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Bovine Enemy #1

The BVD virus has mutated into dozens of strains causing respiratory disease outbreaks in feeder animals and reproductive disease in pregnant cows.It's perhaps the single most important infectious disease agent in the beef industry - bovine viral diarrhea virus - commonly called BVD.The diseases caused by the BVD virus are extremely complex and difficult to grasp. Because of the wide variety of disease

The BVD virus has mutated into dozens of strains causing respiratory disease outbreaks in feeder animals and reproductive disease in pregnant cows.

It's perhaps the single most important infectious disease agent in the beef industry - bovine viral diarrhea virus - commonly called BVD.

The diseases caused by the BVD virus are extremely complex and difficult to grasp. Because of the wide variety of disease syndromes that can occur, the virus is often blamed for many disease problems without diagnostic evidence that it's actually the culprit.

Bovine viral diarrhea is a misnomer for most of the disease problems caused by the BVD virus, because diarrhea is often not seen. The main effects of viral infection in the U.S. today are associated with respiratory disease outbreaks in feeder animals and reproductive disease in pregnant cows, although sudden death in cattle of all ages has been seen.

The virus has mutated into dozens of strains that can infect a variety of organ systems ranging from the digestive tract to the respiratory tract to the reproductive tract. It will continue to mutate.

BVD can cause in utero infections that result in the fetus being infected permanently. When born, these persistently-infected (PI) animals shed large numbers of the virus and are often the primary source of BVD disease in beef herds; exposure to infected animals from outside the herd is not required.

The virus infects many cells of the immune system and impairs the animal's ability to ward off other disease agents. So, while the BVD virus may not kill an animal directly, the immunosuppression allows other infectious disease agents to do serious injury or cause death.

Reproductive Problems Disease problems associated with this virus vary according to the stage of pregnancy when the cow is exposed and on her immune status. If the dam is immune to the exposing strain, the virus is eliminated and no infection occurs in the fetus.

But, if the dam's immunity is insufficient to prevent fetal infection by a particular strain, or if she is PI, several things can happen.

If the developing embryo is infected and killed, an "infertility" problem may occur with cows coming back into estrus late in the breeding season. We see herds with diagnosed BVD problems in which an increased number of open cows are noted. Generally, these reductions in pregnancy rates are in the 5-10% range.

Abortions can occur at any stage of pregnancy, even months after initial infection. Virus cultures may be negative simply because the virus has done damage but is no longer present for culturing. Calves may also be delivered full-term, either dead or weak.

Persistently Infected Calves The PI animals originate in the first 125 days of pregnancy when the virus infects the developing fetus. This occurs before the fetal immune system develops. If the infecting strain doesn't kill the developing fetus, the calf will be born PI and will be tolerant to that particular strain. No immune rejection attempt occurs.

In most semi-closed beef herds, these PI animals will be the primary source of virus. Recent Canadian research shows most PI animals to be nursing calves.

Most producers have observed calves born with "birth defects" as a result of BVD but did not know the cause. From about 90 to 150 days of pregnancy, viral infection of developing organ systems can lead to a variety of congenital defects. The brain, eye and skeleton are especially vulnerable. There are many causes of congenital defects, and the BVD virus is only one of the many that must be considered.

After about 150 days of gestation, the fetus develops a functioning immune system that can protect it from most strains of BVD virus. So, most third trimester exposures do not result in fetal infection or death. However, especially "hot" or virulent strains can cause fetal infection or deaths just like they can in calves and adults.

Because most PIs in beef herds will be found in nursing calves, and because the virus is so immunosuppressive, most will die in early life of scours or pneumonia. A few calves will live for several months; in rare cases, for several years.

In many herds, however, no adult carriers can be found. This presents a diagnostic challenge in eradicating carrier animals from a herd. Nursing calves would have to be tested before the breeding season to break the transmission cycle.

PI calves that survive to weaning are generally stunted and severely underweight for their age. Only a few will be average in weight. Testing "runts" and poor-doing calves at weaning time can be useful in diagnosing the presence of the BVD virus in a herd.

Selection of infected animals for replacement bulls or heifers will continuously expose herd mates to infection.

