economical losses from clinical mastitis in 4 dairy herds in israel

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ISRAEL JOURNAL OF
VETERINARY MEDICINE
ECONOMICAL LOSSES FROM CLINICAL
MASTITIS IN 4 DAIRY HERDS IN ISRAEL
S. Friedman(1)*, E. Shoshani(2),E. Ezra(3)
Vol. 59 (1-2)
2004
1. "Ha'Haklait” and The National Service For Udder Health and Milk QualityP.O.B 3553 Caesaria 38900 - Israel.
2. Extension service, Ministry of Agricultural and Rural Development Bet-Dagan
- Israel.
3. Israel Cattle Breeder's Association (ICBA) - P.O.B 3553 Caesarea 38900 Israel.
* Author for correspondence: E mail: shmulik @mba-labs.or
Abstract
Cows were monitored and sampled for clinical mastitis by the farmers themselves
during a period of one and a half years. A total of 600 aseptic milk samples were
collected when an incidence of clinical mastitis was observed and underwent
bacteriological examinations. Records collected from the Israeli Herd Book during
the mastitis episode included: Monthly milk and Somatic Cell Counts (SCC), the
time of appearance of the mastitis as well as the rate of recurrence of clinical mastitis
during the lactation period. The aim of this study was to quantify the direct damage
derived from milk losses exclusively caused by clinical mastitis. The most severe
effect of clinical mastitis was found when it occurred : (a) during the first 60 days of
lactation (losses of 903 kg milk per lactation); (b) After parturition during the
summer season (1350 kg milk per lactation); and (c) In case of 2 or more recurrences
of clinical mastitis in the same cow, during the same lactation.
Introduction
Mastitis is known as a disease that causes heavy economic losses to milk
producers and to the dairy industry (1. 5, 7, 8, 10). The majority of milk
producers are unable to asses the damage caused by this disease. Mastitis
causes a reduction in the quantity/quality of milk output (9), increased
veterinary expenses due to excessive use of medications. (7), increased risk
of residues in the milk/meat and, consequently the possibility of damage to
public health (9,10). Additional loss to the producer is results from confiscation
of suspected milk followed by imposition of heavy penalties.
The reduction or impairment of profitability caused by mastitis is hard to
asses due to the impact of the many factors involved in the calculation, which
are onnected directly or indirectly to the dairy branch in Israel. I.e. milk quotas,
"summer milk", the policy concerning rewards and penalties, food prices, the
cost of heifer replacement, etc.
In studies carried out abroad, the overall financial damage calculated,
including cases of sub-clinical mastitis, indicated losses amounting to $160 $344 per cow (5,6). It has been found that the annual costs of mastitis per
cow (irrespective of the severity of infection), were around $200-300 in the
USA and France (1,2) and 120 £ in England (3).
Forced culling of cows affected by mastitis results in decrease of infected
cows and reduces the risk of infecting new members of the herd (7,8,9).
Consequently, there is an immediate decrease in the overall milk production
level with a direct impact on the dairy farmer's income (10).
Despite the wide divergence between dairies, it showed that the average
loss for one case of clinical mastitis was about $40 (4) .
The cost of replacement of heifer varies among countries, and depends on
the current market demands. This inflicts more financial damage. The aim of
this study was to quantify the direct damage incurred by milk losses caused
exclusively by clinical mastitis.
Materials and Methods
Cows (n = 970) from four farms (3 cooperative farms consisting of 300
cows/herd, and one familial farm with 100 cows milked twice a day), were
monitored and sampled for clinical mastitis by the farmers for one and a half
years (1998-9). The mean daily milk yield was 36.5 kg/cow in the cooperative
farms and 31.9 kg/cow in the familial farm. The SCC annual averages in all
farms where between 350.000 and 525.000 /ml milk . Postdipping (Iodophors
of 4000 ppm of final concentration ,Zohar Dalia, Israel) and dry cow treatment
(Nafpenzal DC, Intervet, Holland) where used in all the farms. Procedures for
collection and diagnosis of milk samples were performed as described
previously (11,12). A total of 600 aseptic milk samples were collected when
an incidence of clinical mastitis was occurred (based on any observable signs
in the udder and/or milk) and delivered to the national mastitis laboratory
(Israeli Dairy Board, Caesaria) for bacteriological examination. A 0.01 ml' of
milk was streaked on Tryptose Soy Agar ( TSA - Hylab Laboratories, Rehovot,
Israel) containing 7.5% sheep blood and incubated for 48 h at 370C. (12).
