Lecture 8: Transition Cow Health and Disease Flashcards

1
Q

What are some peripartum metabolic changes and challenges? (growing fetus -> lactating)

A

-Fetal growth
-Rumen and gut adaptation to diet changes
-Initiation of lactation
-“opening” of teats and reproductive tract
-Rapid, leave calcium demand
-Decrease DIM
-Negative energy balance
-Fat mobilization
-Hypocalcemia
-Immunosuppression

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2
Q

What are goals, impediments and consequences of a transition cow?

A

Goals
-Calve w/o problems
-Avoid disease
-Make lots of milk
-Get pregnant by 120 DIM

Impediments
-Feed intake
-Severity, timing and duration of negative energy balance
-Environmental factors (moving to different group, reestablish cow hierarchy moving in pairs will reduce)
-Immune function

Consequences
-RP
-Dystocia
-Metritis
-Ketosis
-DA
-Mastitis
-Endometritis
-Anestrus

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3
Q

How to determine the success of the transition period?

A

-Clinical disease incidence (doesn’t take into account subclinical and producers don’t always record)
-Production (easy do it w/ program)
-Measure dry matter intake (weigh feed fed - not eaten but most farms don’t do that)
-Measure body condition score (maintain is good)
-Understand cow experience
*Feed access (make sure every cow has space)
* Lying time (monitor with leg band)
*Housing design (make sure conformable and can lay down)
-Clinical tests: BHB (beta hydroxybutyrate), non-esterified falls acid (NEFA)

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4
Q

What is considered one of the most important determinants of health and performance?

A

Feed Intake
-Measurements of group-average DIM can be useful starting point for early warning
-Ideally would detect individual outliers (but not case on most farms)
-A 1kg decrease in individual DMI in the week before calving is associated with
*2x increase in the odds of subclinical ketosis
*2.9x increase in the odds of metritis

Concept: monitoring food intake can give insight on disease

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5
Q

Why does DIM drop?

A

-Diet composition, BCS (increase will decline DIM but increase infection), parity, and time from calving together explain only 18% of cow-to-cow variation in pre-partum DIM
-Little evidence for lack of rumen/gut space
-Burning NEFA in liver may inhibit DMI (bad sign may decrease DIM)
-Probable roles of insulin (esp. postpartum) and leptin in decrease DIM

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6
Q

What can amplify a drop in DIM?

A
  1. Crowding/lack of feed access (What to make sure they are always eating)
  2. Heat stress (Feed will spoil faster, use of fans or sprinklers)
  3. Excessive dietary changes (Dry cows fed higher fibre so switch of diet makes it harder)
  4. Social changes (Social hierarchy, cows won’t eat for couple days after being moved, move in pairs to help with stress)
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7
Q

What is the time frame for development of mammary glands for lactation, rumen microflora adaptation, and social adjustment to new group?

A

Development of mammary glands for lactation: Takes around 3 w
Rumen microflora adaptation around 10-14 d
Social adjustment to new group 1-2d major effects; up to 1 week

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8
Q

Recap: what are the pariparturient disease?

A

-RP right after calving
-Milk fever right after calving
-Metritis 1-10d
-Ketosis 8-20d
Displaced abomasum 9-20d
-Endometritis 20d–>

*Bottom line: Marjorie of metabolic problems occur in the first 4 weeks of lactation
-25% experience 2 or more diseases

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9
Q

What are the economic impacts of disease?

A
  1. Unrealized milk production (production cows would produce < milk yield)
    2.Treatment costs
  2. Discarded milk
  3. Delayed or non-pregnant*
  4. Culling (removed from the herd)
  5. Health (5% of cows)
  6. Direct costs of most transition diseases (milk fever, metritis, ketosis, DA) $175-$450/case
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10
Q

What is milk fever?

A

Milk fever aka Hypocalcemia, parturient paresis
-Large, rapid net output of calcium unto colostrum (30g of Ca in 1 day)
-All cows have some degree of hypocalcemia in the first 1-2d after calving
-a disease of cows in 3rd + lactation especially jerseys: put more Ca+ into milk
-Ca is a key part of the mechanism of muscle contraction (which leads to direct clinical signs)
-If blood Ca falls too low to support muscle fxn cows become weak and eventually unable to rise

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11
Q

What are clinical signs of milk fever?

