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Large Animal Disease > Equine Vaccinology > Flashcards

Equine Vaccinology Flashcards

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
Q

cells that express immunoglobulin molecules on their surface, which function as antigen receptors

A

B cells

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26
Q

What is the Thelper cell that is primarily active during inflammatory and cytotoxic response

A

Th1: y-IFN, IL-12

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27
Q

What is the Thelper cell that is primarily active during humoral and allergic response

A

Th2: IL-4,5,6,10

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28
Q

In vaccine strategy, what may influence whether a Th1 or Th2 type of response will predominate

A

adjuvant
immunization route
cytokines present during antigen presentation

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29
Q

What T helper cell is predominately present during delayed, type hypersensitivity, cytotoxicity, T- cell mediated autoimmunity, and graft rejection

A

Th1

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30
Q

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

A

True

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31
Q

In the horse, what antibody is important for rapid initial response to antigen stimulation

A

IgM

IgG increases after IgM but is produced in larger amounts and with a higher affinity for antigen

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32
Q

Are IgM or IgG responses longer lasting

A

IgG

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33
Q

What is the difference between MHC class I and MHC class II antigen presentation

A

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

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34
Q

MHC II is present on what cells

A

(Professional APCs: dendritic cells, macrophages, B cells)

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35
Q

MHC class II presents to what cells through the exogenous pathway

A

T-helper cells (CD4)

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36
Q

MHC class I presents to what cells through the endogenous pathway

A

Cytotoxic T cells (CD8)

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37
Q

If you give an intramuscular killed flu vaccine, what is stimulated

A

Enters the body as exogenous antigen

CD4+ Th stimulate the humoral response due to presentation on MHC class II by APC (dendritic cells)

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38
Q

If you give an intranasal modified live flu vaccine, what is stimulated

A

Enters body as endogenous and exogenous antigen

target cell (airway epithelial) presents MHC I to CD8+ CTL: virus infected cells are destroyed

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39
Q

What is the goal of mucosal vaccines

A

to induce a secretory and systemic immune response that closely resembles the immune response after infection

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40
Q

T/F: Mucosal immunity equals systemic immunity

A

False- mucosal immune system can function independently

mucosal surfaces represent the entry site for the vast majority of equine infectious pathogens

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41
Q

What are the 4 types of vaccines

A

1) Inactivated
2) Modified Live
3) Recombinant
4) DNA/RNA

42
Q

What is the first vaccine

A

Edward Jenenr discovered the small pox vaccine using Cowpox virus

43
Q

Why does natural Equine Influenza Virus infection trigger a longer immunity than an inactivated EIV vaccine

A

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
Q

T/F: T cells respond directly to antigens

A

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
Q

antigen that is produced inside of the cells, couples with MHC I and presented on cell surface for CD8

A

Endogenous antigen

46
Q

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

A

Exogenous antigen

47
Q

CTLs can recongize

A

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
Q

T-helper cells recognize

A

antigen ONLY when they are displayed in association with MHC II molecule on the surface of an APC

49
Q

Inactivated vaccines contain antigen meaning that they

A

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
Q

Toxoid vaccine is

A

inactivated toxin
(ie tetanus toxoid)

51
Q

How are inactivated vaccines made

A

1) Chemical treatment (formaldehyde) and heat inactivated
2) Adjuvant addition (aluminum hydroxyphosphate gell, MF59, carbomer, TLR agonsits)

52
Q

What are the downsides to inactivated vaccines

A

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
Q

T/F: adjuvants can steer the type of immune response

A

True
Al salts, oil emulsion, liposomes, saponins, ISCOMS, and cytokines all might help the Th1, Th2, or CTL response

54
Q

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

A

Subunit vaccines

55
Q

Subunit vaccines are biologically safe and typically tolerated but what are the downsides

A

often require high antigenic mass and strong adjuvants to stimulate a protective immune repsonse

56
Q

What are the pros of inactivated vaccines

A

1) Absence of pathogenicity- good for pregnant mare, colostrum deprived foals, and immunocompromised animals

2) No virus replication and spread

57
Q

Inactivated vaccine efficacy is dependent on

A

1) Quantity
2) Quality
3) Virus strain
4) Adjuvant

58
Q

Inactivated vaccine stimulate what part of the immune system

A

strong antibody-mediated immune responses, yet often fail to induce strong cell-mediated immunity

59
Q

aluminum salts are an adjuvant that steer what immune response

A

Humoral

60
Q

What kind of animals are inactivated vaccines good for

A

Pregnant mares
Colostrum deprived foals
Immunocompromised animals

61
Q

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)

