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Characterization of Clinical Mastitis in Primiparous Heifers
Characterization of Clinical Mastitis in Primiparous Heifers V. MYLLYS Milk Laboratory National Veterinary and Food Research Institute FIN40231 Helsinki, Finland H. RAUTALA The Finnish Animal Breeding Association FIN-01301 Vantaa, Finland ABSTRACT
INTRODUCTION
Using data from health records for cows in Finland from between 1983 and 1991, we investigated the general trend for frequency of mastitis in heifers, seasonal variation, breed differences, and etiology of the disease. The performance of the heifers was monitored during first lactation. Treatment of heifer mastitis, defined as mastitis treatment 1 wk before and 1 wk after calving, increased from 1.8 to 4.4% between 1983 and 1991. The increase can be partly attributed to increased milk production, subsequent reduced resistance to mastitis, and the general trend toward more efficient treatment of mastitis. Heifer mastitis was a characteristic disease of well-managed, productive herds with low SCC and a high frequency of mastitis treatments administered by a veterinarian. Of the feeding factors studied, only use of homemade concentrates was associated with higher mastitis frequency. Mastitic heifers had higher genetic potential for milk production than control heifers, but actual milk production was 70 to 80 kg lower than expected. Most mastitic heifers recovered well and were not more susceptible than control heifers to further incidence of mastitis or other diseases. However, heifer mastitis caused more heifers than usual to be culled. (Key words: heifer, mastitis, management)
Primiparous heifers have generally been assumed to be free of IMI before or at parturition. However, high rates of IMI in heifers, usually caused by coagulase-negative staphylococci. have been reported recently (14, 16, 24, 28, 29). The IMI caused by coagulase-negative staphylococci are not severe (28), and virulence of those bacteria is generally less than that of major pathogens, such as Sruphylococcus aureus (1, 12). Mastitis in primiparous heifers, however, may be an economically important disease. The health status of udders of heifers entering the milking herd affects future milk production and quality (11). Even when mild, mastitis may damage the developing milk secretory tissues, leading to reduced milk production (28) that cannot be compensated for by the healthy quarters (30). Subsequent subclinical IMI and teat canal colonization lead to high SCC in the bulk milk (28). Infected heifers can also be a source of pathogenic bacteria, including S. aureus (11, 19), in the lactating herd. Severe mastitis requires the infected heifers to be culled (5). Mastitis control programs attempt to reduce the duration of existing IMI and to prevent new M I . The current trend in food animal practice is that each medical decision be justified economically. Although treatment of mastitis with antibiotics is more effective for heifers than for lactating cows (18), and although preventive intramammary infusions of antibiotics have reduced the number of infected quarters at parturition (13), whether treatment is economically advantageous is unclear. Furthermore, use of antibiotics may cause residue problems in milk and promote development of resistant bacterial strains. Therefore, to minimize the economic losses to dairy fanners, it is important to know why
Received July 26, 1994. Accepted October 6, 1994.
1995 J Dairy Sci 78538-545
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MASTITIS IN PRIMIPAROUS HEIFERS
539
tion of the herd. The total number of heifers included was 50,085. In the second part of the study, for each heifer treated for mastitis, a control heifer (or heifers) was selected from the same herd. Controls had not been treated for mastitis by a veterinarian during the period of 7 d before and 7 d after first calving and had calved within 2 mo before and 2 mo after the calving of the mastitic heifer. There were 3181 cows MATERIALS AND METHODS treated for heifer mastitis and 5784 controls. The data for this study were collected from Parameters measured in the study are presented the Agricultural Data Processing Centre of in Tables 2 and 3. Data were not available for Finland (Suomen Maatalouden Laskentakeskus all parameters from all heifers. For estimation Oy, Vantaa). The data were derived from of the genetic potential of the heifers, progenyveterinary records, milk production records, testing results of their sires were used. and artificial insemination statistics. Milk Statistical analyses were carried out using t production records contained data on produc- test and chi-square test of SAS (20). The t test tion, SCC, body weight, and feeding. The col- was used to analyze differences between varialection procedure was reported by Grohn et al. ble means between mastitic heifers and con(6). For this study, the data were selected only trols. For categorical variables, chi-square tests from those herds with an acceptable system of were used. health records. The requirement was that data be available from over 70% of the dairy farms RESULTS in the area. The breeding values of the sires The frequency of heifer mastitis more than were taken from the official progeny-testing results. Heifer mastitis was defined as clinical doubled during the 8-yr period of study (Figure mastitis that was treated by a veterinarian dur- 1). Differences occurred between the two main ing a period of 7 d before and 7 d after first dauy breeds used in Finland, Ayrshire and Friesian. The frequency of treatments for calving. For estimation of the general trend of masti- heifer mastitis of Ayrslure heifers in 1991 was tis frequency in heifers and for calculation of 3.9% and of Friesian heifers 5.6% (P < .OOl). the seasonal variation in mastitis, and the in- The odds ratio was 1.63 for heifer mastitis of fluence of breed, data collected from between Friesians compared with that for Ayrshires cal1983 and 1991 were used. The total number of culated over the whole study period. Seasonal heifers calving during this period was 419,069, variation is presented in Figure 2. The frequency of heifer mastitis was ranging between 44,382 and 50,309 per year. For a more detailed investigation on the strongly associated with milk production; inbackground and consequences of heifer masti- fection was more frequent (5.8%) for herds tis, health record data from 1991 were used. In with high mean production (>7000 kg/yr) than the first part of the study, we estimated the (3.5%) for herds with low milk production effect of management and feeding in a herd on (<6ooo kg/yr; P < ,001). The odds ratio for the frequency of heifer mastitis. The heifer mastitis in high production herds, comparameters recorded in the study are given in pared with low production herds, was 1.70. In Table 1 . The effects were estimated by divid- the intermediate production class, the proporing parameters into three classes (Table 1) and tion of heifer mastitis was 4.8%. Results from calculating the proportion of heifers treated for the effect on heifer mastitis frequency of other mastitis. Herd data were collected before the herd characteristics and different feeding heifers calved so that the treated heifers were strategies on f m s are presented in Table 1. not included in the statistics. Because milk Heifer mastitis apparently occurred most often production directly influenced the feeding in herds that had high mean milk production, strategies on a farm, its confounding effect was low bulk tank milk SCC, high incidence of accounted for by grouping the results into mastitis treatment, calculated optimal feeding, three classes according to mean milk produc- and ample dietary cereals.
some heifers have clinical mastitis at calving and how mastitis affects their productivity. The aim of this study was to collect retrospectively basic information on heifer mastitis in Finland. Potential predisposing factors behind the disease were investigated, and the performance of the heifers was followed during the first lactation.
