Bovine Endometritis

Several of our tweeters appear to have hit the wine (ahem, Fay Pooley, Jono Frost) but everyone is still keen to carry on with case 2, so here goes…

Straight in there with reasons to do a PNC:

So, issues on our PNC hitlist:
– Uterine involution
– Damage to repro tract
– Check cervix
– Presence of vaginal discharge
– Systemic illness/other concurrent diseases

A quick abbreviations check up:

Now onto our findings:

So what do we want to look at in more detail?

 

And some answers:

So let’s have a diagnosis:

Unfortunately, not just a bulling string!

So let’s move on to treatment options:

If there is a CL present…

If no CL present…

So if there is a CL present, we will treat her with 2ml prostaglandin and recheck at the next visit. However, if there is no CL present then we need to treat with antibiotics, in this case cephapirin (Metricure) which is given intra-uterine via a catheter passed through the cervix.

Another option was raised:

Now we’ve fixed this one, how are we going to prevent other cases occurring?

So it is important to have a clean calving environment, but this is not a key factor in the development of endometritis. What else?

http://twitter.com/MO05EE/status/327526657818783744

So we need to make sure we get the nutrition of our dry cows spot on to try and reduce problems around calving.

http://twitter.com/MO05EE/status/327529094906535937

That little link that has snuck in there courtesy of Mark is a very nice article on strategies for the control of milk fever – definitely worth a read!
 http://inpractice.bmj.com/content/27/2/88.full.pdf+html?sid=7e851fba-95c2-4bcb-87f4-3fbee559cf81 

And a final round up from Wendela!

If only it was always this clean and easy…

 

Summary: uterine infections in cattle
Pathogenesis

Associated with dystocia, assisted parturition, twins,
stillbirths and retained fetal membranes

Reduced DMI and immune function also have an effect

Can be acute or chronic

Local infection of the reproductive tract can spread to systemic
endotoxaemia
Development of disease is dependent on the balance
between host immunity and pathogenicity of bacteria

Healthy cows: clear bacteria in 3 weeks, complete
involution of uterus and cervix in 4-6 weeks

NB/ lochia passed until 23 DIM – this is normal! Do not
treat unless foetid odour (metritis)

Bacterial causes
E. coli
alters the uterine environment, paving the way for other bacteria and viruses.
Associated molecules affect release of GnRH, LH and sensitivity of pituitary to
LH so cow is less likely to ovulate
Arcanobacterium
pyogenes
– most severe endometrial lesions, synergism with anaerobes,
enhances likelihood and severity of disease

Suppressed immune function from 2 weeks pre-partum to 3
weeks post-partum due to drop in energy, vitamin and mineral intake, NEB,
mobilisation of body fat and protein and a massive increase in cortisol

Pathogenic organisms cause PGE rather than PGF production
in response to inflammation, but there is a loss of cyclicity due to no
luteolysis, leading to a prolonged luteal phase

Once a cow is infected, PMNs become less effective

 

Clinical signs

Puerperal metritis = clinical metritis with acute
systemic illness

– Pyrexia (>39.5*C)
– Dullness

– Reduced yield

– Inappetance

– Tachycardia

– Dehydration

Clinical metritis = uterine disease within 21d of parturition, most
commonly in the first 10d

– Enlarged uterus

– Watery red-brown fluid to viscous off white
purulent discharge with a foetid odour

– Graded 1-3, based on % pus in discharge

– Clinical metritis can be present without a fever

Clinical endometritis = clinical disease >3 weeks post-partum

– (Muco)purulent discharge in the vagina

– Graded based on character of vaginal mucus

– Cervix >7.5cm diameter

– No systemic signs

Subclinical endometritis = subclinical disease >3 weeks post-partum

– Chronic inflammation of the endometrium without
clinical signs of uterine disease but with a reduction in reproductive
performance

– Cytology – PMNs >5-18% from flush or
cytobrush

Pyometra = (muco)purulent material in the uterus with
distension and the presence of an active CL

– PGE production from damaged uterine wall, rather
than PGF-2alpha, is an inflammatory mediator without causing luteolysis

– Incomplete closure of the cervix

– Mixed echogenicity on US – snowstorm appearance


Treatment

Principles of treatment:

1.       Reduce
bacterial load

2.       Enhance
uterine defence and repair mechanisms

3.       Halt
and reverse inflammatory changes that impair fertility

 

Metritis

RFM is the greatest risk factor for metritis – reduce RFM
to reduce incidence of metritis

Systemic antibiotics: procaine penicillin or ceftiofur
for 3-5d

Flunixin if systemically sick

Fluid therapy

Consider lavage

Calcium may be indicated

 

Clinical
endometritis

PGF2-alpha in the presence of a CL

– Luteolysis, increased oestrogen levels and
myometrial contractions

– Stimulation of uterine defence mechanisms

Metricure (cephapirin) in the absence of a CL

 

Subclinical
endometritis

PGF2-alpha

Metricure (cephapirin)

 

Pyometra

PGF2-alpha

 

Prevention

All are diseases of immune function in the transition
period

Optimise immune function in transition cows

– Feed intake and energy balance

– Mineral status – selenium and vitamin E

– BCS monitoring

Pick up hypocalcaemia early and treat to try and reduce
RFM