A
  1. Stage 1
    -Unsteady on their feet
    -Cool extremities skin and ears (poor circulation so strength of heart contraction is slow)
    -Can be hyper-excitable (jumpy)
  2. Stage 2
    -Unable to rise: so in sternal recumbency
    -Depressed, head on flank
  3. Stage 3
    -Lateral recumbency
    -Bloat –> death (rumen is filled with gas, can’t get rid of gas)
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12
Q

What is treatment for milk fever?

A
  1. IV calcium injection (only when cows are down)
    -Required to treat stage 2 or 3
    -Short duration of effect (4h) so have to give a secondary long term treatment:
  2. Oral calcium gel, bolus, or drench
    OR
  3. Subcutaneous calcium injection

*if IV is too fast (high height of IV bag) can impact heart contractions so want to do it slow or have IV bag around the level of their head

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13
Q

What are milk fever treatment outcomes?

A
  1. Fully recover
    -Production loss
    -Risk of other diseases
  2. Relapse (if not given secondary treatment)
  3. Downer cow syndrome (Don’t respond to initial treatment)
    -Ischemic necrosis of the hind leg muscles (bc weigh too much putting too much pressure on muscles)
    -Estimated that only 1/3 recover (2/3 euth)
    -Bright/alert, eat/drink, but will not get up
    -Can also be the result of acute toxic mastitis or calving paralysis (flip on back and switch sides multiple times a day or lift with tractor to increase blood flow of muscles
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14
Q

What is different for subclinical hypocalcaemia?

A

-Subclinical hypocalcemia present in 32.3% of sampled cows
-is associated with:
1. Increased odds of DA
2. Greater odds of culling
3. ~3kg/d lower milk yield in early lactation
4. Reduced immune function
5. A difference in early lactation fatty acids metabolism

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15
Q

How do you prevent hypocalcaemia?

A

-Cows have adequate whole-body ca, most of which is stored in bone

Challenge
-Maintain blood Ca by fast enough mobilization of Ca from bone (via PTH)
-Extra dietary Ca is not absorbed as fast as loss in colostrum (although Vit D3 enhances absorption)

Traditional theory
-Restrict Ca intake prepartum <20g/d
- <100g/d is difficult

Current theory
-Balance dietary cations (Na & K) and anions (Cl & S) to create a neg dietary cation anion difference (DCAD)
-ie acidic
-Point is to facilitate mobilization of Ca by producing slight metabolic acidosis (favours the fxn of osteoclast cells)

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16
Q

What is DCAD and what is the ‘chemical equation’ used to illustrate?

A

(Dietary Cation Anion Difference)
DCAD (mEq/kg) = (Na + K) - (Cl + S)

-lowering the DCAD lowers the risk of milk fever
-Adjust dry cow ration by:
*Feeding low potassium forages
*Low ca diets (<0.5%)
*Feeding adequate Mg
*Feeding anionic salts (imput în ration creates neg DCAD)
-N.B intake is critical
*Better to eat and not have anionic salts rather than feed anionic salts and suppress intake

17
Q

What are metabolic fuel sources?

A

-Carbohydrates (glucose) are the primary metabolic fuel
-Cows diets are mostly CHO
-But dietary CHO are converted to fat (fermentation of starch and fibre to VFA)
-Glucose is required for milk (lactose) and fetus (lots of glucose going into milk leaving little for themselves)
-Cow must perform gluconeogenesis (of VFA’s only propionate can -> glucose
-Mobilization fat is a large source of energy, but not a direct substitute for glucose

18
Q

What is the response to NEB?

A

Adaptive
-Spare glucose, shift to fat as fuel (problem Pre-partum fetal demand for glucose, postpartum: udder need for glucose)
-Burn NEFA; increase gluconeogenesis from glycerol, propionate, AA (problem for FA’s to enter Krebs cycle, intermediates require glucose) otherwise NEFA metabolites -> ketones +- fatty liver

-All transitional dairy cows are in NEB (completely normal not consuming enough energy issue how sever and how adapt)
-Issues include
1. The degree and
2.Success of adaptation
3.Ability to maintain DIM prepartum and increase rapidly postpartum (aimed to mitigate immunosuppression, impaired GI and liver function

19
Q

What is ketosis?

