BOVINE VIRAL DIARRHEA • INTRODUCTION • Bovine viral diarrhea (BVD) is a common viral infection of cattle worldwide. • The viruses responsible for BVD are classified as pestiviruses, a group of viruses that includes BVDV type I and type II, Border disease virus of sheep and hog cholera virus. • Although BVD was first recognized as a disease of cattle 50 years ago, the genetics and epidemiology of BVD viruses have only been welldescribed in the last 10 years. • The name bovine viral diarrhea is misleading in that the disease does not specifically affect the digestive tract but rather has immune suppression as a hallmark sign. • Clinical disease associated with BVD virus infection is most common in young cattle (6–24 months old). • The clinical presentation can range from inapparent or subclinical infection to acute and severe enteric disease. • Mucosal disease (MD) is an uncommon but highly fatal form of BVD occurring in persistently infected (PI) cattle and can have an acute or chronic presentation. • MD is induced when PI cattle become superinfected with cytopathic BVDV • . The origin of the cytopathic BVDV causing superinfection is usually internal, resulting from a mutation of the resident persistent, noncytopathic BVDV. • In those cases, the cytopathic virus is antigenically similar to the resident noncytopathic virus and thus does not induce an immune response. • External origins for cytopathic BVDV include other cattle and modified-live virus vaccines. • Cattle that develop mucosal disease due to exposure to a cytopathic virus of external origin often produce antiviral antibody. • Prevalence of persistent infection usually is low, and many persistently infected cattle do not develop mucosal disease, regardless of exposure. • MD is a highly fatal disease complex characterized by profuse enteritis in association with typical mucosal lesions. • Aetiology – Causes • The causative agent of BVD is bovine virus diarrhoea virus (BVDV). Two genotypes have been identified: • BVDV-1, distributed worldwide • BVDV-2, identified mainly in North America and occasionally in Europe. The BVD virus exists as two different biotypes: the noncytopathic (ncp) and the cytopathic (cp) biotypes. • Only the ncp biotype can cause persistent infection of the bovine fetus. • Calves persistently infected with an ncp BVD virus will develop Mucosal Disease if the virus mutates spontaneously into the cp biotype or the calf is infected with a cp virus closely related to its own ncp BVDV strain. EPIDEMIOLOGY • 2 forms of disease bovine viral diarrhoea and mucosal disease were described as distinct diseases with epidemiological differences. oBVD -High morbidity (80-100%), low case fatality rate (0-20%). oMD - Low morbidity (5-10%), high case fatality rate(90-100%). • Both form of disease are manifestations of the antigenically similar virus. • It occurs only in immunotolerant animals ,which are persistently viraemic as a result of congenital infection with a non cytopathic strain in early foetal life and clinical disease in these animals appear between 6 and 24 months of age due to superinfection with a cytopathic strain. • In immunocompetent animals, post-natal natural infection does not produce the disease. Global prevalence of bovine viral diarrhoea • Source of infection 1. Nasal discharge 2. Saliva 3. Semen 4. Faeces 5. Urine 6. Milk 7. Contaminated food and water • Haematophagus flies , e.g. Stomoxys calcitrans and Haematopota pluvialis can transmit the virus. • Route of transmission Direct contact Transplacental transmission Transmission • There are two modes of BVD virus transmission: 1) acute or postnatal infections and 2) fetal infections. • In the acute, postnatal infection, BVD virus is transmitted in nasal secretions from an infected calf to others much like common cold viruses are transmitted between children. • In most cases, the infection results in fever and mild diarrhea. • The calf develops an immune response to the BVD virus and clears the virus without residual problems. Fortunately, acutely infected animals shed small amounts of virus and are inefficient transmitters of BVD viruses. Transmission of BVD from acutely infected calves is of greatest importance in crowded conditions such as feedlots and veal calf barns. • The second mode of transmission is from the cow to her fetus. Intrauterine infection • BVDV can cross placenta and infect foetus of all ages. Outcome of these infections largely dependent on the age of gestation when infection occurs. i. If infected in first month of pregnancy ,pregnancy is terminated either by abortion or resorption of the foetus by dam. ii. If the foetus infected in second to the sixth month of pregnancy , a variety of different syndromes are observed.Foetus may be still aborted or the foetus survives full term with resultant offspring born malformed , weak, dwarfed , stillborn or persistently infected. iii. If infection occurs around three to five months of pregnancy , virus affects the developing nervous system of the foetus. These calves may have eye abnormalities such as blindness and cataracts or bent up front legs. iv. If exposure to a noncytopathic virus occurs between 42 and 125 days of gestation , calves born are persistently infected. • Clinical signs of disease • It usually are seen 