2019, Issue 3 Ruminant Immunology Flashcards
Vaccinating calves in face of maternal ab:
List the broad conclusions from studies that reported initial specific maternal antibody titers against important respiratory and GI pathogens:
Initial specific maternal ab titers vary greatly, depend on factors, such as:
-farm-level practices, ie dam vx and colostrum mgmt
-individual calf level factors, ie dystocia & vigor
-study-level factors, ie geography, inclusion criteria & study design
Vaccinating calves in face of maternal ab:
The time period that maternal antibodies are present in a calf’s circulation is variable and dep on:
specific pathogen
initial dose of abies ingested and absorbed
degree to which dz challenge accelerates catbolism of abs
Vaccinating calves in face of maternal ab:
How long are the half-lives of various maternal ab against common viral pathogens?
-unknown in the field
varies:
BRSV: 5-6.5 months
BHV1: 2-10 months
PIV3: 5-6 months
BVDV 3-7.5 months
Vaccinating calves in face of maternal ab:
The exact ab titer that is protective against a particular disease depends on:
-pathogen
-degree of challenge
-other host, pathogen & environmental factors that influence epidemiologic triad
Vaccinating calves in face of maternal ab:
In experimental studies, why is vaccination in the face of maternal antibodies unlikely efficacious?
Because they are unlikely to exhibit seroconversion (4-fold increase in antibody titer)
Vaccinating calves in face of maternal ab:
What is the effect of vaccination on cell mediated immune response in calves IFOMA?
More research required
– current research says calves may be capable of generating an cell mediated immune response
Vaccinating calves in face of maternal ab:
Are vaccines efficacious at preventing against pathogen challenge in FOMA?
**translations of vaccine efficacy against pathogen challenge in experimental models to vaccine effectiveness for disease protection against natural exposure remains to be clearly demonstrated
Vaccinating calves in face of maternal ab:
If calves are suspected or confirmed failure of TPI, at what age are they likely to respond to parenteral vaccination?
As early as the first week of life
Vaccinating calves in face of maternal ab:
What is a hypothesis to support vaccination in the face of maternal antibodies?
Extend the period of time when antibodies are present by vaccinating in FOMA may be beneficial for clinical protection
**hypothesis not sufficiently tested
Vaccinating calves in face of maternal ab:
Can intranasal vaccination produce a protective immune response in seroneg/seropos calves?
-can induce relevent protection
-short duration
-variable magnitude
-viral shedding may be reduced
-immunologic priming can occur regardless of serologic status at time of intranasal vaccination
Vaccinating calves in face of maternal ab:
Is intranasal or subcutaneous vaccination in FOMA superior?
IN vaccination may be more effective than parenteral vaccination
**responses may be variable & dz protection not complete
Vaccinating calves in face of maternal ab:
intra-nasal vaccination in the FOMA, what are the caveats?
clinical protection is inconsistent
relatively short lived
Vaccinating calves in face of maternal ab:
What are the potential negative effects of vaccinating in the FOMA?
-likely to inhibit seroconversion
-+/- negative effects on cell mediated immunity, pathogen shedding & risk of clinical disease
Vaccinating calves in face of maternal ab:
what are the potential beneficial effects of vaccinating in the FOMA?
-may prolong the presence of antibodies or result in immunologic priming
-can reduce clinical symptoms after experimental pathogen challenge
Vaccinating calves in face of maternal ab:
When would herds benefit from earlier vaccination in calves?
-inadequate pre-calving vaccination
-poor colostrum management
Vaccinating calves in face of maternal ab:
When would intranasal vaccination be an advisable strategy?
-in herds where transfer of passive immunity is good– to circumvent interference by maternal antibodies and provide short-term disease sparing effects (with mucosal immunity)
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
define vaccine efficacy
the percent reduction in disease incidence and pathology in a vaccinated group compared with an unvaccinated group
or
if it has biological activity and stimulates an active immune response agents in the vaccine
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
define vaccine efficiency
ability of a vaccine to improve health outcomes in the production setting
-ie: clinical illness, death loss, improvement in weight gain * clear economic advantage
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
what are factors that compromise safety of a vaccine?
-improper time of administration (ie wildtype virus and concurrent MLV vx admin)
-improper storage and/or handling of vaccine
-disrupted physiology and immunologic status of cattle being vaccinated
-manufacturing errors that may compromise safety of a particular lot group of vaccine
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
What are cellular components that make up endotoxins?
lipopolysaccharide (LPS) cell membrane
peptidoglycans
lipoproteins
other bact components
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
define endotoxin
major components of outer cell membrane of gram neg bacteria
-released from bact cell walls when cell is killed or lysed
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
define exotoxin
diffusible proteins that are primarily produced & actively released from bact during log-phase growth
-heat-liable, highly antigenic proteins
-released when cell walls are lysed
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
What part of bacteria makes a vaccine toxoid?
exotoxins– chemically or heat inactivated
Vaccination management of beef cattle, delayed vaccination & endotoxin stacking:
what are bact exotoxins classified as (according to mode of action)
Type I: membrane acting toxins that bind surface receptors & stimulate transmembrane signals
Type II: membrane damaging toxins that directly affect cell membranes from forming pores or disrupting the lipid bilayers of cell membranes
Type III: toxins that modify an intracellular target molecule by translocating an active enzymatic component into the cell