Introduction
Bovine viral diarrhea virus (BVDV) has caused much confusion among producers, veterinarians, and researchers. Within the last decade, many obscure aspects of this pathogen have been unravel- ed. Type 2 BVDV strains have received much recent press. For the moment, consider infections caused by Type 1 or Type 2 BVDV strains merely different clinical outcomes of the same disease syndrome. The events that need to occur for either viral type to cause disease are very similar. This paper will supply a "simple" description of how cattle acquire BVDV, explain the role that management plays in influencing disease outcomes, and discuss the limitations of vaccines used to control this ubiquitous virus.
Pathogenesis of BVDV
When BVDV infects cattle, the outcomes depend on the level of resistance in the affected animals, the virulence of the infecting viral strain, and the presence of carrier animals. Many dairy producers who have dealt with BVDV wonder how the virus was originally introduced into their herd. This will be discussed later under management strategies. It is important to remember that this virus can infect cattle of all ages and that a healthy, functioning immune system will reduce potential losses. The economic impact of this disease is most devastating when susceptible (non-immune), pregnant animals are exposed to the virus. Transplacental infection of the fetus can create a carrier state which allows the virus to linger in a herd indefinitely.
There are basically three classifications of cattle with regard to BVDV status; unexposed cattle, animals exposed after birth, and those exposed while in the uterus. Even though BVDV has a world wide distribution, some cattle have never been exposed to either a field strain or a vaccinal strain of the virus. These animals are completely susceptible to BVDV. If these animals are maintained in a closed herd (ie. no purchased additions, complete isolation from all other ruminants, and implementation of strict biosecurity measures), disease from BVDV will most likely not occur. Very few, if any, herds in Illinois can be considered truly closed.
Exposure after birth
The results of infection with BVDV after an animal is born vary depending on the strain of the virus and the immunity of the host. In the majority of cases only mild disease is produced. Animals are transiently viremic, generate antibodies, and clear the virus in 7 - 10 days. Postnatal infection with BVDV can also cause immunosuppression enhancing the ability of other agents to cause disease. Respiratory pathogens like IBR and Pasteurella can create significant losses. Stress can also potentiate the immuno- suppression caused by BVDV. Diarrhea in calves has been attributed to BVDV, but most likely the virus is not a primary cause and may work together with other agents. Of primary economic concern is the reproductive failure seen when BVDV is introduced into a breeding herd.
Exposure to BVDV in utero
The major economic impact of this disease ensues when fetal calves are exposed to BVDV. Table 1 demonstrates the various outcomes of fetal infection with the virus. Only the birth of a normal, antibody-negative calf is desirable. This will occur only when the level of resistance (immunity) in the dam is sufficient to ward off the virulence of the infecting viral strain. If the cow can fight off the infection, the fetus will be protected from viral invasion. Persistently infected cattle are usually unthrifty and succumb to disease early in life. They may also appear clinically normal and have the ability to produce antibodies to other infectious agents and other strains of BVDV. These animals may successfully conceive and their calves will be persistently infected as well.
Although fetal losses from abortion, resorption, mummification, stillbirth or birth defects have economic repercussions, the birth of a normal but persistently infected (carrier) calf could be devastating (Table 1, grey shaded box). When infection occurs in early gestation, the developing fetal immune system does not recognize BVDV as a foreign antigen. These calves are born with the virus circulating in their bodies. They do not develop antibodies to the virus because BVDV was present before their immune system was functional. In other words, their immune system "sees" the virus just like any other cell in the body and will not produce antibodies against it. When a fetus is infected later in gestation (after the immune system is functioning), the fetus will produce antibodies and the calf will be born with active immunity to BVDV. This situation is not altogether undesirable, but the added stress of infection, viral clearance, and antibody production on the growing fetus may produce a weakened newborn calf.
All strains of BVDV come in two varieties or biotypes; cytopathic (CP) and non-cytopathic (NCP). For every strain of CP-BVDV, there is a NCP-BVDV. Cytopathic biotypes of the virus will destroy cells in culture. Non-cytopathic isolates replicate in cell culture, but do not destroy the cells and indirect methods must be used to detect their presence. For this reason NCP-BVDV is difficult to identify in the lab. A carrier animal will only have the NCP biotype of BVDV circulating in its system. The virus can be isolated from virtually any secretion or excretion including nasal discharge, saliva, feces, urine, tears, and milk. These calves will shed virus even while carrying maternal antibodies. Cytopathic BVDV alone cannot maintain itself for long in a cattle population and once all susceptible animals in a herd have been infected, it will disappear. The CP biotype can produce all the same clinical manifestations ascribed to NCP-BVDV, except the NCP biotype can survive within PI animals, creating the carrier state.
Acute deaths from mucosal disease will occur only if the carrier animals are exposed to a CP biotype of the same or a very similar strain of BVDV. Economic impact of mucosal disease in the dairy industry is at best minimal. Its occurrence is sporadic with usually less than 5 percent of a herd affected annually. Most mucosal disease occurs between 6 and 24 months of age. Maternal antibodies may protect the carrier calves from superinfection during the first 6 months of life. The source of CP-BVDV may be from transiently infected cattle, "live" vaccine, or mutation of the NCP biotype within the carriers themselves. The carrier animal cannot be "saved", "cured", or "treated." To keep these animals in a herd can have catastrophic economic consequences. Carriers must be identified, eliminated, and prevented from re-emerging in a herd.
