Busting BVDV myths

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The effects of bovine viral diarrhea virus (BVDV) are wide-ranging in terms of reproductive issues, adult and calf health, and production. Much as been written about BVDV over the years and much has been and is still being discovered, but in spite of that misinformation “myths” about BVDV still remain.

Dan Givens, DVM, PhD, Auburn University, discusses the plausibility of the most persistent myths about BVDV. Givens categorizes these myths by:

  • Confirmed Research evidence confirms the truth of this myth.
  • Implausible Worthy of disbelief based on available research evidence.
  • Busted Research evidence confirms the fallacy of this myth.

Myth 1: Commingling heifers such as at synchronization or shortly before breeding presents a low risk of BVDV infection.

Busted. If the heifers to be commingled have not previously contacted each other, then prevalence studies indicate that approximately 4 of 1,000 heifers will be persistently infected (PI) and efficiently spread virus to cause infection of naive, contacted cattle. If the heifers have not been previously immunized, then the negative impact on pregnancy rates and abortions can be severe due to the timing of infection. Prior research indicates infection with BVDV at the time of estrus synchronization can decrease pregnancy rates by 20% to 50% [1–3].

Myth 2: Virus from a persistently-infected calf is not very pathogenic.

Implausible. Pathogenicity (the ability of an organism to infect a host and cause disease) is the product of infectivity (the ability of a virus to invade and establish replication within the host) and virulence (the severity of disease exhibited by infected hosts). Virus from a persistently-infected calf is very infective. To put that in perspective, prior research [4] has shown that if you take about 60 mL of snot or spit from a PI animal and mix it in a farm pond equal to the size of an Olympic swimming pool (50 m X 25 m X 2 m), then you can go to the other side of the pond and 1 mL of collected water will contain enough virus to infect a calf 50% of the time. 

When considering the virulence of BVDV, we must consider that BVDV causes a spectrum of clinical diseases that includes:

  • Severe, acute disease associated with leukopenia, thrombocytopenia, mucosal damage, and enteritis
  • Acute disease associated with immunosuppression and respiratory disease
  • Reproductive losses including early embryonic deaths and later abortions
  • Congenital defects including cerebellar hypoplasia, mandibular brachynathism, and ocular lesions
  • Persistent infections which can be associated with low birthweights, poor growth rates and a decreased life-span. 

While the BVDV strains from PI animals may not often be associated with severe, acute disease because pregnant animals with severe, acute disease will likely abort or die in the course of an outbreak [5], strains of BVDV in PI animals are likely to cause the other clinical diseases that are discussed. Thus, while PI animals may not spread the most notorious of BVDV outbreaks, they are factories of infectious virus and are likely to spread other clinical diseases within the BVD spectrum.

Myth 3: Acute/transient BVDV infections will always present the same in cattle.

Busted. The outcome of acute infection with BVDV is a result of unique interplay of the viral strain, environmental stress, and the animal’s immunity. The outcome of acute infection with BVDV can be severe, acute disease associated with mucosal lesions, enteritis and bleeding disorders with a mortality rate of 25% in some populations [6, 7]. The outcome of acute infection with BVDV can be immunosuppression which is often linked to respiratory disease in some populations [8]. The outcome of acute infection with BVDV can also be clinically undetectable in some populations [9; 10]. Thus, acute or transient BVDV infections will not always present the same in cattle.

Myth 4: A cow or heifer must already carry the BVDV virus before pregnancy in order to produce a PI calf.

Busted. A cow or heifer only has to sustain an infection with BVDV before approximately four to five months of gestation to produce a PI calf. At that point in gestation, the calf’s immune system develops the competence to recognize BVDV as a viral intruder and prevent persistent infection. Just like there is variability in the age at which a calf will reach 65% of its mature body weight, there is variability in the gestational age at which immunocompetence is achieved.

One study describes a set of twin calves in which one was persistently infected with BVDV and the other was not [11]. Another study describes a PI calf that resulted when a pregnant cow was exposed to BVDV at a gestational age of 182 days [12]. However, the vast majority of calves will not be susceptible to persistent infection after 150 days of gestation.

