Experimental Primary Postnatal Bovine Viral Diarrhea Viral Infections in Six-month-old Calves

Wilhelmsen, Catherine L.; Bolin, Steven R.; Ridpath, Julia F.; Cheville, N. F.; Kluge, John P.

doi:10.1177/030098589002700404

Cited by 50 publications

(28 citation statements)

References 19 publications

(2 reference statements)

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“…Moreover, gross and histological lesions in the alimentary tract, as observed especially in animals more than 6 months of age during the outbreaks of BVDV infection in Ontario in 1993 [7], and from where the 24515 BVDV isolate was isolated, were not a predominant finding in our 4 to 4.5 month-old calves, as previously noted for calves less than 6 months of age [7]. Heterogeneity in virulence of BVDV type 2 isolates and in clinical manifestations they produce [11,18,33], animal management and/or exposure to more hostile conditions (for instance, the presence of other pathogens) in their natural environment are factors that might be taken into account to explain clinical and pathological differences among BVDV isolates.…”

Section: Discussionsupporting

confidence: 63%

Clinical response and immunomodulation following experimental challenge of calves with type 2 noncytopathogenic bovine viral diarrhea virus

et al. 2000

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-Eight calves between 16 and 18 weeks of age that were seronegative to bovine viral diarrhea virus (BVDV), bovine leucosis virus and bovine immunodeficiency-like virus were infected (day 0) intranasally with the type 2 noncytopathogenic Canadian 24515 field isolate of BVDV in order to evaluate the effect of BVDV infection on certain clinical, hematological and immunological parameters. All virus-exposed animals developed fever and showed a significant (P < 0.05, 0.01 or 0.001) drop in the number of circulating leucocytes (neutrophils, lymphocytes and monocytes) by day 3 or 5 post-exposure (PE), which continued to the end of the experiment at day 12 PE. BVDV was consistently isolated from the peripheral blood buffy coat cells from day 5 PE, and also from selected tissues (spleen, thymus, mesenteric and submaxillary lymph nodes, small intestine, lungs and thyroid gland) that were collected at the time of euthanasia of the animals at day 12 PE. Diminished significant (P < 0.05) percentages of peripheral blood mononuclear cells (PBMCs) expressing at their surface either B7 and MHC II molecules were observed in virus-exposed calves at days 7, 10 and/or 12 PE, when compared to virus-nonexposed control calves (n = 5). However, no changes in the percentages of PBMCs expressing either B4 or MHC I molecules were observed throughout the experiment. Finally, a significant (P < 0.05 or 0.01) enhanced phagocytic capability of the PBMCs, as analyzed by flow cytometry, was observed in virus-exposed animals at days 3, 5, 7, 10 and 12 PE, when compared to control calves. These results demonstrated the virulence of the 24515 isolate of BVDV in 4 to 4.5 month-old calves, and suggest that type 2 BVDV infection in calves is associated with dysregulation of certain immunological functions. bovine viral diarrhea virus type 2 / clinical response / immunomodulation Vet. Res. 31 (2000) 215-227 215

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Section: Discussionsupporting

confidence: 63%

Clinical response and immunomodulation following experimental challenge of calves with type 2 noncytopathogenic bovine viral diarrhea virus

et al. 2000

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“…2 The occurrence of oral and nasal ulcers associated with acute BVDV infections has been reported. 39 We observed lymphoid depletion in the thymic cortex and/or Peyer's patches of some calves exposed to BVDV. It is highly likely that BVDV caused these lesions as they were not present in control calves not exposed to BVDV and viral antigen and high concentrations of virus were detected in these tissues of all calves exposed to BVDV.…”

Section: Discussionmentioning

confidence: 74%

“…Careful examination of the literature revealed only one previous immunohistochemical study of acute BVDV infection in calves. 39 In that study, small numbers of antigen-bearing cells were found in the gut-associated lymphoid tissue, bronchus-associated lymphoid tissue, and in the cortex, paracortex, and medulla of mesenteric lymph nodes; however, only sections of distal ileum, proximal colon, mesenteric lymph node, and lung were subjected to immunohistochemical examination.…”

Section: Discussionmentioning

confidence: 88%

Distribution of Virus and Viral Antigen in Specific Pathogen-free Calves Following Inoculation with Noncytopathic Bovine Viral Diarrhea Virus

1996

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Abstract. Gross and microscopic lesions and distribution of virus were studied in specific pathogen-free calves (SPF) 10 days post-inoculation (PI) with bovine viral diarrhea virus (BVDV). To investigate possible differences in tissue tropism between BVDV isolates, two clinically and antigenically different noncytopathic (ncp) isolates of BVDV were compared in the study. Four calves were exposed to noncytopathic (ncp) BVDV 7937, and four to ncp-BVDV 126. Two additional calves that were not exposed to virus served as controls. Both ncp-BVDV 7937 and ncp-BVDV 126 induced mild disease characterized by variable fever and anorexia. Lymphoid depletion was evident in Peyer's patch of four calves and the thymus of two calves exposed to BVDV. Differences between these isolates in the distribution of BVDV or BVDV antigen in tissues of inoculated calves were not found. High concentrations of BVDV and BVDV-specific antigen were detected in the thymus, Peyer's patch, and mesenteric lymph node of all exposed calves. BVDV was shown to infect cells of the bone marrow without causing microscopic lesions. High concentrations of BVDV were recovered from the bone marrow of all calves exposed to BVDV and BVDV-specific antigen was demonstrated at this location in six of these calves. Platelet counts of calves exposed to BVDV were significantly reduced during infection, which resulted in thrombocytopenia in one calf. Focal areas of necrosis were observed in squamous epithelial cells of the tonsil and ruminal mucosa. BVDV-specific antigen was found in and adjacent to these foci. Calves exposed to ncp-BVDV 7937 had slightly more severe clinical signs than those exposed to ncp-BVDV 126.

