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Mastitis and Economics: How much do you save by reducing mastitis?

Emma Gratte
Scott R.R. Haskell
Sofie Fröberg
Published: March 09, 2005
  • There are many ways that mastitis affects the overall economics of the farm
  • Subclinical mastitis can cause decreased milk yields
  • Reduced milk quality due to mastitis can lead to reductions in payments for milk
  • Mastitis is one of the three major reasons that cows are culled
  • Mastitis can lead to poor reproduction
  • Other economic costs are discarded milk, treatment costs and the introduction of other diseases

Introduction

The concentration of the milk somatic cell count (SCC) is directly correlated to the infection status of the udder. Nothing affects the SCC the way bacterial infections do. An effective way to monitor the herd infection status is to comprise the testing of bulk tank somatic cell count (BTSCC) and/or SCC on an individual cow level in the daily management routines (Ingalls, 1998). 

Mastitis is of significant economical concern for the milk producer (Table 1) and causes reduced animal welfare in the herd. This text considers the main factors contributing to the serious economical loss derived from mastitis.

Table 1. Estimated annual losses1 due to mastitis in $. Figures from Current Concepts in Bovine Mastitis, National Mastitis Council, 1996 (After Schroeder, 1997)

Source of loss Loss per cow ($) Per cent of total (%)
Reduced milk yield  121.00  66.0
Discarded milk 10.45 5.7
Replacement cost  41.73 22.6
Extra labour 1.14  
0.1
Treatment   7.36 4.1
Veterinary services  2.27 1.5
TOTAL  184.40  100.0

1Assumptions: ⅓ of cows infected in an average of 1.5 quarters; milk loss 388 kg per infected quarter; milk price $0.266 per kg

Milk yield

For every case of clinical mastitis in the herd, there are between 15 and 40 subclinical cases (Bailey, 1996; Crist et al., 1997). Subclinical mastitis should be taken seriously and be thoroughly investigated because it can for example cause considerable losses in decreased milking capacity (Table 2). The proportion of economical loss that could be associated with reduced milk production from subclinical mastitis - can be as much as 80% (Gill et al., 1990). Most commonly at the beginning, the infection does not appear as a clinical case but could gradually develop into one and thereby cause even more damage (Jahnke, 2004).

Table 2. 305-days milk yield in relation to SCC and the difference per class compared with SCC class <50,000 cells/ml milk (After Jahnke, 2004)

1st lactation

 

 

2nd lactation

 

 

SCC class1

Milk yield
(kg)

Diff.
(kg)

Diff.
(%)

Milk yield
(kg)

Diff.
(kg)

Diff.
(%)

<50

8,700

0

0

10,447

0

0

51-100

8,472

-228

-2.6

9,991

-456

-4.4

101-200

8,422

-278

-3.2

9,820

-627

-6.6

201-400

8,392

-308

-3.5

9,716

-731

-7.0

401-800

8,378

-322

-3.7

9,455

-992

-9.5

>800

n. a.2

n. a.2

n. a.2

9,062

-1,385

-13.3

1 Geometric averages x 1,000, 2 Too few cows (0.3% of total number of cows)

A German study, including 18,702 cows, showed that 80% of the total milk yield loss of cows in first lactation and 57% of those in second or higher lactation - was represented by cows with a SCC between 50,000 and 200,000 (Jahnke, 2004). According to a study by Raubertas and Shook (1982), the milk production loss per increased unit of SCC is greatest when the SCC is low (Raubertas & Shook, 1982). Apparently even relatively low SCC gives reduced milk yield, so it’s financially imperative to maintain control of the SCC.

USDA’s (United States Department of Agriculture) National Animal Health Monitoring System (NAHMS) Dairy ’96 Study included 1178 herds in 20 states. The herds were put into three different classes according to BTSCC reported by the farmer for the last six months: low-BTSCC herds with <200,000 cells/ml milk; medium-BTSCC herds with 200,000 to 399,000 cells/ml and high-BTSCC herds with >400,000 cells/ml (Ott, 1999). The biggest group, representing 54.6% of the herds, was the one with medium-BTSCC. Second biggest was the low-BTSCC herd group (29.8%) and the smallest group was the high-BTSCC herd group with 15.6% (USDA/APHIS/VS, 1996). Medium-BTSCC herds produced 372 kg less milk per cow and high-BTSCC herds gave 959 kg less milk per cow than the low-BTSCC herds (Ott, 1999).

