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Exam 3 Flashcards

1
Q

Define acute versus persistent viral infections and relate the difference in the immune responses between these

A

a. Acute: Sudden onset and short clinical course; effective host responses which eliminates the virus from host tissue (host can die which doesn’t effectively solve the problem)
b. Persistent: variable clinical course; virus circumvents acquired host responses, host fails to eliminate virus

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2
Q

Name the four possible pathologic consequences to persistent viral infections

A

a. Repeated episodes of disease (e.g. herpesviruses)
b. Prolonged immune suppression (e.g. feline immunodeficiency virus, FLV)
c. Prolonged inflammatory reactions (e.g. feline enteric coronavirus)
d. Neoplasia (e.g. Feline leukemia virus FLV)

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3
Q

Spell out the epidemiologic consequence of viral persistence

A

Long term sources of infection; virus shedding occurs months-years or lifetime of infected animal (becomes a source of disease for life)

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4
Q

Name the two requirements for a virus to develop a persistent infection

A

a. Evade acquired immune response (antibody and cytotoxic T cell responses)
b. Regulate lytic potential (virus will destroy host cells)
i. Replication occurs within the cell and then the cell lyses to spread virus

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5
Q

List two ways that a normally lytic virus can become non-lytic and persist

A

a. Generate mutant viruses that are nonlytic

b. Regulate gene expression

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6
Q

State the four evasion strategies that a virus might use to evade acquired immune responses

A

a. Infect lymphocyte and/or antigen presenting cells (host doesn’t produce response)
b. Regulate gene expression (viral proteins aren’t produced-> immune molecules absent)
c. Sites of infection aren’t readily accessible to immune response (antibody fails to reach site of infection)
d. Alter/mutate viral protein structure (viral proteins are not recognized by antibody)

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7
Q
  1. Explain how “recrudescence” is different from primary infection and cite an example.
A

a. Recrudescence is “to be raw again” which occurs long after the primary infection
b. Occurs after latent periods (proteins are undetectable by the body) then gets reactivated
i. Herpes Simplex Virus 1 (HSV1) is an example
ii. Regulated gene expression

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8
Q

Tell how infection of sites that are not readily accessible to the immune system can become sites of viral persistence

A

a. Epithelial surfaces are relatively inaccessible to acquired immune responses (IgG, cytotoxic T cells)
b. To become persistent, the virus CANNOT induce inflammation
i. Virus has to be non-lytic and released from apical surface of cell

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9
Q

Define, with respect to herpesvirus infections, what is meant by the term “latent infection”, “recrudescence”, “productive infection”, “non-productive infection”

A

a. Latent infection: “to be hidden”; infectious virus and viral proteins are undetectable
b. Recrudescence: “to be raw again” (symptom-flare up)
c. Productive infection: produces viral proteins
d. Non-productive infection: absent in viral protein = evade detection

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10
Q

Identify how feline immunodeficiency virus establishes life-long infection in cats

A

FIV impairs acquired immune responses (suppresses cytotoxic T cells and antibody responses) produces long-term immune suppression

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11
Q

List the different types of conventional virus vaccines, explain how they are produced, relate the advantages & disadvantages, and specify the types of immunity generated by these

A

a. Live virus
i. Wild type virulent* (e.g. smallpox) ability to produce disease
ii. Attenuated virus (e.g. cowpox) *to reduce in virulence
1. Laboratory attenuated virus (modified live) most popular type
a. Inoculation in unnatural host which triggers adaptive mutation. Progressive adaptation to unnatural host then loses adaptation/virulence for natural host.
b. CDV, passage in embryonated eggs = safe and effective
c. E.g. rabies, canine distemper virus CDV, canine parvovirus, feline calicivirus

b. Inactivated “killed”
i. Virus is propagated and then killed (heat, formalin, UV light, irradiation) then an adjuvant* is added. *a chemical that enhances immune response
ii. E.g. rabies, FIV, canine coronavirus, equine influenza, canine influenza, parvo2

c. The goal is to trigger acquired immunity and then allow the body to create and store memory B cells.

