reproductivedisorders-170511hkk030340.pdf

༄། འབྲུག་རྒྱལ་འཛིན་གཙུག་ལག་སློབ་སྡེ།
རང་འབྱུང་འཐློན་བསྡེད་མཐློ་རིམ་སློབ་གྲྭ།
སྤུ་ན་ཁ་རློང་ཁག།
ལློད་སྦུད་ས།
དློག་ཏྲར་་་འཇིགས་འབྡེལ་རློ་རྡེ།
རང་འབྱུང་འཐློན་བསྡེད་མཐློ་རིམ་སློབ་གྲྭ། སྤུ་ན་ཁ་རློང་ཁག།
ལློད་སྦུད་ས།
5/11/2017
REPROODUCTIVE DISORDERS OF FARM ANIMALS
1

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 In simple language this can be defined as disease affecting
reproduction. In other words it is any condition that leads
to infertility or sterility.
 Infertility: inability to produce viable young one
within a stipulated period characteristic to that
species.
 Sterility: Complete inability to produce due to some
permanent factors.
The reproductive diseases can be broadly classified into
three categories:  Anatomical or Structural defects
 B. Functional Defect
 C. Infectious Causes

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Congenital Acquired
a Aplasia/absence of ovary a Ovaro-bursal adhesion
b Hypoplasia of ovary b Adhesion of uterus
c White heifer disease c Prolapse of cervical
rings
d Double cervix and external os d Fracture of pelvis
e Agenesis or aplasia of fallopian
tube
e Ovarian tumor
f Atresia of vulva f Vulval tumor
g Hermaphrodite
h Freemartins
ANATOMICAL/STRUCTURAL DEFECT
Anatomical or structural defect could be congenital or acquired

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Congenital Defects:
1.Aplasia of ovary:
Means complete lack of development of the ovary. It can
be unilateral or bilateral. If bilateral the animal will be
sterile. In case of unilateral aplasia the animal may
reproduce but the animal will be infertile and it is not
economically viable to maintain such an animal.
2.Hypoplasia of the ovary:
Means incomplete development and the organ is very small.
It could be unilateral or bilateral, complete or partial.

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3.Freemartins:
Occurs in the female member of heterosexual twin in
which allantois-chorionic membranes of the twins fuse
early during embryonic development (as early as 30
days, prior to development of reproductive organs).
fusion allows an exchange of blood between the twins.
 Freemartin is noticed in cattle, sheep, goat, pigs but
not in horse, human, monkey dog and cat as vascular
anastomosis occurs after sexual differentiation in
these species.
 Clitoris is enlarged
and tuft of hairs at
tip of the vulva is
more prominent.

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4.Agenesis or aplasia of F. tube
It could be unilateral or bilateral, complete or
segmental.
5.Atresia of vulva/ Narrow vulva:
The Vulval opening may be absent which has to be
corrected surgically. In case of narrow vulva there will
be normal pregnancy but will lead to dystocia during
parturition. This can be corrected through episiotomy.
6.Intersexuality (hermaphrodite)
 is a situation in which the sexuality of an individual is
confused by the presence of anatomical structures of
both sexes.

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This condition is classified as-
True hermaphrodite- has both male and female gonads
which may be either separate or combined as ovo-testes.
It has been found in horse, goat, cow and pig. Common in
pig and goat than in other species.
Pseudo hermaphrodite
Pseudo hermaphrodite is an individual that has the
external genitalia of one sex, but the internal sex organs
of the other.
It has been observed in pig, goat and dogs.

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7.Segmental Aplasia Of Mullerian Duct/White Heifer
Disease
The disease may constitute an imperforate hymen and
segmental aplasia of the uterus. Absence of anterior
part of the vagina, cervix or the uterine body and horns
(Absence of one horn is called uterus unicornis) are a
common feature in this case.
The defect is associated with single recessive sex limited
gene with linkage to white coat color and commonly found
in white shorthorn heifers.

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8.Para Ovarian Cysts:
 Around 1 cm in d.m. and adjacent to ovary in the
mesosalpinx and may press lumen of the oviduct
 Cysts Of Gartner's Duct
 two in number in cow and located
beneath the mucosa of the floor of
the vagina.