Problematic underestimation often occurs when producers are asked to estimate their milk loss caused by mastitis. The cost of milk loss associated with mastitis reported by milk producers cooperating in the NAHMS, was compared with estimates based on BTSCC and individual cow SCC. The producer estimates had a weighted proportion of 31% of the total cost due to mastitis, while the milk production loss based on the BTSCC had a weighed proportion of 81% (Lightner et al., 1988). Thus, the milk producer usually loses more money on reduced milk yield as a result of mastitis than he or she thinks. Another reason for this could be that the milk production loss is not visible to the producer because the milk is never produced and therefore never seen (Østerås, 2000).

A recent study by Wilson and colleagues (2004) at CornellUniversity showed that clinical mastitis tends to strike high producing animals in second-plus lactation. In other words mastitis often hits the cows with the highest production potential, which expands the loss due to mastitis. According to the study, the estimated loss following clinical mastitis was almost 700 kg for cows in first lactation and 1,200 kg for cows in second or higher lactation (Wilson et al., 2004). Rajala-Schultz reported in 1999 that cows with clinical mastitis did not return to the same production level within the remainder of the lactation, according to Miller and co-workers (2004). There may also be a carryover effect of elevated SCC on the subsequent lactation (Miller et al., 2004). Fetrow and colleagues (2000) mention different studies in this matter showing an impact on the subsequent lactation which varies between 9% and 50%.

Milk quality premium and deduction

When the somatic cells destroy bacteria, enzymes that have been involved in the process are left behind. These enzymes are often resistant to pasteurization and can cause milk fat and protein damage, which can result in serious off-flavours in dairy products. It may also significantly reduce shelf life, quality and yield of dairy products - even when kept properly refrigerated (Ingalls, 1998). Even modest increases in individual cow SCC (<100,000/ml) have been shown to reduce cheese yields (Ruegg, 1999). Therefore most milk purchasers pay premiums for higher quality milk. Controlling subclinical mastitis and producing lower SCC milk generates an opportunity associated with both increased production and increased milk price.

Many dairies have an upper SCC limit for milk that is legally marketable. Bulk tank milk must have an SCC of <750,000 cells/ml to be legally marketable in the US. In many US markets, milk price premiums are paid for milk with low SCC and in some cases, high SCC milk is penalized (Fetrow et al., 2000). In European Union countries (Ingalls, 1998; Miller et al., 2004), New Zealand and Australia the limit is 400,000 cells/ml and in Canada 500,000 cells/ml (Ingalls, 1998). The premium and deduction system varies considerably between countries and between purchasers from the same country. The premium and deduction system of the dairy Arla Foods in Sweden and Denmark is shown in Table 3.

Table 3. The premium and deduction system of Arla Foods in Sweden and Denmark.Milk price in Sweden is

€0.26/kg milk (Arla pers. comm., 2004)

SCC limits (x 1,000 cells/ml) Premiums/deductions (% of milk price)
<200  +2%
201-300 +1%
301-400  0
401-5001  -4% 
>5012  -10%

1 or 2 = If shipped milk exceeds this SCC limit three times in a row a deduction of 20% or 30%, respectively, will follow

An example of the possible premium opportunity for a Swedish farmer in year 2004, by using a 50-cow dairy farm shipping 48,444 kg milk monthly with a 450,000 SCC - is demonstrated in Table 4. The reduction per month and cow would be €10.15 (32 kg x 0.0104 x 30.5). An example of the possible opportunity for a US-farmer in Wisconsin in year 1999, with the same number of cows and the same milk yield per month but a different premium system - is shown in Table 5. According to Cook and Nordlund (2004), not getting SCC premiums represents a big loss for most Wisconsinherds; on average it accounts for 41% of total milk quality loss of €199.52 per cow per year.

Table 4.Example of calculation of milk quality premium opportunity in € for a Swedish farmer delivering to Arla (Arla pers. comm., 2004)

Maximum available SCC premium (at <200,000) 0.0052
Current received SCC premium
(-4% deduct at the last milk checks1)   
-0.0104
Potential premium difference 0.0156
Milk shipped last month 48,444 kg
Current monthly premium opportunity 755.73

 1 For farms shipping milk to Arla the milk check is made once weekly.

Table 5.Example of calculation of milk quality premium opportunity in € for a US-farmer in Wisconsin (After Ruegg, 1999)

 Maximum available SCC premium (at <100,000) 0.0132
Current received SCC premium (€-0.0037 deduct at the last milk checks)    -0.0037
Potential premium difference
 0.0169
Milk shipped last month 48,444 kg
Current monthly premium opportunity 818.70

Culling and replacement costs

Beside low production and reproduction, mastitis is one of the three major reasons why cows are removed from the herd (Young, 2000). The general rate of milk quality related culling, varies across herds and studies. Seegers and co-workers(2003) reported in a review that 5% to 17% of all culling was related to udder disorders and that the proportion reached 28.5% when high SCC and teat injury were included. On a typical Wisconsin dairy farm the milk quality related culling is estimated to be 24% (Cook & Nordlund, 2004). Roenfeldt (2000) reported that within 60 days of a severe clinical mastitis event, 13% of animals are culled and another 8% are dried off early. Furthermore, for clinical coliform mastitis, 23% of cows are either culled or die without completing their lactations.However declared culling reasons are more or less subjective, so they provide information on the farmer’s reactions rather than constituting an objective evaluation of the impact of health disorders on longevity (Seegers et al.,2003).

