170 R
. Rupp, D. Boichard Livestock Production Science 62 2000 169 –180
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initial le plus bas presentent le risque le plus faible de mammite clinique, et qu’il n’y a pas d’optimum intermediaire.
2000 Elsevier Science B.V. All rights reserved.
Keywords : Clinical mastitis; Dairy cow; Somatic cell count; Survival analysis
1. Introduction 1995; Mrode and Swanson, 1996; Boichard and
Rupp, 1997. However, the relationship between SCC and mas-
Because of its high incidence Seegers H. et al., titis is far from being clear. Some authors Coffey et
1997a; Seegers J. et al., 1997b and biological effects al., 1986a; Kehrli and Shuster, 1994; Schukken et al.,
Schukken et al., 1997, mastitis is the most costly 1994 were concerned by the recommendation of
disease in dairy cattle Shook and Schutz, 1994. For continuously decreasing SCC by selection, and ar-
farmers, the economic consequences of mastitis gued that such a trend could impair the cow’s
include losses of milk production Lescourret and capacity for leukocyte recruitment and, therefore, her
Coulon, 1994 or milk sale, increased culling rates, ability to respond to intramammary infection. Ac-
cost for veterinary treatments, and higher Somatic cording to Kehrli and Shuster 1994, cows with
Cell Counts SCC in milk. Although management is very low SCC would be more susceptible to mastitis.
the most effective way to prevent intramammary These arguments were based on early studies report-
infection, selection for mastitis resistance is an ing that moderate cell counts in milk play a protec-
alternative to be considered, at least to prevent any tive role in the defense of the mammary gland
detrimental effect of selection for milk yield on Schalm et al., 1964a,b. These authors found that
udder health. quarters
with moderate
to high
initial SCC
Direct selection against clinical mastitis is dif- 400,000–600,000 cells ml had lower risk of being
ficult, because in most countries clinical mastitis infected after experimental challenge with mastitis
events are not widely recorded, and because the pathogens, and concluded that a cell count of
corresponding heritability trait is very low, close to 500,000 cells ml afforded protection against in-
0.02 Emanuelson et al., 1988; Weller et al., 1992; tramammary infection. Following these results, in-
¨ ¨
Lund et al., 1994; Poso and Mantysaari, 1996. trammamary polyethylene devices were developed to
Conversely, several arguments promote the interest artificially increase SCC and potentially afford
of SCC in the selection for mastitis resistance. As protection to bacterial infection Schultze and Paape,
SCC are routinely recorded in most milk recording 1984; Timms, 1990. Use of such devices was shown
systems, they are available on a large scale at a to be effective against severe coliform infections but
moderate cost. Although detecting short clinical unfortunately led to undesirable milk losses Timms,
events on the basis of monthly test day SCC is 1990. More recently, a study based on an ex-
usually not possible, SCC efficiently account for perimental infection with Staphylococcus aureus on
subclinical and chronic infections. As reviewed by 113 cows Schukken et al., 1994 and using bac-
Mrode and Swanson 1996, the heritability of SCC, teriological tests to define establishment of infection,
close to 0.15, is much greater than for clinical supported that theory and reported that animals
mastitis. In addition, the genetic correlation between resisting infection had higher SCC just prior to
both traits is positive and moderate to high around infection than animals becoming infected 282,000
0.7, suggesting that some genes reduce both cell and 91,000 cells ml, respectively. Whereas selec-
counts and clinical infection rates. Consequently, it is tion against cows with high SCC is supposed to
believed that selection for decreased SCC would reduce mastitis incidence, the question is now raised
reduce susceptibility to clinical and subclinical mas- whether SCC should be decreased to the lowest
titis Colleau and Le Bihan-Duval, 1995. Indeed, possible value or should not be lower than a critical
SCC has already been included in the breeding goal threshold.
and genetic evaluations are routinely published in To answer that question, some authors investi-
several countries Schutz, 1994; Reents and Dekkers, gated the linearity of the relationship between both
R . Rupp, D. Boichard Livestock Production Science 62 2000 169 –180
171
traits. McDaniel 1993 found that regressions of SCC information and to occur from 5 to 35 days
absence or presence of mastitis cases in first lactation after calving. Mastitis events were declared by
cows on PTA for sire somatic cell score were farmers and collected every month by Milk Record-
positive: one unit change in PTA corresponded to an ing technicians until March 1, 1997. Reliability and
increase of 36 in mastitis incidence. Rogers et al. completeness of disease recording was assessed by
1996 found similar results for US bulls used in an additional survey conducted by the Milk Record-
Denmark and Sweden. In two Swedish breeds, ing agents. Herds 36 for which clinical cases
Philipsson et al. 1995 reported a linear relationship recording was considered to be incomplete by the
between Relative Breeding Values RBV for clinical technicians were excluded from the study. Herds
mastitis and SCC, with a 0.35 increase in RBV for without any clinical mastitis event recorded were
mastitis per unit of RBV in SCC. All these studies also discarded. The information collected was the
suggested that SCC could and should be decreased to date of the monthly test following the event. If
the lowest possible value. mastitis occurred around calving 28 to 1 8 days,
Other authors investigated the relationship be- this was additionally stated. Consequently, the confi-
tween SCC at a given time, e.g., the onset of dence interval of the exact date of clinical mastitis
lactation, and occurrence of intramammary infection was 35 days during the lactation average interval
or clinical mastitis later in lactation Coffey et al., between two consecutive test day or 16 days around
1986b; Schukken et al., 1994; Beaudeau et al., calving. Accordingly, for processing this informa-
1998. These studies, however, were carried out with tion, a mastitis during lactation was arbitrarily sup-
a limited amount of data or did not account for the posed to occur 16 days before test day and a mastitis
time period up to mastitis. around calving was supposed to occur the day of
Alternatively, in addition to the presence or ab- calving. The whole data set included 25,833 cows,
sence of mastitis events, survival analysis can also out of them 5156 20 had at least one clinical
account for the length of the time period up to the mastitis in first lactation. To avoid the possible effect
¨ event Grohn et al., 1997, i.e., the number of days
of a previous clinical mastitis event on the first SCC, up to first mastitis. Survival analysis is based on the
1940 cows with a clinical mastitis recorded before 35 concept of hazard rate, defined as the probability of
days after first calving were discarded. Finally, to occurrence of some event at time t, given that it did
study the relationship between early SCC and clini- not happen just before t. This methodology provides
cal mastitis in a range of low to moderate cell estimates of relative risks of an event for groups of
counts, only cows with a first SCC lower than cows defined according to given characteristics. The
400,000 cells ml were considered. Accordingly, objective of this study was to determine if low SCC
2779 cows were discarded. These edited cows were cows are at greater risk to first clinical mastitis than
found to have high mastitis frequency, as 476 17 cows with somewhat higher SCS. Relationship be-
of them had at least one clinical mastitis in first tween SCC at initial test in first lactation and time to
lactation. Finally, cows culled before 35 days and first mastitis later in first and second lactation was
herds with less than three selected cows 692 were assessed by survival analysis.
discarded. After edits, the final data set consisted of 20,422 cows in 2611 herds, with 13 of these cows
having at least one clinical mastitis. Distribution of
2. Material and methods clinical events is shown in Fig. 1.
