26/12/2020
1️⃣0️⃣ Bovine Viral Diarrhoea (BVD)
Bovine Virus Diarrhoea virus (BVDV) is a member of pestivirus in the family Flaviviridae. There are two genotypes (BVDV-1 and BVDV-2) according to their anti-genetic and genetic differences and also there are two biotypes (Donis, 1995), which are Cytopathogenic (CP) and non- cytopathogenic (NCP). (Fig: 1).
The NCP biotype is most commonly isolated in the field; and it replicates in cultured cells without inducing of cell death, and can cross the placenta to set up a persistent and long-standing infection. In contrast, the CP biotype, which arises through mutation of NCP virus (Donis, 1995), induces apoptotic cell death in cultured cells (Zhang et al., 1996) and is unable to establish persistent foetal infections (Brownlie et . al., 1989).
Bovine Virus Diarrhoea virus (BVDV) is the most common viral disease of cattle major reproductive pathogen in the cattle populations in the world-wide (Paton et al., 1998; Houe, 1999). It caused significant negative economic impact (Duffell et al., 1986) Infection of the bull can drop down in semen quality and the isolation of infectious virus in the ej*****te, while infection in the cow leads to poor conception rates, abortions and congenital defects. BVDV reduce the animal’s resistance to other respiratory and enteric pathogens (Ex: Pneumonia). The prevalence of BVDV is primarily due to the efficiency with which the virus crosses the placenta of susceptible females. Calves that survive infection during the first trimester of pregnancy are born with a persistent and long-standing infection. These persistently infected (PI) animals represent between 1.0% and 2.0% of the cattle population and continuously shed infectious virus.
1️✅ BVDV infection and male fertility:
Transmission of the BVDV can be cryo-preserved semen and the effect of distributing BVDV contaminated semen so should be ensured semen from the BVD virus-free (Schlafer et al., 1990). Most cell types within the bull’s reproductive tract are permissive to BVDV but infection of spermatozoa has not been demonstrated conclusively. High viral titres can be isolated from the accessory glands of the reproductive track, te**es and semen of infecteds bulls, sometimes in association with testicular lesions (Barlow et al., 1986). But PI bulls can sire clinically normal offspring. Acute infections are also accompanied by BVDV contaminated ej*****tes that may or may not be associated with a transient dip in semen quality (Kirkland et al., 1997).
✅ Ovarian function following BVDV infection
All of major organs within the female reproductive tract are permissive to the BVDV and the distribution of virus is similar in animals carrying persistent infections (PI).
Virus can be recovered from cells within the oviduct, endometrium, myometrium, as well as placental membranes of the cow (Fredriksen et al., 1991.) within the o***y the virus has been located in luteal,interstitial, granulosa and thecal cells, not only that follicular fluid also (Booth et al., 1995).
Acute NCP infections also alter ovarian function. Viraemia during the pre-ovulatory period reduces the follicle growth rate in the mono-ovulatory cow (Grooms et al., 1998.) but not the super-ovulated cow (Kafi et al., 1997). However, the number of ovulations and the quality of embryos recovered following super-ovulation is dramatically reduced (Kafi et al., 1997).
BVDV infection of the o***y may be prolonged how the BVDV compromises ovarian function is uncertain but three possible mechanisms suggest themselves. Infected pituitary gonadotrophs may be unable to provide adequate gonadotrophic support (Anderson et al., 1987), the suppressed plasma oestradiol levels seen during infection may be sufficient to silence oestrus and prevent ovulation (Fray et al., 1999)., while the leucopenia that accompanies acute infections (Bolin et al., 1985)., may be reflected by a deficient ovarian leucocyte population, these cells being vital for normal folliculardynamics (Adashi, 1990).
✅ Infection during pregnancy and foetal pathology
The foetus is vulnerable to infection when permissible animals come into contact with the BVDV. In broad terms, transplacental infections are particularly very harmful during the first 180 days of pregnancy period and may result in the foetal death, congenital deformity and the birth of PI calves. The BVDV infection of the dam during the pre-implantation period may result in a high incidence of embryo or foetal mortality (Larsson et al., 1994.) while those infections which occur between implantation and the end of the fourth month of pregnancy approximately day 40 to 125.
Which are characterised by;
Foetal death,
Abortion,
Mummification,
Abortion rates as high,
Return to oestrus,
Birth defects of the nervous system and eyes,
Weak/premature calves,
Live persistently-infected calves.
Foetal infections are during mid-gestation 125–180 days, high incidence of congenital abnormality, which may approach 100% following experimental infections. These abnormalities present as alopecia, pulmonary hypoplasia, re****ed growth, thymic aplasia, ataxia, cerebellar hypoplasia and other CNS defects and a range of ocular lesions (Baker, 1995.) Transplacental infections during late gestation are not associated with a significant level of congenital deformity. During this period most infections are followed by the birth of a clinically normal calf with high levels of pre-colostral antibodies. However some late stage abortions and abnormalities have been reported (Moening 1995.) and field level data indicate that infections late in gestation of the cow can compromise the calves’ immune system (Alenius, S., 1999).
✅ Young Calf BVD
Strict biosecurity measures and a robust herd health plan are essential to prevent introduction of BVDV into a herd once it has been eliminated. Effective bio-containment measures are essential on those farms with active infection to reduce the costs of BVD and to, eventually, eradicate BVDV from the herd.