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MYLLYS AND RAUTALA
TABLE 1. Mastitis frequency for individual heifers in relation to herd characteristics.1 Annual production Medium
Low (c6ooo kid
High
~ ~ 7 0 kg) 0 0
( > 7 W kg)
(no.)
(%)
(no.)
(%)
2858 8100 4043
5.8 4.5 3.4 < .001
2432 5341 2165
7.6 5.7 4.5 < ,001
1.9 4.4 1.1 < .a01
4984 4964 4978
2.6 4.2 9.0
2996 3108 4495
3.3 5.4 9.0 < 001
2995 4077 2241
3.4 3.5 2.6 .14
4733 8214 5354
4.6 4.8 4.0 .I2
2949 5386 3866
6.4 5.6 5.2 .12
2310 3 166 3837
3.2 3.6 3.0 .37
5560 6984 5756
4.8 4.7 4.0 ,054
4066 4946 3189
2124 3658 2931
3.7 3.3 2.8 .20
7581 7384 3336
4.5 4.8 4.0 .17
5674 4570 I957
2499 4036 2778
3.0 3.4 3.3 .73
5202 9124 3975
4.9 4.4 4.1 .I5
4428 5990 I783
5.5
5422 2199 1692
3.2 3.4 3.4 .92
8149 5387 4165
4.6 4.5 4.3 .67
2806 3748 5647
6.1 5.1 5.4 .49
5379 2865 1069
3.6 2.7 3.0 ,058
10926 4149 2426
4.5
6390 3032 2779
6.0 5.9 4.7 ,036
1890 3066 4357
2.7 3.5 3.4 .29
3709 5482 9110
3336 3250 5615
4.5 6.1 6.1 .0036
(no.)
(W
Herd SCC (x lO3/ml)
300
1240 3936 2464
P Treated heifers, % of herd
16-35 >35
.M1 2516 2461 1886
P Herd size, no. of cows
cl2 12-17 >I7 P Feed consumption, %2
I07 P Protein intake, %2
<111 11 1-120 >120 P Proportion of grass silage in feed, %
<30 31-40 >40 P Concentrate in feed, 9%
<35 36-40 A0
P Commercial concentrate in feed, % Not in use
1-20 >20
P Homemade concentrate (cereals) in feed, % <21
21-30 >30
4.4 3.1 2.1
P
< .CO1
5.0
3.9 .I 1 3.5 4.7 4.7 ,0096
5.0
5.9 6.2 .047 5.6 5.8 5.6
.86
5.7 6.0 .69
'Table displays total number of heifers in each category and percentage of heifers infected. Probability values have been calculated for each variable stratified according to herd production. 2Percentage from calculated optimum.
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MASTITIS IN PRIMIPAROUS HEIFERS TABLE 2. Characterization of heifers that were treated for mastitis and controls on the same farms.
Mastitis Weight,' kg Duration of pregnancy, d Calving age, d Milk index? kg Protein index? kg Protein index,' 8 Fat index,2 % Milking speed index2 Udder conformation index2
(no.) 2257 2516 3122 1914 1914 1914 1914 1911 979
Control
Jz
SE
492.3 277.0 766.9 103.4 104.6 100.5 100.1 99.4 97.9
.1 .1 1.2 .2 .2 .2 .2 .3 .3
(no.) 4128 4495 5682 3413 3413 3413 3413 3402 656
P
-X
SE
492.4 277.0 767.9 101.2 102.4 101.3 101.4 100.4 98.5
.08 .2 .9 .2 .2 .2 .2 .2 .2
.94 .88 .51 COO1 COO1 ,0032 COO1 .CO10 .11
lHearth girth measurement 1 to 4 mo after parturition. ZBreeding value of the sire. The mean of the population = 100; standard deviation = 10.
Results from the comparison of mastitic heifers and controls are presented in Tables 2 and 3. According to the data in Table 2, the genetic production potential of heifers with mastitis was slightly higher than that for control heifers. However, the actual milk production of heifers with mastitis was slightly less than that of the control heifers (Table 3). Milk SCC was elevated in first test milking for heifers with mastitis (P < .001), but the differences disappeared during later lactation (Table 3 and Figure 3).
DISCUSSION
The increase in the frequency of heifer mastitis during the study period was surprisingly high. During the same period, no major changes took place in the feeding or management of the dairy cows. However, milk production continuously increased. In 1983, the mean milk production was 5738 kg, and, in 1991, it was 6440 kg (25). High milk production is associated with low mastitis resistance, both genetically (3, 26) and phenotypically (21). Also, the frequency of mastitis treatments
TABLE 3. Characterization of heifers that were. treated for mastitis and controls on the same farms. Mastitis
Milk production, kg/305 d Fat production, kg Fat content, 951 Protein production, kg Protein content, 5% Production weighted average SCC, x 1 0 3 ~ Log average SCC Milk in first test milking,' kg SCC in first test milking.1 x 1 0 3 ~ Mastitis treatments,' % Other diseases, % Overall culling, 9b Culling because of mastitis, 8
(no.) 2280 2280 2282 2280 2282
-X
5531.2 241.8 4.4 178.9 3.2
Control
SE 21.4 .9 .01 .7 .CO4
2282 2567 2567
137.0 4.8 19.7
4.8
1181 3181 3181 3181 3181
359.3 9.4 31.4 19.8 8.6
27.6
.06
.08
(no.)
