Lecture 8: Transition Cow Health and Disease Flashcards
What are some peripartum metabolic changes and challenges? (growing fetus -> lactating)
-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
What are goals, impediments and consequences of a transition cow?
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
How to determine the success of the transition period?
-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)
What is considered one of the most important determinants of health and performance?
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
Why does DIM drop?
-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
What can amplify a drop in DIM?
- Crowding/lack of feed access (What to make sure they are always eating)
- Heat stress (Feed will spoil faster, use of fans or sprinklers)
- Excessive dietary changes (Dry cows fed higher fibre so switch of diet makes it harder)
- Social changes (Social hierarchy, cows won’t eat for couple days after being moved, move in pairs to help with stress)
What is the time frame for development of mammary glands for lactation, rumen microflora adaptation, and social adjustment to new group?
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
Recap: what are the pariparturient disease?
-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
What are the economic impacts of disease?
- Unrealized milk production (production cows would produce < milk yield)
2.Treatment costs - Discarded milk
- Delayed or non-pregnant*
- Culling (removed from the herd)
- Health (5% of cows)
- Direct costs of most transition diseases (milk fever, metritis, ketosis, DA) $175-$450/case
What is milk fever?
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
What are clinical signs of milk fever?
- 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) - Stage 2
-Unable to rise: so in sternal recumbency
-Depressed, head on flank - Stage 3
-Lateral recumbency
-Bloat –> death (rumen is filled with gas, can’t get rid of gas)
What is treatment for milk fever?
- 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: - Oral calcium gel, bolus, or drench
OR - 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
What are milk fever treatment outcomes?
- Fully recover
-Production loss
-Risk of other diseases - Relapse (if not given secondary treatment)
- 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
What is different for subclinical hypocalcaemia?
-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
How do you prevent hypocalcaemia?
-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)
