Bovine Viral Diarrhoea (BVD)

Bovine Viral Diarrhoea (BVD) is also known as Mucosal disease.

Bovine Viral Diarrhoea (BVD) is most common disease in young cattle, characterized by fever, inappetence and diarrhoea.

Etiology

Bovine viral diarrhoea virus (BVDV) is a SS-RNA virus, genus Pestivirus in the family Flaviviridae and is closely related to classical swine fever and Ovine Border disease viruses.
There are two biotypes designated as non-cytopathic (NCP) and cytopathic (CP) depending on their effect on tissue culture cells.
The non cytopathic type is most common and most important.
It cross the placenta, invade the fetus and establishes persistent infection in the fetus.
The superinfection of persistent infected animal with cytopathic biotype virus causes mucosal disease.
It occurs usually at 6-24 months or older.

Epidemiology

The disease have been recorded in most of the countries.
Prevalence o infection is high, but the incidence of clinical mucosal disease is low.
Incidence of mucosal disease in herd is usually <5% upto 2 yrs of age.
Morbidity rate: 40%.
Mortality rate: 20 %.

Source of infection

Persistently infected immunotolerant seronegative animals.
The persistent infection develops when infection of foetus with a non-cytopathic strain occurs before 120 days of gestation.
These animals shed the virus in all secretion and excretions (nasal discharge, saliva, semen, faeces, urine, tears and milk).
Excretion of virus in the semen from both persistently and transiently infected bulls.

Transmission

Direct contact with an infected animal.
Nose to nose contact is effective method for transmission of virus from PI animal to susceptible animal.
Transplacental (in utero) transmission from dam to foetus.
Infection may be transmitted through natural service or artificial insemination.
Embryo transfer from persistently infected animals.
Inoculation of pregnant animal with live virus vaccine, their calves may develop disease.
Indirect transmission rarely occur through, farm workers, equipment and biting flies.

Pathogenesis

It depends on multiple interactive factors. Host factors which influence the clinical outcome of BVDV infection include:

Whether the host is immunocompetent or immunotolerant to the virus.
Age of the animal.
Immune status.
Presence of stressors.
Transplacental infection and gestational age of the fetus.
Infection at 0-45 days of pregnancy causes early embroyonic mortality.
Infection at 45-125 days of pregnancy results in persistent infection, the foetus become immunotolerant to the virus.
Infection at 125-175 days of pregnancy results in numerous congenital defects (cerebellar hypoplasia, optic neuritis, ocular defects, retinal atrophy, cataract and microphthalmia). During this period organogenesis of nervous system and development of immune system takes place, which results in generation of inflammatory reaction to the virus. which is responsible for congenital defect in foetus.
Infection at 180 days of gestation to term, the foetus become immuocompetent, eliminates the virus. At birth foetus has antibody to the virus, but virus free.

Clinical manifestation

Inapparent or subclinical infection form

The most frequent form of infection in cattle with high morbidity and low case fatality rate.
This occur in immunocompetent seronegative cattle.
Mild fever, leukopenia, inappetence and mild diarrhoea followed by rapid recovery.

Peracute bovine viral diarrhoea form

Severe form of enteric infection in immunocompetent seronegative animals.
Fever, respiratory distress, severe depression, anorexia, profuse watery diarrhoea, dysentery, conjunctivitis and agalactia.
Abortion in late gestation.
Morbidity rate: 40%, Mortality rate : 25%.

Acute mucosal form

It occur in persistently infected calves at 6-24 month age group.
Morbidity is low and case fatality rate is high (90%).
Fever, tachycardia and polypnoea and lacrimation.
Affected animals are depressed, anorexic, drool saliva, wetting hair around the mouth.
Discrete shallow erosions on inside the lips, gum, dental pad, hard palate, commissures of the mouth and tongue, coronitis ad lameness.
Cooked up appearance of entire oral cavity.
Profuse watery diarrhoea, the faeces is foul smelling which contain mucus or blood.
Straining during defecation.
Dehydration.
Death occurs after 5-7days of illness.

Thrombocytopenia and haemorrhagic form

Bloody diarrhoea, petechial and eccymotic haemorrhage.
Bleeding at venupuncture site.
Epistaxis.
Platelet count < 25000.

Chronic mucosal form

The animal become chronically ill.
There may be intermittent bouts of diarrhoea, inappetence, progressive emaciation, chronic bloat, rough hair coat, hoof deformities, chronic erosions on entire oral cavity and skin.

Unthrifty PI animals form

Calves are smaller body size.
Curly hair coat.
Stunted growth.
High incidence of respiratory disease.

Reproductive failure and neonatal form

Conception failure, increased embryonic mortality, fetal mummification, abortion, premature birth, congenital defect, birth of stunted weak calves.

Sample collection

Live animal-Whole blood, nasal swab, paired sera sample and semen.
The whole blood should be kept room temperature for 5 days for virus isolation before processing.
Dead animal-intestinal tissue, mesenteric lymph node, spleen, lymph node, lungs and liver.

Diagnosis

Based on clinical signs- oral lesions and diarrhoea.
Leukopenia.
Identification of the viral agent from persistently viraemic healthy animals resulting from congenital infection can be readily identified by isolation of non-cytopathic virus in cell cultures from blood or serum.
It is necessary to use an immune-labeling method to detect the growth of virus in the cultures.
Persistence of virus should be confirmed by resampling after an interval of at least 3 weeks.
These animals will usually have no or low levels of antibodies to BVDV.
Indirect immunoperoxidase staining technique is used to detect BVDV antigen in semen.
Identification of antigen in tissue sample-Immunohistochemical methods- immunoflourescence, immunoenzyme staining section in frozen tissue.
Monoclonal antigen capture ELISA.
Nucleic acid based detection methods.
Nucleic acid hybridization probe and RT-PCR.
Serum neutralization test and ELISA are used detect antibodies in serum.

Differential diagnosis

This disease must be differentiated from conditions in cattle causing diarrhoea, erosions/ulcerations of the gastrointestinal tract, reproductive failure, teratology, skin disease, laminitis, poor growth and respiratory tract disease such as vesicular diseases, ingestion of caustic substances, mucosal disease complex:

Clinical diagnosis is a complex problem.
Signs of the different syndromes may appear alone or in combination
Although many of the signs are similar to RP, the mortality in that disease is much higher
The oral lesions are very important, but their absence does not exclude BVD.

Prevention

Vaccination

Modified Live BVD vaccine: Not recommended for pregnant cattle or in stressed populations.
Killed BVD vaccine: This is safer for administration even to pregnant cattle. A booster dose after 3 to 4 weeks of initial vaccination.

Calves should be vaccinated at 4-6 months of age and again when they are 8-12 months old.
Calves less than three months of age generally not vaccinated because of potential vaccination failure associated with the presence of colostral immunity.
Heifers and cows should be revaccinated 30-60 days before breeding and booster dose one month before calving or in the last trimester.

Control

Primary goal of a control strategy is removal of persistently infected animals from a herd.
All cattle should be screened for the virus including calves born in the herd for nine months after initiation the programme.
Newly introduced animals should be tested for the disease before their introduction. Quarantine the newly purchased animals for 30 days.
Implementation of Strict managemental practices.
Cattle should not be allowed to mix with sheep and goats.
Periodical testing of bulls used for artificial insemination.