN CATTLE, IT CAN ALSO PRODUCE CONGENITAL DEFECTS IN THE FETUS. THESE INCLUDE CEREBELLAR HYPOPLASIA, ANENCEPHALY(ABSENCE OF A MAJOR PORTION OF THE BRAIN), AND HYDROCEPHALY. AFFECTED CALVES MAY BE BORN WITH SEVERE DEFECTS OF THE CNS, BUT PROLONGED GESTATION OCCASIONALLY OCCURS IF PITUITARY FUNCTION IS COMPROMISED. BLUE TONGUE VIRUS: TRANSMITTED BY INSECTS, INFECTION CAN OCCASIONALLY CAUSE PROLONGED GESTATION. THE FETUSES OF COWS EXPOSED TO THE VIRUS AT 60–120 DAYS OF PREGNANCY DEVELOPED HYDRANENCEPHALY (BRAIN'S CEREBRAL HEMISPHERES ARE ABSENT), WHEREAS FETUSES EXPOSED LATER IN PREGNANCY DEVELOPED LESS SEVERE CNS DEFECTS.
  • 9. PROLONGED GESTATION ASSOCIATED WITH FETAL DEATH IN CASES OF FETAL MUMMIFICATION, FETAL DEATH IS OFTEN NOT IMMEDIATELY APPARENT. IN SUCH CASES, THE CORPUS LUTEUM PERSISTS IN THE OVARY, AND THERE IS NO VAGINAL DISCHARGE AND NO SIGNS OF ESTRUS. THE ABNORMAL PREGNANCY IN SUCH ANIMALS CONTINUES INDEFINITELY. AFFECTED ANIMALS ARE NORMALLY IDENTIFIED WHEN OWNERS NOTICE THAT EXTERNAL SIGNS OF LATE PREGNANCY, INCLUDING ABDOMINAL ENLARGEMENT, ARE LESS OBVIOUS THAN IN OTHER MEMBERS OF A GROUP. CLINICAL EXAMINATION REVEALS THAT THE FETUS IS DEAD, ALTHOUGH THE DAM IS PREGNANT. RECTAL EXAMINATION REVEALS AN IRREGULARLY SHAPED, CONTRACTED UTERUS WITH A FETAL MASS BUT NO FETAL FLUID WITHIN IT. THERE IS NO FREMITUS IN THE UTERINE ARTERY.
  • 10. DIAGNOSIS WHEN A NUMBER OF CASES OF PROLONGED GESTATION ARE SEEN IN A HERD, A FULL INVESTIGATION SHOULD BE CONDUCTED IN AN ATTEMPT TO IDENTIFY THE CAUSE AND POSSIBLY A PREVENTIVE PROGRAM. TESTS FOR EVIDENCE OF PATHOGENIC VIRUSES OR SEROLOGIC EVIDENCE OF EXPOSURE TO THEM MAY LEAD TO CLEAR EVIDENCE OF VIRUS INVOLVEMENT IN SOME CASES, THE CAUSE OF PROLONGED GESTATION REMAINS UNKNOWN.
  • 11. TREATMENT IN A CASE OF SUSPECTED PROLONGED GESTATION, THE DAM'S BREEDING RECORDS, IF AVAILABLE, SHOULD BE CHECKED TO ENSURE THAT PARTURITION TRULY IS OVERDUE. TREATMENT OF A CASE IN WHICH GESTATION IS NOT GENUINELY PROLONGED MAY RESULT IN THE DELIVERY OF A PREMATURE FETUS THAT IS UNLIKELY TO SURVIVE. RECTAL EXAMINATION OF THE UTERUS AND ITS CONTENTS IS AN IMPORTANT DIAGNOSTIC AID. FETAL PARTS MAY BE PALPABLE, AND IN SOME CASES IT IS POSSIBLE TO DETECT AN ABNORMAL CRANIUM. AN ULTRA SONOGRAPHIC SCAN MAY CONFIRM THE PRESENCE OF FETAL ABNORMALITIES, INCLUDING A THIN-WALLED, FLUID-FILLED CRANIUM.
  • 12. • IN TRUE PROLONGED GESTATION, THE FETUS IS UNLIKELY TO BE OF ANY ECONOMIC VALUE. TREATMENT SHOULD BE AIMED AT FETAL DELIVERY WITH MINIMAL DAMAGE TO THE DAM. • ADMINISTERED BOTH PROSTAGLANDIN F2A AND THE CORTICOSTEROID DEXAMETHASONE BY THE IM INJECTION. • LUTEOLYSIS IS INDUCED BY THE PROSTAGLANDIN, AND THE MATERNAL HORMONE CASCADE THAT PRECEDES PARTURITION IS INITIATED BY THE CORTICOSTEROID. • IN CATTLE'S, 500 MCG CLOPROSTENOL (SYNTHETIC ANALOGUE OF PROSTOGLANDIN F2Α.) AND 20 MG DEXAMETHASONE ARE GIVEN. • A SINGLE DOSE OF THESE TWO DRUGS IS NORMALLY EFFECTIVE. PARTURITION SHOULD BEGIN IN 24–72 HR.
  • 13. • INDUCED PARTURITION SHOULD BE MONITORED CAREFULLY. • ASSISTANCE MAY BE REQUIRED IF THERE IS EVIDENCE OF UTERINE INERTIA OR DAMAGE TO THE ABDOMINAL WALL, EITHER OF WHICH MIGHT MAKE EXPULSIVE EFFORTS INEFFECTIVE • IF THE FETUS IS LARGE AND DYSTOCIA OCCUR THEN TRACTION IS APPLIED IF NOT POSSIBLE THEN GO FOR CAESARIAN SECTION. • AFTER FETAL DELIVERY, UTERINE INVOLUTION MAY BE ENCOURAGED BY ADMINISTRATION OF OXYTOCIN. RETENTION OF FETAL MEMBRANES IS MANAGED IN THE USUAL WAY. • FLUID THERAPY, ANTIBIOTICS, AND TREATMENT WITH NSAIDS SUCH AS FLUNIXIN MEGLUMINE MAY AID RECOVERY AND PROVIDE ANALGESIA.