At the other end of the window of susceptibility, PI dams will always produce PI calves by natural gestation. Insemination of non-viremic, seronegative heifers with BVDV-contaminated semen can result in a low percentage of PI calves [13, 14]. Controlled research does demonstrate that calves are less susceptible to persistent infection at 18 days of gestation compared to 30 days of gestation [15].

Myth 5: Unless it’s PI, BVDV infection in utero doesn’t have that much effect on the calf.

Busted. Limiting the in utero impact of BVDV to persistent infections is a fallacy [15]. Without resulting in PI calves, BVDV can cause cerebellar hypoplasia, microencephalopathy, hydrocephalus, hydranencephaly, porencephaly, hypomyelination, cataracts, microopthalmia, optic neuritis, retinal degeneration, thymic hypoplasia, deranged osteogenesis, and growth retardation. While these calves will not be persistently infected and will be negative for virus if tested at birth, the etiology of congenital defects is a transient BVDV infection that disrupted organogenesis. Diagnostic, pre-colostral serum samples will contain anti-BVDV antibodies as the immune system won the war against this pestivirus but the combination of direct cellular damage by virus and the inflammatory response to BVDV causes multiple battle sites within the calf to be destroyed.

Myth 6: PI calves will always look normal at birth.

Busted. While calves persistently infected with BVDV can present as normal calves, many times they are small and unthrifty [16] or can exhibit a congenital defect such as mandibular brachygnathism [17]. In one study, all neonatal calves presenting with mandibular brachygnathism from a herd outbreak involving abortions and premature births tested positive for BVDV [17]. Natural and experimental reports suggest that BVDV infection between 79 and 90 days of gestation can result in brachygnathism and persistent infection [18]. In another study, the median live calf birth weights were 37 pounds for persistently infected calves in comparison to 65 pounds for uninfected calves [35].

Myth 7: You can always differentiate between an acute infection and mucosal disease based on clinical signs and gross necropsy.

Busted. Mucosal disease is a unique acute episode of severe disease in a calf which is persistently infected with a noncytopathic strain of BVDV. Mucosal disease occurs when the PI calf is superinfected with a genetically similar, cytopathic strain of BVDV [19]. Clinical signs and gross lesions of mucosal disease may include high fever, lethargy, bloody profuse diarrhea and severe erosions, ulcerations, and hemorrhages of the mucosal surfaces of the muzzle, oral cavity, esophagus, rumen, reticulum, omasum, abomasum, and the small and large intestines [19].

In comparison, clinical signs of severe acute BVDV infections of naive cattle may include high fever, moderate to severe depression, bloody diarrhea, hemorrhages and prolonged bleeding from venipuncture sites, and erosive lesions in the esophagus and abomasum [9]. Thus, mucosal disease and severe acute infections with BVDV cannot be accurately differentiated based only on clinical signs and gross necropsy results.

Myth 8: Using bulk tank milk is a good screening tool for PI surveillance in a dairy herd.

Implausible. Composite milk samples from lactating cows can be collected and accurately tested for BVDV by polymerase chain reaction (PCR) [20]. This composite sample should represent less than 400 cows to accurately detect one PI animal in the group [21]. If the composite milk sample tests positive, the animals are tested individually to determine which animal is PI.

However, the critical problem with relying on this approach to screen a dairy herd for BVDV is that most PI animals in the herd will not be lactating but will be in the youngstock spreading virus to the extent allowed by biocontainment practices on the farm. Therefore, a dairy herd may be experiencing significant reproductive losses due to BVDV without having any lactating PI cows on the farm. Thus, a more sensitive screening method for BVDV in the dairy herd might be submission of diagnostic samples from any aborted, premature, underweight, or ill-thrift calves, screening for antibodies in 6- to 12-month-old non-vaccinated heifers and/or assessment of precolostral antibodies in a subset of newborn calves [22].

Myth 9: You don’t have to worry about endemic strains in a herd infecting incoming cattle.

Busted: Strains of BVDV which are maintained by PI cattle in an apparently healthy herd can cause severe outbreaks of disease in incoming naïve cattle [23]. A recent report of such an outbreak involved a 23% mortality rate in 70 naive, recently purchased freshening heifers during expansion of a dairy.

Myth 10: Stress in naïve animals does not predispose them to disease due to BVDV infection.

Busted: The severity of disease resulting from infection with BVDV is determined by virulence of the viral strain, stress of the environment, and the competence of the animal’s immune system. Stressed calves or heifers are much more likely to exhibit disease due to BVDV.