In a DAISY (The Dairy Information System, England) survey reported by Kossaibati, Hovi and Esslemont (1998), it was estimated that 0.2% of 40 clinical mastitis cow cases were fatal. Fatality incidences in the US where estimated to be 2.5% in the year 2001. The cost per culled cow the same year was around €1,092 when adding the cost of delayed filling of the vacated slot (14 days between the cull cow leaving and the replacement heifer producing; €136), to the average value of a cow in the herd (€956) (Fetrow, 2001). In the UK year 2000, a cull cow was assumed to cost €690 per cull (Kossaibati & Esslemont, 2000). 

Østerås (2000) simulated replacement cost at culling, where the replacement cost was the value of a pregnant heifer minus the value of the slaughtered cow that was replaced. This difference was reduced according to the expected lifetime of a cow (e.g. four years) and corrected by the higher milk yield of an older cow (or approximately 1,500 litres less for a first calver). Culling in first lactation month gave a replacement cost of €397 to €794. Cows at month four to six in lactation had the lowest replacement cost of around €199 to €397. Thereafter the replacement cost increased due to the value of an extra calf being born. The most optimal replacement cost was €99 for cows in fifth lactation and the worst established costs was for cows in second or third lactation.

Reproduction

In a study including 1,001 Holstein dairy cows on two commercial dairies, Kirk (2004) found that cows that had a case of clinical mastitis prior to their first breeding, had an extended interval from calving to first artificial insemination. Cows that had mastitis prior to pregnancy diagnosis had decreased conception rates when compared to the controls. In addition, there was an increase in abortions in cows with clinical mastitis compared to cows without. This is in accordance with Hovingh (1999), who observed that cows which were infected by mastitis during the first 45 days after breeding were almost three times more likely to abort than cows without an experienced mastitis event. 

Subclinical mastitis during the first 90 days of lactation can cause the same damaging results on reproduction as clinical cases. When 758 Jersey cows were followed, more than half of the cows were infected with mastitis during early lactation and most of these cases were subclinical rather than clinical. Cows that developed clinical or subclinical mastitis before their first service (during the first 90 days of lactation), had between 7 to 10 increased days to first service compared to uninfected herd mates. Services per conception were to 2.1 for cows with subclinical mastitis and 3.0 for cows with clinical mastitis, compared to 1.6 for uninfected cows. The results only got worse for cows whose subclinical infection developed into a clinical case. The latter increased days to first conception by about 26 days more than uninfected cows and services per conception increased to 4.3. In addition, no matter which kind of causative bacteria (gram-negative or gram-positive) they resulted in the same impact on reproduction. Mastitis after pregnancy had no effect on reproduction (Linderoth, 2003).

Another study including data from 4,555 breedings, found that cows with mastitis within 30 days after insemination had a conception rate of 38%, compared to 46% for cows without mastitis (Kelton et al., 2001).

Linderoth (2003) reports that unpublished results from research at the University of Tennessee show that cows experimentally infected with Streptococcus uberis, demonstrated significant reduction in follicular function. If cows developed clinical mastitis prior to the onset of oestrus, most of them did not show oestrus behaviour. The reason is that clinical mastitis delayed oestrus by a full cycle, despite the fact that ovulatory follicles were the same size as for cows without mastitis. Mastitis-infected cows had reduced oestrogen levels and did not have a surge of luteinizing hormone that is necessary for ovulation. Moreover, higher cortisol levels in the blood of infected cows, indicates that they were stressed due to the mastitis infection (Linderoth, 2003). Clinical intramammary infections often imply release of inflammatory mediators that can have negative effects on luteal function, levels of circulating progesterone and continuance of early pregnancy. These effects are largely linked with the endotoxin release in clinical coliform mastitis. Mastitis at or previously after insemination - may have a negative influence on the establishment and/or maintenance of pregnancy through the hypothalamus-pituitary-ovarian axis (brain to ovary), the uterine-ovarian axis or a nutritional effect on hormone levels (Young, 2000).