Concurrently with this procedure, records collected from the Israeli Herd Book
during the mastitis episode included: Monthly milk and Somatic Cell Counts
(SCC), the time of appearance of the mastitis as well as the rate of recurrence
of clinical mastitis during the lactation period.
The period of clinical mastitis was calculated as 40 days prior to the
bacteriological findings of the udder infection and up to 20 days later (total of
60 days).
Statistical analysis
All data were analyzed by the GLM procedure of SAS (SAS 1990) by the
following model:
Y= µ+Hti + CDIMk+LL +DIM+Um +Sn+e
Y= Milk production.
µ= Overall mean.
H= Herd effect
CDIM= Category of day in milk (DIM) k=1,2,3
L= Lactation number L= 1,2,3,4+
Um=Udder Infection pathogen
Sn = Calving season (1= winter, 2= summer)
e = Error term
Days in Milk (DIM) were divided to 3 categories - 0-60, 61-100 and 101-305
days. Due to small number of cows aged more than 4 lactations they were
grouped to lactation 4.
Results and Discussion
Most of clinical mastitis in our study originated from environmental bacteria;
Escherichia coli was the most dominant bacteria following by Coaguase
Negative Staphylococci (CNS) (Table 1). The high rate of clinical mastitis,
caused by environmental pathogens, might indicate that the sources of the
infecting bacteria in Israeli dairy-farms could be attributed to barn
maintenance. I.e.: untreated open farm yards (which are currently forbidden
by law), unsuitable rest area (less than 15 m2/cow) and lack of hygienic
treatment of the cow before milking. It should be emphasized, though, that
there is a wide diversity amongst the farms involved in this study. Therefore,
one should not conclude that the conditions in all dairy farms in Israel are
similar. The diversity of the environmental bacteria, requires an individual
approach to each farm.
Examination of the occurrence of clinical mastitis showed that 25% of the
infections appeared during the first 60 DIM, 13% between 61-100, and 62%
after 101 DIM. Secretory tissue proliferation is the main factor to enhance milk
production along the lactation curve (Wilde et al.,2000)/ Although the highest
occurrence of clinical mastitis was found during the third phase of lactation,
the greater financial loss occurred during the earlier phases due to
interference of secretory tissue proliferation.. In our study the main damage to
milk production was caused when the clinical mastitis occurred during the first
phase of lactation - a loss of 903 kg milk per lactation (Table 2).
Table 1. Distribution (%) of bacteriological diagnosis of clinical mastitis in 4
farms
Sn= number of samples, (N= number of cows).
Pathogenic
factor
E.coli
CNS
Streptococcus spp.
Nocardia
C. Bovis
Others
Farm 1;
Farm 2;
Farm 3;
Farm 4;
Sn=30 (N=70)
Sn=277 (N=340)
Sn=67 (N=270)
Sn=132 (N=290)
60
20
7
0
0
13
45
17
13
2
7
7
80
6
8
0
0
2
64
4
8
6
0
3
Table 2. Mean milk yield per DIM of standardized lactation (305d) and SCC of
cows,
which
were
infected
with
clinical
mastitis
during
one
of
three
lactation
stages.
Mastitis event
Category
1 (0-60)
2 (61-100)
3 ( >100)
No mastitis
in
DIM
Milk (Kg)
34.00 ± 1.5
35.83 ± 1.3
35.37 ± 1.6
36.96 ± 0.9
SCC (*1000)
670 ± 144
632 ± 227
456 ± 293
873 ± 44
Nocardia spp. Was found as the dominant bacteria causing milk loss while
Escherichia coli, Corinobacterium bovis and CNS had similar effect. However,
due to low number of infected cows, excluding E. coli (n=34, table 5), those
figures should be considered cautiously. The damage of clinical mastitis,
caused by E. coli, was expressed in 1.9 Kg milk loss per milking day and 580
Kg for the entire period of lactation (305 days).
When the effect of the calving seasons was examined (Table 4), it was found
that cows calving in summer (April-September) lost 1350 kg milk per lactation,
when clinical incidents of mastitis developed during the first 60 days after
parturition. In comparison to loss of 420 kg milk per lactation of cows calving
in winter (October-may).
