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 unraveled. This [article] 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 virus.
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. 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 that allows the virus to linger in a herd indefinitely.
There are basically three classifications of cattle with regard to BVDV status:
1. unexposed cattle
2. animals exposed after birth
3. those exposed while in the uterus
Even though BVDV has a worldwide 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 (no purchased additions, complete isolation from all other ruminants and implementation of strict biosecurity measures), disease from BVDV will most likely not occur.
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. Postnatal infection with BVDV can also cause immunosuppression, enhancing the ability of other agents to cause disease. Stress can also potentiate the immunosuppression 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 (PI) 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 PI (carrier) calf could be devastating.
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 noncytopathic (NCP). 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. The occurrence of BVDV 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 CPBVDV 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. Many producers have expanded their operations and purchased additional animals within the last few years. Maintenance of strict biosecurity measures are not commonly practiced. 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. 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.
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 herdmates 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 three to four 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 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.
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.
Ideally, all non-pregnant heifers over six months of age should be exposed to a carrier animal. Natural exposure would provide the highest level of immunity, but the potentially devastating effects of viral exposure to pregnant animals eliminates this as a possible means of herd immunization. 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 be 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.
If killed vaccines are used for primary immunization, two doses within 30 days are required. Frequent boosters every four to six months may also be necessary throughout the animals’ lives. Modified-live vaccines may provide longer duration of immunity. Initial immunization with modified-live vaccines should occur between 4 and 12 months of age.
No vaccination program is 100 percent effective at eliminating disease. Proper handling and usage is essential to success. Immunizing the existing herd may help reduce the economic risk from introduction of BVD virus. Your veterinarian can help design a complete vaccination program tailored to your farm.
Environmental mastitis
The primary environmental pathogens responsible for bovine mastitis include two types of bacteria: coliforms and streptococci other than Streptococcus agalactiae. These other streptococci are often referred to as “environmental” streptococci or “fecal” streptococci. Typically, coliforms are responsible for the peracute, toxic, “watery” mastitis, whereas environmental streptococci cause a less severe type of infection.
While the contagious mastitis bacteria Staphylococcus aureus and Strep. agalactiae are transmitted by infected cows during the milking process, environmental pathogens are found in the cow’s surroundings and transmission occurs in between milkings. The duration of infection for environmental pathogens is shorter than for contagious pathogens.
The rate of new infections by environmental bacteria is typically higher during the dry period than during lactation. Without dry-cow therapy, the rate of streptococcal infection tends to increase dramatically the first two weeks of the dry period and again during the two weeks before calving. Coliform infections can be up to four times greater during the dry period than during lactation and dry-cow therapy has little effect. Infection rates are highest in the early stages and decrease as lactation advances.
Infections tend to be more prominent with each successive lactation. More than 50 percent of coliform infections have been shown to last less than 10 days and nearly 70 percent less than 30 days. Few coliform infections become chronic, with less than 13 percent lasting for more than 100 days. Approximately 60 percent of streptococcal infections last less than 30 days, while up to 18 percent may become chronic and persist more than 100 days.
Improve resistance
Any control procedure employed that tries to improve the cow’s ability to fight off environmental pathogens is reactionary and implies that the cow needs to respond to an infection. It is much more logical to place the majority of our control efforts into reducing or eliminating teat-end exposure to environmental bacteria.
Even so, there are some measures that can be implemented to raise a cow’s level of resistance to infection. These approaches should not replace good hygienic practices but should serve a supplemental role to maintaining a clean environment.
Provision of a stress-free atmosphere for cows, particularly around calving, is essential for mastitis control as well as high production. Stress causes cattle to release naturally produced “cortisone” which has immunosuppressive effects on the body. Cows that are immunosuppressed are much more likely to contract mastitis and it may take longer for them to clear infections.
Many infectious diseases such as bovine viral diarrhea, bovine respiratory disease complex and salmonellosis can cause severe immunosuppression. Reducing stress (including heat stress) and controlling infectious diseases cannot only reduce the impact of environmental mastitis but may also lead to higher production levels.
Deficiencies in dietary selenium, vitamin E and vitamin A (or beta-carotene) have been shown to result in increased incidence of mastitis. Mastitis pathogens can create severe tissue damage, causing the release of free oxygen-radicals. These nutrients work in enzyme systems that act as antioxidants during inflammatory episodes. Supplemental dietary selenium, vitamin E and vitamin A may reduce the severity and shorten the duration of clinical mastitis.
Vaccinations
Control of coliform mastitis has been made possible through the discovery of mutant gram-negative bacteria. Vaccines made from core antigens stimulate production of antibodies that are cross-protective against a wide variety of gram-negative organisms. Heat-killed Escherichia coli J5 mutant bacterin is administered subcutaneously at dryoff, 30 days later and within 14 days of calving.
A California field study demonstrated that the prevalence of clinical coliform mastitis over the first 100 days of lactation was 2.6 percent in vaccinated cows and 12.8 percent in controls. In another trial, vaccinated cows exhibited fewer bacteria in their milk and lower body temperatures after experimental infection. Additionally, milk production and dry matter intake were higher in vaccinated cows.
A third study evaluated a vaccination program in an Ohio herd over a two-year period. Vaccination with the J5 bacterin did not reduce the prevalence of gram-negative intramammary infections (IMI) at calving, but did reduce the incidence of clinical mastitis. In unvaccinated cows, 67 percent of IMI present at calving became clinical during early lactation while only 20 percent of IMI present at calving in vaccinated cows became clinical.
Another gram-negative bacterin-toxoid vaccine has been made from a mutant strain of Salmonella typhimurium (Endovac-Bovi). This is a core antigen vaccine and is to be administered intramuscularly at dry-off and two to three weeks prepartum. Studies have shown that there is a 47 percent reduction in clinical mastitis during early lactation and a 67 percent reduction in repeat episodes of mastitis. Additionally, deaths and involuntary cull rate were 61 percent lower in vaccinated cattle.
Economic losses due to clinical mastitis have been estimated to be $107 per clinical episode. Losses due to decreased milk production and non-salable milk account for 84 percent or almost $90 per case. Use of these bacterins can be a cost-effective control practice. PD
References omitted but are available upon request at editor@progressivedairy.com
—Excerpts from 2007 Midwest Dairy Expo Proceedings
Richard L. Wallace
Dairy Extension Veterinarian
University of Illinois