Discarded milk

If the cow is treated for mastitis, the milk has to be withdrawn for a certain amount of time. The number of days the milk has to be discarded is usually around eight (Østerås, 2000). An American study showed that cows with a higher SCC before a clinical case of mastitis, required longer treatment than those that had low SCC preceding the disease. The milk of the former cows had to be discarded for 9.5 days compared to 7 days for the milk of the latter ones (Ruegg, 2004). Half of the period of discarded milk is due to therapy and half is due to risk of therapeutic residues in milk. To consider the economical loss, the amount of discarded milk during this period has to be multiplied with the milk price the farmer gets (Østerås, 2000). For example, if a cow is producing 23 kg of milk per day, her milk is withdrawn for eight days and the farmer gets €0.2701/kg milk – that constitutes an absent income of €49.70. If some of this milk is given to the calves and not discharged down the drain, the value of saved calf feed should be taken into account (Østerås, 2000).

Treatment costs

Esslemont (2002) estimated the direct cost of a mild, severe and fatal case of clinical mastitis for farmers in the UK in the year 2002 (Table 6). The estimated direct cost for a mild and severe case of clinical mastitis in the US is shown in Table 7.

Table 6a. Treatment costs in € for a mild, severe and fatal case of mastitis in England in 2002 (After Esslemont, 2002) and for b) a mild and severe case in Wisconsin, US, in 2001 (After Fetrow, 2001)

a)

Treatment cost

Mild case

Severe case

Fatal case

Cost of drugs

10.96

69.31

111.76

Herdsman’s cost  €15.66/hour

2.62 (10 min)

7.83 (30 min)

15.66 (60 min)

Veterinary’s cost  €109.65/hour

 - 

45.69 (25 min)

109.65 (60 min)

Average turnout fee/cow

 -  

11.42

27.41

Total

13.58

134.25

501.25

 b)   

Treatment cost

Mild case

Severe case

Cost of drugs

7.43

37.17

Herdsman’s1 cost  €12.74/hour

12.74 (60 min)

50.98 (240 min)

Veterinary’s2 cost  €109.65/hour

 - 

26.55

Total

20.17 

114.70

 1Hours of labour for treatment, segregation, care and milking, 2 Veterinary costs incl. culture and other expenses per case

Increased labour

According to a review article by Blosser (1979), Dobbins (1977) assessed the required additional labour due to mastitis. The extra work included changing of milking units, washing extra equipment, discarding milk, treating cows and additional handling of the cow (Blosser, 1979). Fetrow (2001) estimated the time spent on a cow with severe clinical mastitis to be four hours with additional tasks consisting of treatment, care, segregation and milking. Emanuelson & Hallén Sandgren (1994) assumed milking time to increase by 10 seconds per cow and milking, due to mastitis.

Diseases related to mastitis

At least three metabolic diseases are linked with mastitis. Once the cow has the first complaint, it is common for her to contract a second one.

Ketosis usually hits fresh cows with a bad energy balance. The primary type impairs the animal’s immune system so that she is predisposed to other diseases such as mastitis. A Dutch study showed that ketonemic cows had more severe mastitis than non-ketonemic cows (Kremer et al., 1993). However it could also be the other way round. The cow can have an ongoing mastitis infection which depresses her appetite and thereby makes her prone to the secondary form of ketosis (Palmer Veterinary Clinic, 2004).

If the cow cannot meet the increasing need for calcium near calving (e.g. due to ratio imbalance), she may get hypocalcemia or milk fever. An increased risk for both mastitis and ketosis are among the possible problems arising from the disease (Rice & Grant, 1996). 

Between 80% to 90% of the cases of left displaced abomasums occur during the first month after calving when the cow is most prone to contract new ailments. Mastitis, ketosis and hypocalcemia are all factors that predispose a cow to abomasal displacement (Vieira, 1998).

By preventing mastitis or treating it as promptly as possible, the consequential risk of the cow contracting other ailments is reduced.

All rights reserved. Nothing from this publication may be reproduced in any form or in any manner without prior written permission from the publisher.

References:

Arla Foods in Sweden and Denmark, personal communication (2004-09-14).

Blosser, T.H., 1979. Economic Losses from and the National Research Program on Mastitis in the United States. Journal of Dairy Science, 62:119-127.

Cook, N.B. & Nordlund, K.N., 2004. Where your mastitis money goes. Hoard’s Dairyman, 149, pp 249.

Emanuelson, U. & Hallén Sandgren, C., 1994. Ekonomiskt effektiv mjölkproduktion, hög mjölkmängd och/eller god hälsa? Djurhälsoavdelningen, SHS. Summary of lecture at Gällöfsta (November 1994), 17 pp.

