Reproductive medicine use in practice Flashcards
What is Puerperal metritis?
Clinical metritis but with acute systemic illness (pyrexia (>39.5), dullness, reduced yield, inappetance, tachycardia, dehydration)
What is Clinical metritis?
Uterine disease within 21 days of parturition, most common in first 10 days. Enlarged uterus, watery red brown fluid to viscous off white purulent uterine discharge, with fetid odor. Grade 1-3 dependent on signs of health. Clinical metritis can be present without a fever.
What is Clinical endometritis?
Clinical disease beyond 3 weeks post partum. (Muco)purulent discharge detectable in vagina. Grading system based on character of vaginal mucus. Cervical diameter >7.5cm No systemic signs (Sheldon et al., 2006). What makes it clinical is we can see discharge coming out of vagina but cows appear clinically well.
What is Subclinical endometritis?
Don’t really notice as no discharge but when you swab there is evidence of:
- Chronic inflammation of the endometrium without clinical signs of uterine disease but resulting in significant reduction in reproductive performance. Determined by cytology, PMN’s exceeding 5-18% in samples from flush or cytobrush, can also be present in the absence of bacteria (Santo 2009, Kasimanickam, 2004).
- Incidence 37-74% (Gilbert, 2005)
- They would benefit from treatment in the same way as a cow with clinical endometritis
What is Retained placenta?
Failure to pass the placenta within 24h post partum
What is pyometra?
Pyometra: Uterus with pus in it (also in a way same as clinical endometritis however there is in addition a persistent CL in pyometra)
(Muco)purulent material in the uterus, distension of the uterus, presence of active CL. (In)complete closure of the cervix. Mixed echo density on US.
In short define puerperal metritis, clinicla metritis, clinical endometritis, subclinical endometritis and pyometra.
Puerperal metritis: discharge, ill, <21DIM
Clinical metritis: discharge, not ill, <21 DIM
Clinical endometritis: discharge, not ill, >20DIM
Subclinical endometritis: no discharge, not ill, >18%PMNs>21DIM
>10%PMN >34-47DIM
Pyometra: ‘closed’ cervix, pus, CL
What is the treatment for metritis?
- Systematic antibiotics (amoxicillin/proc penicillin)
- No benefit of ‘intrauterine & systemic’ over systemic only. Systemic antibiotics at the right dose is sufficient to penetrate the uterus
- TLC
- Fluids (oral, IV)
- NSAIDs (>1 day), one dose of flunixin did not improve outcome (outcomes based on whether she comes back in to calf not if it reduces pain) (Drillich et al., 2007)
- Lavage? On farms this is done with a hose pipe until clean water comes out. Evidence zero in this area.
- Animal welfare! They should have some anti-inflammatories
- Herd management protocol: treat cows with at least 2 symptoms of metritis (RP, T>39.5, dullness or inappetance, fetid uterine discharge)
- These animals are ill and need treatment.
What is the treatment for clinical & subclinical endometritis?
If CL is present: PGF2α - Stimulate uterine defences. Luteolysis and subsequent increased oestrogen and myometrial contractions. Some evidence for direct short term contractile effect on uterus. However, 20% of cows anovular until 60DIM.
If no CL is present: cephapirin - improved pregnancy rate; economically preferable to treat all cows with RP, dead calf, owner observed discharge >13 DIM with cephapirin compared to examining and treating at risk cows based on vaginoscopy (cephapirin only registered product to use research shows cows come in to calf week earlier than calfs that don’t get treatment)
•DO NOT GIVE: oxytetracycline (OTC) or Lugol’s iodine: can cause coagulation necrosis of endometrium (Gilbert & Schwark 1992)
What is the treatment for Pyometra?
PGF2α
What are the effects on ovarian function that pathogens have?
Pathogens in the uterus have many other effects on uterus:
- Pathogen associated molecules such as LPS affect the release of GnRH, LH and sensitivity of pituitary to LH; cow less likely to ovulate
- Lower oestradiol concentration at time of maximal follicle diameter; cow less likely to ovulate
- Slower growth of 1st postpartum dominant follicle
- Lower progesterone concentration 5-7 days after ovulation; a response of luteal cells to cytokines secreted by infected endometrium
- Prolonged luteal phase: due to PGF>PGE switch which disrupts luteolytic mechanism
What is the definition of retained fetal membranes?
membranes present >24 hours after calving
What are the risk factors for RFM?
twins, dystocia, stillborn calf, induced parturition, abortion, milk fever, increased age, seasonal effects
What is the pathogenesis of RFM?
Not the lack of uterine motility; failure immune system to degrade placentomes at the end of pregnancy, as low intracellular calcium effects immune function (mononuclear cells).
Riskfactors: suboptimal DMI around the time of calving 2-3 weeks before, high PGF and cortisol levels 1 week prior to parturition are more likely to get a RFM.
What is the impact of cases of RFM?
Only important as risk factor for (endo)metritis. Preg rate 15% less than uninfected cows. Typically 25-50% develop metritis/endometritis if have RFM.