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Monitoring essential as mastitis bacteria changes

Carol Ryan Dumas

Capital Press

Pathogens causing mastitis in dairy cows is changing leading to more clinical cases on dairies. Many of those pathogens do not respond to the drug treatments that have worked in the past, demanding different management protocols and necessitating milk culturing to identify the pathogen and determine treatment.

While dairymen have made a substantial progress in managing mastitis in their herds, controlling the infection in cows’ udders is demanding new concepts in management.

The type of bacteria on larger, well-managed dairies has changed, leading to more cases of clinical mastitis than 10 to 15 years ago, said Pamela Ruegg, professor and extension milk quality specialist with the University of Wisconsin-Madison, during a recent webinar.

Widespread adoption of a five-point plan, developed in the UK in 1950, to control mastitis has brought a huge reduction in infections from contagious pathogens, such as strains of staph and strep.

But clinical mastitis is still a frequent disease on dairy farms. The difference is most mastitis infections today are caused by environmental pathogens originating in moisture, mud and manure.

Some of those environmental pathogens, such as E coli, are not adapted to living in the cow, and the cow’s immune response is often enough to kill the bacteria. But pathogens have changed, and there is now a very diverse group of opportunistic environmental pathogens, such as Klebsiella, that are behaving more like contagious pathogens, causing mild clinical infections and subclinical infections that can be transmitted to other cows.

Ninety-nine percent of all mastitis originates from bacterial exposure to the teat that exceeds the ability of the cow’s immune defense. Infections have been successfully controlled in the past through cow management, milking protocols and drug treatment.

Many of the newer pathogens, however, do not respond to those drug treatments and some lack any FDA-approved treatment. Management of mastitis infection from those environmental pathogens is based on reducing teat exposure, monitoring and culturing milk to identify the type of bacteria and the appropriate treatment, Ruegg said.

One of the most important things the industry can realize is that all cows are not at equal risk from environmental pathogens, and that provides a lot of options for management. Most at risk are high-producing cows and fresh cows, she said.

High-producing cows are at risk because of their high milk-flow rate, which opens the teat sphincter quite wide and leaves plenty of opportunity for bacteria to enter. Fresh cows are at higher risk due to depressed immunity in the dry period and early lactation and stressors associated with transition to lactation.

Clinical mastitis results in abnormal milk, which cannot legally be sold for human consumption, and cows that have a case of clinical mastitis are five times more likely to have future cases, she said.

“We really need to work on preventing the first clinical case. It’s very important,” Ruegg said.

The industry has done a good job in controlling mastitis, targeting certain bacteria and monitoring somatic cell counts (SCC) in milk, which detect a response to infection. But on many farms, the rate of clinical mastitis is very high despite low SCC in bulk tanks. Most dairymen are not monitoring clinical mastitis or culturing milk to identify the pathogen, she said.

“We absolutely must monitor clinical mastitis,” she said.

There needs to be a system in place to detect, monitor and manage clinical mastitis. Part of that is observing foremilk before each milking, keeping health and treatment records, recording when and how often an infection occurs, and scoring cattle as to the severity of the infection.

The industry also needs to culture abnormal milk to identify the bacteria and determine the correct treatment. It is impossible to determine the bacteria by looking at the milk or animal symptoms, she said.



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