Double Jeopardy - Cows with Ketosis
Cows with ketosis more at risk to more severe E. coli mastitis infection
If the most severe symptoms of E. coli mastitis strike a member of your dairy herd, she's probably one of your most valuable milk producers—a fresh, older cow. Learning why these animals are most susceptible would let us help them fight off these infections.
Cows that experience the most severe kind of E. coli mastitis can experience hard quarters, high fevers and diarrhea. They can completely go off feed and, in the very worst cases, die in a short time.
Research that helps us understand how E. coli mastitis occurs, how cows fight back and why some herds and some cows might be more at risk is worth a second look.
To understand such research, we need to understand the cow's own mastitis-fighting methods. When E. coli bacteria enter the cow's teat end, her udder immune system has to "see" the bacteria. This part of her immune system has to recognize that this is a "bad invader." The udder immune system can't fight off the bacteria all by itself—the rest of the body has to help.
The "bad invader" message has to be quickly passed on to the immune system's headquarters, elsewhere in the cow's body. Once it receives the initial message, headquarters has to alert the fighting cells throughout the cow's body. These cells, the white blood cells (WBCs), respond by travelling through the bloodstream and crossing into the infected quarter. If the udder sends the right message, headquarters relays it correctly and the WBCs answer the call, then the cow responds to the E. coli invasion appropriately. Cows that efficiently send messages, and act on them, quickly clear out mastitis infections.
Cows with immune systems that malfunction respond more slowly. Any breakdown or delay in any of these steps lets bacteria multiply in the infected quarter. In the case of mastitis caused by E. coli bacteria, which multiply very quickly, this is a big disadvantage. Cows with slow immune systems have more bacteria to fight and are much more likely to have more severe mastitis.
Researchers try to study each of the steps in the immune response that must occur once E. coli bacteria invade. In 1993, researchers from Holland published a paper entitled Severity of Experimental E. coli Mastitis in Ketonemic and Non-ketonemic Dairy Cows. These researchers wanted to examine the part of the cow's immune system known to be important in fighting off E. coli mastitis—the response of the WBCs to the message "E. coli invasion in the udder." They suspected cows with ketosis had WBCs that read and responded poorly to messages. If so, this would be one of the reasons E. coli mastitis was more severe in fresh cows.
To study this, the researchers used 18 cows, all between lactations 3 and 6 and between weeks 3 and 6 of lactation. Six of the cows were fed a low amount of concentrate for four days to induce ketosis. The other 12 got haylage and an appropriate amount of concentrate for their lactation stage.
To cause mastitis in all 18 cows, the researchers inoculated one quarter (the right rear) with E. coli from a cow with clinical mastitis. They left the other rear quarter alone to use for comparison.
After inoculation, all cows were fed full amounts of haylage and concentrates. Cows, their milk and their blood were examined and tested regularly for seven days.
The results showed ketonemic cows had more severe mastitis than the non-ketonemic animals. But this couldn't be blamed on the WBC response. Just before the researchers caused the mastitis, the WBCs of the ketonemic cows responded just as well as those of the non-ketonemic cows. The researchers concluded that ketosis must be affecting some other step in the immune response of these animals.
This study did have its limitations. The researchers, not natural infection, caused the mastitis. It's possible these experimental mastitis cases differed from those we see on Ontario farms. Ketosis in these cows was caused by limit-feeding. This might not have resulted in all the metabolic changes that occur in cows developing ketosis associated with high milk production or that develop it over a longer time during the late dry period.
Nevertheless, the study did show that E. coli mastitis was more severe in ketonemic cows. Even if the actual cause wasn't found, the study did establish a link between mastitis severity and ketosis.
The study also showed the WBCs were ready to go, provided the message got through, regardless of ketosis. This finding suggests the negative effects of ketosis on the immune system are likely short lived. Once ketosis ends, we can expect a cow's immune system to resume normal activity.
Both E. coli mastitis and ketosis are serious threats to Ontario herds. When Dr. Todd Duffield of Ontario Veterinary College (OVC) blood tested 1,333 cows in 93 Ontario herds, he found 14 per cent of them to be subclinically ketonemic. Dr. Jan Sargent, also of OVC, cultured the milk from 834 cases of clinical mastitis on 65 farms. She found coliform bacteria, the family that includes E. coli, caused 17 per cent of the cases.
Some Ontario herds will typically have a few ketonemic cows that develop severe mastitis. We can watch these more closely, and be quicker to test or treat for both diseases. When only a single cow is affected, the important factors that put her at risk likely relate more to her individually than to the management of the herd as a whole.
A far bigger problem occurs in herds that have whole groups of ketonemic, fresh cows at risk of more severe mastitis. Some herds have problems associated with feed changes, inconsistent close-up dry cow feeding, poor forage quality, periods of overcrowding or uncomfortable housing.
We should look more closely at dry cow feeding and housing in herds with outbreaks of severe clinical mastitis in fresh cows.
This is a proven link between nutrition, or feed delivery, and mastitis. Dry cow feeding programs, feeds and feed delivery must be optimal to prevent ketosis. That way, if invasion of the udder does occur, the cow's immune system will be in top shape for fighting back.
To help high-risk, fresh cows, have them calve in a clean, dry environment. That way they'll have to fight fewer bacteria in the udder. Housing before and after calving needs to be comfortable. To reduce stress, avoid crowding and mixing cows and heifers around calving time.
This research also makes it easier to understand that reducing the severity of an E. coli mastitis case is not simply a case of finding the right drug for the bug. After mastitis symptoms have already appeared, it's much too late for antibiotics to make a difference in the battle, as much research has shown. Only the cow's own immune system gets the message in time to act against E. coli.
On a broader basis, this research provides a good example of why it takes so long to get answers to what seem like simple questions. It takes time to understand all the steps that occur in the battle between the cow and the mastitis bacteria. Once we know more, we'll be able to arrive at good specific techniques to help cows win the war.
Give the cow all the help she needs and she'll look after the rest. And stay tuned for more research that will give us clues on how to help the cow's immune system.
For the original reference: Journal of Dairy Science 76:3428-3436. 1993. Severity of Experimental Escherichia coli Mastitis in Keonemic and Non-ketonemic Dairy Cows. W.D.J. Kremer, E.N. Noordhuizen-Stassen, F.J, Grommers, Y.H. Schukken, R. Heeringa, A. Brand and C. Burvenich.
This article first appeared in the March 2000 Ruminations column of the Ontario Milk Producer magazine.
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