Editor’s note: first in a coliform mastitis series.
The dairy industry has made great strides against coliform mastitis in regard to management and prevention, but it still continues to be an economic problem for producers. “In our practice, coliform mastitis is predominantly manifested as a mild to moderately-severe case of clinical mastitis,” says Dale Moore, DVM, PhD, University of California Veterinary Medicine Teaching and Research Center. “We rarely see acute coliform mastitis anymore. It is still of economic importance, not necessarily because of the loss of cows, but because of the number of cases.”
Gram-negative bacteria that can cause mastitis include Escherichia coli, Klebsiella, Pseudomonas and Serratia. E. coli is the most common pathogen that causes coliform mastitis because it is readily available in the environment.
Coliforms and immunity
Understanding how a coliform infection interacts with the immune system is a bit of a chicken-or-the-egg question. “We are still trying to determine if a cow has an altered immune system which in turn leads to her specific response to a coliform infection, i.e. is she predisposed due to her immune status?” says George Barrington, DVM, PhD, Washington State University. “Alternatively, cows with a coliform infection clearly have alterations in their immune system because of the infection.”
There are some well-recognized immunologic events with regard to exposure to Gram-negative organisms that involve macrophages, neutrophils, endothelial cells, platelets and numerous cytokines. “In any case, we are still characterizing the immune system as it relates to the bovine mammary gland,” says Barrington. Nutrition can play a role in immune response, especially with the addition of components such as vitamin E (see sidebar).
Barrington adds that Ho Park and co-workers first started characterizing mammary lymphocyte populations in 1991. They found significant differences regarding cell-mediated immunity throughout the entire lactation cycle, from early pregnancy to early dry-off to the late dry period and through lactation. “What’s interesting is that we’re correlating the changes in the immune system with when the disease occurs, but we haven’t really matched that information yet to answer the question: Are these changes we see causing the susceptibility to coliform mastitis, or is the coliform mastitis causing the changes? There’s a triangle of effects involving the neuro-endocrine-immune systems, and it may be even more complicated than that.”
The cell wall of Gram-negative bacteria has several different parts. Although cows make antibodies to the entire structure, the outer parts are not consistent across different E. coli strains, so there is little cross-protection, says Moore. The core antigens of the cell wall are closely conserved by most E. coli organisms, and these core antigens are exposed during bacterial growth. A cow with high antibodies to these core antigens is less likely to develop severe clinical cases.
People have been asking what effect the coliform organism itself might have in the disease process, says Barrington. “Researchers are looking at virulence factors with regard to the organisms and whether or not disease occurs. I don’t think that question has been answered. They have looked at toxin genes and things like that, but they haven’t quite matched the expression of various virulence factors in organisms to severity of disease.”
Right now there’s a finite number of virulence factors that we can identify, and we’re able to research, Barrington adds. “With the currently identified virulence factors, there does not appear to be a correlation with disease severity or disease occurrence. That doesn’t say that virulence factors don’t play a role, because we very well may not have identified those virulence factors. Each year there’s more and more information coming out with regard to the mechanisms of these organisms.”
“I think it has to do with exposure and immunity, or, challenge and resistance,” adds Moore. “You can overwhelm immunity or resistance by a large challenge or exposure.”
And as far as her immune system goes, is a dairy cow the same as a beef cow? Not really, says Barrington. “With regard to humoral immunity, a periparturient dairy cow can often deplete her serum IgG1 levels to very low levels, whereas beef cows generally do not. We do not yet know, however if there are periparturient difference in cell-mediated immunity between dairy and beef cows.”
Because coliforms occur naturally in the environment and are often present in bedding, keeping them at bay requires good hygiene practices. Though they are not “contagious” organisms, they can easily spread through feces, soil and other means to contaminate the dairy.
“It’s an index factor of spreadability,” says Greg Goodell, DVM, Greeley, Colo. “If Mycoplasma is on the top end at 100%, that’s the most-spreadable disease in the barn. Coliforms, however, are on the other end of the spectrum. The dry cows don’t lactate, so the producer assumes coliform mastitis cannot be a problem during the dry period. It never dawns on them that they may be infected during the final milking procedure or possibly even after dry-off. The producer assumes only contagious mastitis spreads in the barn.
