But what to do about this dairy herd disease?
Evidence is mounting that Johne’s disease infects the vast majority of U.S. dairy herds and that prevalence within herds is much higher than most producers suspect.
The question is what to do with this information. Because of the disease’s pervasiveness, eradication is not an option, if it ever was. Yet living with the disease, like living with mastitis, creates its own set of risks.
The National Animal Health Monitoring System reported that 68% of U.S. dairy operations were infected in 2007. But the test used did not identify all true positives and prevalence was likely higher, says Jason Lombard, a veterinary epidemiologist with USDA’s Animal and Plant Health Inspection Service.
Lombard suspects almost all herds are infected. “We did see an increase in prevalence as herd size increased, but no regional differences,” he says.
In a 2008 study done by USDA at federally inspected slaughter facilities, 34% of cull dairy cows had Johne’s causative bacteria, Mycobacterium avium paratuberculosis (MAP), present in lymph nodes. More than twice that number had MAP isolated from the surface of their hides, indicating that cross-contamination was occurring during transport to slaughter. (MAP presence in feeder cattle was 1% or less.)
Headlines were made this summer when a Regional Dairy Quality Management Alliance (RDQMA) study of three Northeast dairy herds reported up to 10 times the within-herd prevalence of Johne’s compared to current diagnostic test results.
Ynte Schukken, a Cornell University professor and director of Quality Milk Production Services in Ithaca, N.Y., coordinates the study’s team of scientists from Cornell, USDA’s Agricultural Research Service, the University of Vermont, the University of Pennsylvania and Penn State. The team has been tracking three herds, ranging from 100 to 350 cows, in New York, Pennsylvania and Vermont for five to seven years.
The team performs a serum ELISA test on each animal every three months and a fecal test every six months, and samples cull cows from the herds at slaughter. They found a 5% to 10% Johne’s prevalence with the live animal testing, but a 25% to 30% prevalence at slaughter.
The other amazing finding is that each herd has multiple strains of MAP. Farm A has nine types; Farm B, seven types; and Farm C, six types. Farm A has two types in common with Farm B and four in common with Farm C.
Farm B has one type in common with Farm C. None of the strains were common to all three farms.
“The multiple strains suggest that infections are occurring through multiple routes and coming from outside the farm,” Schukken says. None of the farms are truly closed, occasionally buying a heifer or having heifers raised by a custom grower. The multiple strains also suggest the infections are occurring by different means, which will make controlling the disease even more difficult.
Bob Whitlock, a Johne’s specialist with the University of Pennsylvania’s School of Veterinary Medicine and RDQMA team member, says the study likely understates within-herd prevalence. “We are evaluating just four tissues at slaughter. To get a truer estimate, we would like to test about 50 tissues.”
Whitlock suspects that true within-herd prevalence “probably approaches 50%. It’s very common, spreads commonly and we likely have human exposure as a result.”
Producers shouldn’t give up hope, though. All of the commonly prescribed Johne’s control measures—clean calving pens, feeding colostrum from noninfected dams and separating calves from their dams soon after birth—are critical in preventing spread.
The key, however, is identifying and culling high and superhigh Johne’s shedders. How often you should test is herd-specific, Schukken says. If you have a high prevalence rate, you’ll likely want to do more frequent testing and test individual animals. If you have low prevalence, you might do more pooled samples, taking manure samples of pens of cows to identify potential problem groups.
Mike Collins, a Johne’s specialist with the University of Wisconsin’s School of Veterinary Medicine, recommends judicious use of the milk ELISA test. At about $5 per sample, it’s a cost-effective way to identify the most infectious cows with Johne’s.
The ELISA test should be done either early in lactation—at least two weeks after calving and before breeding—or a few weeks prior to dryoff. The advantage to doing it early is that if the cow is a high positive, she can be tagged “Do Not Breed” and culled at the end of lactation.
If the test is done prior to dryoff and comes back positive, there’s a temptation to calve the cow one more time. Even if the cow is culled, there will be a temptation at the sale barn to resell her for breeding, spreading the problem to someone else’s herd.
In Canada, Rumensin has been shown to significantly reduce the shedding rate of Johne’s-positive cows, says Ken Leslie, a veterinarian at the University of Guelph in Ontario. “It’s quite clear, with fecal-positive cows, that Rumensin has dramatically reduced shedding.”
The study was done with time-release boluses, not direct feeding. But some Canadian producers are feeding Rumensin at label rates as part of their Johne’s control efforts.
Collins says Rumensin does show some benefit, but researchers don’t understand how it works to reduce shedding. “It’s a useful adjunct to a Johne’s control program, but don’t use it alone,” he says. Note that Rumensin is not labeled for Johne’s control in the U.S.
Another effective tool to control Johne’s is the vaccine Mycopar. When given to calves before 30 days of age, it almost eliminates fecal shedding. But it has limited USDA licensure, meaning its use must be approved by your state veterinarian. The problem is that it cross-reacts with bovine tuberculosis (TB) tests. With bovine TB now in at least eight states, state veterinarians are reluctant to allow use.
The Johne’s Disease Integrated Program is working on a vaccine that is not cross-reactive with TB tests and may be available later this decade.