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.