Other Management Articles
- Building A Herd of High-Producing, Healthy Cows with Low Involuntary Culling
- Culling Heifers: When and Why and the Impact on Herd Economics
- Economics Matter in Culling Decisions
- What is an ideal BCS at calving?
- Facts about Somatic Cell Counts
- First Layer of Defense Against Mastitis
- The When and Why of Milking Procedures
- Are Mastitis Vaccines a “Cure All”?
- Growing Heifers to Be Your Best Cows
- A Look in the Mirror
- Fertility Potential: The Bull + The Cow + The Inseminator + The Environment
Clinical and subclinical mastitis are costly and persistent problems faced by the dairy industry. Mastitis is an infection of the mammary gland that occurs when infectious agents from outside enter the udder and begin to multiply.
Nature has provided a wonderful, and often taken for granted, mastitis defense: the teat.
The first line of a teat’s defense is the teat sphincter. This round muscle tightly closes the teat to prevent penetration of infectious organisms. If bacteria manage to pass the teat sphincter, their next obstacle is the teat canal, which is lined with a waxy secretion from the lining cells called keratin. Keratin acts as a sticky trap to catch infectious organisms. The mastitis causing organisms are then washed away by milking. Frequent milking reduces mastitis, if milking procedures are correctly followed. The milk flow flushes out the bacteria and the top layer of keratin. By removing the old keratin, newly formed layers of keratin are exposed, which recreate the defense function.
The teat is not only a physical barrier, but it has active defense mechanisms to help ward off infection. The keratin has chemical properties that can either stop bacterial growth (bacteriostatic) or kill bacteria (bactericidal).
Protection of the udder does not stop at the teat canal. Lactoferrin is secreted into teat cistern and is especially high during the dry period. Its iron binding properties stop bacterial growth. The white blood cells, called somatic cells in the udder, recognize and fight infection. Even the cells lining the teat have receptors that will recognize infectious agents and will signal a response to the cow’s immune system.
We challenge this natural defense system with our management when we change the numbers of pathogens on teat skin, change the resistance of the teat canal to infection, and deliver forces via action of the milking machine that overcome the natural resistance of the teat canal to bacterial invasion.
Pathogen concentration near the teat sphincter is the most obvious challenge. If a clean teat environment is always maintained, there is never any pathogen to enter the teat. There is a direct correlation between hygiene score and increased SCC and mastitis.
Target: <20% above 3 Hygiene score 1
Milking vacuum creates a pressure gradient underneath the teat end, thereby unfolding the teat canal and causing milk to flow from the teat sinus into the liner. Normal milking causes the teat canal to remain dilated for approximately an hour after milking before muscles can fully contract. This provides opportunity for pathogen penetration of the teat end.
High peak milk flow rate can only come from widening of the teat canal. An increase in the teat canal cross-sectional area during milking potentially results in delayed refolding and closure of the teat canal.
Target: cover the entire barrel of the teat with an effective post dip so that a drop forms over the teat opening.
There has been significant shortening of teats over the past 30 to 40 years. Liners tend to slip more frequently on shorter teats—and that liner slip is a major cause of new infections.
Shorter teats have shortened teat canals which shortens nature’s defense mechanisms and is a higher risk for new infections.
Target: Select liners that fit herd teat profiles.
Opening and closing of the liner breaks up the keratin layers within the teat canal. Overly aggressive pulsation may remove too much Keratin and leave a layer of ineffective, immature cells that will not produce the protective layer in time.
Increased teat end vacuum, machine stripping, rough take offs, longer milking times and improper pulsation can all cause edema in the teat wall. Teat end damage can also occur. These issues can cause slower closure of the teat canal and/or hypoxia in teat tissues, slower regrowth of keratin, a greater degree of openness of the teat canal orifice post milking and increased teat-end hyperkeratosis.
Target: Correct equipment settings for vacuum and pulsation and implement strong milking procedures.
Teat dip with softening agents can aid in healing the teat.
A fully involuted udder during the dry period with a teat end sealed completely by the protective keratin and the cistern filled with high levels of lactoferrin and protective somatic cells is almost immune to infection. High producing cows tend to not form the keratin plug until sometimes 30 days after dry, and residual milk can dilute the protective internal secretions.
Target: Provide internal teat sealant to protect the udder until keratin seals. Ensure good hygiene scores post dry to limit opportunities for infection when udders are leaking milk.
High producing cows have higher risk factors for teat end issues. We do not have to give up on production to limit somatic cell and mastitis issues, but we do have to ensure management recognizes the risks and takes steps to minimize them. The risks of mastitis to the welfare of the cow and the dairy business makes pairing of management and genetic selection one of the most powerful choices for a dairy.
The Genetic Connection
Select for reduced Somatic Cell Score (SCS) and increased resistance to mastitis (Zoetis and CDCB Mastitis) to genetically improve the cow’s ability to resist mastitis. Additional selection emphasis on teat length and optimal milking speed can help to reduce problems caused by ill-fitting milking machines or prolonged milking times.