Final Flashcards
what are the fetal malpositions
presentation
position
posture
definition of presentation
signifies the relationship between the longitudinal axis of the foetus and the maternal birth canal
definiton of position
indicates the surface of the maternal birth canal to which the fetal vertebral column is applied
definition of posture
refers to the disposition of the movable appendage of the foetus
maternal causes of dystocia
failure of expulsive forces (uterine or abdominal causes)
primary uterine inertia
- Are the onset of birth, (bitch, sow)
- Fetus remains in intrauterine position
(uterinecontractions fail to be initiated)
Causes:
myometrial defect (overstretching, infection, degeneration, systemitc illness, hereditaty, small litter size)
biochemical deficiencies (E-P ratio, oxytocin, PGF, relaxin, Ca or glucose def)
oligamnion
premature parturion
envoronmetnal disturbances
condition - obsetiy/ malnutrition
- Therapy : hand vaginal stimulation (Ferguson reflex), extraction of fetuss
secondary uterine inertia
consequence of another case of dystocia
at first contractions are normla by thten myometrial exhaustation
cause = uterien damage or prolapse
therapy = eliminate cause, extract fetus, uterotonics in bithcn adn queen
abdominal causes of dysotica
- Inability to strain
- Causes : age, pain, debility, diaphragmatic rupture, tracheal / laryngeal damage
obstruction of birth canal
Bony pelvis
= Congenital = developmental abnormalities of the pelvis are generally rare in animals
= Acquired = fracture, diet, immaturity (juvenile pelvis), neoplasia, disease – exostosis (periostitis)
Soft tissue
= Vulva = congenital defect, fibrosis, immaturity
= Vagina =congenital defect, fibrosis, prolapse, cystocele (bladder, prolapse in vagina), neoplasia, prevaginal abscess, hymen
= Cervix = congenital defect (duplication – cervix duplex), fibrosis, failure to dilate – narrow cervical canal (4 degrees)
= Uterus = torsion, herniation, adhesion, stenosis of the horn or corpus
narrow pelvis
Interfere with the passage of a normally developed fetus
More common in non selective breeding + dwarf breeds
Pelvic inlet of the achondroplastic breeds of dog is flattened in brachycephalic breeds, is a common of dystocia
Therapy : mostly cesarean section, fetotomy
immature, juvenille pelvis
more common in sows, goats and cattle
Prematurely mated animals (the pelvis is not completely ossified)
Rachitis (most often in sow)
Therapy : mostly cesarean section, fetotomy
narrow vulva and vagina
o Most often in primiparous (heifers – overfat body condition)
o Prematurely mated animals (juvenile females)
o Insufficient serous infiltration of the soft parts of the canal
o Scar tissue, connective tissue – bar, wounds, persistent hymen (foals), congenital stenosis, edema of the vulva due to venous stasis
o Simultaneous appearance of a narrow vagina and vulva is possible
o Therapy : mostly operation – episiotomy
narrow vertical canal
- Mostly in cows, sheep and goats
- Disorder of the opening stage . fetal membranes
- Hormonal insufficiency + Insufficient serous infiltration
- Incomplete dilation of cervix in the ewe and doe goat (ringworm) -commonly associated with prolonged gestation and hypocalcemia, hypophosphatemia
- Consequence of uterine torsion
- Scar tissue, wounds, neoplasms
- Protracted labour – 6-12 hours after rupture of the fetal membranes, involutionary processes
- Degree of incompletely open cervix according to Götze
- therapy: medically, manually
= denaverine hydrochloride, misoprostol, fetotomy
stages of cervical canal
- 1 =ring like cervix that adheres closely to the fetus, its hard and easily rupture during extraction of the fetus
- 2 = only legs or head pass through the cervical canal
- 3 = only 2-3 fingers or fists can be inserted into the cervical canal
- 4 = cervical canal is closed (uterine torsion > 180 degree)
dry birth canal
- premature rupture, perforation of the amniotic membrane – leakage of the amniotic fluid
- Prolonged birth, mucosal edema
- Therapy: Fetal fluid supplements as substitutes for amniotic fluid
o form of a water-soluble, cellulose-based obstetrical lubricant
o a substitute such as soap (particularly soap flakes)
neoplasm in birth canal
- Vagina, vulva
- They can bleed and prolapse
- Cysts, lipomas, papillomas, adenomas, carcinomas, mixed tumors
- Neoplasms of the cervix are rare in livestock
- They narrow the birth canal and make birth more difficult
- Mare, cow, bitch
- Therapy: operation
dislocation of the gravid uterus
- Torsion of the gravid uterus uterus rotates about a longitudinal axis
- Ventroversion, ventroflexion and retroversion, retroflexion the uterus rotates around the axis that lies horizontally in front of the pelvis entrace
- Lateroversion or lateroflexion the uterus rotates around the axis that lies vertically in front of the pelvis entrace
- Prolapse of the gravid uterus (Prolapsus uteri gravidi) the uterus moves caudally in the direction of its longitudinal axis – due to heavy vaginal prolapse in cows (no special significance for birth)
ventroversion and ventroflexion
- Gravid uterus is physiologically located on the ventral abdominal wall and ventroverted to a certain degree
- If longitudinal axis of the uterus is vertically =pathology
- Flexion of the gravid uterus more caudally – ventroflexion
- Causes – older animals, in animals with lowered abdomen,overweight,. bicornual gestation in mare, ventral abdominal hernia, placental hydrops (mares)
- Symptoms– during labour
- Fetus is in transverse presentation (in front of the pelvis entrace)
- Therapy – reposition of the gravid uterus (lifting the abdomen with a board or turning the animal on the back if lying down, fetal fluid supplements, reposition of malpresentation, Caesarean hysterotomy, fetotomy)
- Epidural anesthesia!!!