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12
Q

Detail what protective immune response(s) (e.g. IgA, IgG, cytotoxic T cell) is required to prevent rotavirus, influenza, smallpox, CPV2 infections

A

a. IgG= blood, lymph
* systemic infection
b. IgA=mucosal surfaces
* most localized infections (mucosal)
c. Cytotoxic T cells= memory

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13
Q

List 2 advantages of live viral vaccines and 4 disadvantages of live viral vaccines

A

Advantages:

i. requires single dose
ii. stimulate protective immunity comparable with natural infection (IgG, IgA, Cytotoxic T cells)

Disadvantages:

i. May cause disease
ii. Possible mutation to virulent form
iii. Unstable (may be inactivated due to heat, chemicals, UV)
iv. Adverse reactions (anaphylaxis, autoimmune reactions)

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14
Q

List 2 advantages of inactivated viral vaccines and 3 disadvantages

A

Advantages:

i. Safe
ii. Stable

Disadvantages:

i. Multiple doses required
ii. Poor stimulators for IgA and cytotoxic T cells
iii. Adverse reactions (like live but also, and injection site fibrosarcomas)

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15
Q

Explain why inactivated canine coronavirus is an ineffective vaccine for prevention of canine coronaviral enteritis

A

Inactivated vaccines produce primarily IgG which is blood and lymph. Canine coronaviral enteritis affects the GI tract in the host. IgA is needed to get the desired immunity for an enteric virus and that comes from a live/parenteral vaccine.

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16
Q

Describe what immune responses are generated by parenteral injection of live canine distemper virus (infects multiple cell types) versus live rotavirus (strict tropism for enterocytes)

A

a. Immune response for parenteral (unnatural) injection for a live vaccine is both IgA and IgG. Will spread systemically via viremia after injection.
b. Live rotavirus will produce IgG, IgA, Cytotoxic T cells for both systemic and local

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17
Q

Recount why human vaccination with vaccinia (cowpox) virus is not always safe

A

Potential adverse effects (myocarditis and encephalitis)

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18
Q

Define the terms “recombinant DNA subunit vaccine”, “gene-deleted vaccines” and “virus-vectored vaccines”

A

a. Recombinant DNA subunit vaccine (e.g. FeLV): foreign gene is edited into bacterial PLASMID and recombinant plasmid introduced in bacteria (E. coli) which then replicates in the host and provides expression of FeLV in controlled environment.
b. Gene deleted vaccines: only required genes for replication are kept and the rest are deleted. The ones deleted often control virulence in host animal.
c. Virus-vectored vaccines: Large genome with non-essential genes; infectious for intended species; safe for intended species {SPECIES SPECIFIC}

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19
Q

Define the term “protective antigen” and relate the protective antigen of rabies virus and feline leukemia virus

A

a. Protective antigen: viral proteins that stimulate protective immune response
b. Rabies: G protein
c. FeLV: gp70

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20
Q

List the advantages of using a canary poxvirus-vectored vaccine for rabies and FeLV control

A

a. Safe alternative compared to vaccinia virus

b. NO lesion, adjuvant, virus shedding

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21
Q

Identify the function of a restriction endonuclease and describe how these enzymes are used to produce recombinant vaccines

A

Restriction endonuclease: cuts DNA at specific sequence and this allows for precise manipulation of DNA (cut-out or insert genes)

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22
Q

State how a plasmid can be used to produce recombinant subunit vaccines and give an example

A

Plasmid is a minichromosome that can have DNA units inserted and then multiply

E.g. is FeLV where the foreign gene is (gp70) is inserted into plasmid and then replicated

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23
Q

Explain how a gene-deleted vaccine can be used to distinguish “vaccinated” animals from “naturally” infected animals and cite an example

A

a. Vaccinated animals will contain antibodies for a certain virus in their blood compared to naturally infected animals.
b. Excision of thymidine kinase gene produces vaccine suitable for pigs.
c. If surface protein gpE is gene deleted (gpE-) and natural is (gpE+)

