Overcoming Mastitis

To overcome an outbreak of clinical mastitis or to control a high SCC level the following approach has proved very successful.

1. Stop spread of infection i.e. pre spray and dry wipe, wear gloves and spray gloves regularly, disinfect clusters between milkings by dipping clusters in per acetic acid solution. 10mls of serpent to 2 gallons of water and change after 10 dips.

2. Cell count all cows every 3 weeks for 3 times.

3.Carry out a culture on 3 problem cows and 1 sample from bulk tank.

4. Get milking parlour serviced.

5.  Get your milking routine accessed and cow teat condition scored.

6.Cull chronic infected cows.

7.Carry out an aggressive dry cow routine.

8. Once Cell count comes good mind, it post spraying is crucial and pre spray problem cows.

 
During the course of the last 3 years we have carried out many farm visits, we would like to thank all the farmers we have visited for their co-operation and dedication. We would also like to thank all the Dairygold Staff and Teagasc Staff for their support over the years.

There is a solution, it takes effort and dedication but the rewards are significant. There is help available don't feel isolated.

In May 2005 Dairygold in conjunction with Teagasc initiated a joint program on milk quality. The objectives of the program were that two Teagasc milk quality specialists work inconjuntion with the Dairygold milk quality team to reduce the incidence of mastitis and reduce on farm cell counts. The aim of the program is to make farms more profitable and deliver a higher quantity of high quality milk for processing.

Mastitis control is an ongoing challenge in modern day Dairy farming irrespective of herd size and calving pattern. Prevention and control of spread of infection are critical mechanisms to minimize the impact mastitis organisms have on your herd. No two farms are the same, general control measures can be implemented, until the specific problem can be identified.

Individual cell count records are critical to controlling and monitoring the performance of your herd from an SCC point of view. Control the spread of the infection; identify the bacteria involved, identify the cause of the infection, e.g. milking practices, teat preparation, milking parlour functioning, housing facilities. Implement good infection control and dry cow therapy program.

When dealing with an on farm mastitis investigation it is very important to establish the cost an infection is having on herd performance.

Table 1: The Influence of SCC on Lactation Loss

 

 

 

Example milk production loss for herd of 100 cows (25% 1stlactation) having average bulk milk SCC of 200,000 cells/mls v100,000 cells/mls.

 

 

Other losses associated with sub- clinical mastitis include occasional lactation therapy with antibiotics + related losses and culling of chronic cows.

1. For every increase of 50,000 in cell count over 100,000 a 2.5% drop in milk yield occurs.

2. On average an infected cow will have 1.6 cases of clinical mastitis in the year.

3. The costs associated with a severe case of clinical mastitis comes to €590.00. This cost includes all the hidden costs of mastitis.

4. Costs of Mastitis

 

Associated costs, higher culling rate, milk yield loss etc

On Farm Investigations

We have dealt with 3 scenarios over the years we have worked on this program

Scenario 1. A farmer experiencing high cell count but no cases or very few cases of clinical mastitis

Scenario 2. A farmer with a cell count of 150,000 to 250, 000, experiencing a high incidence of clinical mastitis.

Scenario 3.  A very low cell count herd i.e. <100,000 and experiencing a high level of E.coli mastitis.

The costs of mastitis in dairy herds are very significant.

To tackle a mastitis problem the following information is required:

1. SCC records at least 3 recordings 3 weeks apart. Milk recording data in conjunction with herd plus is a Key component to tackling a SCC problem. It gives a great insight into what has been happening on the farm.

2. Treatment records. Tube usage, number of reoccurring cases etc.

3. Bacterial Identification.

4. Examination and scoring of cow teat condition.

5. Detailed milking machine service report.

6.Analysis of milking routines.

7. Housing facilities, road ways and collection yards.

8. Robust treatment regime for both the lactating and dry period.

 Bacterial Challenge and Identification

Mastitis occurs when the udder becomes inflamed because leukocytes are released into the mammary gland in response to invasion of the teat canal, usually by bacteria.
These bacteria multiply and produce toxins that cause injury to milk secreting tissue and various ducts throughout the mammary gland. Elevated leukocytes, or somatic cells, cause a reduction in milk production and alter milk composition. These changes in turn adversely affect quality and quantity of dairy products.

Over coming mastitis is a multi factorial issue. Mastitis can present itself in three forms clinical, sub- clinical and chronic mastitis.

1. Clinical mastitis cases, clots are present with an inflammation of the quarter, a raised cell count generally associated with this condition.
2. Sub- clinical mastitis exhibits no visual difference in consistency of milk, but a high cell count is present.
3. Chronic Mastitis: an inflammatory response that lasts for months and runs from lactation to lactation. It is usually sub-clinical with flare ups of clinical mastitis from time to time.

These conditions result primarily from invasion of bacteria through the teat canal. The teat canal is the first line of defence against infection. A sphincter muscle surrounds the teat canal; this muscle prevents milk from leaking and prevents bacteria entering the teat canal. Between the milking intervals the cells lining the teat canal produce keratin which has bacteriostatic properties and forms a barrier against bacteria.

The understanding of the cows' defence mechanism is important to enable control and prevent new infection and mastitis.

To overcome mastitis, the identification of the problematic agent is significant to help point us in the direction of possible cause. These bacteria can be divided into 2 categories; Environmental Bacteria i.e. Strep Uberis, E.Coli and Strep Dysgalactiae and Contagious Bacteria i.e. Staph aureus, Strep agalactiae.

Environmental bacteria as the name suggests originate primarily from the environment. Infection is picked up from the environment i.e. poor housing bedding, manure, dirty road ways, common clothes and poor teat preparation are prime examples.