lateroversion and lateroflexion of gravid uterus
- Physiologically, gravid uterus is suppressed to the right side due to rumen in ruminants
- The front part of the gravid uterus can be lateroverted, if going more caudally – lateroflexion (parts of the fetus remain in the dislocated part of the uterus and parturition is difficult)
- Mostly in mares
- Lateroversions are not problem during parturition as lateroflexions
- Therapy – same as in ventroflexions
retroversion and retroflexion of uterus
- Physiologically in mares - the tips of the horns verted cranially and directed caudally (without any parts of the fetus)
- Pathological – there are parts of the fetus in verted part of the uterus (e.g. legs to carpal or tarsal joint)
- Mostly in mares
- Therapy – sedation and lifting of the rear part of animal, rectally or vaginally pushing the front part of the uterus, fetal fluid supplements, fetotomy
torsion of gravid uterus
- Rotation of pregnant uterus on its longitudinal axis to the left/right which leads to narrowing of the birth canal
- Cow, rarely mare, small ruminants
Cause - disposition (cattle) – anatomical relations, insufficient fixation of pregnant uterus
Predisposing factors - excessive movements of the foetus/dam, decreased volume of fetal fluid, fall, kicking, relaxed ligaments, fetal overweight, cow tied in the barn for long period
Features - ACW and CW (90-360o) <45 degrees is sufficient to result in dystocia
- Either precervical or postcervical rotation
- Torsio cornualis/ torsio cornuum uteri – place of rotation is one uterine horn or part of horn in small multiparous animals
Signs - parurition not progressing, uneasiness and restless, vulvar lips uneven
Diagnosis: - Vaginal: conically closed, shrinkage of front part of vagina, rotation of mucosa felt
- Rectal: palpation of twisted horn and broad ligaments
Prognosis: - depends on degree of torsion
Therapy - return the uterus to its normal position
- direct: to uterus with foetus
o with extraction – turn foetus opposite to the torsion
o kamer method – try to encourage the foetus to turn/turn ourselves
o cämmer’s torsion fork with canvas cuffs – use of detorsion rod to correct a uterine torsion
o auer-shreiner method: 3 forces simultaneously on uterus and foetus
o snöborgs method: press abdominal wall (similar to above) - indirect: directed to mother’s body (in direction of torsion)
o hold uterus in place and turn over cow (rolling) - C-section: when other methods don’t work, at long duration, foetus is dead and uterine rupture is possible
endometritis in mares
- Inflammation of uterus, differs in etiology, clinical manifestation and duration
- The most common cause of subfertility and infertility
- Every mare 5-15 years old, mates or AI in 3 consequetive estrus without conception thoroughly suspicious on endometritis
physiological endometritis after mating
PMIE
chronic endometirits
degenerative endometritis
physiological endometritis
- Immediately after mating for AI
- Uterine response on bacteria and proteins from semen
- Resistent uterus overcome inflammation in 6-12h
- Healthy endometrium overcome infection in 6-12h
- Time frame 120 – 150h before embryo reaches uterus
PMIE
Predisposing factors
= Inadequate evacuation of inflammation products, inadequate lymphatic drainage of uterus
= Poor contractibility of myometrium
=Bad overall conformation of mare
=Hormonal disbalance
occurs due to failure of natural defence mechanism
signs = vaginal discharge and inflammation
histroy = failure to conceive, irregular cyclicality
Treatment in estrus and post estrus with monitoring of mare – individual approach - flush uterus, repeat until clean
20IV ocytocin post flush
flush 4-6h post mating
cloprosenole but can influence CL
diagnosis of endometritis
Clinical (anamnestic, vaginal, rectal ultrasound)
Ultrasound – accumulation of fluid in uterus
= Fluid in utero 6h mating – normal
= Fluid in utero 12h or more after mating or AI = worrying
= Fluid in utero 24h or more after mating or Ai =endometritis
Laboratory (cytological, bacteriological)
= Cytological smear of endometrium or low volume flush
= Bacteriological cultivation of microorganism
=Proper evaluation based on combining both tests
= If in doubt, cytological smear more significant (number of neutrophilic leukocytes)
prevention of PMIE
- Decrease number of mating or AI
- Avoid mating out of full season
- Ultrasound monitoring of ovulation
- Start therapy immediately Induce ovulation with hCG or synthetic GnrH for LH (buserelin and deslorelin)
- AI with extenders containing antibiotics
- Minimal contamination technique
chronic endometritis
Untreated PMIE become chronic endometritis
cause = poor conformation, trauma, inadequeate vulva/cervical sphincter
bacteria = strep equi, e.coli, p.areuginosa, k.pneumonia
3 natural barriers:Rima vulve, vestibulo-vaginal ring and cervix
Diagnosis: history, vaginal, rectal, US, endoscopy, cytology
therapy:
surgical correction of anatomical defects (cassock, correction of urethral flow and correction of laceration)
ATB, flushes
for chronic mycotic = clotrimazole, amphotericin
pyometra as consequence of chronic endometirits
- Multicausal etiology
o Fibrotic cervix, adhesia of cervix
o Chronic endometritis - No visible signs
- Intermittent purulent discharge
- Irregular cyclicity
- Poor prognosis for future fertility
- Uterus permanently damaged
- Endometrium replaced with granulation tissue
- Atrophy and fibrosis of endometrium
- Recurrent disease
endometriosis
- Direct link to early embryonic mortality and cervical fibrosis
- Senile atrophy of uterine glands older pluriparous mares (>15g)
- Endoscopic and PHD finding
endometrial cysts
- Lymphatic and real endometrial (usually due to drainage of lymph)
- Doesn’t involve direct in fertility
- Could disturb embryo mortality
- Laser and caterisation during endoscopy, if indicated
cause of infertility in cows
functional ovaires
displaying oestrus behaviour
narrow vagina
ovulation disorders
abortion
dystocia
detachment of placenta
subfertility/reduced fertility in cow causes
acquired/ environmentally induced - more frequent, alimentary “starvation sterility”
congenital/hereditary - lower %, often incurable, lesions of sexual organs, inherited anestrous, sub oestrus, cysts
temporary (cysts, endometritis) and permanent (incurable)_
cause of sub fertility in cattle
physiologic disturbance path anatomic, infectious, management, nutritional, hormonal
what it sterility
an absolute inability to reproduce
infertility
considered (same as) sterility or denotes a delayed or irregular production of annual live calf
subfertility
most forms of functional infertility results in anestrus = failure of cows to display oestrus
inflammatory disease can compromise fertility
reduced fertility = heifers that don’t conceive in optimal period and cows that didn’t conceive until 150th PP
infertility - steriliy = heifers that due to hereditary, most often incurable lesion in the genitals cannot conceive
parameters most commonly used in fertility analysis and assessment are
- Days open <90d
- % of conception at first AI > 60%
- Insemination index <1.5
- Conception index 60%
- Intercalving period – calving interval
- Abortions (between 45-265 days of pregnancy) <3%
- Age at first calving 24months
- Culling rate and reasons for culling – indicator of the prevalence of subfertility in herds (reproduction problems, low production)
impaired development of reproductive organs is due to
- Absence of gonad stimulating action of the pituitary gland
- Consequence of chronic diseases, deficient nutrition, very poor housing conditions of female calves
infantilism
general developmental delay, including genitals
- can be the result of poor housing, deficient diet, chronic diseases - acquired!
- detected during gynaecological examination of heifers at breeding age (16-24 months)
- Clinical finding:
o poorly developed sexual organs (as in a calf) that are not active - vulva, vagina, uterus as in a calf
o Anestrus
o prone to obesity
o Dif. dg.: freemartins, ovarian hypoplasia, ovarian atrophy
freemartinism
