Bovine Viruses (Lecture 4+5) Flashcards
Give 5 animals that can be a host for BVDV
Deer, rabbits, sheep, goats, pigs, (moose, llamas)
what 4 criteria must an animal meet to be a reservoir of BVDV
Must be susceptible to BVDV
must shed the virus
must maintain BVDV in the pop
must have contact with cattle
true or false, BVDV usually occurs in pigs with no clinical signs
true, if signs do show up its abortion, poor conception rates, still born
If a cow is infected with BVDV at 1month gestation, 2-4months, and 5-9months, what are the outcomes?
1mon= early embryonic death and return to estrus
2-4mon= calf with persistent infection and antibody negative, possible abortion or malformation
5-9mon= able to recognize virus as nonself and establish antibodies and be normal, or possible abortion or malformation (blindness tremors)
When is it most dangerous for a fetus to become infected with BVDV
60-120 days as they’ll become persistently infected and persistent shedders of the virus
list the pathogenesis of BVDV
- oronasal infection
- tonsils
- regional lymphnodes
- blood circ
- lymphoid tissue of gi tract and lungs
- thymus bone marrow and spleen
7 all other organs
BLV infects
b lymphocytes
infection of BLV leads clinically to
- asymptomatic stage
- persistent lymphocytosis
- leukemia/lymphoma
how does BLV transmit between animals
transmission of infected cells via
blood, colostrum, milk, in the uterus, breeding
BRDC is associated with
winter and the first 40 days on feed
what are the 4 important viruses associated with BRDC
- BHV1
- Bovine parainfluenza 3
- bovine respiratory syncytial virus
- BVDV
describe the epidemiology of BRSV and BPIV3
spread through direct contact between animals and aerosols, 70% of infections happen in calves under 2 years old and humans are passive vectors
describe the pathogenesis of BRSV and BPIV3
- virus enters through the resp tract
- damage to mucosa
- invade epithelial cells of the resp tract
- replicate in the resp tract
- infect more animals through hosts snot
which BRCV replicate well in the pulmonary alveolar macrophages
Bovine parainfluenza 3
what causes the damage in cattle infected with BRSV? The virus itself or the bodies response to it?
the immune system- pro-inflammatory genes are upregulated and extensive mast cell degeneration
true or false, BRSV is more pathogeneic in neonates compared to young calves (6 weeks)
false
When does the peak clinical signs of BRSV occur
4-6 days after infection
which is more severe BRSV or BPIV3
brsv
Ovine herpes virus 2 infection in bovine has ____ mortality and ____morbidity
high, low
what is the pathogenesis of BHV1
- nose to nose contact or aerosols
- enters epithelial and eventually nerve cells in the upper airway
- lysis of infected cells
- lysis of ciliated epithelium in the trachea limits primary innate defense
BHV1 is excreted via snot for how many days? when most infectious
10-17 days, peak at 4-6 days
how long will BHV-1 live in the environment for at 4deg, in frozen semen?
1 month, may survive more if in feed, in semen 1 yr
which group of rotaviruses are the major cause of rotavirl infection in domestic animals
A
BRV causes diarrhea in calves
1-2 weeks of age
BRSV and BPIV3 are alike in pathogenesis and epidemiology list at least 2 differences between them
bovine parainfluenza virus replicates well in the pulmonary alveolar macrophages leading to phagocytosis and prostaglandin production suppressed , BRSV does not
In BRSV infection its the host immune system that causes damage thorough mast cell degeneration
BRSV is more pathogenic in young claves instead of new borns
BPIV3 is generally less severe
what are the clinical outcomes of BHV infection
respiratory disease, infectious bovine rhinotracheitis, necrotic lesions on nasal and mucosal regions , abortions up to 100 days after infection, high morbidity, relatively low mortality
How would you clean the environment of BHV
BHV is enveloped so it will be susceptible to detergents and natural solvents like acetone, ether and chloroform
how does rotavirus cause diarrhea
rotavirus replicates in the enterocytes leading to osmotic diarrhea via altered metabolism of enterocyte membrane proteins. it also increases cell leakiness by increasing intracellular ca2+ disrupting the tight junctions
replicating virus produces a toxin which induces secretory diarrhea