6–12 days after infection and last 1–3 days. • Transient leukopenia may be seen with onset of signs of disease. • Recovery is rapid and coincides with production of viral neutralizing antibody. • Gross lesions seldom are seen in cases of mild disease. • Lymphoid tissue is a primary target for replication of BVDV, which may lead to immunosuppression and enhanced severity of intercurrent infections. • Acute Infections: Non-Pregnant Cattle • In the naive, non-pregnant, immunocompetent animal, BVD is normally mild it is estimated that 70 to 90% of BVDV infections cause no obvious clinical signs. • When clinical disease does occur in these animals, morbidity is high amongst cattle of 6-12 months of age. • Following a 5-7 day incubation period, pyrexia and leukopenia is seen. • Viraemia arises on days 4-5 days post-infection, and continues until around day 15. • Clinical signs more commonly include depression, anorexia, occulo-nasal discharge, decreased milk production and oral lesions, with a rapid respiratory rate resembling pneumonia sometimes apparent • Acute Infections: Pregnant Animals • When acute BVDV infection occurs during pregnancy, the dam may show any of the clinical manifestations that are seen in non-pregnant animals. • BVDV is able to cross the placenta and infect the developing foetus and so there may be additional outcomes of infection that depend on the stage of gestation. • If infection becomes established at the time of insemination, conception rates may be reduced, and early embryonic death is increased when the virus is introduced at a slightly later stage • Foetal infection in the first trimester (50-100 days) may also result in death, although expulsion of the foetus often does not occur until several months later. • An additional effect of foetal infection before 120 days gestation is the birth of persistently infected (PI) calves. • Congenital defects can arise from transplacental infection between days 100 and 150. • Infection in the third trimester trimester (over 180-200 days) elicits a response from the fully-developed immune system, giving rise to normal but seropositive calves. • Persistent Infections • Foetal infection with a non-cytopathic BVDV virus before 120 days gestation may result in the birth of calves persistently infected with and tolerant to bovine viral diarrhoea virus. • Persistently infected animals can be identified at birth as being antigen-positive but seronegative. • 50% of persistently infected cattle die within the first year of life. Animals may be undersized and slow-growing, and are predisposed to other diseases. • Persistent infection with BVDV is the prerequisite for developing mucosal disease. • Mucosal disease is an invariably fatal condition of 6-18 monthold cattle[. • Disease follows a course of several days to weeks and intially presents as pyrexia, depression and weakness. • Anorexia leads to emaciation, and animals suffer watery, foulsmelling and sometimes bloody diarrhoea. • Dehydration ensues. As suggested by the name, lesions are localised to mucosal surfaces. • These include the oral mucosa, tongue, external nares, nasal cavities and conjunctiva, where large lesions cause excessive salivation, lacrimation, and oculo-nasal discharge. • The coronet and interdigital surface are also affected, causing the animal to become disinclined to walk and eventually recumbent. PATHOLOGICAL FINDINGS Multiple small erosions of BVDV/MDV Coalescing erosions/ulcers Comparison normal and necrotic Peyer's Patch Mucosal disease Ulcerated nose Mucosal disease Ulcerated tongue Photomicrograph of a spleen section showing necrosis of the red pulp (HE staining; magnification, ϫ 10); and Photomicrograph of a prescapular lymph node section showing lymphoid depletion and hemorrhagic areas (HE staining; magnification, ϫ 10) • Diagnosis • The genetic material of BVD may be detected by polymerase chain reaction (PCR), a sensitive and specific technique. • Viral proteins can be detected in tissues by BVD-specific antibodies tagged with a fluorescent dye (FA test) or an enzyme immunocytochemistry). • Indirect evidence of BVD infection is provided by serum neutralizing antibody (SN) titers in any unvaccinated cattle. • A blood test called the "BVD ELISA"" can used to identify PIs • Treatment • Acute BVDV infection is usually mild and does not require treatment, and treatment of more severe cases is symptomatic and supportive. • There is no known treatment for mucosal disease and cases are euthanased on welfare grounds; recovery is most unlikely. • Control Control of BVD is based on four equally important aspects: • Elimination of PI’s – Those PI’s found under Diagnosis should be isolated and culled • Biosecurity – Maintaining biosecurity involves avoiding introduction of animals into the herd and/or implementing stict isolation / quarantine of introductions until proven negative, and restricting access of livestock to external sources of infection. • Vaccination – To eliminate PI’s is not sufficient alone to keep out infection and prevent it from continuing to spread. Bovilis BVD is licensed for foetal protection. • Monitoring – This varies depending on the nature and risk status of your herd. Appropriate screening programmes can be discussed with your local veterinary practitioner.
