Материал: Bovine Viral Diarrhea Virus Diagnosis, Management, and Control

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INTRODUCTION

Pathogenesis is defined as “development of disease.” After infection with BVDV, clinical signs of disease are highly variable (Baker, 1995; Nettleton and Entrican, 1995) because of complex interactions between the etiologic agent and the infected host. Genotype (BVDV 1, BVDV 2—also now recognized as two distinct species of virus), biotype (noncytopathic [ncp], cytopathic [cp]), and virulence of individual BVDV strains are determinants for the outcome of infection on the virus side. Immune competence, immune status, and possibly other factors determine the outcome on the host’s side. Both host and viral factors vary widely causing the broad range of clinical signs and lesions.

For discussion on pathogenesis of BVDV infections, the following syndromes are distinguished: acute BVDV infection, transplacental/intrauterine infection, persistent infection, and mucosal disease (Figures 7.1 and 7.2). Susceptible cattle of all ages may contract a primary, transient BVDV infection termed acute BVDV infection irrespective of the clinical course (subclinical, severe acute, or protracted). The transient acute infection causes severe complications if the infected animal is pregnant. BVDV will cross the placenta and infect the fetus causing transplacental/interuterine infection. There are several outcomes of fetal infections; the most important is infection of the fetus leading to the birth of persistently infected (PI) calves. Persistent infection is the prerequisite for the development of fatal mucosal disease later in life. Finally, to close the circle of infection, animals with persistent infection and mucosal disease are the main sources of virus in outbreaks of acute BVDV infections (refer to Figure 7.2).

ACUTE INFECTION

Acute infections of cattle with BVDV develop when susceptible (seronegative), immune-competent cattle become infected with BVDV. Seropositive cattle, dependent on the levels of antibody titers, are usually not susceptible. The virus sources are often PI animals, while horizontal infection from acutely infected cattle is less likely (Traven et al., 1991; Niskanen et al., 2000). Iatrogenic transmission by contaminated instruments, vaccines, or semen has also been described (Coria and McClurkin, 1978; Barkema et al., 2001; Niskanen and Lindberg, 2003).

ROLE OF VIRAL AND HOST FACTORS IN

PATHOGENESIS

The most important determinant for the outcome of acute BVDV infection in susceptible animals is the virulence of the individual BVDV strain. Historically, acute BVDV infections have received little attention, because they were predominantly subclinical (Moennig and Plagemann, 1992; Hamers et al., 2001), and the unspecific signs of transient fever and listlessness did not incite high awareness. Until the early 1990s, there were only a few reports about acute BVDV infections causing severe clinical signs or with special affinity for the respiratory tract (Potgieter et al., 1984). Over the last 15 years, however, there has been an increasing interest in acute BVDV infections because of an increase in incidence of field cases of acute BVDV infection associated with severe clinical signs and mortality in all age groups (Perdrizet et al., 1987; Pritchard et al., 1989; Hibberd et al., 1993; David et al., 1994; Carman et al., 1998).

Highly virulent BVDV strains isolated from the outbreaks that had severe economic impact in North