most common non-inflammatory condition - 92% of heifers born to bull twins
results in infertility involving tubular reproductive tract
what are chimeras
individual animals that contain two cell types originating from separate zygotes
signs of freemartinsim
heifers have the bullish appearance and behaviour of male animals
vulva is small and shrivelled with very pronounced clit, urination is strong jet directed upwards
internal repro organs abnormal
rectally: cervix and uterus often missing
least masculinised form more common - hypo plastic ovaries, short vagina and absent cervix
cause of freemartinism
day 28-30 of pregnancy = fusion of chorioallantoic part of placenta meaning common blood supply between twins
exchange of humeral and cellular elements between fetes –> 2 chimeras
testicular development occurs before ovaries I cows + antimullerian hormone from male inhibits growth of female
RBC, WBC, antimullerian germanitave embryonic stem cells androgens enter the female blood stream
50th day of feral development = initial freemartin development
75th day = masculinisation
diagnosis of freemartinism
clinic exam: rectal, length of vagina test
<7cm = freemartin, do chromosome testing if 7-14cm
false positive if persistent hymen
false negative if normal legnth
PCR = finds XX and XY in same animal, fast and accurate
karyotyping = blood lymphocytes in metaphase - spread and examine for XY cells
skin grafting - freemartin heifer will accept skin from male twin
prognosis of freemartins
most female cattle that are blood chimeras are often sterile freemartins
barren so use for fattening - not for mating
hermaphoriditism
mixing of sexual characteristics of both sexues in 1 individual
type of hermaphrodism
ambiglandular
testicular
ovarian
ambiglandular
bilateral = 1 testis + 1 ovary or 1 ovartestes on either
unilateral = testis and ovary/ ovotestes on 1 side and ovary or test on other
alternate = testis on 1 side, ovary on the other
rodents and pigs
testicular
in goats, sheep, cattle and horse
only testis on both sides but external genitalisa resemble female
cause = androgen insensitivity
XY male and production of testosterone normal but due to intracellular androgen insensitivity - mesonephric duct system doesn’t develop
vagina = short or normal, no cervix, small or absent uterus and testes in normal ovary position
maybe inherited in cattle as X-linked trait
ovarian
cause = enzymopathies in steroid conversio
chromosomal factors
heterosexual twins in cows
more rare than testicular
white heifer disease
segmental aplasia of mullein ducts
prenatal, hereditary, lack of development of portion of mullein duct system (except ovaries)
signs of WHD
various degrees of aplasia of vagina, cervix, uterus and oxiducts
imperforate hymen - blockage of caudal part of 1 uterine horn
uterine unicorni –> accumulation of endometrial secretions in cranial horn that presses on bladder and rectum
animals are cyclic and develop cyclic structureus
maybe oviduct obstruction -> hydrosalpinx
recessive gene related
aplastic secretion usually a band of CT and muscle with no lumen, mucosal epithelium or glands
diagnosis of WHD + control
rectal palpation and vaginal exam
selective careful breeding
congenital repro problems (cow)
ovarian hypoplasia
congenital lesions on ovaries
abnormalities of uterine tubes
aplasia uteri
aplastic cervix
cervix duplex
uterus didelphys
vagina subsepta
hymen feminis persistens
ovarian hypoplasia
hereditary and recessively transmitted to offspring
if unilateral - can conceive
if bilateral - not cyclic
partial = can conceive but will have a small reserve of follicles and stop cycling before being ready to mate
signs = small functionless ovaries with undifferentiated parenchyma, infantile genital tract and not cycling
congenital lesions on ovaries
very easy to diagnose
hypoplastic ovaries don’t respond to eCG or GnRH so no oestrus
don’t use bulls with small, asymmetrical testes for breeding
abnormalities of uterine tubes, uterus and cervix
depending on site of aplasia cow is infertile of subfertile
partial/segmented aplasia more common than complete
aplasia uteri
= no uterus
in WHD, freemartin and hermaphoridte
if isolated portion of horn present secretions can accumulate which cause dilation and can be misdiagnosed as pregnancy
hypoplastic cervix
vulnerable to ascending infection
cervix duplex
1 = duplication of lumen - each horn connects to vagina by separate canal-normal conception
2= 1 cervix opening in to a double of uteri sometimes 1 channel not patent
lower results with mating/AI
bulls transmit to 3-9% of offspring so exclude from breeding
uterus didelphys
complete absence of fusion of 2 paramesonpehric canals
AI in ipsilateral horn-conception and AI possible
vagina subsepta
= dorsoventral post cervical band and vertical vaginal bands
if adjacent to cervix - can interfere with sperm, calving or placenta passing
diagnosis = vag exam and palpation
therapy = pull as causally as possible and cut with scissors or fetotom knife
hymen feminis persistense
rare, increase in circular fold narrows vaginal entrance and interferes with mating
hereditatry
surgery not advised
acquired repro problems cow
ovaritis
ovarian neoplasia
lesions of uterine tube
mucometra
uterine tumours
uterine adhesions
ovaritis (oophoritis)
very rare
cause = brucellosis, TB usually accidental finding PM
ovarian neoplasia
rare
granulose cell tumours - looks like honeycomb on US
fibromas
GCT can produce ovarian steroids = anestrus or constant heat
lesions of uterine tube
occlusion of lumen = secretion accumulation
hydrosalpin = congenital stenosis of infection
phyosalpinx = can occur to upper-inffection of hydrosalpin with t.pyogenes or ascending uterine infection
mucometra
rare consequence of untreated cystic ovaries
affected cows unable to conceive
thinning of uterus wall and degeneration of endometrium
differentiate from 9-11 weeks of pregnancy on rectal using US
uterine tumours
rare in cattle - often in incidental finding but can affect fertility
rectal - can be mistaken for mummified foetus
leiomyoma, fibromyoma, fibroma
uterine adhesions
cause = perimetritis, uterine rupture, dystocia
signs = fibrous tags over surface animal often sterile
can involve omentum intestines, abdomen wall adhesions may after c-section
lesion of cervix
normal bacteria in caudal vagina, E.coli, strep, staph, T.pyo
inflammation post dystocia
cervicitis with puerperal metritiscommon if delayed uterine involution/ RFM
rare = laceration, fibrosis and obstruction of cervical canal –> infertility
conditions of vagina, vestibule and vuvla
cysts of earth’s canal
obstretcial damage to perineum and vagina
laceration or bruising, scarring and distortion and fibrosis
next birth –> narrowing of birth canal
urovagina
in cachet and old cows
prevalence in carols and holstein
pelvic and uterine ligaments loosen, anus and vulva moves forwards and vulva lies horizontally
vagina pulled cranially and hangs over edge of pelvis - urine leaks out of vulva and some goes into vagina
sometimes covers cervix –> endometritis
ovulatory conditions - cow (physiologically)
2-3 waves during cycle (wave 7-10d)
1st follicular waves 4th d pp
follicular recruitment 3-6 follicles 4mm
-> after recruitment, 1 follicle separates and grows until ovulation or atresia
biggest follicle secretes inhibit and oestrogen and blocks FSH so smaller follicles go into atresia
average diameter of ovulatory follicles = 14.8mm heifers, 17.4mm cows
anovulatory conditions
follicle growth only until recruitement
> static ovaries <6mm, small ovaries
cause3 = severe malnutrition during puerperium
repeat checking + US to confirm
follicular growth only until 1 selection, but not to ovulatory size
v. common, small static ovary, no CL, but ovulatory size follicles
progesterone low
cause = NEB, suckling calves, disease
cause of anovulatory condition
NEB = increase NEFA, BHB and somatotropin, decreased insulin, IGF-1, leptin and glucose
leptin = decrease in correlation with frequency of LH pulses
interval until 1st ovulation PP coincides with exit from NEB
6 weeks pp - drop of 1 BCS tolerated
No LH > no ovulatory growth, no estradiol produced
