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Large Animal Disease > Equine Vaccinology > Flashcards

Equine Vaccinology Flashcards

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1
Q

What is passive immunization

A

transfer of preformed antibodies

eg: colostral antibodies, tetanus and botulinum antitoxins/antisera, rattlesnake antivenin, etc

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2
Q

What are examples of passive immunization

A

colostral antibodies, tetanus and botulinum antitoxins/antisera, rattlesnake antivenin, etc

preformed antibodies

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3
Q

What is the goal of passive immunization

A

to provide immediate protection to individuals that are lacking active immunity

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4
Q

What is the goal of active immunization

A

to elicit protective immunity and immunological memory resulting in successful elimination of the pathogen

ie vaccination and infection

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5
Q

What are the goals of vaccination

A

Animal Health
-prevent and control infectious diseases
-improve animal welfare

Public Health
-decrease cost of animal production
-prevent incidence of zoonotic disease
-reduce use of other drug and resides

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6
Q

What might influence your decision to vaccinate an animal

A

Risk of exposure
Cost
efficacy*
overall health
regulations
pregnancy
zoonotic risk
adverse effects
pregnancy
population factors
severity of disease

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7
Q

T/F: the development of an immune response after vaccination means that a state of immunity has been achieved

A

False- vaccines must induce the appropriate immune response at the right site

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8
Q

What should you consider with state of immunity to an infection

A

What do we want?
Antibodies or cellular response?
Immunologic memory?
How do we accomplish this?
What branch of immune system?

*Varies between disease agents

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9
Q

What is the pathogenesis of Equine Influenza

A

1) Inhalation of infectious virus
2) Infection and replication in respiratory epithelial cells
3) Following release- virus spreads throughout the respiratory tract (fairly localized infection )

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10
Q

What is the immunity of equine influenza

A

Mucosal IgA - protective immunity (produced at site of infection)

Systemic IgG is important for resistant and recovery from infection

CTL: clearance of virus- do not protect against infection

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11
Q

T/F: CTL response is important for equine influenza immunity

A

False- it is important for the clearance of the virus but does not protect against infection

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12
Q

What is the primary factor causing protective immunity against Equine Influenza

A

Mucosal IgA

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13
Q

What is the function of Systemic IgG in equine influenza

A

primarily resistance and recovery from infection

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14
Q

What immune response should the ideal equine flu vaccine induce? *

A

Should induce a long-lasting mucosal (IgA) and systemic antibody response (Ig) to protect against infection and reduce virus shedding

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15
Q

What is the pathogenesis of Equine-Herpesvirus-1

A

1) Inhalation of infectious virus
2) Infection and replication in respiratory cells and infection of leukocytes
3) Travel to regional lymph nodes and second round of virus replication occurs
4) Cell associated viremia
5) Infiltrate uterus and CNS- leukocyte infiltration, thrombosis, tissue destruction causing abortion and EHM

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16
Q

Immunity to equine herpesvirus-1

A

Mucosal IgA: protective immunity if strong response

Systemic IgG: likely no effect, some reduction of virus shedding?

CTL: Clearance of virus- protection of viremia associated sequelae

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17
Q

What part of the immunity to equine herpesvirus is important in Clearance of virus- protection of viremia associated sequelae

A

CTL

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18
Q

What immune response should the ideal EHV-1 vaccine induce?

A

Should induce a strong and long lasting mucosal (and systemic) antibody responses as well as a cytotoxic T- cell response

to protect against infection, reduce virus shedding, and prevent complications

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19
Q

T/F: the type of protective immune response can vary between disease agents

A

True

If extracellular (antibodies, complement)

if Intracellular: CTLs, activated macrophages

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20
Q

Rhodococcus equi or HerpesVirus is intracellular how might the immune response target intracellular pathogens

A

CTLs, activated macrophages

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21
Q

Rabies virus prior to neuroinvasion is extracellular, how might immune response target extracellular pathogens

A

Antibodies, complement

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22
Q

CD8+ T cells are

A

Cytotoxic T cells (CTL)

Role: to kill other cells in the body (e.g virus infected cells)

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23
Q

CD4+ T cells are

A

T helper cells

Role: to assist other effector cells to fight off pathogens

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24
Q

CD4+ T cells are Thelper cells, what are the different types?