Esslemont, D., 2002. What is mastitis really costing you?  Dairy farmer, December, pp 30-31.

Fetrow, J., Stewart, S., Eicker, S, Farnsworth, R. & Bey, R., 2000. Mastitis: An economic consideration. In: National Mastitis Council Annual Meeting Proceedings, pp 3-47.

Gill, R., Howard, W.H., Leslie, K.E. & Lissemore, K., 1990. Our industry today. Journal of Dairy Science, 73:3340-3348.

Jahnke, B., 2004. Noch nicht krank, doch schon sehr teuer. Neue Landwirtschaft, 4: 59-62.

Kelton, D.F., Petersson, C., Leslie, K.E. & Hensen, D., 2001. Associations between clinical mastitis and conception on Ontario dairy farms. In: National Mastitis Council Annual Meeting Proceedings, pp 228-229.

Kossaibati, M.A., Hovi, M. & Esslemont, R.J., 1998. Incidence of clinical mastitis in dairy herds in England. The veterinary record, 143:649-653.

Kremer, W.D.J., Noordhuizen-Stassen, E.N., Grommers, F.J., Schukken, Y.H., Heeringa, R., Brand, A. & Burvenich, C., 1993. Severity of Experimental Escherichia coli Mastitis in Ketonemic and nonketonemic Dairy Cows. Journal of Dairy Science, 76:3428-3436

Lightner, J.K., Miller, G.Y., Hueston, W.D. & Dorn, C.R., 1988. Estimation of the costs of mastitis, using National Animal Health Monitoring System and milk somatic cell count data. Journal of the American veterinary medical association, 192: 1410-1413.

Miller, R.H, Norman, H.D., Wiggans, G.R. and Wright, J.R., 2004. Relationship of Test-Day Somatic Cell Score with Test-Day and Lactation Milk Yields. Journal of Dairy Science, 87:2299-2306.

Ott, S.L., 1999. Costs of Herd-Level Production Losses Associated With Subclinical Mastitis in U.S. Dairy Cows. National Mastitis Council Annual Meeting Proceedings, p. 152.

Østerås, O., 2000. The cost of mastitis- an opportunity to gain more money. Proceedings of British Mastitis Conference, pp. 67-77.

Raubertas, R.F. & Shook, G.E., 1982. Relationship Between Lactation Measures of Somatic Cell Concentration and Milk Yield. Journal of Dairy Science, 65:419-425.

Seegers, H., Fourichon, C. & Beaudeau, F., 2003. Production effects related to mastitis and mastitis economics in dairy cattle herds. Veterinary research, 34:475-491.

USDA/APHIS/VS (United States Department of Agriculture/Animal and Plant Health Inspection Service/Veterinary Services), 1996. Part III: Reference of 1996 Dairy Health and Health Management National Animal Health Monitoring System, 33 pp.

Wilson, D.J., González, R.N., Hertl, J., Schulte, H.F, Bennett, G.J., Schukken, Y.H & Gröhn, Y.T., 2004. Effect of Clinical Mastitis on the Lactation Curve: A Mixed Model Estimation Using Daily Milk Weights. Journal of Dairy Science, 87:2073-2084.

Related Links:

Negative influence of subclinical mastitis.
Bailey, T.,1996., Dairy Pipeline, October

Somatic Cells, Mastitis and Milk Quality.
Ingalls, W., 1998.

Effect of clinical mastitis on production and reproduction.
Kirk, J.H., 2004.

The cost of clinical mastitis in UK dairy herds.
Kossaibati, M.A. & Esslemont, R.J., 2000.

Don’t let subclinical mastitis zap reproductive efficiency.
Linderoth, S., 2003. Dairy herd management.

Ketosis.
Palmer Veterinary Clinic, 2004

Dairy Cow Health and Metabolic Disease Relative to Nutritional Factors.
Rice, D.N. & Grant, R., 1996. University of Nebraska-Lincoln Cooperative Extension.

Milk quality: Reclaim lost profits
Roenfeldt, S., 2000.

Treatment of Clinical Mastitis.
Ruegg, P.L., 2004.

Mastitis Control Programs: Bovine Mastitis and Milking Management.
Schroeder, J.W., 1997. North Dakota State University Extension Service.

Left Displaced Abomasum Prevention.
Vieira, E.A., 1998.

Can mastitis have an effect on reproduction?
Young, A., Dairy management. November 2000.

Information from Penn State University 

University of Kentucky Cooperative Extension Fact Sheet  

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