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“…According to their cytopathogenicity in cultured cells, BVDV strains fall into two biotypes: non-cytopathic (NCP) strains, which cause no cytopathic effect, and cytopathic (CP) strains, which induce apoptotic cell death (Zhang et al, 1996;Grummer et al, 1998;Brock, 2003). NCP strains are the most frequently isolated strains on farms; these strains give rise to mild infections with moderate symptoms, characterized by a short febrile period, transient leukopenia and lymphoid depletion caused by apoptosis, especially severe in lymphoid tissues of the intestinal tract, leading to a local immunosuppressive state (Wilhelmsen et al, 1990;Walz et al, 2001;Liebler-Tenorio et al, 2003a, b).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis in lymphoid tissues of calves inoculated with non-cytopathic bovine viral diarrhea virus genotype 1: activation of effector caspase-3 and role of macrophages

Pedrera

Gómez-Villamandos

Romero-Trevejo

et al. 2009

Journal of General Virology

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The mechanisms responsible for lymphocyte apoptosis in bovine viral diarrhoea have not yet been clarified. Previous work suggests that bovine viral diarrhea virus (BVDV) is only directly responsible for the destruction of a small number of lymphocytes. The aim of this study was to clarify, in vivo, the role of macrophages in lymphocyte destruction through indirect mechanisms linked to the biosynthetic activation of these immunocompetent cells on ileal Peyer's patches, as well as the distribution and quantification of apoptosis. Eight colostrum-deprived calves were inoculated intranasally with a non-cytopathic strain of BVDV genotype 1 and killed in batches of two at 3, 6, 9 and 14 days post-inoculation (p.i.). The progressive depletion of Peyer's patches was found to be due to massive lymphocyte apoptosis, with an increase in cleaved caspase-3 and TUNEL-positive cells. Lymphoid depletion was accompanied, from 3 days p.i., by a significant rise in macrophage numbers both in lymphoid follicles and in interfollicular areas. Some macrophages showed signs of viral infection, together with subcellular changes indicative of phagocyte activation and, in some cases, of secretory activity. However, the number of macrophages that showed positive immunostaining for tumour necrosis factor-a and interleukin-1a, cytokines with a proven ability to induce apoptosis, remained low throughout the experiment in lymphoid follicles, where most apoptotic cells were found. These results thus appear to rule out a major involvement of macrophages and macrophage-secreted chemical mediators in the apoptosis of follicular B lymphocytes during BVDV infection. INTRODUCTIONApoptosis is a form of cell death recognized as an essential mechanism in morphogenesis and homeostasis of organs and tissues. The main morphological changes during apoptosis (cellular shrinkage, membrane blebbing, chromatin condensation at the nuclear periphery and nuclear fragmentation into apoptotic bodies) are the final result of a complex biochemical cascade of events (Huppertz et al., 1999;Rathmell & Thompson, 2002). The apoptosis cascade includes an initiation stage with induction of the cascade by external and internal stimuli, an execution stage with activation of effector proteases called caspases (cysteine-containing aspartic acid-specific proteases) and the apoptotic death stage including nuclear and cellular collapse (Huppertz et al., 1999;Hengartner, 2000). In vitro studies have elucidated two regulatory apoptosis pathways (intrinsic and extrinsic). Both pathways induce apoptosis via activation of the effector caspase-3, which, once activated, irreversibly executes cell death, so that activation of caspase-3 can be considered a hallmark of apoptosis (Stennicke et al., 1998;Huppertz et al., 1999).Apoptosis may also be involved in the immunopathogenesis of some viral diseases. There are several potential mechanisms by which viruses activate the apoptotic pathway. Some viruses may do so through the direct action of a specific viral protein (Noteborn et al., 1994;Zh...

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Experimental Primary Postnatal Bovine Viral Diarrhea Viral Infections in Six-month-old Calves

Cited by 50 publications

References 19 publications

Clinical response and immunomodulation following experimental challenge of calves with type 2 noncytopathogenic bovine viral diarrhea virus

Clinical response and immunomodulation following experimental challenge of calves with type 2 noncytopathogenic bovine viral diarrhea virus

Distribution of Virus and Viral Antigen in Specific Pathogen-free Calves Following Inoculation with Noncytopathic Bovine Viral Diarrhea Virus

Apoptosis in lymphoid tissues of calves inoculated with non-cytopathic bovine viral diarrhea virus genotype 1: activation of effector caspase-3 and role of macrophages

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