pp anestrus= if esters not noticed 60 d after calving
ovarian cyst cow
cysts = diameter > 2.5mcm but continues to grow and persist in absence of CL from follicle that didn’t ovulate (10d+)
benign = look like follicular cysts but don’t inhibit cycle/ovualtion/waves. CL present
most cysts disappear by 60d pp but some persist = chronic
how to help with anovulatory conditions in cattle
improve energy status during transition period
prevent disase
decrease frequency of suckling to 1-2 x1d in beef cows
GnRH agonist, prostaglandins or progestogens
differential of ovarian cysts cattle
corpus hemorrhagicum
vaculoalted LC
non-ovarian cyst
abscess
tumour
types of ovarian cyst in cattle
follicular
= thin wall, fluctuating, progesterone <1ng/ml. 15-45d post calving
luteal
= wall > 3mm, progesterone >1ng/ml formed from unovulatoed follicle and theca cells luteinise or formed from follicular cysts
signs of ovarian cysts cattle
follicular = 80% anestrus, unequal esters or persistent anestrus, masculinisation
luteal = anestrus
risk factors of ovarian cysts cow
dystocia, RFM, NEB, obesity, increased temp, older, feeding oestrogen type components
cause of ovarian cysts cattle
neuroendocrine imbalance
therapy of ovarian cyst cattle
follicular
= treat, don’t wait for regrression
= GnRH - leads to increase LH and lutenisation of cyst (oestrogen -> progesterone)
= then PGF2a 7-10d later + increase P4 - restores hypothalamic response to estradiol and ovualtion occurs
= 72% cows regain cyclicality in 28-30d post GnRH
= 20% remain in anestrus - P4 remains low during lutenisation and response of hypothalamus to estradiol doesn’t change
= intravag progesteagen for 9-12d = cyst regression + grow of follicular wave. Esters 7d after removal
= cyst aspiration
luteal
= PGF2a most effective
= GnRH or hCG good, but unsure what type of cysts
= GnRH then PGF2a 7-9d later, don’t rupture - haemorrhage and adhesions
prevention of ovarian cysts cow
decrease stress, treat infection, prophylactic GnRH 12-14d post birth
no effective treatment for multiple cysts so cull
persistent CL
anything that interiors with production or release of PGF2a
cause = uterine infections, insufficient involution, uterine abnormalities
treatment = PGF2a
absent/ delayed ovulation
oestrus and ovualtion sized follicle that doesn’t ovulate and regress or ovulates late (normal 25-35h after esters)
delayed = 48 h between statrt of esters and ovulation
cause = insensitivity of hypothalamus to estradiol, weak LH surge
aetiology = NEB, heat, stress, increaction, fast metabolism
delayed ovulation = decreased conception due to old oocyte - improper fertilisation, poor development potential old sperm
Changes in uterine tube environment (slow passage of zygote)
-prevention = GnRH with/before AI
inactive ovary
no cyclicality, small, oftenn flat follicles, no CL
cause = malnutrition, NEB, uterine infection
therapy = hormones eCG, rectal ovarian and uterine massage
ovarian atrophy
small, hard, smooth ovaries without any formation
cause = prolonged non-stimulation of ovaries by hypothalamus - pituitary gland
aetiology = def Ca, P, Cu, Co, Fe, I , vitamin A, O, E, malnutrition, chronic disease, hoof problems, parasites
physiological atrophy = sterile
atrophy is high producing = atrophy lactations
therapy = treat primary cause GnRH, eCG, hCG, CIDR, vitamins, minerals, antiparasititics
don’t confuse with hypoplasia of ovaries (congenital and irreversible) –> will be no reaction after hormones, no germinative layer
bartholin gland cyst
= under mucosa of vestibule of vagina 2-10cm big, unilateral in older cows
cause = atresia/obstruction of excretory ducts
signs = disturb urination, interfere with mating, vaginitis
DD= tumour, prolapse, absecess
if puncture - amber liquid
treat = hold top of cyst and cut with scissors along wall of vagine rinse inside with 10% betaine
will reoccur if just punctured
pneumovagina
vulva not acting as a seal, aspiration of air and maybe faeces
leads to dilation of vagina and maybe uterus and bacterial contamination
cause = aging, vulva conformation, BCS, trauma
treat = none if mild, vulvoplastiy.caslick, treat underlying cause - BCS
AI to increase subfertility
prognosis = severe cases unlikely to breed successfully
tumours of vagina and vulva
fibropapillomas
= pedunculate, remove surgically
don’t affect fertility but can interfere with parturition
other tumours = rare
> SCC or lymphoma
anestrus in cow
due to:
- pregnancy, persistent CL, ovarian cysts, anovulatory anestrus (normal)
anovulatory anestus.= normal-restoration of gonadotropin secretion and ovarian follicular activity occurs pp
pp anestrus = dairy cow not in heat by 60d pp
true anestrus
cow not in heat because of inactive ovaries - in high yield cows and beef suckler cows
predisposition = stress, lameness, nutriton, breed, season
expression of estus
decrease in intensity of esters signs = increase number of cows in silent heat
high yield cows = decrease oestrogen conc = decrease intensity of heat signs
silent heat
normal cyclic activity but weak abscent heat signs
cause = failure of oestrus detection, heat stress, erotism, def beta carotene, P, Cu, Co
aids to detect oestrus
tail pain - removed when mounting
Lamar heat mount detector - clearer result than pain, turns red when mounted
heat watch
pedometers
repeat breeder cow syndrome
= normally cyclic cow with no clinical abnormality which has failed to conceive after 3 successive insemination
pathologic conditions of repeat breeder cow syndrome
subclinical endometritis
= chronic uterine damage
luteal deficiency
= insufficient progesterone so suboptimal growth of blastocyst so not enough IFN-1 for luteloysis
delayed ovulation
= extended follicular phase and decrease signs of oestrus
- increase progesterone concentration > allows follicular growth but postpones LH surge
- 2 wave cycles = old follicles
treatment of repeat breeder cow syndrome
intrauterine ATB 10-12h post insemination
- uterus can recover before embryo arrives in uterius at day 4-5
- give GnRH at time of insemination
cause and factors of repeat breeder cow syndrome
cause = unclear but mulitfactorial
-> cow, bull, environment
factors: age, genetics, infection of repro tract, nutrition, embryo mortality
structural defects of sheep
karyotype alteraions
uncommon = aplasia/hypopalstia of ovaries/PMD, bilateral hydrosalpinx etc
intersexuality common in goats –> PIS -> always breed horned with non-horned to prevent
EED small rum
asymptomatic absorption of embryo, no discharge
notice repeat breeding in longer period than normal (17d)
infertility in ewess
fetal deeath
mummification - sterile, persists CL, resorption of liquid
macerate - infection, endometritis, purulent discharge, fatal death and emphyseam
bloody abortion - if occurs 45-70d of pregnancy - perivulvuar and tail area dirty with bloody discharge
trauma in small rum
sheep= very resistant, maybe unnoticed
towards end of pregnancy - distended abdomen >5% abortion rate
most common cause = 3Ps
protector dog = too aggressive
pastor = too many sheep in truck
passage = narrow aisle
sheep need 50cm each at feeding station
stress in small rum
housing, ventilation, flood
functional factors in ewes
lower fertility at beginning and end of season - first few cycle anovulatory
don’t mate too early
cysts uncommon
first 2 weeks of pregnancy embryos not attached to uterus grow on secretion (uterotropha)
at 3 weeks placenta starts to develop .> placentomest 80-100
4-10 weeks placenta development, foetus grows slowly
management factors in sheep
good esters detection and AI methods
proper implantation of male effect
1 ram to 30-50 ewes
flushing, hormones, BCS, feeding
avoid mixing pregnant and non-pregnant ewes
newborns need colostrum within 2-4h (IgG)
male management
poor results if inexperience rams with maiden ewes
dont’ put male in repro programme too young
peak breeding = 3-4y
check testicles regularly
out of season = decrease libido, decrease sperm production and semen quality
structural defects in goats
pallidness interest syndrome (PIS) = XX female to male intersexuality associated with polled goats