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24
Q

Describe general steps in pathogenesis for many picornaviruses

A 
Oral exposure=>
replication in intestinal epithelia and lymphoid tissue=>
Viremia=>
brain (CNS deficits) 
skin (vesicular lesions)
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25
Q

Porcine Teschen Virus 1

A

i. European: CNS; vaccines

ii. USA: mild, no vaccines

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26
Q

Avian Encephalomyelitis Virus

A

i. Mostly in chicks 1-21 days old, CNS disease
ii. Transmission: feces, egg–borne
iii. Vaccination of breeding flock since maternal immunity is passed

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27
Q

Avihepatoviruses (Duck Hepatitis Virus)

A

i. Ducklings <21 days
ii. Adults have disease just no symptoms
iii. Rapid transmission
iv. Vaccinate breeding flocks since maternal antibodies passed along

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28
Q

Equine Rhinitis A Virus

A

i. Respiratory virus
ii. Subclinical or persistent infection is common
iii. Killed vaccine available

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29
Q

Swine Vesicular Disease Virus

A

i. Outside of USA

ii. Vesicles same as FMDV

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30
Q

Seneca Valley Virus

A

i. Vesicular disease in pigs, History in NC, can appear differently even on same animal
ii. Same as FMDV and cant distinguish between FMDV and vesicles

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31
Q

List four reasons why Foot and Mouth Disease Virus (FMDV) is highly contagious

A

a. High titer droplets
b. Stable virus
c. Short incubation (excretion before symptoms)
d. Transmitted in infected products (trade restriction)

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32
Q

Describe why we vaccinate breeding flocks.

A

Vaccinate breeding flocks to allow passive immunity from mom to young

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33
Q

Recall that swine vesicular diseases have indistinguishable appearances and that all vesicular diseases are reportable.

A

Vesicular disease is undistinguishable from FMDV in swine. All vesicular diseases are reportable and can be tested.

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34
Q

Describe site of FMDV persistence and impact on spread to others

A

a. Can be recovered from saliva of infected animals but not transmitted to co-housed animals
b. Persistent virus cattle can be transmitted

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35
Q

Recall FMDV immunity is specific for >70 subtypes and lasts <1 year

A

SUBTYPES are sufficiently different from each other to make immunity in vivo SUBTYPE SPECIFIC; and IMMUNITY lasts only <1 YEAR (not lifelong)

36
Q

Describe four impediments to vaccination against FMDV.

A

a. Immunity is subtype specific and there are about 70 subtypes
b. Immunity only lasts <1 year
c. Cannot differentiate infected/carriers from vaccinated animals
d. Vaccination can mask presence of persistent virus and when removed it causes outbreak

37
Q

Recall any one of many reasons why FMDV spread through UK in 2001.

A

Some of the farms infected were farms that practiced FMDV vaccination??

38
Q

Name the three types of equine encephalitis viruses here in the United States

A

a. EEE (Eastern Equine Encephalitis)
b. WEE (Western Equine Encephalitis)
c. VEE (Venezuelan Equine Encephalitis)

39
Q

Compare the enzootic and epizootic/epidemic transmission cycles of the three equine encephalitis viruses

A

a. EEE/WEE Transmission
i. Birds and mosquitos are enzootic
ii. Epizootic: People/horses (dead end); avian species are not

b. VEE Transmission
i. Enzootic: Rats and mosquitos
ii. Epizootic: People (dead-end); Horses are not

40
Q

Define a “dead-end host”

A

Do not replicate large enough viral proteins in the bloodstream and cannot pass along to mosquitos (vectors)

41
Q

Name two strategies for controlling equine encephalitis virus infections and one strategy for monitoring virus activity in a region

A

a. Control: vaccination, restrict movement, and pesticide control
b. Monitoring: Sentinel Program (caged birds are strategically placed in a variety of locations and checked for antibodies of the virus)

42
Q

State the primary clinical concern for horses infected with equine arteritis virus

A

Abortion can occur even if the mare has subclinical infection

43
Q

Explain how equine arteritis virus and porcine respiratory and reproductive syndrome (PRRS) viruses are able to persist in the male reproductive tract