Bedding is a culprit
Don Gardner, DVM, Huddleston, Va., says over the years he’s seen a lot of sawdust used as bedding in Virginia and a lot of coliform mastitis because of it. “My clients have come to understand that fresh sawdust is a gold mine for coliform bacteria. We’ve found if we stockpile it for three or four months and let it generate some heat, we get a reduction in the amount of bacteria. Fresh sawdust, right from the mill and used as bedding, leads to a peak of clinical cases nine days later. You don’t see the problem with sand or shavings from a furniture mill where it’s been kiln-dried. We have found that sawdust or shavings can be made a poorer growth media for bacteria if either is mixed 50-50 with dry agricultural lime. The lime by itself doesn’t make a good bedding media because it packs and becomes hard and uncomfortable.”
Gardner’s first choice for bedding is sand, but a lot of freestall operations that have liquid manure systems have historically felt they couldn’t use sand for bedding because they couldn’t get the sand out of the pits. “There are new super agitation pumps now available that can handle these sand bars that develop in these pits. This has opened up the use of sand for bedding for a lot of dairies that have these liquid systems.”
Barrington adds that shavings are an excellent growth media for these organisms. Even in what looks like clean shavings, there can be higher counts of coliforms than in actual fecal material. “It depends on the type of shavings, such as white fir, red fir and cedar that are our choices in the Northwest. There’s a difference in the wood products, irrespective of how they’re handled.”
Managers cannot do much about environmental conditions, but they can choose what type of bedding they use, adds Barrington. “They can manage the pens such that contamination is minimized.”
Lynne Dzuba, DVM, Newton, Wis., adds that if clients have to use shavings they know may cause problems whether it’s due to bacteria or poor environmental conditions, it is worth the extra expense to bed heifers with those shavings and get a dried product for the cows.
In California, many producers use dried manure solids for bedding, sometimes mixed with rice hulls, says Moore. “A few are using sand for freestall bedding, but mostly we’re using a lot of organic materials. As long as the stalls are properly bedded and groomed, we do not see much clinical coliform mastitis.” An exception is when freestalls have a wet area at the back of the stall due to poor dimensions or lack of a brisket board. “Stall dimensions and bedding can be factors influencing the positioning of the cow,” says Moore. “The cows need to be moved back enough so they are manuring in the alley, not the stall.”
Not all of Moore’s clients use freestalls, however. Most of the cows in that area of California are put into corrals with shades. “If the corrals are not properly maintained, the cows can get new infections. Subsequently, they could turn into a clinical case once they freshen. A lot of new infections probably originate in the dry period and then manifest as clinical after freshening. However, we can see coliform mastitis at any time of the year, and at any state of lactation. It depends primarily on stall or corral maintenance and the weather.
“Facilities management seems to be the big issue we deal with in recognizing potential causes or sources of bacteria in the udder,” she says. “This is an important area for veterinarians to start making some observations and recommendations.”
In many parts of the country coliform problems are seasonal problems. Hot, dry weather causes cows to stand or rest in or near wet areas to cool down, exposing teats to soil or bedding that is full of pathogens.
“Last summer we had hot weather and the cows were hot, spending a lot of time lying down in new shavings,” says Barrington. “Within a week we saw three or four cases in one small herd milking about 100 cows. We saw three Klebsiellas and one E. coli, and these were in vaccinated cows. Maybe they would have died if they hadn’t been vaccinated, but they were an economic problem.”
Gardner sees problems in summer pastures with trees where cows congregate and create a mudhole from urination. “From stomping and swishing flies they get their udders dirty. We always see an elevated level of coliform mastitis during one of those hot periods,” he says. “Now we use electric fencing to keep them out of those areas.”
Hot, dry weather doesn’t always mean dry cows. Moore says sophisticated cooling systems that drip or mist water can also be a problem because that water ends up somewhere – sometimes in the back of the stall. Cooling systems used in the holding pens can also produce wet cows in the milking parlor.
