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Udder Health is a Management Decision

Richard Vanderwal

Abbotsford Veterinary Clinic Ltd.,
Abbotsford, B.C., Canada V2S 5Z5

Take Home Messages

Udder health management is a focussed strategy built on specific milk quality goals.
The level of mastitis in a herd is a dynamic interaction between the rate of new infections and the duration of existing infections.
The keys to reducing the duration of new infections is to analyze antibiotic and supportive therapy rationale and options. The objective is to make management decisions on the basis of herd records and an understanding of the udder defense systems.

Udder Health is a Management Decision

Volumes have been written on the subject of mastitis control, yet mastitis remains the most expensive disease of dairy cattle. Why does this situation continue or exist and what can we contribute to the discussion?


Mastitis is a disease.
Mastitis is a symptom of udder management disease.
Udder management disease is the result of unreasoned management decisions that allow the negative interactions of milking system and housing variables to take effect.
Udder health is a focussed strategy to keep the mammary system operating at peak efficiency.

Develop RIGHT SYSTEMS to Reduce the RATE of Infection

Quantifying the Problem (assessing the enemy) -- there are only four ways to get mastitis:

there is only one way in.
there are only four or five major pathogens.
milking systems related: Staph spp, Strep. spp.
environmentals: coliforms E.coli, Klebsiella)

How tough can it be?

Assessing Udder Defence. An udder infection comes in one way through the teat end. The cow's first line of defence is the teat canal and its structure. The second line of defence are somatic cells, whose job is to attach to and engulf bacteria. The presence of specific antibodies (immunity) makes the somatic cells much more efficient at their job. If the bacteria gets past these two lines of defence it is able to enter the small milk sacs and milk ducts, where they begin an irritating inflammatory reaction that sends more somatic cells to the area. Bacteria that have reached this far may be able to sequester away in body tissue. The teat end is the point at which all the strengths and weaknesses of a milking system interact.

Anatomy The teat canal is not so much a single channel from teat end to teat cistern as a delicate web of tiny channels that open at the base of the teat into a common channel. It is within the walls of this web that the strongest defence against incoming bacteria exists. A small protein called ubiquitin acts as a general antiseptic in the teat canal against a wide range of bacteria. In a healthy teat, this lining also produces the keratin plug that mechanically traps debris and bacteria. The healthy sphincter muscle that surrounds these structures is really an active flutter valve that resists distention, tending to always contract closed.

Another area prone to irritation is where the teat meets the udder. Inside, the circular folds of the teat are vulnerable to irritation from chafing when the milk flow has ceased and the teat cup has crawled up to the base of the udder. The inside lining of the teat is a delicate membrane, and it is not designed to be shut off from its blood supply and rubbed repeatedly with no milk as a lubricant. The result is injured tissue that serves as a potential breeding ground for bacteria, especially Staph.

What is the Key to Reducing New Infection Rates? In essence there are two keys to reducing the new infection rate:

1. reduce the numbers of bacteria in the area that could be a problem (establish sanitary barriers), and
2. foil the mechanisms that allow entry into the udder (establish optimum milking machine performance).

Sanitation barriers are designed to physically remove and neutralize potential contaminants. The goal is to milk a sterile cow with a sterile unit:

Pre-dip. Starting with a clean udder, pre-dipping is designed to replace water preps and reduce the number of bacteria on the outer surface of the teat. It works, especially against Strep. uberis and coliforms.

Post-dip. Post-dipping is still the most effective single act to reduce the new infection rate (by 50%). The keys to an effective teat dip are its ability to kill bacteria, remain active on the teat, prevent chapping, and promote healing.

Backflush. Backflush disinfects teat cup liners between cows to eliminate cow to cow transfer of bacteria, and establishes the stated goal of a "sterile unit". It is very effective in problem Staph herds.

Free stall management. A basic rule is that where the udder lies is clean and dry. Always.

Dry cow hygiene. It is very important to protect the teat end against any moisture in the early dry-off period. The other high-risk time is the day or two before calving.

Milking system performance. If not operating properly, the milking machine can serve as:

an insult to the teat end tissue, or
a tool for implanting bacteria into the udder.

The most important contributors to these are ineffective pulsation and droplet impacts. Milk droplet impacts are the results of vacuum fluctuations -- it is difficult to quantify the influence on new infection rates, but liner slips and sudden vacuum drops are the primary contributors. Other factors have solutions that lie in levelling out the milk flow (alternating pulsation), removing the need for the formation of milk slugs (lowline/no lifts), increasing milk flow rates away from the cow (air vents), and maximizing the opportunity for vacuum to get back to the teat end (large bore lines, no restrictions, or sensors).

Pulsation creates the action on the teat liner and teat wall that exposes the teat end to vacuum during the milk phase, and then rests or massages the teat wall in a rest phase. Pulsation rates and ratios are industry standardized. Milk-rest ratios vary, and the influence of vacuum fluctuations in the system influence the actual action of rubber on teat.