A

Th1: inflammatory and cytotoxic response (y-IFN, IL-12)

Th2: humoral and allergic response (IL-4/5/6 and 10)

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25
cells that express immunoglobulin molecules on their surface, which function as antigen receptors
B cells
26
What is the Thelper cell that is primarily active during inflammatory and cytotoxic response
Th1: y-IFN, IL-12
27
What is the Thelper cell that is primarily active during humoral and allergic response
Th2: IL-4,5,6,10
28
In vaccine strategy, what may influence whether a Th1 or Th2 type of response will predominate
adjuvant immunization route cytokines present during antigen presentation
29
What T helper cell is predominately present during delayed, type hypersensitivity, cytotoxicity, T- cell mediated autoimmunity, and graft rejection
Th1
30
T/F: if the appropriate immune response to a pathogen is to be induced by vaccination, the vaccine must induce the appropriate T-helper response Inducing the wrong T-helper response may even be detrimental
True
31
In the horse, what antibody is important for rapid initial response to antigen stimulation
IgM IgG increases after IgM but is produced in larger amounts and with a higher affinity for antigen
32
Are IgM or IgG responses longer lasting
IgG
33
What is the difference between MHC class I and MHC class II antigen presentation
MHC I: located on virtually all nucleated cells in the body Endogenous pathway MHC II: present on antigen presenting cells (Professional APCs: dendritic cells, macrophages, B cells) Exogenous pathway each pathway activates different cells
34
MHC II is present on what cells
(Professional APCs: dendritic cells, macrophages, B cells)
35
MHC class II presents to what cells through the exogenous pathway
T-helper cells (CD4)
36
MHC class I presents to what cells through the endogenous pathway
Cytotoxic T cells (CD8)
37
If you give an intramuscular killed flu vaccine, what is stimulated
Enters the body as exogenous antigen CD4+ Th stimulate the humoral response due to presentation on MHC class II by APC (dendritic cells)
38
If you give an intranasal modified live flu vaccine, what is stimulated
Enters body as endogenous and exogenous antigen target cell (airway epithelial) presents MHC I to CD8+ CTL: virus infected cells are destroyed
39
What is the goal of mucosal vaccines
to induce a secretory and systemic immune response that closely resembles the immune response after infection
40
T/F: Mucosal immunity equals systemic immunity
False- mucosal immune system can function independently mucosal surfaces represent the entry site for the vast majority of equine infectious pathogens
41
What are the 4 types of vaccines
1) Inactivated 2) Modified Live 3) Recombinant 4) DNA/RNA
42
What is the first vaccine
Edward Jenenr discovered the small pox vaccine using Cowpox virus
43
Why does natural Equine Influenza Virus infection trigger a longer immunity than an inactivated EIV vaccine
Because it induces high levels of IgA in nasal mucosal secretions wheras vaccination using a killed vaccine induces no IgA response plus there is difference in IgG subisotypes
44
T/F: T cells respond directly to antigens
False they recognized processed antigens that are associated with an MHC molecule present on the surface of either infected cells or on the surface of specialized antigen presenting cells (APCs)
45
antigen that is produced inside of the cells, couples with MHC I and presented on cell surface for CD8
Endogenous antigen
46
antigen that is produced outside of the cell and is taken up into the cell by endocytosis or phagocytosis. APCs then degrade ingested antigen into peptide fragment and coupled with MHC II for CD4 recognition
Exogenous antigen
47
CTLs can recongize
any cell that is infected with an intracellular pathogen and is displacing components of that pathogen on its surface bound to an MHC I molecule
48
T-helper cells recognize
antigen ONLY when they are displayed in association with MHC II molecule on the surface of an APC
49
Inactivated vaccines contain antigen meaning that they
enter the body as exogenous antigen, which is phagocytosed by APCs and presented by MHC II molecules and typically results in humoral immune response unlikely to induce a CTL response that is essential for defense against some viral infections