A

Infects the epithelium in the seminiferous tubules and is spread via sperm (equine), affects the bulbourethral gland in swine and is shed in sperm (swine)

44
Q

Name the biggest infectious disease problem of swine here in North Carolina

A

PRRS (porcine respiratory and reproductive syndrome)

45
Q

State why we think PRRS virus vaccines does such a poor job of protecting swine from this disease

A

Antigenic variation of virus strains (the virus mutates and the new population has no immunity)

46
Q

Recognize the two important pestiviruses found here in the United States and one pestivirus that is an important foreign animal disease (used to be in the US)

A

a. Bovine Virus Diarrhea (BVD both 1+2) & Border Disease
b. Classic Swine Fever (Hog Cholera)

47
Q

Tell the two important disease types that Bovine viral diarrhea virus (BVDV) is capable of causing

A

Both Acute and Persistent

48
Q

Tell the two biotypes of BVDV

A

a. Non-cytopathic (normal)

b. Cytopathic (mutation can arise)

49
Q

Recognize that BVDV can cause immunosuppression and make other infections more severe as well as interfere with vaccination

A

Acute infection can generate immunosuppression (especially in calves) shipping fever is an opportunistic cold.

50
Q

Describe the complex pathogenesis of “mucosal disease”

A

a. Non-cytopathic disease mutates to cytopathic

b. Superinfection with cytopathic biotype from environment

51
Q

Explain the ear notch method for identifying BVDV persistently infected calves

A

Since the BVDV virus can cross placenta then the calf is born with a persistent infection. A segment of ear is notched and tested (ELISA)

52
Q

Define the pathogenesis of border disease virus

A

Transmission and pathogenesis is similar to BVD (Fetal infection less than 2 month)

53
Q

Name the two flaviviruses that are both important animal and human pathogens found in the United States and how they are transmitted

A

a. West Nile Virus: transmitted by avian to mosquitos and then to host (horses) similar to WEE and EEE
b. Zika Virus: Spread by mosquitos through in utero infection; can also be spread through seminal fluids in males

54
Q
  1. Explain why pigs are such an important intermediary host for avian influenza viruses that can lead to new mammalian-adapted virus strains
A

Pig has both receptors (2,3 linked sialic acid)

55
Q

Identify the likely origin of the first canine influenza virus and recognize that there is a new second influenza virus strain

A

a. Originated from horses, canine influenza 1

b. In 2015, avian strain H3N2 mutated to canine influenza 2

56
Q

Spell out what a “fowl plague” strain of influenza virus is and what two hemaglutinin types are associated with these strains

A

a. H5 and H7

b. Severe systemic infection; cost lots of $$$

57
Q

Define “antigenic drift” and “antigenic shift”- cite an example of each

A

a. Antigenic drift: slow accumulation of mutations in envelope proteins that allow escape from immunity from virus. Point mutations.
eg. H3N2 epidemic

b. Antigenic shift: sudden appearance of a new antigenic virus type that the population has little or no immunity. Re-assortment.
eg. H1N1 pandemic

58
Q

Recognize that canine distemper virus in the US is primarily a problem in unvaccinated populations of dogs (like human measles)

A

It can spread easily through a shelter (few outbreaks in NC shelters)

59
Q

Distinguish the three types of Newcastle disease virus and briefly describe their associated diseases

A

a. Lentogenic: mild respiratory
b. Mesogenic: moderate systemic infection (resp & GI)
c. Velogenic: severe systemic infection (resp, GI, and CNS)

60
Q

Recognize the link between strength of immune response (weak, moderate, strong) and the different outcomes of a canine distemper infection in dogs

A

a. Excellent immune response: subclinical infection and virus could invade 2-8 years later
b. Moderate immune response: mild illness, virus persists in CNS, death 4-9 weeks later
c. Poor immune response: severe disease and death

61
Q

Recount how Rinderpest virus (cattle plague) was eradicated in 2011

A

Bourgelat created vx

62
Q

Describe how Nipah and Hendra viruses are transmitted to pigs and horses (and sometimes people)

A

Contraction with Nipah and Hendra viruses come from direct contact with infected bats

63
Q

What calicivirus can readily jump species?