A

-Produced from excessive rate of breakdown of body fat–> incomplete oxidation –> increase in ketones
-Increased ketone bodies in blood
1. Beta-hydroxybutyrate
2. Acetoacetate
3. Acetone
-Blood glucose is low (see heart diagram)

20
Q

What are clinical signs of ketosis?

A
  1. Decreased feed intake/off feed
  2. Decreased milk production
  3. Firm dry manure
  4. Loss of body weight
  5. Ketones in milk or urine
  6. Nervous signs (occasional)
    -May be under-recognized tip of the iceberg in many cases (lot of subclinical)

Subclinical ketosis
-Elevated circulating level of ketone bodies w/o the presence of the clinical sings of ketosis
- around 40% cumulative incidence up to 2 w postpartum (very common)
-Precision ulta best test to use

21
Q

What are associations of ketosis with health and performance? Not *

A

-Subclinical ketosis in early lactation is associated with:
-4-8x increased risk of LDA
-Decreased milk production
-Increasd severity of mastitis due to impaired neutrophil function
-50% decrease in pregnancy at first AI
-50% increase in risk of anestrus at 60DIM

22
Q

What are the treatment options for ketosis?

A

-Provide additional energy to decrease ketone body generation (propylene glycol orally 300g once/d for 3-5d)
-Dextrose IV once
-Corticosteriods proven to NOT be affective
-Correct primary nutritional or management problem that is limiting permpartum DIM or producing fat dry cows

23
Q

What is displaced abomasum (DA)

A

-Common after ketosis (6-8x more likely)
-Physical shift of abomasum from ventral abdominal up to left (80-90%) or right side (10%)
-Associated wit accumulation of gas and lack of abomasa motility (could be related to low level Ca or low level feed intake
-Restricts passage of feed
-Leads to anorexia, +- diarrhea, drop in milk, further ketosis (becomes worse)
-Ping abdomen to diagnose, flick side and hear ping actually called ping test

24
Q

What are risk factors for LDA?

A
  1. Fat cows (BCS>or equal 4)
  2. Twins
  3. Dystocia
  4. Retained placenta
  5. Milk fever
  6. Hypocalcemia
  7. Ketosis* talked about before (6-8x more likely)
  8. Metritis
    -Intake DIM during the transition period
    -Feeding and management practices that prevent other postpartum disorders reduce the risk of LDA
    -Anything that impacts DMI will increase risk for DA
25
Q

What is the treatment for DA?

A
  1. Rolling –> 60% will relapse
  2. Surgery
    a. Numerous surgical approaches or blind toggle bar suture (left/right flank incision)
    b. All yield 80-95% “success”
26
Q

How do you manage transition cows to prevent disease? not *

A

-Prevention evolves more than a good truncation ration, we also need to consider:
1.”cow comfort” (stall design, ventilation/heat abatement ie sprinklers, floors not slippery)
2. Access to water
3. Calving mangament
4. Post calving -grouping
a. by stage of lactation
b. By parity

27
Q

What are some concepts of the transition check list?

A

-Goal: optimize metabolic health and immune fxn (can prevent lots of things)
-Means: manage cows to maintain feed intake (max feed intake)
-Feed access (decent bunker space and feed lots for left overs)
-Pen design (not too crowded and comfortable for cows to eat)
-Lying time (Well designed tells and adequate clean, dry bedding)
-Pen management (<24h in calving pen, separate heifers if possible, minimize group changes)
-Transition diet (meet but not exceed energy, water ad lib, adequate vit E and selenium goal of BCS 3-3.5 at calving
-Monitoring (clinical disease incidence)

28
Q

What are the take-home messages?

A

Goals for a transition cow includes:
-Calving w/o problems
-Avoiding disease
-Producing lots of milk
-Being pregnant by 120DIM

-Majority of peri-parturient disease occurs shortly after calving, thesis include RP, metritis, DA, endometritis, ketosis, and milk fever these are influences by the cows nutrition, DMI and energy requirements
-Prevention of periparturient disease is key