-x
4275 4275 428 1 4275 4281
5564.0 245.3 4.4 180.6 3.2
4281 4794 4794
123.6 4.9 20.3
2328 5784 5784 57 84 5784
201.9 8.8 31.8 16.1 4.6
P SE 15.7 .7 ,008 .5 ,003 2.8 .os .06
12.0
.22 .0020 ,0038 ,048
.15 ,011 .28 COO1 COO1 .42 .68 COO1 401
'Takes place within 1 mo after parturition. 'Mastitis treatments >7 d after parturition. Journal of Dairy Science Vol. 78, No. 3, 1995
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MYLLYS AND RAUTALA
The differences in mastitis frequency among Ayrshires and Friesians were essentially the same as in progeny-testing data, which revealed that Ayrshire cows had a mastitis frequency of 6.9%and Friesians 9.8%. The difference in heifer mastitis between the two breeds probably represented the general -. mastitis resistance of each. 83 84 85 86 87 88 89 90 91 Seasonal variation in heifer mastitis freYear quency was small, but two peak periods were Figure 1 . Heifer mastitis treatment between 1983 and identified. The first peak occurred late in 1991 for Finnish dauy breeds, Ayrshire (1) and Friesian spring, just before the transition from confined @I. housing to pasture, when mastitis frequency also increased in older animals (26). At that time, the air temperature may rise, and the quality and quantity of homegrown fodder can in general has increased with the increased awareness of the importance of proper treat- be expected to be poorest following long storment of mastitis to maintain milk quality and age. The second peak occurred in late summer the severe penalties set by dairies on milk with when the weather is warm and humid. Heifer mastitis was more frequent for wellhigh SCC. In 1983. 18.1% of cows were treated for mastitis; in 1991. 27.4% were managed herds of high production, low bulk treated. Obviously, the increase in heifer milk SCC, but with a high requirement for mastitis frequency can partly be explained by treatment of clinical mastitis by a veterinarian. As the data on mastitis in this study were these two phenomena. Heifer mastitis during period of 7 d before treatment data, not actual disease data, and 7 d after first calving made up about one- management decisions were of great importhird of all the mastitis treatments for first tance. The high frequency of mastitis treatment lactation cows. The situation is similar for all indicates a general tendency to treat even mild mastitis treatments, independent of cow age cases of mastitis in line with good farming (26). Thus, the predisposing factors for mastitis practice. Some evidence exists for the association of around calving are likely to be similar in heifmastitis with generous concentrate feeding (7, ers and older cows, even if the sources of the 21), excessive protein in feed (17), and high pathogenic organisms differ. The immune blood urea concentrations (4). However, in function during the periparturient period is imthose studies, the frequency of heifer mastitis paired (8), and the mammary gland is susceptidid not vary according to the proportion of ble to mastitis during transition times, such as concentrates and silage in feed, or calculated drying off and colostrogenesis (15). protein content, but the type of concentrate seemed to be associated with frequency of heifer mastitis. Because homemade concentrates and commercial concentrates were alternatives, it was not possible to determine whether homemade concentrate predisposed 3.5 heifers to mastitis or whether commercial concentrates protected heifers from mastitis. More detailed data on feeding of the individual heifp 1.5 ers just before calving is needed to explain the * 0.5 relationship between feeding and heifer masti04 : : : : : : : : : ; : 1 tis. J F M A M J J A S O N D Month According to Erb et al. (3, older heifers have more mastitis than younger heifers. Also, Figure 2. Mean seasonal variation of heifen treated for mastitis between 1983 and 1991. Bars indicate standard in practice, pregnancies that are longer than errors of the mean. normal are associated with a longer heavy .
I
,
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MASTITIS IN PRIMIPAROUS HEIFERS
543
support those theories. When heifers with mastitis were compared with healthy control heifers, calving age, duration of pregnancy, and size of the animals were not associated with frequency of heifer mastitis. Good milking speed has been associated with more udder diseases and higher SCC (10, First test milking Z), but results of our study indicated the 70 I reverse. The heifers with mastitis were, according to sire progeny-testing results, genetically slower milkers than the controls. Bad udder 6o SO conformation may predispose a cow to mastitis (22), but the data we examined showed no differences between the heifers with mastitis and control heifers for progeny-testing results of the sires. 10 Heifers with mastitis tended to be geneti% 0 cally higher producers of milk with lower fat 201> 151and protein contents, but differences were 500 1001 10 100 small. According to breeding indices of the sires, the expected 305-d milk production of Second test milking the heifers with mastitis should have been 43 70 I kg higher than that of the control heifers, but, 60 -in fact, production was 33 kg lower. Thus, r heifer mastitis caused a pioduction loss of 70 50 -to 80 kg per cow, which is indicative of some -udder secretory tissue damage. This figure was x 40 30 -rather low compared with production losses 20 -from other types of mastitis. Timms and Schultz (27) reported production losses of 821 and 1153 kg from infections of coagulasenegative staphylococci and from Sruphylococ201> 151cus uureus, respectively. Conversely, the de10 100 500 1001 crease in production has been reported to be small, especially with young cows (5)or when Third test milking mastitis incidence was followed by low SCC (9). Our results are in accordance with those latter results. The influence of heifer mastitis on SCC 50 was clearly seen in the first test milking, which took place within 1 mo after parturition. During the later lactation, the heifers with mastitis and control heifers were represented equally in the very low SCC class (IlO,OOO), indicating 10 that mastitis did not permanently harm the 0 udder tissue. The heifers with mastitis seemed 201> 151to accumulate in the SCC class of 10,000 to 10 100 500 1001 50,000 instead of in the classes 50,000 to 500,000, where the control heifers were more scc (x103/rnl) frequently represented. We have no explanaFigure 3. The SCC in milk of heifers treated for tion for this result. There was no significant mastitis (open bars) and for control heifers (solid bars) during first lactation, as determined by monthly test milk- difference in mean logarithmic SCC for the entire lactation between heifers with mastitis ings after parturition.
feeding period, which could predispose heifers to mastitis, for example, by inducing early milk letdown. However, the results did not
,
1
!
