The USA is unique in that in
every major dairy breed, you have two choices for ranking indexes—AIPL (USDA)
“Net Merit” and each breed association’s TPI (Holstein), JPI (Jersey), etc.
Holstein USA’s “TPI” (and its
Canadian corollary, LPI) is calculated from milk production and type
classification traits, weighted roughly 60%/40%. Jersey USA’s “JPI” is somewhat
similar, more heavily weighted to butterfat yield, then protein, then type.
None of these indexes put as much emphasis on health, fertility and longevity
as “Net Merit”—which is a curious switch from the traditional view of breed
associations, founded on the belief in “longevity” as cow profitability.
“Net Merit” over time has
been transformed from an index weighted 70% on “milk pounds” (1970) to 0% on
“milk pounds” today—placing roughly equal emphasis on fat + protein, health,
fertility and associated assumptions relative to cow size and feed efficiency.
Net Merit became “lifetime” net merit in response to the loud complaints of
commercial dairying—“cows turn over too fast”.
PTA- SCS (somatic cell
score) is the key “health” component in “Net Merit”. Why is this?
Not just because mastitis
is the scourge of dairying, the biggest source of lost income during any cow’s
lactation. A somatic cell is not just a “mastitis” cell—it is any cell
with a nucleus, thus it could be a bacterial or viral cell, it could be a spent
white blood cell, it could be a shed skin cell.
Thus the level of SCC in any
individual cow’s milk indicates the total functioning of her immune system in
fighting infections and protecting health.
Canadian Dairy Network (the
research agency that calculates Canadian genetic evaluations) in a major study
of the production patterns of dairy cows over their lifetimes concluded that
SCS is an indicator of the potential productive longevity of dairy cows. They
found (1) the sires with higher SCS ratings, had the earlier-maturing, faster
aging daughters, less productive than their evaluations suggested in second and
later lactations (if they even had mature lactations); (2) the sires with lower
SCS ratings, produced daughters that matured better, lasted longer, and
exceeded early age estimates of productivity in their mature lactations.
The summary conclusion: if you are seeking longevity, pay
attention to SCS ratings. In other words, SCS is not just about
mastitis. Thus we cannot blame higher SCS scores on bad milking habits or
maladjusted vacuum systems. Fragile health is a heritable condition.When
we ignore SCS ratings in favor of bigger numbers, like PTA Milk, we can
accumulate problems as well as add to generations of “single trait” selection
in genetics.
An example of this is that the
highest SCS cows in many herds are “lame” cows with clean udders on CMT tests. Foot
rot, heel warts and laminitis will all elevate SCC levels, simply because the
immune system is producing leucocytes in volume to reach these furthest extremities,
where blood flow is small. Infection fighting cells, once “spent,” are expelled
by the body through the udder.
The cell counting machines at
the dairy labs add them up in the SCC totals.
Even extraordinary high
butterfat% and protein% levels in milk will elevate SCS a bit, because the
thicker (more milk solids density) milk draws some skin cells along during
final milking. Again, a basically benign cell gets counted the same as an
infection cell. But this usually stays within 10% of the SCS levels on lower
testing cows. (There is no evidence that higher SCS levels will affect cheese
yields—possession of the “B” Kappa Casein gene and the level of protein % have
the greatest positive impact on cheese production from any given volume of
milk.)
Are you prepared for
the coming 400,000 SCS limits on “legal” milk? Many of us, under the
existing system that uses 750,000 as the legal limit, see our herds range from
200,000 to 500,000 according to the season. Thus the new 400,000 limit exposes
too many dairymen to penalties and diversion of milk to sub Grade A processing
at a lower milk price. While a lower SCS limit forces us to pay more attention
to milking system maintenance, cow stall bedding, hoof care, vaccination,
post-calving cow health, milking prep procedures and teat dipping, without
considering the genetic links to health, it can still feel like a losing
battle.
Chronically high SCS
levels are NOT “normal” and only environmental
I listened to a Holstein USA
fieldman advise southern dairyman that “sire SCS data is meaningless, all high
SCS scores are the fault of bad milking machines”—his further advice was that,
unless sires are +2.50 for Type, they cannot help you breed good
udders—meanwhile, the average herd SCS in the southern USA is dangerously close
to the coming legal limit.
Increasingly, astute dairymen
are coming to recognize that too much of their advice on genetics is coming
from opinion rather than research-based and observationally verified fact.
Advice that is not leading you to solutions other than “cull the bad ones” is
poor genetic theory and expensive in reality.
The facts are this—SCS
has as high a level of heritability as most type traits other than udder
traits.
We all pay a great deal of
attention to linear type data—why then ignore SCS data??
The dollars and cents of
the SCS scoring that adds up to PTA- SCS
AIPL standardizes each
breed’s SCS average at 3.00. Thus an average bull will be SCS 3.00. It is a trait where lower score is
better—thus bull books that say “+3.30 SCS” are incorrectly stating this,
given you might interpret the worst scores as better than the best scores.
Each log point of SCS
represents approximately 70,000 cells for a Michigan dairyman (the average of
all milk tested through MMPA in 2010 was slightly over 210,000 raw count).
Thus the difference between
really healthy SCS and problematic SCS looks like this: (Dec 2011)
080H 1067
Atlantic SCS 2.48 +0.2 PL 200H 1758 Leheros SCS 3.31 -0.8 PL
006H 1124
Tycoon Red SCS 2.50 +6.1 PL 007H 2236 Elton *BL SCS 3.19 -1.2 PL
054H 0480
Legend SCS 2.51 +2.0 PL 029H 8343 Convincer *CV SCS 3.18
-3.3 PL
076H 0500
Refresh *RC SCS 2.52 +4.5 PL 200H 7030 Talent *RC SCS 3.18 +2.6 PL
076H 0569
Hi Tech SCS 2.55 +4.3 PL 011H 3073 Luke SCS 3.16 -3.8 PL
006H 1152
Zade SCS 2.57 +6.2 PL 200H
0044 Morty SCS 3.11 -4.1 PL
Further correlations will
often show up as differences in levels of UDC (Udder Composite) or FLC (Feet
and Leg Composite) to indicate type-related sources of rising SCS levels, or
differences in the DPR (Daughter Pregnancy Rate) to indicate slower fertility
that can, with SCS, contribute to shorter herdlife. Now consider how multiple
generations can add up negatively into big SCC differences.
In other words …
Health traits, primarily SCS,
and fertility traits, primarily DPR, add up to major impacts on the cow
Productive Life length. Individual exceptions aside, the pattern is clear from
the above examples.
Genetics has changed since Hoover was
President
Mostly, what has changed is the presentation of the
data. Old assumptions as to the value of PD (now PTA) volumes for milk, fat and
protein, and the value of type score information, need to catch up to what we
have learned by more recent genetic studies of health and fertility patterns.
There are “pretty” cows that act frail, “milky” cows
that lack fertility, and “functional but plain” cows that can live productively
forever even if only herd average as heifers.
These variations are explainable by looking at all
the data, and rather than just a blind look at your favorite trait number
or ranking index, can help you to a more profitably precise selection of
AI sires.
The most total value (herd equity plus milk
check cashflow) cows come from genetic packaging of type, production and health
in a positive balance, leading to longevity.
Taking shortcuts to save a couple bucks on a straw
or gain a phantom 500 pounds on PTA Milk is where we miss out on accumulating
gains in productive longevity.
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