Develop a RIGHT APPROACH to Pharmaceuticals to Reduce the DURATION of Infections

The reason to consider pharmaceutical intervention in cases of mammary infection is to reduce the duration of infection. The basic principles of treating any infection are:

selection of an effective antibacterial agent,
achieving a therapeutic concentration at the site of infection,
adequate duration of therapy, and
supportive therapy where needed.

An Udder Closer Look. Any bacteria that passes the teat canal may encounter the second line of defence - the somatic cells or leucocytes. These leucocytes track down and engulf bacteria, and should then kill them. Leucocyte efficiency is reduced by milk protein, butterfat, and by an absence of specific antibody. There is also evidence that engulfed bacteria may go dormant and survive in the leucocyte. This becomes important if antibiotics are used that cannot penetrate the cell. Both groups of antibiotics have difficulty with intracellular bacteria: bacteriostatic antibiotics need an actively dividing bacteria to be effective; bactericidal antibiotics are less effective inside leucocytes because of the higher pH.

The next step in the infection is the tissue reaction in the small milk sacs and milk ducts. The ducts can be quickly obstructed by somatic cells and swollen shut by edema. Further reaction results in cellular debris that clogs the passages; a severe reaction will cause fibrosis/scarring as a way for the body to sequester the infection. This accounts for much of the ineffectiveness of intramammary treatments a physical inability to move into and be active in the target tissue. Therapy of mastitis cases is carried out with pharmaceuticals that include antibiotics, anti-inflammatories, fluids, and oxytocin. To give an overview of the steps and pitfalls, here is a schematic of the action sequences of drug activity:

Antibiotics. How do antibiotics work? The basic assumption is that if bacteria are sensitive to an antibiotic, we need to get the antibiotic in contact with the organism, and it will kill them. So step one is to choose the right antibiotic based on culture and sensitivity, then supply that right antibiotic in enough concentration to clean up the infection.

Our discussion so far has shown that antibiotic therapy for clinical mastitis has a variable success rate the efficacy of such treatments should be critically evaluated. Some of the factors that affect antibiotics efficacy are:

animal factors stage of lactation, amount of milk, milking routine, and type and duration of infection.
drug factors pKa (dissociation constant) of drug, lipophilic activity, ionized or non-ionized fractions, type of activity: bacteriostatic or bactericidal, frequency and route of administration, and combinations to exploit synergy and/or extend spectrum of sensitivity.
microbial factors type of bacteria and natural or acquired resistance.

Anti-inflammatories and Fluids. Systemic products including cortisones and flunexin (sic) are utilized to control the tissue reaction to infection, thus maintaining tissue integrity and blood supply to the area. This allows somatic cells to work more effectively. Because of this consideration, these products need to be used early.

Oxytocin remains very effective in completely emptying the mammary gland of bacteria and endotoxins if given early and often. Complete and frequent milkouts are very underrated in their usefulness early in infections.

Fluids are important to maintain healthy cell function and circulation. Cows with acute mastitis need to be encouraged to drink with TLC or intravenous hypertonic saline.

How Do Treatment Goals Vary with Different Types of Infections? Acute bacterial infections that produce endotoxins (e.g. coliforms: E.coli, Klebsiella ) result in more clinical signs from the effects of the endotoxin than from the bacteria itself. Thus treatment strategy must be aimed at the critical links. Physical blockage of udder tissue is a significant barrier to drug action. Early frequent strip-outs, fluids, and anti-inflammatories are as, or more important than, antibiotics.

Organisms which bind poorly to cell linings can be successfully eradicated by creating high antibiotic levels in the intramammary milk (e.g. Strep ag.). Chronic mastitis is an udder tissue disease, not a milk disease. Most organisms attach to the cell linings, and have varying abilities to cause deeper tissue damage. High tissue levels of antibiotics are necessary to get at these organisms. This can only be done by systemic antibiotics, administered intramuscularly or intravenously. The udder has an excellent blood supply. A new infection will still have a good blood supply at the site of infection; an old infection has had the opportunity to separate itself from the body with non-vascularized scar tissue as a microabscess, and thus the antibiotic is unable to reach the organism (e.g. Staph.).

NMC 1994 lists reasons why antibiotic therapy of clinical mastitis may fail. Note that these are generic; you need to target specific therapy for specific bacteria.

Drug cannot reach all infection sites.

microabscess formation
ducts blocked with milk clots
poor drug distribution in the udder due to edema, etc.
abscessation and scarring
intracellular bacteria
Inadequate concentration of drug to effect killing.
Bacteria resistant drug.
bacteria not in rapid growth phase required for some drugs to act
organism is not vulnerable to drug's action
drug has wrong spectrum
acquired immunity by organism
emergence of L-forms, acapsular forms that resist beta-lactam antibiotics.
Re-infection of affected quarters.

Summary of Current Therapy Results: For lactating animals, the overall cure rate estimates are 25 to 40%. The high range is optimistic. The overall cure rates include spontaneous cures from the cow's immune system independent of antibiotics.