The impact of stress is exemplified by the fact that experimental inoculation of calves with isolates of highly virulent BVDV type II in controlled, low-stress environments does not result in development of lesions or clinical signs that are as severe as those for infections occurring in commercial production settings [9]. Recent severe outbreaks of BVDV have been associated with high stress events in the dairy environment such as a snowstorm with ambient temperatures of -4°F shortly after transportation of naive cattle [23].

Myth 11: The dam of every PI calf is a PI herself.

Busted. Persistent infection in a calf occurs when the dam is infected with noncytopathic BVDV prior to approximately 125 to 150 days of gestation [24]. This can occur following an acute or persistent infection of the dam. Prior research demonstrates that 93% of PI calves do not come from a PI dam [25].

The non-PI cow that experiences an acute infection and subsequently gestates a PI calf throughout pregnancy will not spread BVDV after postpartum uterine discharges cease. This cow will also exhibit the greatest immunity to subsequent disease due to BVDV. Thus, culling dams of PI calves without testing to see if the dam herself is PI is clearly poor management in almost all circumstances.

Myth 12: It is OK to let pregnant cows be exposed to calves up until five months of gestation.

Implausible. As discussed previously, persistent infection in a calf occurs when the dam is infected with noncytopathic BVDV prior to approximately 125 to 150 days of gestation. Therefore, if a non-vaccinated and previously non-exposed pregnant cow was exposed to a PI calf during this period of gestation, she is likely to develop an acute infection. This acute infection puts her fetus at risk for becoming persistently infected.

In most dairy situations maintaining adequate separation of early pregnant cows from calves is very feasible. If the calves have previously been tested for BVDV then they represent little risk to the pregnant cows. However, as PI calves will have a higher death rate than uninfected calves during the first year of life [26], developing heifers are a common source for BVDV transmission to other cattle on the farm.

Myth 13: The freezing and thawing of semen will kill BVDV.

Busted. Bulls acutely or persistently infected with BVDV can shed infectious virus in semen [27–30]. Viral transmission can occur in seronegative heifers following insemination with infected semen [13, 14, 31, 32]. The virus does persist in semen following processing and cryopreservation [13]. Seroconversion was detected in 161 cows out of 162 following insemination with semen from a PI bull. Additionally, sperm separation procedures such as washing, Percoll gradient, glass wool filtration, and glass bead filtration do not completely
remove BVDV associated with the spermatozoa [33].

Straws of semen stamped with CSS can be used with great assurance that the semen is free of BVDV. Certified Semen Services (CSS) requires bulls and mount animals to be healthy and free of infectious disease (www.naab-css.org/about_css/disease_control-2002.html). Animals are tested for BVDV and must be negative within 30 days prior to entry to the AI center. Whole blood or serum is tested by viral isolation or antigen capture ELISA. Upon arrival to the AI center, animals are held in isolation until two consecutive negative virus isolation results are obtained 10 days apart. If BVDV is detected in whole blood or serum, the animal is retested in 21 days to determine if the infection is acute or persistent.

Bulls that were acutely infected will have virus isolation performed on semen collected 30 days preceding and following the date of viremia. The semen must have negative results from each collection code prior to distribution. Before the semen can be released from any bull in the AI center they must undergo virus isolation test of processed semen. This is semen that is completely extended and frozen. Any bull that has a persistent testicular infection is not eligible for semen collection and must leave the resident herd.

Myth 14: Multiple low-birth weight calves should raise suspicion of disease due to BVDV.

Confirmed. While calves persistently infected with BVDV can present as normal calves, many times they are small and unthrifty [16]. In one study, the median live calf birth weights were 37 pounds for persistently infected calves in comparison to 65 pounds for uninfected calves (Givens et al., in preparation).

Myth 15: Having one dose of killed BVDV vaccine in an animal is better than no vaccination at all.

Busted. One should note that a single dose of killed BVDV vaccine does not follow the manufacturer’s recommendations and will not provide appropriate or adequate protection against BVDV. One dose of a killed BVDV vaccine only serves to provide producers with a false sense of security. The severe acute BVDV outbreaks of disease in the early to mid-1990’s were only described in herds not vaccinated or “not vaccinated according to the manufacturer’s recommendations [34].”

