Changes

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.

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.

1.2.3 Persistent Infection- Immunotolerant Animals.

====Persistent Infections====

 

Immunotolerant Animals.

Infection of the foetus with non-cytopathic virus before 120 days gestation may result in the birth of immunotolerant and persistently infected (PI) calves. The immune system, although competent, recognises the antigen as “self” rather than “foreign” and no response is mounted. The calf therefore develops a tolerant state to the virus which persists into neonatal life. Although no antibodies are produced against the original, transplacental-infecting strain, heterologous BVDV strains can elicit a response in PI cattle. Therefore, these may prove seropositive if tested (Bolin, 1985).

Infection of the foetus with non-cytopathic virus before 120 days gestation may result in the birth of immunotolerant and persistently infected (PI) calves. The immune system, although competent, recognises the antigen as “self” rather than “foreign” and no response is mounted. The calf therefore develops a tolerant state to the virus which persists into neonatal life. Although no antibodies are produced against the original, transplacental-infecting strain, heterologous BVDV strains can elicit a response in PI cattle. Therefore, these may prove seropositive if tested (Bolin, 1985).

PI cattle are predisposed to other diseases, and have a reduced survival rate (Houe, 1993) with 50% dying within their first year (Duffell and Harkness, 1985). This increased susceptibility may be due to BVDV-associated immunosupression, considered in section 1.2.5. Animals may be undersized and slow-growing, and persistent infection is the prerequisite for mucosal disease.

PI cattle are predisposed to other diseases, and have a reduced survival rate (Houe, 1993) with 50% dying within their first year (Duffell and Harkness, 1985). This increased susceptibility may be due to BVDV-associated immunosupression, considered in section 1.2.5. Animals may be undersized and slow-growing, and persistent infection is the prerequisite for mucosal disease.

1.2.4 Mucosal Disease

====Mucosal Disease====

Mucosal disease (MD) primarily affects 6-18 month-old cattle and is invariably fatal (Brownlie et. al, 2000). Baker (1995) summarises the characterising symptoms, which last several days to weeks. These include pyrexia, depression and weakness. Anorexia gives emaciation and dehydration. Foul-smelling, sometimes bloody, watery diarrhoea develops 2-3 days after the onset of disease. Animals are often euthanised for humane reasons.  

Mucosal disease (MD) primarily affects 6-18 month-old cattle and is invariably fatal (Brownlie et. al, 2000). Baker (1995) summarises the characterising symptoms, which last several days to weeks. These include pyrexia, depression and weakness. Anorexia gives emaciation and dehydration. Foul-smelling, sometimes bloody, watery diarrhoea develops 2-3 days after the onset of disease. Animals are often euthanised for humane reasons.  

As suggested by the name, lesions develop on mucosal surfaces including the oral mucosa, tongue, external nares and the buccal and nasal cavities (Brownlie, 1985). Coalition of lesions gives larger areas of necrosis (Baker 1995), leading to excessive salivation, lacrimation, and ocular discharge.  The coronet and interdigital surface are also affected, causing the animal to become disinclined to walk and eventually recumbent (Brownlie, 1985). Lesions of the abomasum and small intestine are seen on post-mortem examination, and congestion of the large intestine mucosa results in a stripy, thickened appearance (Brownlie, 1985). Figure 1.5 shows examples of tongue and small intestine lesions.

As suggested by the name, lesions develop on mucosal surfaces including the oral mucosa, tongue, external nares and the buccal and nasal cavities (Brownlie, 1985). Coalition of lesions gives larger areas of necrosis (Baker 1995), leading to excessive salivation, lacrimation, and ocular discharge.  The coronet and interdigital surface are also affected, causing the animal to become disinclined to walk and eventually recumbent (Brownlie, 1985). Lesions of the abomasum and small intestine are seen on post-mortem examination, and congestion of the large intestine mucosa results in a stripy, thickened appearance (Brownlie, 1985). Figure 1.5 shows examples of tongue and small intestine lesions.

MD occurs when animals persistently infected with noncytopathic BVDV are superinfected with an antigenically similar cytopathic strain. Cytopathic virus arises from the persistent noncytopathic virus by mutation (see 1.1.4), and may then be transmitted to cause MD in animals PI with the same noncytopathic strain. Immunotolerance induced by the noncytopathic strain prevents superinfecting virus being recognised by the immune system; the biotypes are “homologous” to the immunotolerance (Brownlie, 1990). “Heterologous” superinfection with a non-related cytopathic biotype causes an antibody response and mucosal disease does not usually occur.

MD occurs when animals persistently infected with noncytopathic BVDV are superinfected with an antigenically similar cytopathic strain. Cytopathic virus arises from the persistent noncytopathic virus by mutation (see 1.1.4), and may then be transmitted to cause MD in animals PI with the same noncytopathic strain. Immunotolerance induced by the noncytopathic strain prevents superinfecting virus being recognised by the immune system; the biotypes are “homologous” to the immunotolerance (Brownlie, 1990). “Heterologous” superinfection with a non-related cytopathic biotype causes an antibody response and mucosal disease does not usually occur.

===Laboratory Tests===

===Laboratory Tests===