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2.Acquired Defects: -
1. Ovaro-bursal adhesion may be due to following
conditions:
a. Infectious causes e.g. extension of
peritonitis due to traumatic
reticulitis into the Ovaro-bursal area.
 Fibrous strand of varying thickness
extends from fimbriae or bursa to ovary.
ii. Peritoneal tuberculosis
iii. Defective manipulation of ovaries like enucleating of
C.L leading to bleeding and adhesion.

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Adhesion of uterus:
Adhesion of uterus to omentum, intestine or to
abdominal wall may occur following caesarean operation.
Stenosis of Cervix:
may occur as a result of severe cervicitis or due to
traumatic injuries. Forceful introduction of AI gun also
leads to this condition.
Fracture of pelvis:
This leads to malignment of the pelvis. This increases the
chances of dystocia.
Tumors:
of the vagina, cervix and uterus causing obstruction.

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FUNCTIONAL/ PHYSIOLOGICAL DISORDERS
usually affects individual animals in a herd. But, in
aggregate it constitutes an important cause of
infertility, related to endocrinological disturbances
influenced by heredity, diseases, nutrition and stress.
 Functional form of Infertility includes problems like;
Anestrus,
 sub estrus/ silent heat,
 Ovulatory defects like Delayed ovulation, Anovulation,
Cystic Ovarian degeneration (COD).
 COD was reported to be most common cause of infertility
followed by subestrus, anestrus and anovulation /
delayed ovulation.

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1.Anestrus:
 is a condition when an animal doesn't come to heat and
is the most common condition affecting fertility in
cattle.
A. True Anestrus:
 is when ovary is non-functional and will be devoid of any
palpable structures. Anestrus is most commonly observed
after parturition and post service when conception does
not occur.
Causes:
 Inadequate or lack of pituitary hormone.
 Malnutrition. This is the most common cause of anestrus.
Inadequate level of carbohydrate, proteins, minerals like P, Cu, Co,
Fe etc., and vitamins like vitamin A.

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 Chronic debilitating diseases such as heavy
Endoparasitism.
 Seasonal influences
 Anestrus are more common during the winters.
Treatment:
A. Improved nutrition
 Cereals, concentrates and mineral mixtures.
 Periodic deworming.
B. GnRH - Inj. Buserelin (Receptal) - 5 ml I/m.
C. CIDR 1.9 g of Progesterone for 7-12 days + PGF2a
during removal of implant.
Oestrus occurs 48-96 hours after its removal and the
cows should be inseminated at 48 and 72 hours.
D. Norgestomet s/c implant +5mg E2 for 9-10 days.
Estrus@2-3 days after removal-AI (48-72hrs later)

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B. Anoestrus Due To Persistent Corpus
Luteum/Pathological Anestrus
Corpus Luteum is responsible for maintenance of
pregnancy through progesterone it secretes. It is
functional and persists on the ovary only during
pregnancy if not it regresses. If it persists in non
pregnant animals it is termed as PCL or Retained CL.
 Retained CL is often associated with other pathological
conditions of the uterus, which causes the uterus to
react as gravid uterus.
I) Mummification
ii) Maceration
iii) Pyometra
iv) Early embryonic death.
v) Luteal cyst

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1. Mummification:
It is a condition wherein the fetal fluid and soft tissue is
reabsorbed leaving just a mass of bone and skin tightly
enclosed by the contracted uterine walls.

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Causes:
 No definitively known cause. Various theories are:
1.Genetic factor
2.Infection and
3.Torsion of umbilical cord
more commonly from 3rd. month of gestation.
The condition is not diagnosed until the end of
gestation period because the animal is in Anoestrus due
to PCL
Diagnosed by rectal examination. A tightly enclosed mass
of the conceptus can be felt.

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Characteristic Features In Mummification Are:
 Failure of udder development
 Failure of abdominal enlargement
 Failure of parturition
 Absence of placentomes and fetal fluids
 Hard and firm fetus
 Absence of fremitus
 Presence of corpus Luteum

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Treatment:
Expulsion using traction if cervix is dilated.
Estrogen inj. daily for 4-7days until the cervix dilates,
if cervix is closed or inadequately dilated.
Supportive treatment with antibiotics.