A

San Miguel Sea Lion Virus

64
Q

Describe possible consequences of local rather than global decisions about purposeful release of viruses (to control animal populations).

A

Viruses are easily mutated or species develop resistance

65
Q

Describe indicated details for reoviruses: Avian Viral Arthritis Virus, Porcine and Bovine Rotaviruses, African Horse Sickness Virus, Epizootic Hemorrhagic Disease Virus, Blue Tongue Virus.

A
  1. Only occurs between viruses in same genus; can cross species to humans
  2. pH stability and proteolytic activation determines tropism
66
Q

Avian Viral Arthritis Virus (reoviruses)

A

a. Enters via oral/nasal/trachea
b. Most common infection in 5-7 week old birds (high morbidity, low mortality)
c. Immunize breeder flocks (maternal antibodies protects for 4 weeks)

67
Q

Porcine and Bovine Rotaviruses (reoviruses)

A

a. Many serotypes
b. Enters oral and travels intestines where infects epithelial cells of villus (not crypt)
c. Resistance by local immunity (IgA) or MLV

68
Q

African Horse Sickness Virus (reoviruses)

A

a. Never seen in western world
b. Transmitted by culicoides (gnats, biting midge)
c. Replicates in lymphoid tissue
d. Vasculitis is central
i. Acute: highly virulent strain of naïve horses; 25-90% loss; pulmonary edema from fluid in lungs
ii. Chronic: poorly virulent or pre-exposed horses; moderate edema in lungs and heart lesions;
iii. OFTEN SEE A COMBO OF BOTH
iv. 9 serotypes but immunity to one does not guarantee to others; control culicoides or MLV (mix 9 serotypes)

69
Q

Epizootic Hemorrhagic Disease Virus (reoviruses)

A

a. Infects ruminants and spread by culicodes with high mortality rate
b. Can present with similar symptoms such as blue tongue (in cows & deer)
c. Enzootic in some areas and will result in a few annual deaths
d. Epizootics will usually result in large number of deaths

70
Q

Blue Tongue Virus (reoviruses)

A

a. 24 serotypes, 5 in the US
b. Infectious disease in ruminants and spread by culicoides
c. Disease affects most lambs (affects breeding stock)
d. Culicoides bites and infects lymph nodes-> blood-> vascular endothelial cells
e. Cyanotic lesions in sheep {INTRAUTERINE TRANSMISSION}
f. Host still remains viremic long after recovery
g. 3 MLV available

71
Q

Vesicular Exanthema of Swine Virus (calicivirus)

A

a. Clinically indistinguishable from FMDV (&SVDV, VDV)
b. Vesicular exanthema of swine emerged from SMSL virus
c. CAN INFECT & CROSS MANY SPECIES (21 ANIMAL HOST)

72
Q

Feline Calicivirus

A

a. Cannot distinguish from FHV & main cause for respiratory disease
b. Severity varies
c. Recovered cats are immune but will shed disease for months (stress increases shedding)

d. Evolves easily (RNA GENOME)
i. Virulent Systemic disease variant
1. Constant mutating from FCV
2. Subclinical to pneumonia
3. Although vaccinated against FCV cats can catch the VSD variant

e. Vaccination: Feline Viral Rhinotracheitis Calicivirus Panleukopenia (FVRCP)
f. Vaccinate for multiple diseases so its convenient (MLV) Intranasal=IgA

73
Q

Rabbit Hemorrhagic Disease Virus (calicivirus)

A

a. rapid, lethal (<1 day following nasal discharge)
b. no vx in US that prevents masking and spread (AU took advantage for pop control)
c. rabbits became immune after virus took a toll on population
d. RHDV2 is mutated strain; slower death and affects younger rabbits

74
Q

Infectious Pancreatic Necrosis Virus (birnavirus)

A

a. Salmonoid fish: lethal disease in young fish grew in hatcheries
b. Lifelong carriers
c. No vaccine so disinfection of water is main treatment
i. Outbreak requires complete restock in fish

75
Q

Infectious Bursal Virus (birnavirus)

