Periparturient Disease Management Flashcards
(25 cards)
describe the peripartum period
- 60d before calving to 30d after calving
- go from:
-lactating and pregnant to
-non-lactating and pregnant to
-lactating and non pregnant - changes in cow routine:
-stop getting milked
-vaccinations, foot trims
-moved to different pens: different set-up, social changes
-different rations: lactating, far-off dry, close-up dry, fresh
~a very confusing time for a cow~
describe transition challenges (9)
- parturition
- social change
- hormonal changes
- diet changes
- metabolic changes
- negative energy balance
- negative calcium balance
- negative protein balance
- negative vitamin balance
what does transition success look like? (9)
- eutocia and live calf
- pass placenta quickly
- eucalcemia
- adequate quantity and quality of colostrum
- feed intake ramps up quickly: rumen adaptation to new lactation diet
- milk production ramps up
- no mastitis
- uterus involutes normally
- return to reproductive cyclicity
what does transition failure look like?
- dystocia
- stillborn calf
- retained placenta
- dyscalcemia
- inadequate quantity and quality of colostrum production
- reduced feed intake
- low milk production
- mastitis
- uterine disease
- delayed return to repro cyclicity
- displaced abomasum
- early removal and replacement
- death
what are the 5 important parts of cow anatomy that can go wrong?
- lungs
- rumen
- liver
- uterus
- mammary gland
describe the 5 key aspects of transition management?
- minimize DMI depression prepartum
- minimize risk and effects of dystocia
- minimize risk and effects of hypocalcemia
- minimize risk and effects of uterine disease
- maximize DMI postpartum
describe DMI depression prepartum
- there is a normal drop
-due to discomfort, big baby, hormonal secretion by calf, and hormones for preparation for calving - how to minimize: remove obstacles/stressors on feed intake
-eliminate overcrowding: increased feed and lying space
-feed a properly balanced TMR
-feed 3-5% refusals (leftover feed/give a little extra/do NOT want pregnant girls to run out of feed)
-control environmental obstacles: heat stress
-group similar animals together: social stress
-reduce pen changes: social stress
-prevent fat cows (have a greater drop in DMI)
describe minimizing the risk and effects of dystocia
- calf factors: size and presentation
- human factors: timing (yank too soon = bad) and procedures
- cow factors: pelvic size, body condition, calcium status (calcium required to squeeze uterus)
management interventions:
1. sire selection: prevention; influence calf size and shape
2. heifer growth: prevention
3. proper nutrition: prevention
4. employee training: mitigation
describe minimizing the risk and effects of hypocalcemia
hypocalcemia is the gateway disease! (review calcium management lecture)
describe minimizing the risk and effects of uterine disease
- uterine involution:
-slower than horses
-approx 60-90d until ready to breed again
-must physically involute to a smaller size - uterine clearance of bacteria
-bacterial contamination (but not infection) in most at calving
-difference between contamination and infection is immune competency
describe metritis complex
- retained fetal membranes
- acute puerperal metritis (1-14 DIM)
- clinical metritis
- subclinical metritis
- purulent vaginal discharge (clinical endometritis)
- pyometra: >30 DIM, must have a corpus luteum
what are some risk factors and effects of metritis complex
risk factors:
1. retained fetal membranes
2. dystocia
3. stillbirth
4, twinning
5. low feed intake
effects:
1. treatment costs
2. decreased milk production
3. increased culling/death
4. poor repor
5. other diseases: mastitis, ketosis, DA)
describe retained placenta/retained fetal membranes
- fetal membranes >12 hours post partum
- not usually a systemic risk!! (unlike horses)
- monitor for fever/metritis
- will rot out in 3-5 days
- usually associated with calcium balance
treatment: wait longer, monitor
-do NOT give oxytocin or PGF2a or pull on it!!