✅Transmission
The virus is contracted from contact with infected cattle; it is also readily sexually transmitted. Those animals infected as adults usually recover from the virus and become immune. BVDV is however readily transmitted across the placenta from cow to calf. Animals that are infected in-utero are born permanently (persistently) infected with the virus. These animals excrete large volumes of virus all of their lives and are the main route of infections in other animals. Identifying and removing these animals is the mainstay of eradication schemes for the BVDV. It needs only one persistently infected animal to be introduced into a susceptible herd to cause very significant financial losses
✅ Clinical signs
Cattle exposed to BVD virus may show few clinical signs, producing protective antibodies within three to four weeks. In some situations, BVD virus infection may temporarily lower immunity to other infectious diseases exacerbating these clinical infections particularly in young calves. Despite its name diarrhoea is not often seen. The low head carriage and wide stance. This calf was also very unsteady on its feet.
BVD virus infection may temporarily lower immunity to other infectious diseases such as
1️⃣ Salmonellosis,
2️⃣ Respiratory infections (Chronic pneumonia),
3️⃣ Coccidiosis,
4️⃣ Mucosal disease.
✅ Mucosal disease
Mucosal disease occurs when persistently infected (IP) animals become superinfected with cytopathic BVD virus (changes in the BVD virus within the PI animal). Mucosal disease is most commonly seen in 6 to 12 month-old calves, and is usually seen as sudden onset depression, fever and anorexia, with excess salivation. Ulcers appear in the mouth and on the muzzle. There are purulent discharges from the eyes and nostrils. There is profuse diarrhoea with shreds of gut mucosa/blood present during the terminal stages. There is rapid weight loss followed by death within 5-10 days.
✅ Diagnosis
Exposure to the virus can be diagnosed by serology. Active infection (either acute or PI) can be diagnosed by PCR based tests. Many different types of samples can be used for BVDV testing including blood, hair plucks and skin biopsies
Persistent infection - Such cattle have often been treated several times for digestive and respiratory infections. PI animals should be disposed of immediately as they act as a source of BVD infection. It is not possible to clear the virus from these animals. Mucosal disease in PI animals is always fatal.
✅ Facter affecting for economic losses by BVDV
Production losses
Deaths
Effect on fertility
Increased replacement rate
Reduced market value of stock
Veterinary and treatment costs
Effects on concurrent disease processes
Increased labour costs and management time
✅ General principles of disease control
1️⃣ Prevent the introduction of new diseases onto an operation from outside sources (Biosecurity)
Reduce the movement of infectious diseases on the farm once biosecurity has been breached (Biocontainment)
✅ Key Principles of Biosecurity
Keep a closed herd
If buying in cattle - only purchase from BVDV accredited herds
If buying in cattle from non BVDV accredited herd blood test and isolate before introducing to herd
Prevent contact with cattle on neighbouring farms
Key Principles of Biocontainment which will lead to eradication
Screen all of all animals
Vaccination - all heifers and cows after screening
Culling - all PI animals immediately
2️⃣ Vaccination
✅ Reference:
1️⃣ Duffell, S.J., Sharp, M.W., Bates, D., 1986. Financial loss resulting from BVD-MD infections in a dairy herd. Vet. Rec. 118, 38–39.
2️⃣ EU Thematic network on control of bovine viral diarrhoea virus (BVDV). BVDV Control QLRT – 2001-01573 Position paper.
3️⃣ Houe, Hans, A. Lindberg, and V. Moennig. "Test strategies in bovine viral diarrhea virus control and eradication campaigns in Europe." Journal of Veterinary Diagnostic Investigation 18.5 (2006): 427-436.
4️⃣ Lanyon SR, Hill FI, Reichel MP,et al. Bovine viral diarrhoea: Pathogenesis and diagnosis. Vet J. 2014;199(2):201–9.
5️⃣ Lanyon, S. R., Hill, F. I., Reichel, M. P., & Brownlie, J. (2014). Bovine viral diarrhoea: pathogenesis and diagnosis. The Veterinary Journal, 199(2), 201-209.
6️⃣ Lanyon, S.R., Hill, F.I., Reichel, M.P. and Brownlie, J., 2014. Bovine viral diarrhoea: pathogenesis and diagnosis. The Veterinary Journal, 199(2), pp.201-209.
7️⃣ Lanyon, Sasha R., et al. "Bovine viral diarrhoea: pathogenesis and diagnosis." The Veterinary Journal 199.2 (2014): 201-209.
8️⃣ Lindberg A, Brownlie J, Gunn GJ, et al. The control of bovine viral diarrhoea virus in Europe: today and in the future. Rev Sci Tech. 2006;25(3):961-79.
9️⃣ Lindberg, Ann LE, and Stefan Alenius. "Principles for eradication of bovine viral diarrhoea virus (BVDV) infections in cattle populations." Veterinary microbiology 64.2-3 (1999): 197-222.
1️⃣0️⃣Peterhans E, Bachofen C, Stalder H, et al. Cytopathic bovine viral diarrhea viruses (BVDV): emerging pestiviruses doomed to extinction. Vet Res. 2010;41(6):44.
1️⃣1️⃣ Saatkamp HW, Beek PMJC, Moen AR, et al. Financial-economic analysis of Bovine Viral Diarrhoea Virus control in Dutch dairy herds. Proceedings of the 12th International Symposium on Veterinary Epidemiology and Economics, Durban, South Africa, 2009.