Most PI calves will be from normal cows that lacked immunity to protect the fetus in utero. However, the dams of any calves that test positive for the virus should also be tested to ensure they are not also PI carriers.

PIs can develop a chronic fatal "mucosal disease." Most researchers now believe mucosal disease results from a mutation of the persisting strain of the virus.

These animals develop severe ulceration of the mucosal surface of the entire alimentary tract, from the nose and mouth to the anus, as well as diarrhea and fever. They subsequently die.

It's important to note that all calves out of PI dams will be PIs; however, most PI calves will be from non-carrier dams that did not have sufficient immunity to prevent fetal infection.

Prevention Of Reproductive BVD Protecting weaner calves and cows from respiratory and sudden death forms of BVD appears to be a much simpler task than protecting fetuses from in utero exposure. Both killed (K) and modified-live virus (MLV) vaccines are available and both types of vaccine will confer acute disease protection when given as directed.

Killed vaccines require two doses and generally give about six months of protection in weaned calves. The MLV vaccines only require one dose and give up to three years of protection. There appears to be satisfactory cross-protection between strains, and recent research has shown at least one Type 1 vaccine will protect against Type 2 challenge in older calves.

In calves less than five months of age, colostrum antibodies will impair the protective response. Research has shown that cell-mediated immunity will develop to the infectious bovine rhinotracheitis (IBR or rednose) and bovine respiratory syncytial virus (BRSV) fractions of multivalent MLV vaccines given to young calves despite high levels of colostrum antibodies. This hasn't been shown to occur with the BVD virus fraction.

Two doses of a MLV vaccine should be given to replacement heifers with the second dose given about one month before breeding. Using two different products with different strains of the BVD virus may broaden protection.

Both antibody and cell-mediated immunity will result from MLV vaccines. Developing the immune heifer cannot be over emphasized. A yearly booster of MLV vaccine given three to four weeks before breeding when cows are open is recommended. Do not give MLV BVD vaccines to pregnant cows.

To help identify carrier animals, rapid and economical tests from diagnostic laboratories are now commercially available. These rapid tests are called "BVD microtiter virus isolation" or "BVDV ELISA."

Essentially, serum is used, and virus is detected with the use of antibodies that react to all strains. Calves less than three months old that have received colostrum present a special problem, so culture of unclotted blood is recommended. Whole herd eradication should not be undertaken without full knowledge of the time, cost and pitfalls.

To get a handle on BVD, producers must understand the terms relating to the disease. Among the terms, are "cytopathic" (CP) vs. "noncytopathic" (NCP) and "Type 1" vs. "Type 2."

This means that the virus strain being cultured has the ability to kill (cytopathic) or not kill (noncytopathic) the tissue culture cells needed to propagate the virus. It has no bearing on whether the strain can kill an animal.

In 1993, dairy cattle were dying suddenly in Canada and the northeastern U.S. Genetic typing found that these BVD virus isolates were different than the recognized strains in existence. The new mutations were deemed Type 2 strains. Many states now report that Type 2 isolates are more common than Type 1.

Whether a BVD virus isolate is CP, NCP, Type 1 or Type 2 does not indicate ability to cause disease; in vaccines, it is no indication of degree of vaccine efficacy. Some vaccine companies are now producing vaccines with both Type 1 and 2 strains.

Fetal Protection The greatest BVD threat is from fetal infections, say Lynn Woodard and Hana Van Campen, from the University of Wyoming Department of Veterinary Sciences. Therefore, special consideration must be given to protecting the unborn fetus. But, they say adequate research into fetal protection after vaccination of the dam with BVD vaccines is lacking.

"With a single exception, no current vaccines on the market have proven fetal protection in a peer-reviewed publication," says Woodard. "Older literature indicates that protection is very poor, but most of these trials were lacking in design and numbers."

Recently, one Type 1 MLV vaccine was shown to provide about 80% protection against a Type 1 challenge that infected all the control fetuses.

"We're waiting for the results of the Type 2 challenge study," adds Van Campen. "We're aware of at least one other major company that's testing its vaccines for fetal protection."

Adding Type 2 strains should broaden protection, but Woodard says producers and veterinarians should be cautious of claims that are not substantiated by published research.