If you keep your cows in an environment that has low nutritional value for these bugs to grow, you’re going to automatically reduce the exposure, adds Gardner. “If it’s the time of year where the temperature is not conducive for bacterial growth, you are going to reduce exposure.”
It all comes back to what was learned in first or second year veterinary school – the host-agent-environment interaction. “We try to classify these things as ‘contagious’ or ‘environmental’, but certainly some of those ‘environmentals’ act as contagious when the host-agent-environment interaction weighs itself toward the spread of that disease,” says Barrington. “The balance among those three issues is crucial. What is the host’s immune status? What’s the nutritional status? The environment has a huge role. Sometimes we try to pigeonhole these organisms into how they should act, but we’re always surprised when they don’t act the way we suspect.”
“Everyone – the producer and the veterinarian – needs to remember that this is a multifactorial disease,” says Goodell. “How many times have you seen a herd where the cows are up to their navels in slurry and mud and management claims they lose one cow a year? Either they catch every cow and half the herd is in the sick pen, or they truly don’t have a mastitis problem.
“Maybe some emphasis should be placed on the fact that other factors can cause a breakdown in the immunology of a cow in her effort to protect herself against E. coli mastitis,” Goodell continues. “It’s not always the wet cow in the parlor or the dirty cow in the dry lot. From a producer and veterinarian’s standpoint, we always tend to go with what’s easiest and not consider other sources of disease.”
There are a multitude of ways coliforms can spread, most of them through some sort of fecal contamination. Moore notes that issues like crowding can be a factor in coliform mastitis. Lactating cows lying in the alleyways because of overcrowding or overcrowded dry cows in the close-up pens can lead to problems. “In general, we are looking for any source of fecal contamination.”
Equipment may also play a role. Unstable vacuum at the teat end may have the potential for causing impacts on the teat end. “If there is a large drop in teat-end vacuum, we can see a higher incidence of new infections,” says Moore.
Liner slippage is another one, a cause of turbulence, Moore adds. “A real problem might be teat-end lesions as a place to harbor bacteria. They are kind of loosened up when pre-dipped and then impacted with liner slippage. A problem we’ve seen is settings on the automatic take-offs. There’s no milk coming through the cluster. and the take-off hasn’t shut off yet.”
Goodell agrees. “Most of the dairies I work with, even though they have automatic take-offs, cannot keep the labor from milking on manual and either overmilking the cow or pulling off the last several machines on a side to speed the parlor up.”
Economics of coliform mastitis
The literature says each case of mastitis costs between $107 and $180. Goodell says actual numbers in terms of drug costs, milk loss during the time the cow was in the sick pen and labor costs can run $80 on a cow treated with intramammary antibiotics. “It’s much lower on a coliform cow with a mild case of mastitis, although if you have a run of moderate or severe cows it can go twice as high.”
Acute cases into the veterinary teaching hospital can cost hundreds of dollars, say Barrington and Moore. “We need to have a better understanding of the cost versus benefit considerations when treating severe cases, ” says Barrington. “We should also admit that euthanasia may be the most reasonable option, for example, with some Klebsiella cases.”
If you can classify the cases based on severity, outcome or whatever system is in use, you can help identify the costs, says Barrington. “You might be able to tell a producer what the cost is for a mild case, and if he understands, it will build your argument when you start throwing in the severe cases.”
Milk loss during treatment and withdrawal times is significant. Treatment costs for individual cases of acute coliform mastitis can also be significant, says Moore. “Death loss requires replacement with another cow, which can be $1,400-$1,900 depending on the region of the country,” she says. There can also be substantial economic losses tied to coliform mastitis and its effect on reproduction. “If you lose an early pregnancy, it may not be as costly as losing a pregnancy later in gestation.”