extreme = complete sex reversion
females with PIS = developmental abnormalities of sexual system
functional factors in goats
irregular esters cycles and start and end of season
cystic ovarian disease in dairy breeders
- signs = persistent esters, nymphomania, short inter-oestrus interval
- follicles = >10mm, >10 d
- therapy = GnRH, 1500-2500IV hCG, 10d post PGF2a
repeated arbortion = probs also genetically induced by hyuperactivity of adrenal cortex
pseudopregnancy
hydrometra, mucometra, cloud burts
accumulation of aseptic secretion within uterine lumen
signs = cyclic activity stops due to spontaneously persistent CL, abdomen distension, cloud burst at time of expected delivery, does looking for kids
diagnosis = US - no foetus or placetnomes and fluid in uterus
therapy = prostaglandins 2x in 12d
RFM in goat
should be out within 3-4 h (12h+ RFM)
aetiology = infection, Se deficiency
signs = metritis, depression, fever, anorexia, foul smelling dishcarge
diagnosis = vaginal exam as goats eat placenta
therapy = intrauterine ATB, no manual removal, 5IV oxytocin few times per day, ATB parenterally penicillin if in time or oxytetracycline if disease
antitetatnus
management factors of goats
optimal mating time
feeding - deficiency of Vitamin A, I or Mn
stress induced abortion. transport, chased by dog, weather
sarannen esters synchro protocl
sponge placemat for 11 days
d9 = IM eCG + PGF2a at 2pm
d11= sponge removal at 2pm
d12 = estrus detection 24-36h post removal
d13= AI 43+- 2h after sponge removal at 9am
= 65%rate
infections in goat
Q-fever
lepto
brucellosis
listeria
camplobacter
too
salmonella
chlamydia
pregnancy toxeamie
cause = nutrition, toxemia, multiple fetus, BCS
unable to eat enough –> fat related –> converted to FA + glycerol for metal growth –> KB near birth –> abortion
toxemia due to too much metal metabolic products
signs = lethargy, muscle tremors, grinding teeth, opisthotonus, ataxia, coma, hypoglycaemia, ketonuria, increased BHBA, decrease Ca, increase K
therapy = bicarbonate, Ca, glucose precursos
No IV glucose due to hepatic lipipodsis + end of pregnancy insulin resistance
No PO glucose because digestion in ru,en causes FA formation
toxic agents in sheep
can cause malformation or abortions
estrogenic herbs = contain phytoestrogens so cause edema, infertility, udder hypertrophy, abortio, genital proplase
overeating –> ruminal tympana –> increased abdomen pressure –> mechanincal abortion
teratogenic plants - alkaloids cross placenta and act on fetus
mycotoxins
nitrate and nitrites from fertilisers lead to hypoexmia of fetus
Cl cpompoudns, bromates, DMSO
legume - clover, alfalfa
infectious agents - small rum
non-specific less important due to long anestrus afterr lambing (heal before next repro season)
RFM uncommon
bacterial/fungal = lesiosn with exudate between endometrium and choroid, diffuse or focal, edema, congestion, haemorrhage or vili necrosis. autolytic fetus
viral = macro no placental changes, fetus not autlytic
sample = fetus, placenta, vagina, maternal serum
negative fetal finding doesn’t exlcude infection becasue fetus becomes immunocompetent around 80d and doesn’t proceed antibodies befores
specific infection in sheep
Q-fever
brucella
lepto
chlamydia
salmonela
toxo
campylobacter
listeria
pestivirus
schmallenberg Virus
anestrus in pigs
esters 7 d post weaning normal -> weaning to esters interval 2-11 d
anestrus due to active, inactive or cystic ovaries
gilt management
don’t induce esters if under 210d old and 105kg (puberty at 210d)
-> decreased maternal instincts, litter size and milk production
puberty can be delayed due to: breed, housing, nutrition, climate, stress
always correct nutrition and environment first before using drugs
breed gils at 250-260d old
normal in pigs
return to esters <8%
abortion <2%
farrowing rate 95%
30 weaned/sow/year
biological methods with pigs
flushing - protein and energ
supplements VitA, E and Se
male effects
h0use with cyclic sows
hormonal estrus induction
gonadotropicn
PG600 = hCG + eCG + heat 3-6 d later
second litter syndrome (pig)
mating at young age has no negative effect on 1st litter but decrease feed intake during 1st lactation has influence on 2nd litter size
transport induced esters pig
for puberty stimulation too
in esters within 7 d post transport
inducing ovulation in acyclic female (PIGS0
eCG/hCG –<estrus 3-6 d layer
regulating luteal phase in cyclic
- regumate 15-20mg/pig/d esters 2-8 d after last progesterone in pig
sows that return to esters within 21+/ 3d and fail to conceive = repeat breeders
EED if return to esters in 25d
seasonal infertility - pig
anestrus
lower fertility end of summer and start of autumn
sigh program: 200lx 16h/day
improve nutrition, decrease stress and stocking density
therapy = gonadotropins
empty/open sow
non-pregnay sows serviced again 6-d after 1st service
hsould be les than 1%
detect pregnancy 30 d post mating
mycotoxins in pigs
in food or bedding
can impair fertility and cause abnormal development of fetuses
zearlenon - oestrogen mycotoxin -> repeat breeding, heat signs, vaginal and rectal prolapse, pseudopregnancy
porcine parvovirus
on 60% of farms
infection:
d35= death and resorption
d35-70 = mummification
d7-114 = immunocompetence, maybe slight weakness of piglets
vaccinate gilts 2x before AI
circovirus PCV2
oronoasla/horizojtal route of transmission
causes repro problems in sow herds
infects embryo after transplacental transmission
signs = embryonic and fetal death, loss of whole litter at any stage of pregnancy, mummification
vaccine available
PRRS
rest disease in nurses and finishing pigs
possible transplacetnal transmission during early prengnayc
late term abortions, mummified foetuses, weak piglets
Light programmes pig
to optimise fertility
200lux for 16h at eye level then 8hr darkness
lactational unit = 8h light, 16h dark
breeding unit = 16h light, 8h dark
synchorno of estrus in gilts
regroup and place next to boar
synthetic progestaen PO for 14-18d + estrus in 4-6d
gonadotropins 1-2d after progestagen
after weaning
PG600 directly after weaning to improve weak heat
progestagens to extend weaning - esters in interval to avoid 2nd litter syndrome
CL In pigs unresponsive until 12-24d post ovulation
natural CL regression due to endogenous PG at 14-17d
timin of AI in pig
standing estrus lasts 48h
ovautlin 32h after start and lasts for 2-4h
sperm viable for 24h, ova 2-4
AI 0-24h before ovulation
2nd AI 12-24h after first
embryonic and fetal death in pigs
embryonic = <30d of pregnancy.- stress, feeding, season, antural mechanism
fetal loss = mummification and stillbirth
preweaning mortality
stillbirth = dystocia, pregnancy duration, infection, parturition duration, interval between piglets, BCS, temp, human help
management of lactation in pigs
prevent excessive weight loss during by optimising nutrition
decrease suckling to decrease metabolic burden andto increase repro rates
weight loss >12.5% = decreased farrowing rate and litter size
kskip a heat - serve at 2nd oestrus post weaning as better pregnancy rates and litter size
problems in lactational management if long wean -estrus period and poor 2nd litter
sows that become fat during prenugnac - decrease feed during lactation
poor lactation nutrition = decreased follicle development during and adter lactation, decrease ov rate, decrease ova quality and increase embryonic moortality
thin sows = prolonged wean-oestru, decreased preg rates and litter size
induction of lactation estrus - pig
can be done in 70-90% of sows
success depends on parity and breed
pro = lactation period extend whilst sow is pregnant, allows piglets to be better developed when weaned
daily temporary removal of whole litter can induce estrus esp if with boar contact
cystic obarian disease pig
persistent pathological filled fluid structures 20-300m each, can be mulitple
no LH surges so fillciels continue to grow
cause = stress, GnRH, therapy at wrong time, early induction of ovualtion after birth
diagnosis = US
cull as often poor repsonse to therapy
vulvular discharge syndrome - pig
cause = overstocking, bedding, feral contamination, AI.mating
signs= white-grey secretion, bad smell