i
t
%i+.l
Journal of Dairy Science Vol. 78, No. 3, 1995
544
MYLLYS AND RAUTALA
and control heifers. The weighted mean SCC were 13,000 higher for the entire lactation for heifers with mastitis. The difference occurred entirely during the 1st mo postpartum, indicating good recovery from heifer mastitis. This finding is in agreement with the results of Pyorala and Pyoriila US), who reported that heifer mastitis is more easily cured than mastitis in older cows. During later lactation, the heifers with mastitis were not treated for mastitis more than control heifers, which indicated that heifer mastitis did not become a chronic disease with recurrent clinical episodes and that mastitic heifers were not more prone to mastitis than controls in general. The puerperal diseases occur as a complex (2). Heifer mastitis was not similar. Occurrence of other diseases was no more frequent in heifers with mastitis than in controls. The most severe consequences were seen as a 4% increase in culling of heifers with mastitis. This result is in agreement with results of Erb et al. (3, who established that mastitis is an important predictor of culling. CONCLUSIONS
Awareness of the importance of proper treatment of mastitis, increased milk production, and subsequent lower mastitis resistance may partly account for the increase in heifer mastitis between 1983 and 1991. Heifer mastitis was a disease of well-managed herds with high milk production, low SCC, and high frequency of mastitis treatments administered by veterinarians. The disease as such was "benign"; production losses were small, mastitis did not predispose the heifer to more mastitis or other diseases later in lactation, and the recovery rate was high, as judged by SCC, although mastitis resulted in increased culling. ACKNOWLEDGMENTS
We are grateful to Tapani Hellman from the Agricultural Data Processing Centre for collecting and processing the data from the records. This work was funded in part by the foundation of Walter Ehrstrom. REFERENCES 1 Birgersson. A., P. Jonsson, and 0.Holmberg. 1992. Species identification and some characteristics of
Journal of Dairy Science Vol. 78. No. 3, 1995
coagulase-negative staphylococci isolated from bovine udders. Vet. Microbiol. 31:181. 2Curtis. R. C., H. N. Erb, C. J. Sniffen, R. D. Smith. and D.S . Kronfeld. 1985. Path analysis of dry period nutrition, postpartum metabolic and reproductive disorders, and mastitis in Holstein cows. J. Dairy Sci. 68: 2347. 3Emanuelson. U,.B. Danell, and J. Philipsson. 1988. Genetic parameters for clinical mastitis, somatic cell counts, and milk production estimated by multipletrait restricted maximum likelihood. J. Dairy Sci. 71: 467. 4Emmert, M., and K. Wendt. 1991. Untersuchungen des Z u s m n h a n g e s zwischen futterungsbedingten Stoffwechselstarungen und Eutergesundheitsschlden bei Milchrindern. Monatsh. Veterinaermed. 46538. 5 Erb. H. N., R. D. Smith, P. A. Oltenacu, C. L. Guard, R. B. Hillman. P. A. Powers, M. C. Smith. and M. E. White. 1985. Path model for reproductive disorders and performance, milk fever, mastitis, milk yield. and culling in Holstein cows. J. Dairy SCI. 68:3337. 6Grohn. Y.,H. Saloniemi, and J. S y v a j h i . 1986. An epidemiologic and genetic study on registered diseases in Finnish Ayrshire cattle. 1. The data, disease occurrence and culling. Acta Vet. Scand. 27:182. 7 Johnson, D. G., and D. E. Otterby. 1981. Influence of dry period diet on early postpartum health, feed intake, milk production, and reproductive efficiency of Holstein cows. J. Dairy Sci. 64:290. 8Kehrli. M. E., B. J. Nonnecke, and J. A. Roth. 1989. Alterations in bovine neutrophil function during the penparturient period. Am. J. Vet. Res. 50:207. 9 Macmillan, K. L., G. F. Duirs. and D. M. Duganzich. 1983. Associations between dry cow therapy, clinical mastitis, and somatic cell count score with milk and fat production in ten New Zealand dairy herds. J. Dairy Sci. 66:259. lOMadsen, P., S. M. Nielsen, M. D. Rasmussen. 0. Klstrup, N. E. Jensen, P. T. Jensen. P.S.L. Madsen, B. Larsen, and J. Hyldgaard-Jensen. 1987. Investigation on genetic resistance to bovine mastitis. Frederiksberg Bogtrykkeri, Copenhagen, Denmark. 1 I Matthews, K. R., R. J. Hannon, and B. E. Langlois. 1992. Prevalence of Sfaphyiococcus species during the penparturient period in primiparous and multiparous cows. J. Dairy Sci. 75:1835. 12Myllys. V., T. Honkanen-Buzalski, H. Virtanen, S. Pyortilti, and H.-P. Muller. 1994. Effect of abrasion of teat orifice epithelium on development of bovine staphylococcal mastitis. J. Dairy Sci. 77:446. 13 Oliver. S. P.. M. J. Lewis, B. E. Gillespie, and H. H. Dowlen. 1992. Influence of prepartum antibiotic therapy on intramarnmary infections in primigravid heifers during early lactation. J. Dairy Sci. 75:406. 14 Oliver, S . P.. and B. A. Mitchell. 1983. Intramammary infections in primigravid heifers near parturition. J. Dairy Sci. 66: 1180. 15 Oliver, S . P., and L. M. Sordillo. 1988. Udder health in the periparturient period. J. Dairy Sci. 71:2584. 16 Pankey, J. W., P. A. Drechsler. and E. E. Wildman. 1991. Mastitis prevalence in primigravid heifers at parturition. J. Dairy Sci. 74:1550. 17 Pedersen. P. S . 1975. Prevention of mastitis in cows. Page 249 in Seminar on Mastitis Control. F. H. Dodd,
MASTITIS IN PRIMIPAROUS HEIFERS T. K . Griffen. and R. G. Kingwill, ed. Int. Dairy Fed., Brussels. Belgium. 18 Pyorda, S., and E. Pyorda. 1994. Efficacy of bovine clinical mastitis therapy during lactation. Page 42 in Proc. XVII Nordic Vet. Congr., Reykjavik. Vol 2. Icelandic Vet. Assoc., Reykjavik, Iceland. 19 Roberson, J. R., L. K.Fox, D. D. Hancock, C. C. Gay, and T. E. Besser. 1994. Coagulase-positive Staphylococcus intramammary infections in primiparous dairy cows. J. Dairy Sci. 77:958. 20SAS@ Users Guide: Statistics. Version 5 Edition. 1985. SAS Inst., Inc., Cary, NC. 21 Schukken, Y. H., F. J. G r o w e r s , D. van de Geer, H. N. Eh, and A. Brand. 1991. Risk factors for clinical mastitis in herds with a low bulk milk somatic cell count. 2. Risk factors for Escherichia coli and Staphylococcus aureus. J. Dairy Sci. 741826. 22 Seykora. A. J., and B. T. McDaniel. 1985. Udder and teat morphology related to mastitis resistance: a review. J. Dairy Sci. 68:2087. 23 Slettbakk, T.. A. J~rstad.T. B. Farver, and D. W. Hird. 1990. Impact of milking characteristics and teat morphology on somatic cell counts in fust-lactation Norwegian cattle. Prev. Vet. Med. 8:253.
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24 Sobiraj, A., H.-U. Ostertag, D.Peip, H. Bostedt, and G . Kielwein. 1988. Clinical and bacteriological findings concerning the incidence of mastitis in first lactating heifers during and shortly after parturition. Tieraerztl. Praxis 16:243. 25 Statistical Yearbook of Finland. 1984-1992. Central Statistical Office, Helsinki, Finland. 26 Syvajiirvi, J., H. Saloniemi, and Y.Grohn. 1986. An epidemiologic and genetic study on registered diseases in Finnish Ayrshire cattle. IV. Clinical mastitis. Acta Vet. Scand. 27:223. 27 Timms, L. L., and L. H. Schultz. 1987. Dynamics and significance of coagulase-negative staphylococcal ininfections. J. Dairy Sci. 70:2648. 28Tnnidad. P., S. C. Nickerson, and T. K. Alley. 1990. Prevalence of intramammary infection and teat canal colonization in unbred and primigravid dairy heifers J. Dairy Sci. 73:107. 29 Wildman, E. E., J. K. O’Neil, P. A. Drechsler, and J. W. Pankey. 1990. Prevalence of mastitis in primiparous cows. .I. Dairy Sci. 73(SuppI. I): 257(Abstr.) 3OWoolford. M. W. 1985. The relationship between mastitis and milk yield. Kiel. Milchwirtsch. Forschungsber. 37924.
