Non-Infectious Infertility in Cattle

Question 1

describe freemartinism (congenital condition)

Answer 1

1. results from 92% of heterosexual twins
   -fusion of chorio-allantoic portions of the twin placentas (28 dpc)
   -common blood supply between twin fetuses
2. exchange of humoral (AMH) and cellular elements between fetuses
   -freemartin calves are blood cell chimeras (60 chromosomes = 58 + 2)/animals that contain two cell types originating from separate zygotes
3. testicular development occurs before ovarian development, so AMH from testis of male fetus inhibits development of paramesonephric (mullerian) ducts in the female
4. results in reduced development of mullerian ducts: small genital tract, hypoplastic ovaries, short vagina, and absent cervix
   -increased development of wolffian ducts: development of epididymides, vasa deferentia, and vesicular glands

Question 2

describe diagnosis of freemartinism

Answer 2

1. history of heterosexual multiple births
2. appearance of external genitalia: small vulva, enlarged clitoris, anestrus
3. palpation or ultrasound of internal repro tract
   -speculum reveals short vagina (1/3) and no cervical os
   -use a vaginal probe: ID 80% of cases
4. PCR: sex chromosome XY and XX in same animal; detect in 1/10,000 blood cells containing Y chromosome ($40)
5. karyotyping: culture blood lymphocytes; metaphase chromosome spreads examined for XY cells (laborious work and expensive)

tx: remove females from herd (no way to get preg); male fertility may or may not be affected

Question 3

describe segmental aplasia of mullerian ducts (congenital condition)

Answer 3

1. autosomal recessive genes (if you see it, CULL THEM)
   -also called white heifer’s disease; high prevalence in short horn females
2. lack of development of a portion of the mullerian ducts (aplasia); involves vagina, cervix, uterus, and oviducts
3. presentation ranges from an imperfonate hymen to absence of part of repro tract
   -may see absence of one horn (uterus unicornis)
   -most commonly affects caudal portion of one horn
   -accumulation of endometrial secretions = hydrometra in cranial horn

Question 4

describe diagnosis of segmental aplasia of the mullerian ducts

Answer 4

1. can be misdx as pregnancy, pyometra, mucometra, or ovarian cysts; but NO cardinal signs of pregnancy is how you tell not preg
2. palpation or USG and inability to pass a pipette into both uterine horns
3. can still get pregnant on normal side (allows gene to circulate in herd!)

Question 5

describe uterus didelphys/incomplete fusion of the mullerian ducts (congenital condition)

Answer 5

1. autosomal dominant gene that results in failure of complete fusion of mullerian ducts
2. mostly affects the cervix, resulting in double external cervical os
   -both external openings may join into a normal internal cervical os
   -or one side may end in a blind diverticulum
3. may cause difficulty passing an AI pipette
4. may cause dystocia if fetal parts pass both external cervical canals
5. fertility IS affected: AI in cervical os contralateral to ovulating ovary; will never fertilize

Question 6

describe ovarian hypoplasia (congenital condition)

Answer 6

1. congenital defect characterized by deficient morphologic and functional development of one or both ovaries
2. ovaries small, hard consistency without palpable structures
3. inherited condition!
4. can be uni or bilateral
   -unilateral: repro tract can be normal; worse because she will reproduce and pass this on!!
   -bilateral: undeveloped repro tract; steer appearance, small pelvic
5. ddx: atrophy by nutritional deficiency

Question 7

describe causes of anestrus (8)

Answer 7

1. high milk yield (>70lb/day)
   -high yielding dairy herds show increased incidence of anestrus
   -directing energy to milk production can result in delayed cyclicity
2. under-nutrition:
   -limited energy intake or lower body reserves (BCS)
3. negative energy balance
4. metabolic diseases

(any energy deficit decreases release of GnRH and frequency of LH pulses)

5. dystocia, RFM, puerperal metritis, pyometra
6. mastitis: cortisol, endotoxins, cytokines, and prostaglandins have negative effects on LH
7. presence of a calf:
   -inhibits GnRH and LH secretion via hypothalamic opioid peptide-B endorphin, serotonin, and dopamine
8. heat stress: high cortisol levels reduce GnRH and LH