Goodell says in the western states, producers will get paid a bonus for being under 200,000 cells, but the amount of fluid milk they have to dispose of to get there overshadows the benefit. “If you walk into a herd on a drylot dairy that has contagious pathogens taken care of and they are only dealing with environmental mastitis, it’s not uncommon to see a bulk tank cell count over 300,000 in August. To the producer that’s normal, and it’s difficult to talk them into changing anything because the price they receive for the fluid milk is much greater than the price they receive as a bonus for the lower bulk tank SCC.”
It’s the same in the mid-Atlantic region, says Gardner. “As far as quality premiums, producers just laugh them off. If you look at things you’d have to do to lower SCC to less than 200,000, it will not pay to initiate those for the quality premium alone.”
“In a lot of our herds, if they stay under 400,000 cells, they’re pretty happy,” says Moore. “Our somatic cell count limit in California is 600,000 cells per mL, lower than the rest of the country. Producers are going with 300,000 to 380,000 cells for many herds. It’s economical. They’re not pulling a lot of cows out to go to hospital to be treated. Nobody’s dying because they don’t have acute cases of coliform mastitis. The motivation to do anything more is fairly low because the returns are small.”
Another motivational issue that dairy advisors have to deal with is a building level of resentment from producers regarding a continually increasing level of quality demands from processors without a comparable level of compensation for these improvements. “GM, Ford and Chrysler sell a much better car with many, many improvements over the one they sold in 1980,” says Gardner. “However, the consumer doesn’t pay 1980 prices. Dairy producers are being asked to provide processors with 2002 quality milk for 1980 prices.”
It goes back to the goal of the producer, says Goodell. “You can tell them they’re going to be a little less profitable per cow by keeping the herd cell count at less than 200,000, but if their goal is to have the lowest SCC, they’re going to say they don’t care. They have pride in the product they’re delivering.”
In Wisconsin, Dzuba says there is a milk quality program called “Milk Money.” “They’re trying to get people to sign up and work as a team with veterinarians and extension agents. It started through Wisconsin Extension with a program developed by Dr. Pamela Ruegg. She offered training workshops throughout the state, and she invited veterinarians to come to the workshops. We learned about the protocols to follow to set up meetings, how to get people interested, how to do the economic analysis to show people the profits they can make by lowering their cell counts. The people most interested are those at 200,000. Those at 400,000 don’t seem to care.”
Technology, such as individual milk meters, can catch a lot of problems, says Goodell, but type and economics of a dairy would determine whether they would be profitable. He says a drylot situation can pay for a milk metering system in a short amount of time, but in a freestall situation it may not be feasible. “Problems come at different times of the year in a drylot dairy vs. a freestall dairy, such as when a downpour in a drylot can cause 18% of your cows to be in the sick pen for a month. A freestall barn is rarely impacted by those events. In the drylot situations, there will be someone who spends more time on the computer looking for cows than in a freestall system. In a freestall system, that person will be spending more time on stall maintenance and bedding.”
“I look at the individual producer’s goals,” says Goodell. “Otherwise, the economics won’t let it go much further.” n
Next: Case definitions, diagnostics and reproductive effects.
This information was obtained from a Bovine Veterinarian roundtable event sponsored by Immvac.
Vitamin E and selenium
The role of vitamin E and selenium and the prevention of mastitis is a vital one. Dale Moore, DVM, PhD, says vitamin E and selenium are important for a healthy cow immune system. “Research has indicated that adequate supplementation is important in fighting infections. Deficiencies of selenium, vitamin E and vitamin A increase both the number of new infections and clinical cases of mastitis.”
Vitamin E and glutathione peroxidase (an enzyme which contains selenium) protect mammary tissue from damage by free oxygen radicals produced by neutrophils and macrophages when killing bacteria. If udder tissue becomes damaged, less milk will be produced. “Neutrophils from cows deficient in vitamin E and selenium also have reduced ability to kill ingested bacteria. Current research suggests vitamin E at 1,000 IU and selenium at 0.3ppm is optimal during the close-up dry period,” says Moore.
Greg Goodell, DVM, uses one subcutaneous does of an injectable vitamin E in the treatment of coliform mastitis. “Clinically, this appears to be part of a successful treatment plan when including NSAIDs, with or without antibiotics.”