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Journal of Dairy Science Vol. 78. No. 3, 1995
INTRODUCTION
Using data from health records for cows in Finland from between 1983 and 1991, we investigated the general trend for frequency of mastitis in heifers, seasonal variation, breed differences, and etiology of the disease. The performance of the heifers was monitored during first lactation. Treatment of heifer mastitis, defined as mastitis treatment 1 wk before and 1 wk after calving, increased from 1.8 to 4.4% between 1983 and 1991. The increase can be partly attributed to increased milk production, subsequent reduced resistance to mastitis, and the general trend toward more efficient treatment of mastitis. Heifer mastitis was a characteristic disease of well-managed, productive herds with low SCC and a high frequency of mastitis treatments administered by a veterinarian. Of the feeding factors studied, only use of homemade concentrates was associated with higher mastitis frequency. Mastitic heifers had higher genetic potential for milk production than control heifers, but actual milk production was 70 to 80 kg lower than expected. Most mastitic heifers recovered well and were not more susceptible than control heifers to further incidence of mastitis or other diseases. However, heifer mastitis caused more heifers than usual to be culled. (Key words: heifer, mastitis, management)
Primiparous heifers have generally been assumed to be free of IMI before or at parturition. However, high rates of IMI in heifers, usually caused by coagulase-negative staphylococci. have been reported recently (14, 16, 24, 28, 29). The IMI caused by coagulase-negative staphylococci are not severe (28), and virulence of those bacteria is generally less than that of major pathogens, such as Sruphylococcus aureus (1, 12). Mastitis in primiparous heifers, however, may be an economically important disease. The health status of udders of heifers entering the milking herd affects future milk production and quality (11). Even when mild, mastitis may damage the developing milk secretory tissues, leading to reduced milk production (28) that cannot be compensated for by the healthy quarters (30). Subsequent subclinical IMI and teat canal colonization lead to high SCC in the bulk milk (28). Infected heifers can also be a source of pathogenic bacteria, including S. aureus (11, 19), in the lactating herd. Severe mastitis requires the infected heifers to be culled (5). Mastitis control programs attempt to reduce the duration of existing IMI and to prevent new M I . The current trend in food animal practice is that each medical decision be justified economically. Although treatment of mastitis with antibiotics is more effective for heifers than for lactating cows (18), and although preventive intramammary infusions of antibiotics have reduced the number of infected quarters at parturition (13), whether treatment is economically advantageous is unclear. Furthermore, use of antibiotics may cause residue problems in milk and promote development of resistant bacterial strains. Therefore, to minimize the economic losses to dairy fanners, it is important to know why
Received July 26, 1994. Accepted October 6, 1994.
1995 J Dairy Sci 78538-545
538
MASTITIS IN PRIMIPAROUS HEIFERS
539
tion of the herd. The total number of heifers included was 50,085. In the second part of the study, for each heifer treated for mastitis, a control heifer (or heifers) was selected from the same herd. Controls had not been treated for mastitis by a veterinarian during the period of 7 d before and 7 d after first calving and had calved within 2 mo before and 2 mo after the calving of the mastitic heifer. There were 3181 cows MATERIALS AND METHODS treated for heifer mastitis and 5784 controls. The data for this study were collected from Parameters measured in the study are presented the Agricultural Data Processing Centre of in Tables 2 and 3. Data were not available for Finland (Suomen Maatalouden Laskentakeskus all parameters from all heifers. For estimation Oy, Vantaa). The data were derived from of the genetic potential of the heifers, progenyveterinary records, milk production records, testing results of their sires were used. and artificial insemination statistics. Milk Statistical analyses were carried out using t production records contained data on produc- test and chi-square test of SAS (20). The t test tion, SCC, body weight, and feeding. The col- was used to analyze differences between varialection procedure was reported by Grohn et al. ble means between mastitic heifers and con(6). For this study, the data were selected only trols. For categorical variables, chi-square tests from those herds with an acceptable system of were used. health records. The requirement was that data be available from over 70% of the dairy farms RESULTS in the area. The breeding values of the sires The frequency of heifer mastitis more than were taken from the official progeny-testing results. Heifer mastitis was defined as clinical doubled during the 8-yr period of study (Figure mastitis that was treated by a veterinarian dur- 1). Differences occurred between the two main ing a period of 7 d before and 7 d after first dauy breeds used in Finland, Ayrshire and Friesian. The frequency of treatments for calving. For estimation of the general trend of masti- heifer mastitis of Ayrslure heifers in 1991 was tis frequency in heifers and for calculation of 3.9% and of Friesian heifers 5.6% (P < .OOl). the seasonal variation in mastitis, and the in- The odds ratio was 1.63 for heifer mastitis of fluence of breed, data collected from between Friesians compared with that for Ayrshires cal1983 and 1991 were used. The total number of culated over the whole study period. Seasonal heifers calving during this period was 419,069, variation is presented in Figure 2. The frequency of heifer mastitis was ranging between 44,382 and 50,309 per year. For a more detailed investigation on the strongly associated with milk production; inbackground and consequences of heifer masti- fection was more frequent (5.8%) for herds tis, health record data from 1991 were used. In with high mean production (>7000 kg/yr) than the first part of the study, we estimated the (3.5%) for herds with low milk production effect of management and feeding in a herd on (<6ooo kg/yr; P < ,001). The odds ratio for the frequency of heifer mastitis. The heifer mastitis in high production herds, comparameters recorded in the study are given in pared with low production herds, was 1.70. In Table 1 . The effects were estimated by divid- the intermediate production class, the proporing parameters into three classes (Table 1) and tion of heifer mastitis was 4.8%. Results from calculating the proportion of heifers treated for the effect on heifer mastitis frequency of other mastitis. Herd data were collected before the herd characteristics and different feeding heifers calved so that the treated heifers were strategies on f m s are presented in Table 1. not included in the statistics. Because milk Heifer mastitis apparently occurred most often production directly influenced the feeding in herds that had high mean milk production, strategies on a farm, its confounding effect was low bulk tank milk SCC, high incidence of accounted for by grouping the results into mastitis treatment, calculated optimal feeding, three classes according to mean milk produc- and ample dietary cereals.
some heifers have clinical mastitis at calving and how mastitis affects their productivity. The aim of this study was to collect retrospectively basic information on heifer mastitis in Finland. Potential predisposing factors behind the disease were investigated, and the performance of the heifers was followed during the first lactation.
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540
MYLLYS AND RAUTALA
TABLE 1. Mastitis frequency for individual heifers in relation to herd characteristics.1 Annual production Medium
Low (c6ooo kid
High
~ ~ 7 0 kg) 0 0
( > 7 W kg)
(no.)