-uterus is already hypermotile, increasing squeezing (oxytocin) will just make her more uncomfy
-no CL anymore so PGF2a will have no effect
describe post-partum uterine discharge
- also called lochia
- character depends on time after calving
-thick = good
-watery = inflammation
-fetid/stinky = bad
-some blood is okay for first week
-white = WBC = okay
describe acute puerperal metritis
-clinical metritis is the same but no systemic signs!
clinical signs:
1. usually with 10d post partum
2. all layers affected
3. large flaccid uterus
4. fetid, reddish brown water discharge
5. systemic signs (APM only): fever, inappetance, obtundation
treatment:
1. systemic antibiotics:
-all mucous membranes leaky with systemic inflammation
-broad spectrum
-gram negative anaerobes
-protect the body, not necessarily enter the uterine lumen
-NOT intra-uterine abx
- NSAIDS
- fluids
-usually cows that end up with metritis did not eat well pre-partum!
describe endometritis
- only the endometrial layer is affected
- subclinical endometritis: need to dig deeper to diagnose
-or clinical endometritis AKA purulent vaginal discharge: can see inflammation - dx:
-cytobrush
-metri-check
describe pyometra
- not a systemic risk in cattle
- delays pregnancy
- uterus full of pus, closed cervix
- corpus luteum: MUST have, so this happens later after calving
-makes progesterone: immune dampening
-present after first ovulation (>30d after calving)
treatment:
-remove CL with PGF2a
describe maximizing DMI postpartum
- post-partum feed intake vs. energy needs:
-energy output peaks before energy input peaks, so body weight drops - barriers to feed intake:
-ration is not balanced or mixed well
-feed not available 24/7 or unreachable
-feed access: high stocking density, low bunk access
-water access
-social stress: young timid cows with older bullies, frequent mixing of cow groups
-heat stress
describe glucose in cows
- not absorbed like in monogastrics
-must be made in the liver via gluconeogenesis - homeorhesis: short term adaptation to support physiologic state (lactation)
-strategic post partum insulin resistance in peripheral tissues to save glucose for the mammary gland to make lactose
how does energy imbalance occur?
- drop in feed intake (type 2 ketosis)
- causes energy imbalance
- causes the body to mobilize fat (NEFAs)
- liver is then overloaded with NEFAs
- which causes ketone production and fatty liver, which means ketosis so further drop in feed intake and cycle
describe fat mobilization
- fat stored as triglyceride (glycerol + 3 NEFA)
- broken down by hormone sensitive lipase
- NEFA travels to
-tissues for energy
-mammary gland for milkfat synthesis
-liver:
–exported as VLDL
–stored (fatty liver)
–used for energy:
—complete beta oxidation via the krebs cycle for energy
—incomplete beta oxidation via pentose phosphate shunt to make ketones
describe ketosis diagnosis
- hyperketonuria:
-urine strips to detect aceto-acetate
-color range results
- 0.20$ per strip - hyperketonemia:
-BHBA: number results
-meter is $30, $1.50 per test - hyperketolactia:
-powder tests for aceto-acetate: 0.75$
-strips for BHBA $1.70 - measured in the 1st 2 weeks of lactation
-normal serum BHBA: 0-1.2mmol/L
-sub-clinical hyperketonemia: >1.2 or 1.4mmol/L
-clinical ketosis: typically >3.0 mmol/L
describe ketosis treatments
- IV dextrose:
-500ml dose is common
-spikes serum glucose then returns to normal in 2 hrs
-spikes serum insulin
-excess glucose secreted in the urine, along with electrolytes
-recommendations: reserve for more severe cases, or hypoglycemic cows, maybe use a lower dose (250ml) - systemic steroids: NOT HELPFUL
-cause hyperglycemia
-block effect of insulin
-lower milk production (reduce drain)
-recommendations: unlikely to help, side effects on immune system - insulin: NOT HELPFUL
-decreased fat breakdown
-increases use of BHB as an energy source
-recommendations: cattle are already insulin resistant in early lactation, especially those in ketosis and this is high cost and unlikely to help - propylene glycol:
-absorbed and enters TCA cycle
-converted to proprionate in rumen
-recommendations: 300ml once a day for 2-5days
-SHOULD BE FIRST LINE TREATMENT - +/- vitamin B12 as a potential appetite stimulant
describe the veterinarian’s role in periparturient disease management
- surveillance plan
- monitor incidence of fresh cow disease
- monitor feed intake data
- monitor social stress: pen moves, stocking density
- train employees on calving management
- monitor calcium status (and urine pH if neg DCAD diet)
- train employees in uterine disease detection and treatment
- adjust SOPs and monitor effects