The discussion continues:

NMC '94 p.38 (J. Hallberg et al): " These data clearly indicate that antibiotic therapy of clinical mastitis in the lactating dairy cow reduces the number of pathogens in milk post- treatment, increases the number of quarters returning to normal milk, and increases the number of 'cured' quarters when compared to non-treated controls. These benefits will increase the safety and quality of milk by reducing a potential source of bacteria and elevated somatic cell count."

NMC'94 p.40 (W.Guterbock): "To date there has been no published evidence that the economic benefits of antibiotic treatment of mild clinical mastitis outweigh the risks and costs. It would appear that these antibiotics were of benefit in the Staph and Strep infections, and of marginal or no benefit in the coliform infections."

Antibiotic therapy of Strep. ag. mastitis is effective and predictable. This statement cannot be repeated with much confidence for Strep. non- ag., Staph. spp. or coliform pathogens. This reinforces the theme of targeting therapies carefully.

Dry Cow. The most effective time to treat subclinical mastitis is at dry-off. The major advantages are:

reduced incidence of new infections in dry period,
higher therapeutic antibiotic levels,
longer antibiotic levels,
a higher cure rate, and
reduced risk of antibiotic residues in milk.

Vaccines -- Their Effect on Duration of Infection. How do vaccines work? We have referred to milk somatic cells as the second line of defence in the udder. These cells can do their job better and faster when specific antibodies are in the udder. The function of antibodies is to coat or label bacteria so they can be recognized more easily, and then phagocytosed. Vaccinations are used to increase the udder concentrations of specific antibodies. Commercial vaccines are available against E.coli. The search for an effective Staph. aureus vaccine continues.

Drug Therapy and Managing Drug Residues. There is zero tolerance for drug residues in milk. Every day, every dairyman's job involves the production of quality milk.

The most common reasons for residue problems are:

human error and inattention to detail during milking,
inadequate records +/or communication,
inadequate withdrawal times on commercial and off-label products, and
treated cows.

Clearly the most effective way to avoid drug residue is to remove the reasons for drug use, especially clinical mastitis. Milk from treated cows should be tested with a residue test-kit before it is re-introduced into the bulk tank. On-farm testing kits are available and need to gain wider use.

Urine splash has been recognized as a possible contributor to positive residue tests. In B.C., Drs. Lorne Fisher and Merv Wetzstein have generated some interesting data on this subject.

Develop the RIGHT MONITORS to Guide Udder Health Management Decisions

Herd udder health monitoring needs to be part of veterinary record analysis. DHIA provides an excellent starting point with somatic cell count programs they are a great motivator in udder health programs by developing an early and accurate awareness of subclinical mastitis trends.

Parameters to be evaluated:

Somatic Cell Counts. A low somatic cell count indicates good udder health in a nonspecific way. Individual cow values and trends both need to be evaluated. Factors increasing SCC are:

active infections,
age of animal,
stage of lactation,
high stress,
inadequate nutrition, and
vitamin E, Cu, Zn, vitamin A.

Rate of Clinical Cases. Records of abnormal, discarded milk, and treated cows are useful. Dairymen are encouraged to record and sample clinical cases.

C and S. Culture and sensitivity testing is still the backbone of relevant information for veterinarians. By defining the causative organism, we can focus on:

reducing the rate of infection by identifying the source of the problem, and
reducing the duration of infection by specifying treatments with a knowledge of bacterial sensitivity.

Data from DHIA can be used to generate udder health monitors.

Parameters we use in a HERD PERFORMANCE TARGET SCREEN are:

SCC averages for two-year olds and older cows.
Percent of two-year olds and cows whose SCC increases over 200,000.
Percent of two-year olds and cows with a SCC over 250,000.

Patterns seen with this information:

High SCC and high rate of clinical cases this herd usually requires an overhaul of people, cow, housing, and milking equipment management. Most of the problem involves contagious mastitis; environmentals may overlap.
High SCC and low rate of clinical cases a moderate case of the above herd contagious mastitis, and no udder health program are key similarities.
Low SCC and high rate of clinical cases this herd usually is well managed, yet has an environmental mastitis problem, usually E.coli or Klebsiella. Management must key on where the udders lie and on milking technique. C and S provide good information as to the source(s).
Low SCC and low rate of clinical cases - goals reached.


A significant portion of good udder health management relies on reducing the rate of new infections.

If infections occur, the limited effectiveness of antibiotic therapies, the risks of antibiotic residues, and the financial losses associated with milk holdbacks all reinforce that mastitis therapies must be specific, targeted, and monitored. The goal is to reduce the duration of any infections this needs clinical case milk culturing, and a specific therapy plan for the different types of mastitis seen.

The production of a top quality product and economics should be a real motivator. Based on the economics of reducing milk loss, reducing cull rates, and reducing treatment costs, it is clear that udder health management programs have a place on every dairy farm. Our consumer expects top quality in "nature's most complete food".

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