50
Toxoid vaccine is
inactivated toxin (ie tetanus toxoid)
51
How are inactivated vaccines made
1) Chemical treatment (formaldehyde) and heat inactivated 2) Adjuvant addition (aluminum hydroxyphosphate gell, MF59, carbomer, TLR agonsits)
52
What are the downsides to inactivated vaccines
1) Induce strong antibody-mediated immune responses, yet often fail to induce strong cell-mediated immunity 2) Multiple administrations often needed due to some proteins altered -Multiple injections (cost) and shorter duration of immunity 3) Local reactions (adjuvant) 4) Contain non-immunogenic components (adjuvants) and proteins that arent immunoprotective
53
T/F: adjuvants can steer the type of immune response
True Al salts, oil emulsion, liposomes, saponins, ISCOMS, and cytokines all might help the Th1, Th2, or CTL response
54
vaccines that contain purified porteins that are naturally produced by the pathogens and that are known to be immunogen responsible for induction of a protective immune response Ex: tetanus toxoid, strep equi vaccines
Subunit vaccines
55
Subunit vaccines are biologically safe and typically tolerated but what are the downsides
often require high antigenic mass and strong adjuvants to stimulate a protective immune repsonse
56
What are the pros of inactivated vaccines
1) Absence of pathogenicity- good for pregnant mare, colostrum deprived foals, and immunocompromised animals 2) No virus replication and spread
57
Inactivated vaccine efficacy is dependent on
1) Quantity 2) Quality 3) Virus strain 4) Adjuvant
58
Inactivated vaccine stimulate what part of the immune system
strong antibody-mediated immune responses, yet often fail to induce strong cell-mediated immunity
59
aluminum salts are an adjuvant that steer what immune response
Humoral
60
What kind of animals are inactivated vaccines good for
Pregnant mares Colostrum deprived foals Immunocompromised animals
61
vaccines that contain microorganisms that have retained the ability to replicate in vivio and eict similar immune response to what is found after natural infection (antibodies and cell-mediated)
Modified Live Vaccines
62
What is a major advantages and cons of using combination vaccines
-Only one injection site, less reaction than multiple -Less cost Cons: but if given together, does it induce the same response? if theres a reaction, what was it from (although likely adjuvant)
63
What is the 4 way vaccine in horses
EEEV WEEV Influenza Tetanus
64
What is the 5 way vaccine in horses
EEEV WEEV Influenza Tetanus EHV 1/4
65
How was the FluAvert (Intervet) Modified live vaccine produced
Serial passage at gradually reduced temp Cold adapted vaccine strain, given intranasal administration mutated form that results in the attenuation of virulence of the microorganisms and thus replication of these vaccine strains in the host should not be associated with disease signs
66
What are the pros of modified live vaccines
1) Potential protection after one dose (replicates) 2) Immunity similar to natural infection -May induce mucosal immunity and stimulates cellular immunity (inactivated doesnt do mucosal)
67
What are the cons of modified live vaccines
1) Reversion to pathogenicity 2) Not for pregnant animals, immuno-compromised animals or neonates 3) Mild clinical signs and shedding (diagnosis) 4) Contamination during production with other viruses (BVD) 5) Vaccine storage (very important)
68
What are some examples of equine modified live vaccines
1) Equine Influenza (FluAvert) 2) RacH strain (cell culture adapted) for EHV-1 3) Non-encapsulated strain of S.equi (Pinnacle)
69
a vaccine that allows selection of specific antigen required to induce a fast and strong B and T cell mediated immune response without the potential of retaining residual virulence uses a live vector (poxvirus, adenovirus) for delivery of the contagion target gene into the host
Recombinant Vaccine
70
What is needed to produce recominant DNA vaccines
knowledge of immunogen responsible for inducing the protective immune response
71
What is the premise of the recombinant vectored equine influenza vaccine
Influenza HA gene(s) inserted into canarypox virus that is given to animal enters host cell and produces a strong B and T cell mediated immune response