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Treatment
Estrogen injection- Stilbestrol.
40-80 mg I/m, Estradiol - 5 -8 mg.
Estrogen brings about following changes, which lead to
expulsion of conceptus, uterine contraction, relaxation of
cervix and knocks off CL.
The conceptus and uterus are sterile in mummification.
2. Fetal Maceration
 Fetus succumbs to bacterial or viral infection resulting
in death, emphysema and maceration characterized by
abortion or dystocia. Usually results dystocia due to
insufficient dilatation of cervix.

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Symptoms:
Foul, fetid reddish grey Vulval discharge. On rectal
examination an emphysematous fetus or macerated
bones could be found.
On rectal examination in the cow, fetal bones may be
palpated in the uterus either floating in pus or
crepitating with little pus around them. The uterine wall
is thick and heavy and the cervix usually large and hard.
 History of chronic, fetid, mucopurulent discharge
from the vulva over a period of several weeks or
months.
Generalized symptoms of elevated temperature and
pulse and anorexia are usually not present

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Treatment:
 The prognosis is poor.
 Treatment in the cow is difficult.
 Bones are attached with endometrium and endometrium
is severely damaged.
 Slaughtering the animal is an option.

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Retention of Fetal Membranes/Retention of
Placenta
 Condition where all or part of the placenta or
membranes are left behind in the uterus during the
third stage of labor.
 In a normal condition, a cow’s placenta is expelled within
a 3 -8 hour period after calving.
 If placenta is not expelled for 12 hours or more after
parturition considered ROP.

5/11/2017
REPROODUCTIVE DISORDERS OF FARM
ANIMALS
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Causes of ROP
1. Immature Placentomes:
 Premature delivery or abortion leads to retention
because of immature placentomes.
2. Delayed Gestation
3. Lack of Uterine Contractions
4. Placentitis or Cotyledinitis:
 Brucella abortus, tuberculosis, Vibrio fetus, IBR,
Staphylococcus aureus, E. coli,
5. Uterine Atony:
 Associated with dystocia, hypocalcaemia, hydropic and
other pathological conditions
6. Severe Deficiency of Selenium, Vitamin A, D, E

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ANIMALS
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Treatment
1. Oxytocin 50-100 IU in cattle/buffalo may be injected
2. Oxytocin is not drug of choice if fetal membranes are
retained inside.
3. If case is reported late after 24 hours then prime the
uterus with estrogen by giving 1-2 ml estrogen and then
after 30-60 min give oxytocin.
4. Estrogen pulls the fetus and activates the receptors of
oxytocin, relaxes cervix.
5. PGF2α is drug of choice in habitual cases but should be
given within one hour after parturition.

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ANIMALS
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Manual Removal:
 Not a preferred method.
 If placenta is hanging
 Epidural
 Separation of Placentome with fingers carefully.

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C. Anoestrus Due to Undetected Heat/ silent
heat:
 Inability or ignorance of the owner to detect heat
 The weak heat or silent heat may be attributed to
inadequate estrogen level.
 Ascertained only by rectal palpation and detecting CL,
ovulation fossa on the ovaries and changes in the
reproductive tract.
 Heat stress, nutritional deficiencies.
Treatment:
 Estrogen Inj. at 17th days of the oestrus cycle and
repeated on the 20th day.
 Improved nutrition

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D. Repeat Breeding Syndrome ( FI)
cows or heifers, having regular estrous cycles and
appears normal on superficial clinical examination, fails
to become pregnant following three or more consecutive
breeding.
leads to long service period and inter-calving interval.
Causes:
1.Anatomical abnormalities
kinked cervix,
Ovaro-bursal adhesions,
Tumors of bovine reproductive organs ,
Persistent hymen. Persistent Hymen (Rupture during
AI)

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2. Infectious causes
Turbid cervico vaginal mucus indicates uterine infections.
Unsterilized instruments for insemination and injudicious
use of intrauterine medications, lead to endometritis
(intrauterine infusion of: antibiotics or Lugol`s iodine
(0.25%, 20-30 ml, Intrauterine, alternate day two
infusions).
3.Nutritional Reason:
 conception of the animal is related to the body
weight(225-250 Kg) jersey (250-275kg HF heifer)
 Underweight animals always have less chances of
conception.
 Strictly follow the deworming calendar/ schedule.

