Brsv

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BRSV Etiology

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1) ss, -sense, enveloped RNA virus
2) Paramyxoviridae, genus pneumovirus
3) Structural proteins designated L, G, F, N, P, and M
4) Antigenic variation on the G protein points to existance of 2 subgroups of BRSV
5) High prevalence worldwide
6) labile; buddy to HRSV which is much more severe (people)

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BRSV surface proteins

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1) F and G
2) F fuses infected cells to uninfected cells to form giant cells (syncitia)
3) G has a viral receptor to attach to the host cell
4) both induce protective antibodies
5) Matrix protein attaches envelope to nucleocapsid
6) Nucleoprotein binds RNA
7) Phosphoprotein is a polymerase co-factor
8) Non-structural proteins help resist IFN alpha and beta

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BRSV Epidemiology

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1) cattle are natural host
2) worldwide distribution
3) High seroprevalence (up to 70%)
4) severe clinical signs mainly seen in calves
5) Vacc w/ inactivated vacc has led to exacerbated clinical signs
6) Morbidity = 60-80%
7) Mortality up to 20%
8) most commonly seen in fall and winter (virus sensitive to high temps; animals closer together in winter)
9) Transmission = direct contact
10) may persist in infected animals

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Transmission

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Virus containing aerosols

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Pathogenesis

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Aerosol exposure--> infection of ciliated and non-ciliated epithelia in respiratory tract--> cytopathic changes and necrosis in infected cells lead ot necrotizing bronchiolitis and bronchiolitis obliterans (occluded bronchiole lumen). Infx of alveolar epi leads to interstitial pneumonia--> dyspnea and forced expiration, characteristic for clinical BRSV infx--> Lung emphysema + possible edema
2) Host response plays an important role in BSRV pathogenesis (up-reg of cytokines, chemokines--> macrophages, lymphocytes, neutrophils)

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Clinical signs

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1) Incubation 2-5 days
2) Possible clinical pictures: a) asymptomatic, b) upper respiratory (cough, seromucoid nasal and ocular discharge), c) Lower respiratory (depression, anorexia, high fever, increased resp rate, abdominal dyspnea, open mouth breathing, subcu emphysema, abnormal bronchovesicular sounds, d) severe drop in milk production, e) secondary bacterial complications, f) NO ABORTION, g) clinical signs last 1-2 wks

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BRSV lesions: Macroscopic

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lungs not collapsing when thoracic cavity opened, broncho-interstitial pneumonia, consolidation in cranio-ventral lungs, emphysematous distention in caudo-dorsal lung, lymph node enlargement, suppurative bronchopneumonia possible (superinfection)

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BRSV lesions: Microscopic

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1) broncho-interstitial pneumonia
2) bronchiolitis
3) alveolar collapse
4) peribronchiolar infiltration
5) syncytia in bronchial lumen, bronchiolar epi, alveolar wall
6) emphysema and edema w/ rupture of alveolar walls in caudo-dorsal portion of lung

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Diagnosis

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1) clnical signs
2) gross and histologic lesions
3) FA
4) IHC
5) VI difficult (labile)
6) ACE
7) RT-PCR
8) serology on paired sera

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BRSV: Immune Response

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1) Passively acquired Ab don't prevent infection but reduce severity
2) CMI plays a role in recovery: CD8+ T-cells in the blood 1 wk after infection and in the lung 10 days post infection

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Prevention and Control

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1) Management
2) MLV (2 doses at 3 wk intervals)
3) Safe for pregnant cattle
4) Contamination of vaccines w/ BVDV has occurred
5) MLV vacc induce neutralizing and fusion-inhibiting Ab
6) induction of CD8+ T cells
7) MLV also stimulates CD4+ T cells
8) Immunity is short-lived-- need frequent boosters
9) Inactivated vaccines induce lower levels of VN Ab than MLV. Only stimulate CD4+

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BRSV Management

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1) separate dairy calves at birth from the dam
2) Try to limit exposure to adult cattle
3) Colostrum feeding (vacc dam in dry period
4) General recommendations to control respiratory disease-- housing, ventilation, etc.
5) Vaccination

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BRSV Treatment

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1) Antimicrobials-- secondary bacterial pneumonia
2) NSAID
3) corticosteroids
4) Antihistamines
5) Antivirals?
6) IBR-PI3 intranasal vaccination