metritis = >100ml
cervicitis = not so much
vaginitis = less quality
bladder = >100ml at urination
take blood sample adn swab of discharge –> acitinobaculium suis
post partum dysgalactia syndrome pigd
+ post mating endometritis
bacteria is usually from environment –>coliform
treatment = ampicillin, trimethoprim, fluids, NSAIDs, oxy
pseudo lactation
physiological in bitch
prevalence = afgans, beagle, boxer and rare in cats
usually 1-3 m after oestrus but also 3-4 d post OVH in diestrus
pathogenesis of pseudolactation
physiologically,i diestrus is similar between pregnant and non-pregnant bitches
trigger= progesterone decrease and prolactin increase, increase tissue sensitivity to prolactin
- different molecular types of prolactin with different bioactivity
- prolactin secretion in pituitary is under tonic inhibitory contorl of hypothalamus, mediated by direct inhibitory action of dopamine, or indirect serotonin (dopamine secretion suppressant)
signs of pseudlactation
6-8 weeks after estrus and can last 30-90d
covert = no signs, physiologic condition
overt = divers signs
behavioural changes, physical changes in caudal mammary gland, aggression
often self limitig but can occur after every oestrus
complications of pseudolactation and DD
rare - vomiting, anorexia, PUPD, tumours, mastitis, CEH
DD = rule out pregnancy, mastitis, tumour, pyometra
diagnosis of pseudolactation
signs and histroy
hormonal tests no due to specific physiology of sexual cycle of bitch
therapy of pseudolactation
mild = no treatment, prevent maternal behaviour, elizabethan collar
therapy if strong bevhaioural changes lasting longer than 4 weeks
drugs = antiprolactinemic, serotonin antaognist with dopamine eeffect I hgih dose (metergoline)
- dopamin agonist are prolactin inhibitors that exert effect by direct stimuatlion of dopamine D2 receptors
eg caergoline 5ug/kg PO for 7-9 d pergolide, bromcriptine
ovariohysterectomy is anestrus
no milking, tranquilliser but not phenothiazines
treat all bithces due to risk of mamary gland neoplasm
what is feline mammary fibroepithelial hyperplasia
benign, progesterone assocaited fibroglandular proliferation or 1 more more mammary glands
can occur in males or females
most common in, intact cats 6m-13yr
when = 1-2 weeks after estrus or 2 w after hormonal therapy
pathogenesis of feline mammary fibroepithelial hyperplasia
not completely understood
growth + development of mammary gland under progesterone control
-> progesterone in stromal and epithelial cells –> activation of specific cascade –> mammary gland proliferation
-> maybe changed regulation leads to disturbed response to progesterone
progesterone –> ductal branching
estrogen –> ductal elongation and bifurcation
progestogens cause stimulation and proliferation of epithelial cells and ductal canal to hyperplasia
high proliferative index
blood progesterone in normal conc
pathomorpholical characteristics - feline mammary fibroepithelial hyperplasia
firm, well-circumscribed unencapsulated mass, solid and smooth
possible ulcerations and necrosis
micro=profieration of glandular, fibre - epithelial elements
therapy and prognosis of feline mammary fibroepithelial hyperplasia
prognosis = good but relapse possible if no OBH
supportive therapy
treatment:
- OVH or ovariectomy = gold standard –> regression in 3-4 week, if not mastectomy
agleprisoton = competitivee progesterone antagonist 10mg/kg SC 1st then 3rd day, control day 7 repeat if needed, regression within 4-8 weeks
dopamine agonist for suppression of lactation
cabergoline for 5-7 days
bromocriptine 0.25mg/kg PO for 5-7 days side effects = ticks
clinical findings of fibroepithelial hyperplasia
15-18cm excessive enlargement that appeared very rapildy
can be: bilateral whole chain enlargement asymmetric (non-pregnant) solitary mass in any gland
skin = tense and erytheamtous
palpation = firm, compact conssitency soft, gelatinous mass
lab = normal
large masses = problems walking
Greg queen = no milk, weak kittens
complications of feline mammary fibroepithelial hyerplasi
mastitis in lactating queens
ulceration due to overstretched skin
maybe hemorrhagic/purulent exudate
increase temp, lethargy, anorexia
LN involvement
diagnosis of mammary fibroepithelial
signs = spread of development
biopsy = FNA or excision - large amount of mitosis = false malignanyc
US - increased echogenicity
DD = neoplasia, FEH = bigger and softer
congenital abnormalities in bithc
ovarian genesis rare and only affects fertility if bilateral
ovarian dysplasia in bithc with abnormal number of chromosomes
intersex - pseudohermaprhodites
vulvar hypoplasia and perivulvar deermatitis
neoplasia in bitch
ovarian tumours uncommon, increase in older
granulosa cell tumour
uterine tumour uncommon - fibroeiomyoma
tumours of cervix rare
vagina and vestibule tumours more common - begging liopma etc
transmissible venereal tumour - dog
affects vagina and external genitalia of bitch and penis in dog
transmission through coitus and sniffing and licing etc
lesions = friable, multilobulated max size after 5-7 weeks and can regress spontaneously within 6 months
metastasis uncommon
therapy = surgical debunking and them vincristine for 3-6 seeks
intratumoural injection with vincristine and interleukin 2
hydro/muco/hematometra bitch
accumulation of sterile serous/mucoid fluid
diagnosis = unlarged uterus US/x-ray no systemic inflam (WBC normal)
treatment = ovariohystercotmy
hematometra = rodenticide toxicity, torson of uterine horn, rule out recent pregnancy
cystic endometrial hyperplasia - bitch
acute/chronic post astral disease of adult intact bitches leading to inflammatory exudate in uterus
cause = repeat exposure of endometrium to progesterone
predisposing = 2 month diestrus
secondary anestrus. -bitch
proonged interests period in failure to cycle 10-18 months of previous cycle
cause= silent heat, hypothyroidism, exogenous glucocorticoids
basenjis and wolf dogs = only 1 cycle per year
inducstion of estrus
- eCG, FSH, LH estrogen
- GnRH analogues
- dopamine agonists (cabergoline)
pyometra
progesterone mediated uterine disease occurring during diestrous
bacterial infection with opportunistic organisms from vagina secondary to CEH
most common organism = e.coli
types of pyometra
open
= 4-8 weeks post estrus, vulvar discharge, less systemically ill
closed
= abdo distension, minimal discharge, more systemic signs
signs of pyometra
fever
hypothermia
dehydration
lab and diagnosis of pyometra
lab
= neutrophilic (penia if endotoxemia)
= normocytic, normochromic aneamia
= WBC left shift
= azotemia, increased ALP and ALT
= hyperglobulinemia, hypoalbumineam
diagnosis = gen and gyno exam
x-ray or us
therapy for pyometra
ovariohysterectomy
medical =have to be of breeding age, vital to program, open Cervi and not systemically ill
PGF2a dinoprosvt 2x 1d cloprotenol or alphaprostol fluids, pain relief, atb antipgroestins = no sidde effects compared to prostaglandins
persistent anestrus dog
primary = lack of cycling by 24month old
dd= previos ovariohysterecotmy silent head
- > check serum progesterone conc every month, = presence of cantonal luteal tissue
therapy = FSH SC.IM for 6-8d
hypothyroidism - dgo
can cause infertility by interfering with gamete maturation
-> thyroidd hormoens support granulosa cell function in developing follicles and are needed for normal placental trophoblast function
signs = irregular/proglonged interests period, prolonged proestrus decrease intensity/ducration of estrus, spotnaneous abortion, mummification, pups with low birth weight
diagnosis = fT4, canine TSH
treatment = thyroxine 2x1d
normal cycle in 4-6 m after adeuqate therapy
causes of primary anestrus dog
persistent anestrus
hypothyroidism
systemic disease
hyperadrenocirticms
progesterone
ovarian aplasia
immune mediate oophoritis
persistent estrus dog
combo of proestrus and estrus greater than 6 weeks
cause = presence of functional ovarian follicular cysts
granulosa cell tumour
PSS - due to delayed metabolism of hormones
irregular estrus - dog
uterus needs 1390-150d for endometrial involution and repair