A

Modified Live Vaccines

62
Q

What is a major advantages and cons of using combination vaccines

A

-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
Q

What is the 4 way vaccine in horses

A

EEEV
WEEV
Influenza
Tetanus

64
Q

What is the 5 way vaccine in horses

A

EEEV
WEEV
Influenza
Tetanus
EHV 1/4

65
Q

How was the FluAvert (Intervet) Modified live vaccine produced

A

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
Q

What are the pros of modified live vaccines

A

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
Q

What are the cons of modified live vaccines

A

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
Q

What are some examples of equine modified live vaccines

A

1) Equine Influenza (FluAvert)
2) RacH strain (cell culture adapted) for EHV-1
3) Non-encapsulated strain of S.equi (Pinnacle)

69
Q

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

A

Recombinant Vaccine

70
Q

What is needed to produce recominant DNA vaccines

A

knowledge of immunogen responsible for inducing the protective immune response

71
Q

What is the premise of the recombinant vectored equine influenza vaccine

A

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
Q

What is the typical vector for vectored vaccines

A

canarypox

73
Q

What is a chimera vaccine (recombinant)

A

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
Q

What is the difference between vector-based vaccines and chimera vaccines

A

same idea but the virus vector in chimeras is that it uses an antigen of interest in the same family of the pathogen

75
Q

What are the pros of recombinant vectored vaccine

A

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
Q

What are the cons of recombinant vectored vaccines

A

1) Require 2 vaccine doses
2) Pre-existing immunity to poxvirus?
-Vaccinia based vectors (not demonstrated in horses)

77
Q

How might vaccine titers in pigs have regulatory considerations

A

Pseudorabies- need to be culled (seropositive)

78
Q

The concept of differentiating infected from vaccinated animals

A

DIVA concept

79
Q

What is most important for neutralization of equine influenza

A

hemagglutinin (HA)

80
Q

less effective in preventing infection of equine influenza but reduce release of virus from cells

A

neuraminidase (NA)

81
Q

The recombinant vaccine for equine influenza only contains the

A

hemagglutinin (HA) immunity for neutralization of the virus

not the NA

a good way for DIVA strategy

82
Q

What is the DIVA strategy of equine infleunza

A

recombinant vaccine with only HA gene so you are able to tell from natural infection (which has anti-NA antibodies)

83
Q

What are the core vaccines for horses

A

Tetanus
Rabies
West Nile Virus
EEE/WEE

84
Q

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

A

Core vaccines

85
Q

vaccine where risk may vary regionally from population to population within an area or between individual horses within a given population

A

risk based vaccines

86
Q

Can you get infected when working with a horse with EEEV

A

No- horse is not a replication host for WEEV or EEEV

87
Q

Can you get infected when working with a horse with VEEV

A

Yes- horse can amplify

but cannot WEEV or EEEV

88
Q

What should go into determining the horse’s risk assessment for determining risk based vaccination

A

1) Horses
2) Environment
3) People (ie vet)

89
Q

What are the different risk based vaccines in horses

A

Diarrhea- Potomac HF, Rotavirus, Cl perfringens

Respiratory: influenza, EHV (rhino), EVA, Strangles

Others: Anthrax, Botulism, Leptospira

90
Q

Does WNV vaccination influence fetal loss

A

scientific data does not support an association

91
Q

What influences vaccine failures

A

1) Inadequate response
2) Inadequate timing
3) Vaccine/pathogen match

92
Q

T/F: very few (if any) vaccines protect all animals from disease

A

True

93
Q

T/F: vaccines may lessen severity of clinical signs and prevent shedding of contagion

A

False

true they might lessen the severity of clinical signs but not all prevent the shedding of contagion

94
Q

Vaccination provides a supplement to

A

other practices aimed at reducing exposure and increasing resistance

95
Q

a lethal inherited condition in Arabians where both T cell and B cell function is impaired

A

Severe combined immunodeficiency (SCID)

96
Q

What are the clinical signs of Severe combined immunodeficiency (SCID

A

once foals off colostral protection, highly susceptible to infections
die before 5 months of age

97
Q

How do you diagnose Severe combined immunodeficiency (SCID

A

CBC is absolute lymphopenia

no antibodies so low serum immunoglobulin

thymic hypoplasia

look for homozygous gene in foal

98
Q

How do you treat Severe combined immunodeficiency (SCID

A

affected foals invariably die by about 5 months of age. there is not therapy available at the time for these foals

99
Q

What are the risk-based vaccines that protect against diarrhea causing agents in horse

A

Potomac Horse Fever
Rotavirus
Cl perfringens

100
Q

What are the risk-based vaccines that protect against respiratory diseases in horse

A

Influenza
EHV (Rhino)
EVA
Strangles

Large Animal Disease (7 decks)

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