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4. Managemental Causes
 not inseminated at right time (A.M-P.M rule )
 Double insemination is recommended for crossbreds.
5.Hormonal aberrations
 cystic ovarian degeneration (COD) is one of the major
causes of RB
 Delayed ovulation is also associated with this malady
(LH).
 Delayed function of CL either alone or in combination
with lowered secretion of P4 during luteal phase

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6.Poor Semen Quality Or Faulty AI Techniques:
 Involves all steps from semen collection to AI
 Correctness and precision of these steps are mandatory
in achieving high success rate with AI.
7. Immunological reason:
 Sperm antigens are recognized as foreign material by
female’s immune system and antibodies develop against
sperm antigen
 Treatment is just change the bull next time.

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Functional Form Of Infertility – Ovulatory Defects
The defects associated with ovulation are:
 Delayed ovulation (Aging of sperm or death of ovum or
spermatozoa)
 Anovulation.
 Cystic ovarian disease (COD)/Cystic Ovarian
degeneration
Reasons:
Endocrine reasons.
(quantity of LH released is insufficient or its timing is
incorrect.

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Mechanical reason:
 Adhesion of the ovarian bursa to the surface of the
ovary. There is no treatment if Ovaro-bursal adhesions.
But LH is hCG (Chorulon) @ 3000 IU in adult cattle may be
tried.
Anovulation
 As the name indicates the mature Graafian follicle
fails to ovulate.
 The animal has normal cycle, normal reproductive
tract but fails to conceive. This is due to:
 Inadequate level or absence of L.H.
 Ovaro-bursal adhesion.

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Delayed Ovulation:
Ovulation takes place 48-72 hours after the onset of
oestrus but the spermatozoa would be dead by then.
Cause: Due to low level of LH.
Treatment: As in Anovulation.
Treatment:
 L .H preparations (HCG- human chorion Ganadotrphin)-
3000 IU. I/V. when the animal is in heat.
 Inj. Receptal - 5 ml I/m.
 Improve feeding.

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Cystic Ovarian Degeneration (C.O.D)/Cystic
Ovaries
Contain one or more persistent fluid filled structures
larger than a mature follicle i.e. >25 mm in diameter in
one or both ovaries. Seen more commonly in the high
producers at around 15-45 days after calving.
 Arise as a result of anovulation of a Graafian follicle.
 Instead of regression and atresia, or luteinization
followed by regression, the follicle increases in size,
there is degeneration of granulosa cell layer and cyst
persists for at least 10 days. E2 (Nymphomania)

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Cyst May Be Follicular Cyst Or Luteal Cyst
Follicular cyst
It is a thin walled fluctuating structure. There may be
multifollicular cyst (these cyst may have demarcation
between them). Bigger the cyst - more estrogen
production.
structure on the ovary that is at least 25 mm in size in
the absence of any corpus Luteum.
 Diagnosis is through USG
Very thin outer wall with black fluid extending to
its outer edges

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ANIMALS
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Clinical signs;
1.Nymphomania
2.Edematous swelling of vulva, frequent and copious
discharge of clear mucus.
3.Shortened interval between successive heats.
4.Sterility hump.
 Relaxed sacrosciatic ligaments

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Treatment of Follicular Cyst

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Luteal Cyst.
 When the wall of follicular cysts gets luteinized, it
results in formation of luteal cyst
 Progress into luteal cysts by forming a thicker wall of
luteal tissue around their outer edges.
 Structure functions as a persistent corpus Luteum and
produces Progesterone.
 Luteal cysts are never multi follicular i.e. luteal cysts
are single on one ovary.

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Clinical Signs
If animal remains anestrus for long time, then it shows
masculinization
Although these animals will attempt to mount other
cows, but unlike the nymphomaniacal cows they will not
stand to be mounted by other cows

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Follicular Cyst Luteal cyst
Thin walled Thick walled
Soft Hard
Nymphomania Anestrus
Plasma Progesterone never rises 0.5
ng /ml
Progesterone levels rises more than 2.5
ng/ml
Differential Diagnosis Of Follicular And Luteal Cyst

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