interestrus less than 4 months = usually infertile due to incomplete eenodmtrail repair
treatment = induce anestrus -> mibolerone, testosterone cyprionate IM
split estrus - dog
most common at first and second estrus
signs = vulvar swelling, serosanginous discharge, no ovulation, follicles regress and proestrus signs disappear
cause = premature atresia and regression of follicles due to insufficient secretion of LH
-> normal estrus 1-3 weeks laterr
-> progesterone remains basal despite showin estrus signs
mate at correct time in relatio to OV
vaginal prolapse dog
= protrusion of oedematous vaginal tissue into vagina lumen and through vulva lips
cause = unknown (no hyuperestrognism) but is due to estrogen sitimualtion during estrus and protestrus
1= slight.moderate eversion of vaginal tissue through vuvlar lips
2= prolaspe of cranial floor and lateral walls trhough vulvar lips
3= prolaspe of entire vaginal circumference as a donnut shaped mass
signs = discharge, dysruia, anuria
treatmet = can regreess spontaneously so keep clean and dry
surgery = for type 3 - circumferential excision of prolapsed tissue -> can recur so OVH
anestrus in queen
physiological in autumn-winter
cause = inadequate photoperiod prevent follicular wavesa t start of mating season (need 14_h)
stress
congeintal abnormlaities (rare)
luteal cysts or neplasia (rare)
treatment
- induced estrus with FSH 2mg IM then 0.5-1mg IM each day for 4 more days
hCG IV
ovulation oof mature follicles with hCG 250iV IM or GnRH 25mg
persistent estrus quee
lasts 2 follicular cycles but endocriniolgoical changes are normal
fertility decrease due to inadequate mating time
follicular cyst queen
heat and signs for 21d+
treatment = 250-500 IV hog or 25mg GnRH
OVH
anovulatory cycles queen
in half of queens bred only once
if not mated enough - no LH surge or mated in 1st 2 d in estrus
diagnosis = serum progesterone con
ovulation = when progesterone >1.5ng/ml
pyometra queen
less common than in bithces
bacterial infection of uterus due to hormonal changes in cats
signs = variable, decreased appetite, PUPD, vomiting
pus contianing blood is open cervix
therapy = OVH
medical treatment maybe if open cervix not severely ill and for valuable breeding females
end of season pregnancy rate depends on ( horse)
stallion fertility
mare fertiliyt
stud management
pregnancy mare manageemtn
reasons for fertility failure in hrse
no conception -> fails to cycle, normal cycle but no conception
conception but loss befroe check
early pregnancy but loss post day 11 diangosis
abortion (up to day 300)
stillbirth or non-viable foal
causes of infertility/subfertility in horse
structural
- inherited
- injuries to genital tract
- age related deegeneration of ovaries and endometrium (defective bulva most common problem)
infectious
- endometritis, metritis, pyometra
functional
- no oestrus behaviour
- shortened lutal phase
- ovulatory dysfunction/multiple ovulation
ovary problems in horses
no follicular growth
ovulatory failure
poor oocyte quality
chromosomal abnormality
oviduct problem in horse
blockage
infection/inflammation
failure to pick up oocyte
poor environment
uterus problem in horse
infection/inflammation
fibrosis
poor environment
mechanical problem
cervix problems - horse
tears
adhesion
fibrosis
inflammation
vagina, vulva and vestibule problems in horse
urine pooling
air
vaginitis
foreign material
breeding soundness exam In horsse
age, health, history, BCS, repro history
exam external genitalia and mammary gland
palpation + US of internal tract
vaginal insepction - cervical function
endometrial fucntion - bactiology and cytology
endometrial biopsy
hysteroscopy
endocrine exam
further exams - karyotyping
urine pooling horse
more common in older mares
urine enters cervix during estrous and can pass into uterus causing endometritis and infertility
treatmetn = correct predispoing factors, uterine lavage, urethral extension surgrey –> vaginaloplasty of transverse folds
perineal laceration in horse
= rectovaginal fistula (cloaca)
cause = dystocia in young maiden mares due to rigidity of birth canal
first aid = debridement, cleaning and hemostasis, parenteral broad spec ATB for 5 days, NSAIDs and tetanus jab daily cleaning + monitor uterine involution
can do elective surgery at least 10 weeks post birth, if foal survives bss done after weaning
surgery = modified Goetze technique –> stage 1 repair = appropriate stripping of mucodsal surface, residual shelf between rectum and vagina in mobilised and fixed as caudally as possible
persistent hymen - horse
can cause accumulation of fluid within vagina and uterus due to impaired natural drainage
rupture with scalpel
granulosa theca cell tumour -in hourse
age 5-9 y old
signs = behaviour changes, anestrus, lymphoma, clitoral enlargement, aggressiveness
diagnosis = rectal + US - 7-40cm, spherical mass with honeycomb/multicystic appearance
hormonally active AMG >4ng/ml
therapy = unilateral ovariectomy
prognosis = good, most return to normal cyclic activity
fibrosis of cervix in horse
older mare
cervix can’t relax properly during esturus so fluid accumulates in uterus –> post breeding e
endometritis common
ovarian cyst adenoma In horse
unilateral
not hormonally active –> anestrus
endometrial biopsy - mare
biopsy = taking piece of uterus surface to detect inflammation or degenetation
indication = prepurchase exam, barren mare, past infertility, abortion, pyometritis or mares needing repro surgrey
when = estrus - cervix in open and more easily penetrated and mare more resistant to endometritis
diestrus = endometrial glands more active and may give better picture of their function
categories of endometrial biopsy mare
I : normal pathologic changes, small and sparsely scattered, foaling rate 80-90%, factors affecting foaling rate = overall management
IIA: mild changes, 50-80%, overallmanagement and endometria changes
IIB: moderate changes, 10-50%, “”
III: severe changes, widespread inflammation, scarring, atrophy of glands in physiological breeding season, 0-10%, severe changes in endometrium
endocrine diagnostic of ovarian function - mare
progesterone
- normal range <1.0ng/ml oestrus, anestrus
- >1.0ng/ml diestrus, pregnancy, persistent CL
estradiol 17B
- no significance
testosterone
- 20-45pg/ml = increase in estrus, transitional phase
anti-mullerian hormone
- 0.1-4ng/ml = no changes in normal mare , >4ng/ml = GTCT
twins in mares
number 1 cause of abrtion (in late pregnancy - 7 months +)
1 twins = breed, older mares, heredtiary repeatable
- check for twins at 14-18d (before fixation) 30d (before cups
if to term 25% live birth, 14% live to 2 weeks
twins between 5-30days –> manual destruction terminate wit PGF2a
between 35-70days -> terminate with PGF2a transvaginal US guided allantocentesis (TUGA)
EED - mares
causes = uterine pathology
fibrosis –> uterine gland failure (need secretion to support embryo due to delayed placental attachment)
if allowed, can do ET
progesterone supplemtnation
diagnosis = palpation, hormonal assay, best = US, check GSD, CRL and FHR
= loss of conceptus before organogenesis is complete
- embryo <40d
- fetus >40d
- early fetal deeath 40-150d
- abortion from 300th d
- stillbirth 300-320 need ICU
gestational age measurement in horse
AV = amnionic vesicle diameter
GSD = gestational sal diameter
CRL = crown-rump length
head length
eye length
trun diameter
FHR = fetal heart rate
infectious infertility in horse (signs)
irregular cycle, anestrus, mated tail and crsuty hair on rum, white exudate, red mm
primary causes of abortion in horse
twins
herpesvirus
placentitis
older mares
less pregnancy rates, less oocytes/mebyros collected
less EED
oviductal embryos smaller and of lesser quality
uterine embryos - decreased collection rates and quality and delayed development
15-20y = shorter follicular phase, smaller follicles, more double ovulation
20y+ = longer follicular pahse, intermitten ovulation, failure to ovulate
failure of ovulation in horse
no apparent, problem with oestrus
doppler US - increased blood flow in follicular wall, sudden appearnace of echogenic particles in follicular fluid
hemorrhagic anovulatory follicle in horse