A recent field report describes the failure of one dose of killed BVDV vaccine to prevent congenital defects in 19 of 37 (51%) offspring resulting from a subsequent, natural challenge with BVDV [17]. Two initial doses of killed BVDV vaccine administered three to four weeks apart are critical to stimulate an anamnestic immune response in vaccinates. Experience provides examples of cows that have received a single dose of killed vaccine for the last eight years without an initial two-dose series of vaccination that gave birth to PI calves after encountering a natural challenge with BVDV. 

References

[1]    McGowan MR, Kirkland PD, Rodwell BJ, Kerr DR, Carroll CL. A field investigation of the effects of bovine viral diarrhea virus infection around the time of insemination on the reproductive performance of cattle. Theriogenology 1993;39:443–9.

[2]    McGowan MR, Kirkland PD, Richards SG, Littlejohns IR. Increased reproductive losses in cattle infected with bovine pestivirus around the time of insemination. Vet Rec 1993;133:39–43.

[3]    Virakul P, Fahning ML, Joo HS, Zemjanis R. Fertility of cows challenged with a cytopathic strain of bovine viral diarrhea virus during an outbreak of spontaneous infection with a noncytopathic strain. Theriogenology 1988;29(2):441–9.

[4]    Rodning SP, Marley MS, Zhang Y, et al. Comparison of three commercial vaccines for preventing persistent infection with bovine viral diarrhea virus. Theriogenology 2010 May;73(8):1154–63.

[5]    Ridpath JF, Neill JD, Vilcek S, Dubovi EJ, Carman S. Multiple outbreaks of severe acute BVDV in North America occurring between 1993 and 1995 linked to the same BVDV2 strain. Vet Microbiol 2006 May 31;114(3-4):196–204.

[6]    Pellerin C, van den Hurk J, Lecomte J, Tijssen P. Identification of a new group of bovine viral diarrhea virus strains associated with severe outbreaks and high mortalities. Virology 1994;203:260–8.

[7]    Corapi WV, French TW, Dubovi EJ. Severe thrombocytopenia in young calves experimentally infected with noncytopathic bovine viral diarrhea virus. J Virol 1999;63:3934–43.

[8]    Fulton RW, Ridpath JF, Saliki JT, et al. Bovine viral diarrhea virus (BVDV) 1b: predominant BVDV subtype in calves with respiratory disease.Can J Vet Res 2002 Jul;66(3):181–90.

[9]    Kelling CL, Steffen DJ, Topliff CL, Eskridge KM, Donis RO, Higuchi DS. Comparative virulence of isolates of bovine viral diarrhea virus type II in experimentally inoculated six- to nine-month-old calves. Am J Vet Res 2002 Oct;63(10):1379–84.

[10] Ridpath JF, Neill JD, Peterhans E. Impact of variation in acute virulence of BVDV1 strains on design of better vaccine efficacy challenge models. Vaccine 2007 Nov 19;25(47):8058–66.

[11] Schoder G, Mostl K, Benetka V, Baumgartner W. Different outcome of intrauterine infection with bovine viral diarrhoea (BVD) virus in twin calves. Vet Rec 2004 Jan 10;154(2):52–3.

[12] Ellsworth MA, Fairbanks KK, Behan S, et al. Fetal protection following exposure to calves persistently infected with bovine viral diarrhea virus type 2 sixteen months after primary vaccination of the dams. Vet Ther 2006;7(3):295–304.

[13] Kirkland PD, Mackintosh SG, Moyle A. The outcome of widespread use of semen from a bull persistently infected with pestivirus. Vet Rec 1994;135:527–9.

[14] Meyling A, Jensen AM. Transmission of bovine virus diarrhoea virus (BVDV) by artificial insemination (AI) with semen from a persistently- infected bull. Vet Microbiol 1988;17:97–105.

[15] Grooms DL. Reproductive consequences of infection with bovine viral diarrhea virus. Vet Clin North Am Food Anim Pract 2004 Mar;20(1):5–19.

[16] Stokstad M, Loken T. Pestivirus in cattle: experimentally induced persistent infection in calves. J Vet Med B Infect Dis Vet Public Health 2002 Dec;49(10):494–501.