Contagious Bacteria are pathogens primarily spread during the milking routine. Infection is spread from infected cows to clean cows via common clothes, milker's hands and infected liners are the main areas.

In addressing a mastitis problem the first area to assess is the teat opening and general skin condition. A general check on teat condition is required i.e. signs of odema, tenderness and uneasiness in cows when the cluster is removed. The teat opening is scored based on the degree of damage caused to the teat end during the milking procedure, this condition is called hyperkeratosis. The condition of the teat is scored based on a score card from 1 to 5

1 = Perfect or normal appearance, no ring evident on teat opening

3 = Moderate hyperkeratosis, few rough projections from teat opening, smooth slightly rough ring.

5 = Advanced protrusion; sphincter appears to be turned inside out, very rough teat end, flowered head at opening of teat.

The teat end serves as the body's first line of defense against infection. A smooth muscled sphincter, which surrounds the teat canal, functions to keep the teat canal closed, prevents milk from escaping, and prevents bacteria from entering the teat. The cells lining the teat canal produce keratin, a fibrous protein with lipid components (long chain fatty acids) that have bacteriostatic properties. This keratin forms a barrier against bacteria. During milking, bacteria may be present near the opening of the teat canal, either through dirty and wet conditions at the teat end, through teat end lesions or colonization, on contaminated surfaces of milking units (liners or claws), or cow prep procedures. Trauma to the teat renders it more susceptible to bacterial invasion, colonization, and infection because of damage to keratin or mucous membranes lining the teat sinus. The canal of a damaged teat may remain partially open.

There are a number of areas that affect teat end condition.

1. Over milking
2. Excessive Vacuum
3. Faulty pulsation
4. Removing clusters under vacuum
5. Blocked air bleeds.

Once established what bacteria is the causative agent and teat ends have been assessed, stopping the spread of infection is crucial. To aid this process a thorough teat preparation program and disinfection program of liners is essential. Pre spray or pre dip all teats prior to milking and dry wipe with a paper towel, apply clusters, on removal of clusters dip clusters in a per acetic acid solution( e.g. serpent) change after 12 dips and apply to next cow. Post spray/dip all cows post milking. This process minimizes the transfer of infection and we have achieved significant progress on farm level in stopping clinical mastitis and dropping herd cell counts.

Once the spread of infection has been curtailed diagnosis of cause is the next step. A detailed look at milking equipment is required.


Milking Equipment:

Areas of common concern:

                                                      Target Level

1. Vacuum level                                 48 kpa
Excessive vacuum is a common problem due to faulty regulators and
inaccurate vacuum clocks.


2. Pulsation Ratio                              68:32 or 65:35

3. Pulsation Rate                              55 to 60 pulse per min

4. D phase                                       >20%
The rest phase of the pulsation cycle should be greater than 20% of the cycle.

5. Adequate vacuum reserve
This is an inability of the vacuum pump to maintain a stable vacuum when
applying or removing clusters. Inadequate reserve is a common occurrence
where extensions to plant have occurred and vacuum pumps have not
increased proportionately.

6. Flooding of receiver jar.
 Occurs with diaphragm pumps, has a major impact on teat end vacuum.

7. Slope in milk line inadequate 1:60
Very common fault in milking parlours should have a constant even fall to the
receiver jar.

8. Milk entries not in top third of milk line.

9. Poor cluster alignment

10. Liner slip.

11. Frayed or damaged rubber fittings and liners.


Milking Practices

Milking procedures vary widely from farm to farm and from our on farm investigation have a significant effect on mastitis incidence. We have noticed a wide variation in milking practices and routines which have a dramatic effect on SCC levels in a herd.

1. Poor teat preparation.
No preparation of dirty cows or no pre-spraying of infected cows.

2. No infection control, infection spreading from cow to cow during milking process.

3. Taking clusters off under vacuum.
Buttons faulty or air admission holes blocked.

4. Under milking of cows.
Due to use of old liners, poor vacuum or poor pulsation settings.

5. Over milking of cows.
A common problem in large parlours with no cluster removers. It is quiet common in small parlours that are poorly designed.

6. Poor fore milking technique.
No gloves worn and spreading infection from cow to cow via hands. Gloves should be sprayed with a teat spray before fore milking cows.

7. Poor post milking spraying.
15 mls per cow per milking should be used with a drop of teat disinfectant visible at the end of the teat. Poor equipment with damaged nozzles and poor pressure will not give adequate cover.

Milking practices contribute significantly to mastitis spread and infection within a herd.

Treatment of clinical and sub clinical mastitis during the lactation period can be very varied. In many instances response to treatment can be only for a short period of time, thus you see fluctuating cell counts from month to month.

For many cases treatment of Staph aureus infections will require treatment with injectable antibiotics in conjunction with intra mammary infusions.

For the majority of farmers, getting a clinical cure is not an issue i.e. the clots disappear; getting a sub-clinical cure is a lot more problematic. We have found where farmers have used the CMT test kit to monitor treatment regimes and continued treatment for a longer period a clinical cure and subclinical cure have been achieved.

Dry cow therapy can have a dramatic effect of somatic cell counts in dairy herds. This is significant opportunity to administer long acting antibiotics with or without a sealer to kill infections within a quarter. Intramammary infusions can last up to 54 days post insertion.

We have achieved very good results where cows have been CMT tested prior to drying off and problem quarters individually treated prior to dry cow therapy.

The response to treatment can be as low as 50% cure rate for staph aureus infections. With such a poor response to treatment in the lactating period, controlling the spread of infection and preventing new infection is the key to maintain a low SCC herd.