(%)
(no.)
(%)
2858 8100 4043
5.8 4.5 3.4 < .001
2432 5341 2165
7.6 5.7 4.5 < ,001
1.9 4.4 1.1 < .a01
4984 4964 4978
2.6 4.2 9.0
2996 3108 4495
3.3 5.4 9.0 < 001
2995 4077 2241
3.4 3.5 2.6 .14
4733 8214 5354
4.6 4.8 4.0 .I2
2949 5386 3866
6.4 5.6 5.2 .12
2310 3 166 3837
3.2 3.6 3.0 .37
5560 6984 5756
4.8 4.7 4.0 ,054
4066 4946 3189
2124 3658 2931
3.7 3.3 2.8 .20
7581 7384 3336
4.5 4.8 4.0 .17
5674 4570 I957
2499 4036 2778
3.0 3.4 3.3 .73
5202 9124 3975
4.9 4.4 4.1 .I5
4428 5990 I783
5.5
5422 2199 1692
3.2 3.4 3.4 .92
8149 5387 4165
4.6 4.5 4.3 .67
2806 3748 5647
6.1 5.1 5.4 .49
5379 2865 1069
3.6 2.7 3.0 ,058
10926 4149 2426
4.5
6390 3032 2779
6.0 5.9 4.7 ,036
1890 3066 4357
2.7 3.5 3.4 .29
3709 5482 9110
3336 3250 5615
4.5 6.1 6.1 .0036
(no.)
(W
Herd SCC (x lO3/ml)
1240 3936 2464
P Treated heifers, % of herd
16-35 >35
.M1 2516 2461 1886
P Herd size, no. of cows
cl2 12-17 >I7 P Feed consumption, %2
<111 11 1-120 >120 P Proportion of grass silage in feed, %
<30 31-40 >40 P Concentrate in feed, 9%
<35 36-40 A0
P Commercial concentrate in feed, % Not in use
1-20 >20
P Homemade concentrate (cereals) in feed, % <21
21-30 >30
4.4 3.1 2.1
P
< .CO1
5.0
3.9 .I 1 3.5 4.7 4.7 ,0096
5.0
5.9 6.2 .047 5.6 5.8 5.6
.86
5.7 6.0 .69
'Table displays total number of heifers in each category and percentage of heifers infected. Probability values have been calculated for each variable stratified according to herd production. 2Percentage from calculated optimum.
Journal of Dairy Science Vol. 78. No 3. 1995
54 1
MASTITIS IN PRIMIPAROUS HEIFERS TABLE 2. Characterization of heifers that were treated for mastitis and controls on the same farms.
Mastitis Weight,' kg Duration of pregnancy, d Calving age, d Milk index? kg Protein index? kg Protein index,' 8 Fat index,2 % Milking speed index2 Udder conformation index2
(no.) 2257 2516 3122 1914 1914 1914 1914 1911 979
Control
Jz
SE
492.3 277.0 766.9 103.4 104.6 100.5 100.1 99.4 97.9
.1 .1 1.2 .2 .2 .2 .2 .3 .3
(no.) 4128 4495 5682 3413 3413 3413 3413 3402 656
P
-X
SE
492.4 277.0 767.9 101.2 102.4 101.3 101.4 100.4 98.5
.08 .2 .9 .2 .2 .2 .2 .2 .2
.94 .88 .51 COO1 COO1 ,0032 COO1 .CO10 .11
lHearth girth measurement 1 to 4 mo after parturition. ZBreeding value of the sire. The mean of the population = 100; standard deviation = 10.
Results from the comparison of mastitic heifers and controls are presented in Tables 2 and 3. According to the data in Table 2, the genetic production potential of heifers with mastitis was slightly higher than that for control heifers. However, the actual milk production of heifers with mastitis was slightly less than that of the control heifers (Table 3). Milk SCC was elevated in first test milking for heifers with mastitis (P < .001), but the differences disappeared during later lactation (Table 3 and Figure 3).
DISCUSSION
The increase in the frequency of heifer mastitis during the study period was surprisingly high. During the same period, no major changes took place in the feeding or management of the dairy cows. However, milk production continuously increased. In 1983, the mean milk production was 5738 kg, and, in 1991, it was 6440 kg (25). High milk production is associated with low mastitis resistance, both genetically (3, 26) and phenotypically (21). Also, the frequency of mastitis treatments
TABLE 3. Characterization of heifers that were. treated for mastitis and controls on the same farms. Mastitis
Milk production, kg/305 d Fat production, kg Fat content, 951 Protein production, kg Protein content, 5% Production weighted average SCC, x 1 0 3 ~ Log average SCC Milk in first test milking,' kg SCC in first test milking.1 x 1 0 3 ~ Mastitis treatments,' % Other diseases, % Overall culling, 9b Culling because of mastitis, 8
(no.) 2280 2280 2282 2280 2282
-X
5531.2 241.8 4.4 178.9 3.2
Control
SE 21.4 .9 .01 .7 .CO4
2282 2567 2567
137.0 4.8 19.7
4.8
1181 3181 3181 3181 3181
359.3 9.4 31.4 19.8 8.6
27.6
.06
.08
(no.)