[17] Blanchard PC, Ridpath JF, Walker JB, Hietala SK. An outbreak of late-term abortions, premature births, and congenital deformities associated with a bovine viral diarrhea virus 1 subtype b that induces thrombocytopenia. J Vet Diagn Invest 2010; 22:128–31.

[18] Ross CE, Dubovi EJ, Donis RO. Herd problem of abortions and malformed calves attributed to bovine viral diarrhea. J Am Vet Med Assoc 1986;188:618–9.

[19] Brownlie J, Clarke MC. Experimental and spontaneous mucosal disease of cattle: a validation of Koch’s postulates in the definition of pathogenesis. Intervirology 1993;35:51–9.

[20] Saliki JT, Dubovi EJ. Laboratory diagnosis of bovine viral diarrhea virus infections. Vet Clin North Am Food Anim Pract 2004 Mar;20(1):69–83.

[21] Hill FI, Reichel MP, Tisdall DJ. Use of molecular and milk production information for the cost-effective diagnosis of bovine viral diarrhoea infection in New Zealand dairy cattle. Vet Microbiol 2010 Apr 21;142(1–2):87–9.

[22] Schefers J, Munoz-Zanzi C, Collins JE, Goyal SM, Ames TR. Serological evaluation of precolostral serum samples to detect Bovine viral diarrhea virus infections in large commercial dairy herds.J Vet Diagn Invest 2008 Sep;20(5):625–8.

[23] Amiridis GS, Billinis C, Papanikolaou T, Psychas V, Kanteres D. Postparturient outbreak of fatal bovine viral diarrhoea in imported pregnant heifers on a dairy farm in Greece. Vet Rec 2004 May 29;154(22):698–9.

[24] Brock KV, Grooms DL, Ridpath J, Bolin SR. Changes in levels of viremia in cattle persistently infected with bovine viral diarrhea virus. J Vet Diagn Invest 1998;10:22–6.

[25] Wittum TE, Grotelueschen DM, Brock KV, et al. Persistent bovine viral diarrhoea virus infection in US beef herds. Prev Vet Med 2001 Apr 13;49(1-2):83–94.

[26] Barber DM, Nettleton PF, Herring JA. Disease in a dairy herd associated with the introduction and spread of bovine virus diarrhoea virus. Vet Rec 1985;117:459–64.

[27] Paton DJ, Goodey R, Brockman S, Wood L. Evaluation of the quality and virological status of semen from bulls acutely infected with BVDV. Vet Rec 1989;124:63–4.

[28] Kirkland PD, Richards SG, Rothwell JT, Stanley DF. Replication of bovine viral diarrhoea virus in the bovine reproductive tract and excretion of virus in semen during acute and chronic infections. Vet Rec 1991;128:587–90.

[29] Revell SG, Chasey D, Drew TW, Edwards S. Some observations on the semen of bulls persistently infected with bovine virus diarrhoea virus. Vet Rec 1988 Jul 30;123(5):122–5.

[30] Howard TH, Bean B, Hillman R, Monke DR. Surveillance for persistent bovine viral diarrhea virus infection in four artificial insemination centers. J Am Vet Med Assoc 1990;196(12):1951–4.

[31] McGowan MR, Kirkland PD. Early reproductive loss due to bovine pestivirus infection. Br Vet J 1995;151:263–70.

[32] Kirkland PD, McGowan MR, Mackintosh SG, Moyle A. Insemination of cattle with semen from a bull transiently infected with pestivirus. Vet Rec 1997;140:124–7.

[33] Bielanski A, Dubuc C, Hare WCD. Failure to remove bovine diarrhea virus (BVDV) from bull semen by swim up and other separatory sperm techniques associated with in vitro fertilization.Reproduction in Domestic Animals 1992;27:303–6.

[34] Carman S, van Dreumel T, Ridpath J, et al. Severe acute bovine viral diarrhea in Ontario, 1993-1995. J Vet Diagn Invest 1998;10:27–35.

[35] Rodning SP, Givens MD, Marley MSD, Zhang Y, Riddell KP, Galik PK, Hathcock TL, Gard JA, Prevatt JW, Owsley WF.  Reproductive and economic impact following controlled introduction of cattle persistently infected with bovine viral diarrhea virus into a naïve group of heifers.  Theriogenology, 2012; 78(7):1508-16.



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