Question 8

describe prevention and control of postpartum anestrus

Answer 8

1. nutritional plan according to milk yield
2. optimal nutrition during the transition period
3. minimize stress
4. bull effect: biostimulation (teaser bulls; sterilized)
5. use temporary calf removal (48, 2, or 96hr)
6. appropriate herd health program: biosecurity, vx, dx
7. hormones: progestagens
   -CIDR: controlled internal drug release
   -for post partum cows (approx 60 dpp): CIDR + GnRH + PGF2a
   -if low BCS = waste of time and money

Question 9

describe cystic ovarian follicles (acquired, noninfectious)

Answer 9

1. anovulatory follicular structures that persist for long periods of time
   -larger size than a follicle but persistent follicles behave similarly
   -at least 2cm in diameter and persist in absence of a functional CL
2. prevalence of 10% of dairy cows annually, prolonged intercalving interval
   -less frequent in beef cows
3. may be single or multiple structure, thin walled, several layers of granulosa cells secrete E2
4. 4 potential outcomes:
   -luteinization: almost all follicular cysts become luteal cysts

-persistency: 70d; remains dominant; releasing E2 and inhibin

-regression: replaced by another follicle that ovulates (self correction in 20% of cases)

-turnover: most of the cases; cyst decreases size and replaced by a new follicular structure that develops into a new cyst

Question 10

describe follicular persistency and oocyte variability

Answer 10

1. dairy cattle have a high metabolic rate (milk)
   -blood flow to liver is higher in higher producers
   -due to increased metab rate, steroid metabolism is greater in higher producers so will have lower levels of progesterone (more metabolism)
2. progesterone is negative feedback to hypothal, when high we get lower LH pulses
   -when progesterone low, more frequent and LH pulses
3. so more frequent LH pulses, stimulation for follicular development without ovulation
   -allows follicle (or cyst) to keep growing!
   -aka high milk yield = more persistent follicular cysts!

Question 11

describe pathogenesis of follicular cycts

Answer 11

1. LH pre ov surge is absent, insufficiency, or improperly times
   -dominant follicle continues to grow (large and anovulatory, high E2 and inhibin)
2. no reduction in GnRH content in hypothal
   -no reduction in LH content in pit
   -no reduction in GnRH receptors in pit
   -cows respond to GnRH injection with release of LH (good for tx purposes)
3. decreased sensitivity of HH to E2
   -injection of E2 fails to cause positive feedback (not good)
4. loss of negative feedback by P4
   -LH is released (wasted in high pulses), leading to absence of surge
5. other factors: oxidative stress, neg energy balance reduced liver function, low circulating IGF-1, increased heat shock proteins in ovaries

Question 12

describe a luteal cyst

Answer 12

1. develops from follicular cyst
   -theca and granulosa cells luteinize over time
2. thickened walls as cells luteinize (>3mm)
3. secretes P4 at different levels: luteal or subluteal

Question 13

describe diagnosis of ovarian cysts

Answer 13

1. behavioral and physical characteristics:
   -most cows do not exhbit estrus
   -nymphomania: frequent and prolonged estrus
2. transrectal exam:
   -structure >2cm
   -no functional CL
   difficult to determine follicular from luteal
3. ultrasound: can tell follicualr versus luteal
   -wall thickness = 90% accruate

Question 14

descrbe treatment objectives of ovarian cysts

Answer 14

objectives:
1. increased secretion of P4 after treatment (endog or exog)
2. decreased pulsatility of endogenous LH
3. sensitize hypothalamus to E2

Question 15

describe use of GnRH and PGF 7 days apart to treat ovarian cysts

Answer 15

1. GnRH or HCG causes luteinization of dominant cyst
   -nondom don’t respond
2. ovulation of dom foll. present in ovary, estrus in 20d
3. P4 produced by cyst reduced LH pulsatility
4. induce atresia of cysts and development of an ovulatory follicle
5. P4 produced by cysts sensitizes HH and uterus for PGF2a
6. HH responds to high E2 and release a preov surge of LH

basically give GnRH to luteinize a dominant cyst (reset cycle as cyst will become a CL and promote normal follicular development)

PGF2a then causes regression of any luteal tissue (that CL you just made out of the dominant follicular cyst) and restore normal cycle

Question 16

describe use of progesterone to treat cysts

Answer 16

-can inhibit LH secretion to help cyst regress

-CIDR can be used to constant source of progesterone, then give GnRH and then PGF2a to trigger/induce ovulation in a postpartum cow or a cow with a cyst)