72
What is the typical vector for vectored vaccines
canarypox
73
What is a chimera vaccine (recombinant)
piece of pathogenic virus put into a close relative of virus viral antigens of interest are synthesized denova within infected cells to stimulate humoral and cellular immunity
74
What is the difference between vector-based vaccines and chimera vaccines
same idea but the virus vector in chimeras is that it uses an antigen of interest in the same family of the pathogen
75
What are the pros of recombinant vectored vaccine
1) Elicit immune strong humoral and cell-mediated immune response 2) Failry rapid induction of immunity 3) No shedding of vaccine virus 4) No potential for residual virulence
76
What are the cons of recombinant vectored vaccines
1) Require 2 vaccine doses 2) Pre-existing immunity to poxvirus? -Vaccinia based vectors (not demonstrated in horses)
77
How might vaccine titers in pigs have regulatory considerations
Pseudorabies- need to be culled (seropositive)
78
The concept of differentiating infected from vaccinated animals
DIVA concept
79
What is most important for neutralization of equine influenza
hemagglutinin (HA)
80
less effective in preventing infection of equine influenza but reduce release of virus from cells
neuraminidase (NA)
81
The recombinant vaccine for equine influenza only contains the
hemagglutinin (HA) immunity for neutralization of the virus not the NA a good way for DIVA strategy
82
What is the DIVA strategy of equine infleunza
recombinant vaccine with only HA gene so you are able to tell from natural infection (which has anti-NA antibodies)
83
What are the core vaccines for horses
Tetanus Rabies West Nile Virus EEE/WEE
84
vaccines that protect from diseases that are endemic to a region with potential public health significance, are virulent/highly infectious and those posing a risk of severe disease
Core vaccines
85
vaccine where risk may vary regionally from population to population within an area or between individual horses within a given population
risk based vaccines
86
Can you get infected when working with a horse with EEEV
No- horse is not a replication host for WEEV or EEEV
87
Can you get infected when working with a horse with VEEV
Yes- horse can amplify but cannot WEEV or EEEV
88
What should go into determining the horse's risk assessment for determining risk based vaccination
1) Horses 2) Environment 3) People (ie vet)
89
What are the different risk based vaccines in horses
Diarrhea- Potomac HF, Rotavirus, Cl perfringens Respiratory: influenza, EHV (rhino), EVA, Strangles Others: Anthrax, Botulism, Leptospira
90
Does WNV vaccination influence fetal loss
scientific data does not support an association
91
What influences vaccine failures
1) Inadequate response 2) Inadequate timing 3) Vaccine/pathogen match
92
T/F: very few (if any) vaccines protect all animals from disease
True
93
T/F: vaccines may lessen severity of clinical signs and prevent shedding of contagion
False true they might lessen the severity of clinical signs but not all prevent the shedding of contagion
94
Vaccination provides a supplement to
other practices aimed at reducing exposure and increasing resistance
95
a lethal inherited condition in Arabians where both T cell and B cell function is impaired
Severe combined immunodeficiency (SCID)
96
What are the clinical signs of Severe combined immunodeficiency (SCID
once foals off colostral protection, highly susceptible to infections die before 5 months of age
97
How do you diagnose Severe combined immunodeficiency (SCID
CBC is absolute lymphopenia no antibodies so low serum immunoglobulin thymic hypoplasia look for homozygous gene in foal
98
How do you treat Severe combined immunodeficiency (SCID
affected foals invariably die by about 5 months of age. there is not therapy available at the time for these foals
99
What are the risk-based vaccines that protect against diarrhea causing agents in horse
Potomac Horse Fever Rotavirus Cl perfringens
100
What are the risk-based vaccines that protect against respiratory diseases in horse
Influenza EHV (Rhino) EVA Strangles

Large Animal Disease (7 decks)

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