A

a. highly contagious dz in chickens, most susceptible 3-6 wk old chicks
b. replicates in gut-associate macrophages and lymphoid cells
i. enteric infection, d+, death
ii. primary viremia spreads to bursal ln
iii. compromised immune, secondary viremia, damages kidney
c. maternal Ig protects 1-2 wks, chick has immunity w/o dz
d. incubating eggs can be vaccinated

76
Q

Chicken Proventricular Necrosis Virus (birnavirus)

A

Enlargement of proventriculus with tendency to rupture at production $$

77
Q

Describe important clinical consequence of antigenic relatedness, high recombination frequency, and high mutation frequency of coronaviruses.

A

a. Coronaviruses are RNA viruses and mutate easily (makes new virus!) which makes them hard to vaccinate against.
b. Can span many species and target each differently (enteric, systemic, resp.)
c. Exacerbate disease by inducing the creation of antibodies (immune-mediated disease)
d. Similarity in disease (serum titers similar)

78
Q

transmissible gastroenteritis virus (coronaviruses)

A

a. Enteric virus in swine (affects pigs of all ages)
b. Fatal in young pigs

c. Epizootic: virus enters a nonimmune herd
i. Usually fatal
ii. Dependent on milk diet
iii. Replacement of sloughed cells poorly

d. Enzootic: virus maintained since non-immune pigs enter herd
i. Colostrum/milk antibody IgA passed from mom (MILDER)
ii. Develops early response to disease and repopulates cells better
iii. mortality but low

e. Transmitted via fecal/oral route for 10 weeks
f. Infects mature villus epithelial cells
g. Best protection is infection with virulent virus (feedback system)

79
Q

porcine respiratory coronavirus

A

PRCV is variant of TGEV (PRCV protects against TGEV)

80
Q

porcine epidemic diarrhea virus (coronaviruses)

A

a. High mortality in young pigs, Older pigs usually recover
b. Was foreign now widespread in USA
c. Fecal/oral route
d. Requires major effort to control spread

81
Q

porcine delta coronavirus

A

New coronaviruses emerging constantly (SADS-Swine Acute Diarrhea Syndrome)

82
Q

bovine coronavirus

A

a. Important cause of
b. Similar to TGEV in swine
c. MLV to treat; vaccinate mom before she calves

83
Q

turkey coronavirus

A

a. 100% morbidity with 50% mortality
b. Enteric and respiratory disease
c. Control via depopulation/decontamination

84
Q

infectious bronchitis virus (coronaviruses)

A

a. Morbidity can be 100% and 25% mortality in young birds
b. Decrease egg yield and quality
c. MLV offered (enteric and respiratory disease in poultry)

85
Q

canine coronavirus

A

a. The younger the more severe (TGEV in pigs)
b. Can infect cats
c. Enteric disease and have implications for FIPV

86
Q

feline enteric coronavirus

A

a. Enteric disease and can mutate to FIPV

b. Restricted to intestinal epithelium

87
Q

Describe how feline infectious peritonitis virus (FIPV) emerges, spreads, causes dz, and how immunity affects dz outcome

A

a. Emerges from Feline Coronavirus (2 biotypes)
i. Feline Infectious Peritonitis Virus (FIPV)
ii. Feline Enteric Coronavirus (FECV)
iii. BOTH INDISTINGUISHABLE

b. Recombination is frequent and antibodies are indistinguishable
c. FCoV infected cats are not immune to FIP
d. FIPV can easily mutate from FECV in infected cat (FIPV cannot spread to new host)
e. Can present as effusive (wet) and non-effusive (dry)

i. Effusive: peritoneal/pleural effusion {NO CELL MEDIATED IMMUNITY}
ii. Non-effusive: pyogranulomatous lesions in the kidneys, liver, CNS, eyes {PARTIAL CELL MEDIATED IMMUNITY}

f. aerosol/oral FECV ® infects macrophages (enhanced by antibodies) / mutates to FIPV ® immune complexes on blood vessels ® next based on cell-mediated immunity
g. Palliative treatment

I&I (1 decks)

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