-x
4275 4275 428 1 4275 4281
5564.0 245.3 4.4 180.6 3.2
4281 4794 4794
123.6 4.9 20.3
2328 5784 5784 57 84 5784
201.9 8.8 31.8 16.1 4.6
P SE 15.7 .7 ,008 .5 ,003 2.8 .os .06
12.0
.22 .0020 ,0038 ,048
.15 ,011 .28 COO1 COO1 .42 .68 COO1 401
'Takes place within 1 mo after parturition. 'Mastitis treatments >7 d after parturition. Journal of Dairy Science Vol. 78, No. 3, 1995
542
MYLLYS AND RAUTALA
The differences in mastitis frequency among Ayrshires and Friesians were essentially the same as in progeny-testing data, which revealed that Ayrshire cows had a mastitis frequency of 6.9%and Friesians 9.8%. The difference in heifer mastitis between the two breeds probably represented the general -. mastitis resistance of each. 83 84 85 86 87 88 89 90 91 Seasonal variation in heifer mastitis freYear quency was small, but two peak periods were Figure 1 . Heifer mastitis treatment between 1983 and identified. The first peak occurred late in 1991 for Finnish dauy breeds, Ayrshire (1) and Friesian spring, just before the transition from confined @I. housing to pasture, when mastitis frequency also increased in older animals (26). At that time, the air temperature may rise, and the quality and quantity of homegrown fodder can in general has increased with the increased awareness of the importance of proper treat- be expected to be poorest following long storment of mastitis to maintain milk quality and age. The second peak occurred in late summer the severe penalties set by dairies on milk with when the weather is warm and humid. Heifer mastitis was more frequent for wellhigh SCC. In 1983. 18.1% of cows were treated for mastitis; in 1991. 27.4% were managed herds of high production, low bulk treated. Obviously, the increase in heifer milk SCC, but with a high requirement for mastitis frequency can partly be explained by treatment of clinical mastitis by a veterinarian. As the data on mastitis in this study were these two phenomena. Heifer mastitis during period of 7 d before treatment data, not actual disease data, and 7 d after first calving made up about one- management decisions were of great importhird of all the mastitis treatments for first tance. The high frequency of mastitis treatment lactation cows. The situation is similar for all indicates a general tendency to treat even mild mastitis treatments, independent of cow age cases of mastitis in line with good farming (26). Thus, the predisposing factors for mastitis practice. Some evidence exists for the association of around calving are likely to be similar in heifmastitis with generous concentrate feeding (7, ers and older cows, even if the sources of the 21), excessive protein in feed (17), and high pathogenic organisms differ. The immune blood urea concentrations (4). However, in function during the periparturient period is imthose studies, the frequency of heifer mastitis paired (8), and the mammary gland is susceptidid not vary according to the proportion of ble to mastitis during transition times, such as concentrates and silage in feed, or calculated drying off and colostrogenesis (15). protein content, but the type of concentrate seemed to be associated with frequency of heifer mastitis. Because homemade concentrates and commercial concentrates were alternatives, it was not possible to determine whether homemade concentrate predisposed 3.5 heifers to mastitis or whether commercial concentrates protected heifers from mastitis. More detailed data on feeding of the individual heifp 1.5 ers just before calving is needed to explain the * 0.5 relationship between feeding and heifer masti04 : : : : : : : : : ; : 1 tis. J F M A M J J A S O N D Month According to Erb et al. (3, older heifers have more mastitis than younger heifers. Also, Figure 2. Mean seasonal variation of heifen treated for mastitis between 1983 and 1991. Bars indicate standard in practice, pregnancies that are longer than errors of the mean. normal are associated with a longer heavy .
I
,
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I
MASTITIS IN PRIMIPAROUS HEIFERS
543
support those theories. When heifers with mastitis were compared with healthy control heifers, calving age, duration of pregnancy, and size of the animals were not associated with frequency of heifer mastitis. Good milking speed has been associated with more udder diseases and higher SCC (10, First test milking Z), but results of our study indicated the 70 I reverse. The heifers with mastitis were, according to sire progeny-testing results, genetically slower milkers than the controls. Bad udder 6o SO conformation may predispose a cow to mastitis (22), but the data we examined showed no differences between the heifers with mastitis and control heifers for progeny-testing results of the sires. 10 Heifers with mastitis tended to be geneti% 0 cally higher producers of milk with lower fat 201> 151and protein contents, but differences were 500 1001 10 100 small. According to breeding indices of the sires, the expected 305-d milk production of Second test milking the heifers with mastitis should have been 43 70 I kg higher than that of the control heifers, but, 60 -in fact, production was 33 kg lower. Thus, r heifer mastitis caused a pioduction loss of 70 50 -to 80 kg per cow, which is indicative of some -udder secretory tissue damage. This figure was x 40 30 -rather low compared with production losses 20 -from other types of mastitis. Timms and Schultz (27) reported production losses of 821 and 1153 kg from infections of coagulasenegative staphylococci and from Sruphylococ201> 151cus uureus, respectively. Conversely, the de10 100 500 1001 crease in production has been reported to be small, especially with young cows (5)or when Third test milking mastitis incidence was followed by low SCC (9). Our results are in accordance with those latter results. The influence of heifer mastitis on SCC 50 was clearly seen in the first test milking, which took place within 1 mo after parturition. During the later lactation, the heifers with mastitis and control heifers were represented equally in the very low SCC class (IlO,OOO), indicating 10 that mastitis did not permanently harm the 0 udder tissue. The heifers with mastitis seemed 201> 151to accumulate in the SCC class of 10,000 to 10 100 500 1001 50,000 instead of in the classes 50,000 to 500,000, where the control heifers were more scc (x103/rnl) frequently represented. We have no explanaFigure 3. The SCC in milk of heifers treated for tion for this result. There was no significant mastitis (open bars) and for control heifers (solid bars) during first lactation, as determined by monthly test milk- difference in mean logarithmic SCC for the entire lactation between heifers with mastitis ings after parturition.
feeding period, which could predispose heifers to mastitis, for example, by inducing early milk letdown. However, the results did not
,
1
!