Management's role in BVDV control
Management practices can facilitate the spread of BVDV within and among herds. As mentioned earlier there are few, if any, truly closed dairy herds in Illinois. Many producers have expanded their operations and purchased additional animals within the last few years. In many herds, exposure to wild ruminants cannot be eliminated. Maintenance of strict biosecurity measures such as shower-in, shower-out procedures seen in large farrowing units are also not commonly practiced on Illinois dairies. In fact, many animals are potentially exposed every spring and summer at county fairs and cattle shows.
When purchasing pregnant cattle, the possibility exists that any one of them may be carrying a persistently infected fetus. Using blood tests to screen herd additions has merit, but results need to be interpreted cautiously. Serology detects antibody production while virus isolation is an attempt to identify BVDV in the sample. Table 2 demonstrates the various outcomes possible depending on the animals' BVDV infection status. Blood test results can only provide evidence of the dam's status. Currently, there are no tests to determine the BVDV status of the fetus. Newborn calves from new herd additions must be bled prior to receiving colostrum. Colostral antibodies may confound current testing procedures. These calves should be considered persistently infected until evidence to the contrary is presented.
Transmission of BVDV occurs by direct or indirect contact with a carrier or transiently viremic animal. Postnatally infected cattle shed very little virus for a very short time, while PI cattle shed tremendous amounts of virus for life. Transplacental infection is possible and this is probably the only circumstance in which transmission occurs efficiently from a transiently infected animal. When feeding pooled milk, it is likely that infective milk would be mixed with that of herd mates containing neutralizing antibody, thus reducing the probability of transmission from this route. Although BVDV will not live long outside of an animal's body, the virus can be transferred from place to place on contaminated clothing, boots, and vehicles. Use of common instruments such as nose grips and communal water troughs can aid the spread of the virus. Fortunately, BVDV is susceptible to most disinfectants and contaminated items can be salvaged.
Limitations of vaccination for BVDV
Bovine viral diarrhea virus is primarily a reproductive disease, and vaccination programs should focus on reproductive events. The desire to vaccinate all animals in a herd once a year must be discouraged. A distinction must be made between vaccination and immunization. Vaccination could be considered the process of injecting an animal with a biological product regardless of the results. Immunization, on the other hand, involves vaccination and the production of a protective immune response, such as antibodies. With regard to BVDV, far too much vaccination transpires and very little immunization results. Killed vaccines contain much more viral antigen than "live" vaccines. This is required so that the vaccinated animal's immune system is overloaded with antigen and will mount an immune response. Killed vaccines require a second dose in 3 - 4 weeks to booster the initial vaccination and insure some level of protection. This protection is short lived and may need boosters every three to four months. Alternately, virus from modified-live vaccines multiply within the animal's body until an immune response occurs and the virus is cleared. This is very similar to natural infection except the vaccinal virus has been "modified" so that the disease does not occur, but antibody production does. This type of immunization is long lasting and no further vaccination may be necessary.
These concepts must be kept in mind when preparing to vaccinate a dairy herd for BVDV. Killed BVDV vaccines can be used on any animal, irrespective of its age, pregnancy status, and/or level of immunity. But, these vaccines must initially be boostered and then repeated multiple times a year for adequate protection. If proper immunization is to occur with modified-live BVDV vaccines, the vaccinates must not possess protective antibodies to BVDV. These antibodies will prevent the vaccinal virus from replicating and improving the immune status. There is some evidence that rotating vaccines may supply broader protection against the many strains of BVDV found in the field.
Referring back to table 2, any animal which is antibody positive would not be protected by a modified-live vaccine. Vaccination would occur, but not immunization. For example, a two month old calf with colostral antibodies still present would not be immunized by a modified-live vaccine, but a six month old calf whose colostral protection has waned would respond. The practice of vaccinating fresh cows with modified-live vaccines needs closer scrutiny. In fact, vaccinating at this time may provide added stress to an already overworked immune system.
Ideally, all non-pregnant heifers over six months of age should be exposed to a carrier animal. Natural exposure would provide the best immunization, but the potentially devastating effects of viral exposure to pregnant animals eliminates this as a possibility. Alternatively, vaccination of healthy heifers with a modified-live vaccine at least twice between 6 and 12 months of age should furnish sufficient immunity for life. Shedding of vaccinal virus has been postulated, so young stock immunized in this manner should isolated from pregnant animals. These heifers could be boostered annually, prior to each subsequent calving, with a killed vaccine. The yearly booster vaccination could be included within the scope of a complete dry cow program.
Summary
If expansion plans are on your horizon or you simply want to buy a few replacements, consider the implications of bringing BVDV into your herd. Even if BVDV is already present within your herd, a different viral strain or biotype can wreak havoc in susceptible cattle. The recent outbreaks of Type 2 BVD have occurred in unprotected (poorly immunized) herds. The magnitude of the losses in an infected herd will be relatively large when reproductive problems occur on an epidemic scale, as with initial horizontal spread to nonimmune pregnant cows. These losses will be considerably lower but longer lasting when endemic infection is maintained in the herd through the presence of carriers. Dr. E. J. Dubovi (Cornell University) has a relatively simple message for controlling BVDV, "Keep the virus from reaching the fetus!"
Source: Dick Wallace, University of Illinois Extension