cause = older age, late in breeding season, post induction of luteolysis, moves with bushings, NSAID or glucocorticoids drug
pathogen = impaired prostaglandin synthesis in follicular wall inhibits ovulation
conception not possible as oocyte stays in follicle
DD = GTCT
90% will form CL/ lutenisation –> spontaneously or induction with PGF2a
10% won’t lutenist -> can take 6-8weeks, no echogenic particles on US, no P4 < 1ng/ml in blood, no inhibitor effect on cycle disappears in weeks-months
rare= development of ovrian hematoma –> abdomen disteress, blood in abdo
no therapy
oestrus reoccurs spontanelously
induce luteolysis with PGF not before 8 days after start of lutenisation
prophylaxis = no induction of esturs and ovulation when follicles of preov size aresent
causes of anestrus in horse
winter anestrus/spring transition
lactation anesturs
siletn heat
multiple ovulations
dietrus ovulation
recent steroid aministraiotn
GTCT
persists CL
-> therapy PGF2a
abortion post d35-> eCG secreted by endometrial cups
endometrial swab in horse
need :clean uterine culture: for some stallions prior to breeding
culture and ctyology
when = late oestrus best because uterine flora decreaes with increase in estrogen
dog mammary tumour stage
use elston and ellis (Nottingham) method
–> tubule formation 1-3, nulclear pleomorphism 1-3 mitotic counts 1-3
total 3-5= grade 1, 6-7= grad 2 , 8-11 = grade 3 all is malignant
increased malignancy = decreased survival
cats mammary tumour staging
modified methdos
same grades of malignancy
grades of tumour
1= well-differentiated carcinoma
2= moderaltey differentieated
3= poorly differentiated carcinoma
TNM classification
T = primary tumour size
T1 = <3cm (d), <1cm (cats)
T2= 3-5cm 1-3cm
T3 = >5cm. >3cm
T4 = inflammation
N = lymph node invovlement
N0 = no mets (cyto/histo)
N1 = mets to ipsilateral LN
N2 = mets to contralateral LN
M= metastatic disease
M0 = no distant
M1 = distant mets
molecular classification of tumour
immunohistochemicl markers.in canine mamary neoplasms
-> ER, PR, HER2, p63, P-cadherin
molecular subtypes
- Lumina A = best prognosis
Luminal B
basal like = poor prognosis
tripple negative ER, PR, HER
prgnosis of tumour
positive.= small breeds (benign), males, ER + PR expression
negatives = >3cm, ulceration, LN involvment, mets, lymphovascualr infiltration
dogs 2 year survival = 75-90%, >3cm = 14m
cats stage 1/2 - 12-29m
4=1m
<3cm post op = 9 months
treatment of tumour
surgery
adjuvant jormone, chemo, radiatio, desmopressin, anti-cox2 treatemtn
not without surgery
anti-cox 2 inhibitors
- selective = firocoxib
- non-selectve meloxicam
in combo with chemo
for IMC = improved quality of lif
mammary tumour bitch
unspayed
influence of sex hromones/castration
<50% malignant
<25% mets to lungs
mammary tumour queen
lower prevalence than bithces
influence of sex hormones/castration
>90% malignant
mets to lung
mammary gland
= modified apocrine sweart gland, tubuloalveolar gland
- parenchyma (alveoli)
> simple columnar secretory epithelium lined with my-epithelial cells, covered by basal lamine
stoma = CT
ducts = lactiferous, papillary
vessels and verse
vascularisation of mammary gland
T1+T2 = cranial superficial epigastric, lateral thoracic and intercostal arteries
A1 = cranial superficial epigastric with anastomses to caudal one
A2 + 1 = caudal superifical epigastric
veins follow artery pattern but small veins cross the midline = potential depostion of maligant cells in adjacetn gland
AT1 = cranial thoracic
T2 = caaudal thoracic
A1 cranial abdomina
A2 caudal abdomianl
I inguinal
lymphatic drainage (bitch)
axillary LN = both thoracic
superficial inguinal = caudal abdo + inguinal gland
cranial abdo gland can be axillary +/or superifical inguinal
in neoplasic thoracic glands - superficial cervixal or ventral thoracic LN involved
both abdo glands drained by axillary, superficial inguinal + popliteal
inguinal drained big popliteal lymph lymph centre
IVEP
in vitro embryo production (IVEP)
-> in vitro maturaion, in vitro fertilisation, in vitro culture
oocytes from slaughterhouse
- aspiratie follicles 2-8mm -4-12 ooytes/ovary
- transport to lab-saline and ATB
- 32-37oC within 2 h
oocytes from live animals
- transvaginal follicle aspiration 2-8mm - ovum pick up
- stimulated (FSH or eCG) or unstimulated cows
equipment for opu
opu device
US with sector probe
needle guiding syste
vacuum pump
application of opu
alternative to MOET - 100 embryos/year/donor
calves from more bulls
can get offspring from infertile but, important cows
grading oocytes
G1 = compact cumulus - oocyte complexes (COCs) unexpanded cumulus mass with >3 layers of cells, homogenous, evenly granular ooplasma
G2= COCs with 2-3 layers of cells, homogenous, evenly gradnular ooplasma
G3= partially/wholly denuded oocytes with expanded or scatteed cells or with an irregular and dark ooplasm
G4 = expandded or scattered cumulus cells
in vitro maturation
G1 + G2
media, gonadotropins, esrtadiol, cystamine for 24hr at 39oC + 5% CO2
expansion of COCs and resumption of meiosis
maturation rate = % metaphase II oocytes, average of 85-90%
risk factors for mammary tumours
age
= risk increase wihth age (median 8y)
breed + genetic
= poodles, English sprigner, GSD, maltese, yorkiie
= no common genetic mtatuion found yet but BRCA 1+2 genes involve in English springer spangles= beagles = familial susceptibility
hormones and growth factors
= castration = best way to prevent
= befreo 1st heat = 0.5% risk
= before 2nd heat = 8%
= befoer 3rd heat = 26%
= preventative effect 0 after 4yr old
= number of pregnancies = no influencee
= more than 3 pseudolactation = incrase risk due to mechanic compression of acini and release of carcinogenic free radical
COX-2 expressin
- in jhumans
= cox-1 = in many tissues
= cox 2 - not innormal cells, induced by growht factors, inflam, oncogens, more frequent In malignancy
diet
= thin at 9-11 months old, decrease risk
obesity = decrease serum globulin - increased serum estrogen
adipose tissue = inreased estradiol production
high intake red meat
molecular pathogenese sin tumours
stem cells
= primary places of neoplastic transformation
estrogen
= growth factor production, direct genotoxic effect
progesterone
= synthesis of GH + it’s receptors(effects on mammary gland
mammary tumour in cats
rare
10-12 yr old
2x higher risk in siamese
high mortality and almost always malignant
OVH in 1st year = 90% preventive
mammary tumour signs
1 or more nodules in mammary gland
usually clinically health
severity of signs depemnds on extent and location of metastasis
-> lungs , live,r bone, brain, spleen, kidney, skin, eye
initial work up for tumour
age, age at OVH
history = duration of signs, repro cycles, lactation, progetsterone therapy
general condition and physical exam –> look at all mam glands in dorsal recumebcny and check LN
diagnosis of mamary tumour
blood and biochem
x-ray of thorax, CT will see 1mm
US
FNA + cytology = prediction of malignancy. 4 sampes per mass. good to differentiate from mastocytoa
check LN - biopsy/FNA for staging
treatment of mammary tumour
surgery = gold standard
exception = inoperable, higly metastic tumours or IMC
surgeries for mammary tumour
lumpectomy
simple mastectomy
regional mastectomy
unilateral
bilateral mastectomy
classification of tumour
epithelial
- simple adenoma/carcinoma -> invasive but good pronosis if completely removed
- epithelial and myoepithelial -> complex adeoma/carcinaoma > rare metasasis, prognosis semi good if compleelt removed
mesenhycma
- fibroadenoma/fibrosarcona, less than 5% of all mammary tumours
combo of epithelial and mesenchyma - very aggresive and poor prognosis
repro tract formation
- Epithelial and primordial germ cells migrate to the sexually undifferentiated gonad
- At the beginning of development, there are two channel systems: Wolffian and paramesonephric (Müller)
- Normally one goes and the other continues. In male fetuses= Wolff canals
- Anti-Müller hormone from testes = regression of Müller channels
- Müller canals develop into the fallopian tube, uterus, cervix, and vagina
- The formation of the external genitalia is influenced by the hormone gonads