i
t
%i+.l
Journal of Dairy Science Vol. 78, No. 3, 1995
544
MYLLYS AND RAUTALA
and control heifers. The weighted mean SCC were 13,000 higher for the entire lactation for heifers with mastitis. The difference occurred entirely during the 1st mo postpartum, indicating good recovery from heifer mastitis. This finding is in agreement with the results of Pyorala and Pyoriila US), who reported that heifer mastitis is more easily cured than mastitis in older cows. During later lactation, the heifers with mastitis were not treated for mastitis more than control heifers, which indicated that heifer mastitis did not become a chronic disease with recurrent clinical episodes and that mastitic heifers were not more prone to mastitis than controls in general. The puerperal diseases occur as a complex (2). Heifer mastitis was not similar. Occurrence of other diseases was no more frequent in heifers with mastitis than in controls. The most severe consequences were seen as a 4% increase in culling of heifers with mastitis. This result is in agreement with results of Erb et al. (3, who established that mastitis is an important predictor of culling. CONCLUSIONS
Awareness of the importance of proper treatment of mastitis, increased milk production, and subsequent lower mastitis resistance may partly account for the increase in heifer mastitis between 1983 and 1991. Heifer mastitis was a disease of well-managed herds with high milk production, low SCC, and high frequency of mastitis treatments administered by veterinarians. The disease as such was "benign"; production losses were small, mastitis did not predispose the heifer to more mastitis or other diseases later in lactation, and the recovery rate was high, as judged by SCC, although mastitis resulted in increased culling. ACKNOWLEDGMENTS
We are grateful to Tapani Hellman from the Agricultural Data Processing Centre for collecting and processing the data from the records. This work was funded in part by the foundation of Walter Ehrstrom. REFERENCES 1 Birgersson. A., P. Jonsson, and 0.Holmberg. 1992. Species identification and some characteristics of
Journal of Dairy Science Vol. 78. No. 3, 1995
coagulase-negative staphylococci isolated from bovine udders. Vet. Microbiol. 31:181. 2Curtis. R. C., H. N. Erb, C. J. Sniffen, R. D. Smith. and D.S . Kronfeld. 1985. Path analysis of dry period nutrition, postpartum metabolic and reproductive disorders, and mastitis in Holstein cows. J. Dairy Sci. 68: 2347. 3Emanuelson. U,.B. Danell, and J. Philipsson. 1988. Genetic parameters for clinical mastitis, somatic cell counts, and milk production estimated by multipletrait restricted maximum likelihood. J. Dairy Sci. 71: 467. 4Emmert, M., and K. Wendt. 1991. Untersuchungen des Z u s m n h a n g e s zwischen futterungsbedingten Stoffwechselstarungen und Eutergesundheitsschlden bei Milchrindern. Monatsh. Veterinaermed. 46538. 5 Erb. H. N., R. D. Smith, P. A. Oltenacu, C. L. Guard, R. B. Hillman. P. A. Powers, M. C. Smith. and M. E. White. 1985. Path model for reproductive disorders and performance, milk fever, mastitis, milk yield. and culling in Holstein cows. J. Dairy SCI. 68:3337. 6Grohn. Y.,H. Saloniemi, and J. S y v a j h i . 1986. An epidemiologic and genetic study on registered diseases in Finnish Ayrshire cattle. 1. The data, disease occurrence and culling. Acta Vet. Scand. 27:182. 7 Johnson, D. G., and D. E. Otterby. 1981. Influence of dry period diet on early postpartum health, feed intake, milk production, and reproductive efficiency of Holstein cows. J. Dairy Sci. 64:290. 8Kehrli. M. E., B. J. Nonnecke, and J. A. Roth. 1989. Alterations in bovine neutrophil function during the penparturient period. Am. J. Vet. Res. 50:207. 9 Macmillan, K. L., G. F. Duirs. and D. M. Duganzich. 1983. Associations between dry cow therapy, clinical mastitis, and somatic cell count score with milk and fat production in ten New Zealand dairy herds. J. Dairy Sci. 66:259. lOMadsen, P., S. M. Nielsen, M. D. Rasmussen. 0. Klstrup, N. E. Jensen, P. T. Jensen. P.S.L. Madsen, B. Larsen, and J. Hyldgaard-Jensen. 1987. Investigation on genetic resistance to bovine mastitis. Frederiksberg Bogtrykkeri, Copenhagen, Denmark. 1 I Matthews, K. R., R. J. Hannon, and B. E. Langlois. 1992. Prevalence of Sfaphyiococcus species during the penparturient period in primiparous and multiparous cows. J. Dairy Sci. 75:1835. 12Myllys. V., T. Honkanen-Buzalski, H. Virtanen, S. Pyortilti, and H.-P. Muller. 1994. Effect of abrasion of teat orifice epithelium on development of bovine staphylococcal mastitis. J. Dairy Sci. 77:446. 13 Oliver. S. P.. M. J. Lewis, B. E. Gillespie, and H. H. Dowlen. 1992. Influence of prepartum antibiotic therapy on intramarnmary infections in primigravid heifers during early lactation. J. Dairy Sci. 75:406. 14 Oliver, S . P.. and B. A. Mitchell. 1983. Intramammary infections in primigravid heifers near parturition. J. Dairy Sci. 66: 1180. 15 Oliver, S . P., and L. M. Sordillo. 1988. Udder health in the periparturient period. J. Dairy Sci. 71:2584. 16 Pankey, J. W., P. A. Drechsler. and E. E. Wildman. 1991. Mastitis prevalence in primigravid heifers at parturition. J. Dairy Sci. 74:1550. 17 Pedersen. P. S . 1975. Prevention of mastitis in cows. Page 249 in Seminar on Mastitis Control. F. H. Dodd,
MASTITIS IN PRIMIPAROUS HEIFERS T. K . Griffen. and R. G. Kingwill, ed. Int. Dairy Fed., Brussels. Belgium. 18 Pyorda, S., and E. Pyorda. 1994. Efficacy of bovine clinical mastitis therapy during lactation. Page 42 in Proc. XVII Nordic Vet. Congr., Reykjavik. Vol 2. Icelandic Vet. Assoc., Reykjavik, Iceland. 19 Roberson, J. R., L. K.Fox, D. D. Hancock, C. C. Gay, and T. E. Besser. 1994. Coagulase-positive Staphylococcus intramammary infections in primiparous dairy cows. J. Dairy Sci. 77:958. 20SAS@ Users Guide: Statistics. Version 5 Edition. 1985. SAS Inst., Inc., Cary, NC. 21 Schukken, Y. H., F. J. G r o w e r s , D. van de Geer, H. N. Eh, and A. Brand. 1991. Risk factors for clinical mastitis in herds with a low bulk milk somatic cell count. 2. Risk factors for Escherichia coli and Staphylococcus aureus. J. Dairy Sci. 741826. 22 Seykora. A. J., and B. T. McDaniel. 1985. Udder and teat morphology related to mastitis resistance: a review. J. Dairy Sci. 68:2087. 23 Slettbakk, T.. A. J~rstad.T. B. Farver, and D. W. Hird. 1990. Impact of milking characteristics and teat morphology on somatic cell counts in fust-lactation Norwegian cattle. Prev. Vet. Med. 8:253.
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24 Sobiraj, A., H.-U. Ostertag, D.Peip, H. Bostedt, and G . Kielwein. 1988. Clinical and bacteriological findings concerning the incidence of mastitis in first lactating heifers during and shortly after parturition. Tieraerztl. Praxis 16:243. 25 Statistical Yearbook of Finland. 1984-1992. Central Statistical Office, Helsinki, Finland. 26 Syvajiirvi, J., H. Saloniemi, and Y.Grohn. 1986. An epidemiologic and genetic study on registered diseases in Finnish Ayrshire cattle. IV. Clinical mastitis. Acta Vet. Scand. 27:223. 27 Timms, L. L., and L. H. Schultz. 1987. Dynamics and significance of coagulase-negative staphylococcal ininfections. J. Dairy Sci. 70:2648. 28Tnnidad. P., S. C. Nickerson, and T. K. Alley. 1990. Prevalence of intramammary infection and teat canal colonization in unbred and primigravid dairy heifers J. Dairy Sci. 73:107. 29 Wildman, E. E., J. K. O’Neil, P. A. Drechsler, and J. W. Pankey. 1990. Prevalence of mastitis in primiparous cows. .I. Dairy Sci. 73(SuppI. I): 257(Abstr.) 3OWoolford. M. W. 1985. The relationship between mastitis and milk yield. Kiel. Milchwirtsch. Forschungsber. 37924.
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