It was found that 22% of the cows had two or more recurrences of mastitis
during one lactation period, either with the same bacteria species or with a
different one. A new or recurrent infection was defined when it appeared two
or more times during the same lactation and when a clinical mastitis
reappeared 20 days after the previous occurrence. E. coli was the dominant
pathogen diagnosed more than once in the same lactation (table 5). Out of
the "recurrent cows": 13% had mastitis three or more times during lactation.
We hypothesize that there are few cows in each farm, which are more
succeptible to environmental bacteria than others due to udder and teat
structure or different heredity/immunity status. Culling of cows with recurrent
clinical infections in the same lactation period, might reduce the financial loss
at a later stage.
Table 3. The effect of type of pathogen on milk yield per DIM during the
period of clinical mastitis*.
Type of pathogen
Milk
E.coli
32.7 ± 0.8
C. bovis
32.5 ± 2.4
Nocardia spp.
30.4 ± 1.9
Coagulase Negative
32.5 ± 1.2
Staphylococci (CNS)
Strep. disgalactia
32.9 ± 1.6
No growth
34.5 ± 1.0
* a period of 40 days prior to bacteriologic result and 20 days after = a total of 60 days.
Table 4. The effect of clinical mastitis event on milk yield and SCC by
interaction between calving season and stage of lactation.
Mastitis event in DIM
Calving Season
Category
Milk
SCC
Winter (Oct - March) 1 (0-60)
35.9 ± 1.2
685 ± 158
2 (61-100)
36.7 ± 1.0
699 ± 161
3 (>100)
36.6 ± 1.0
396 ± 185
No mastitis*
37.3 ± 0.9
87 ± 47
Summer (April-Sept.) 1 (0-60)
32.1 ± 1.0
654 ± 185
2 (61-100)
35.0 ± 0.9
564 ± 183
3 (>100)
34.1 ± 1.1
516 ± 146
No mastitis*
36.6 ± 0.9
87 ± 67
* - cows in which clinical mastitis and SCC higher than 200,000 did not occur during the entire
lactation period.
Table 5. Recurrence rate of pathogen which caused clinical mastitis in a cow
during a lactation period.
Type of pathogen
E.coli
Serratia
A. piogenes
Nocardia spp.
Staph. aureus
CNS
Strep. dysgalactia
No. growth
Others
Total
Recurrence rate in %
36.56
3.23
1.08
7.53
1.08
9.68
2.15
37.63
1.08
100
No. of cows
334
3
1
7
1
9
2
35
1
93
Conclusion
The damages discussed in this paper refer only to milk loss. It does not
include damages incurred by use of medications, extra work, disposal of milk,
fines, death of cows, and the cost of replacing heifers.
From a literature survey and results of another study we performed (in
preparation), it was found that sub-clinical mastitis might cause a greater
damage in terms of milk loss' compared to clinical mastitis' due to its high
prevalence and duration.
Although sub-clinical mastitis causes the greatest damage to milk
producers (13), clinical mastitis is also a significant contributor. The most
severe effect of clinical mastitis was found in our work, when it occurred (a)
during the first 60 days of lactation; (b) after parturition during summer (1350
kg milk per lactation) and (c) when recurrences appeared more then twice
during the same lactation.
In order to minimize the damage from clinical and sub-clinical mastitis it is
necessary to focus on preventive actions at the farm-medical level rather than
to resort to syringe and antibiotics. Appropriate and continuous maintenance
of the cows, housing, prevention of stress actions, and a fully hygienic milking
routine will minimize the damage caused by clinical mastitis.
Reference:
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programmers and related costs in French dairy herds. 48th Annual meeting of
the European association for animal production Vienna (Austria),1977.
2. Blowey, R.W :An assessment of the economic benefits of a mastitis control
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3. Fourichon, C, Horet. P, Seegers. H, Sorensen J.T. , Beaudeau F.,
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10. Beck Hs. Wise Ws, Dodd FH.: Cost benefit analysis of bovine mastitis in
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11. Brown, R. W., Barnum, D. A., Jasper, D. E., McDonald, J. S. and Schultz,
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Microbiological Procedures for the Diagnosis of Bovine Mastitis, 2nd edn.
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13. Philpot, W.N and Nickerson, S.C .Mastitis: Counter Attack, Babson
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