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VETM 422 Virology > Lecture 16: Equine Viruses 2 > Flashcards

Lecture 16: Equine Viruses 2 Flashcards

1
Q

Viral features of equine herpesvirus

A
  • dsDNA, enveloped
  • lifelong infection
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2
Q

What are the types of equine herpesvirus? which are relevant and how prevalent are they

A
  • Types 1-5: only 1 and 4 are prevalent and economically important
    o Type 1: respiratory disease, abortion, neurological disease
     Seroprevalence 30%
    o Type 2: conjunctivitis
    o Type 3: genital lesions (coital exanthema)
    o Type 4: respiratory (main), can induce abortion
     Seroprevalence up to 100% (almost all animals infected and carrying virus)
    o Type 5: equine multinodular pulmonary fibroses
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3
Q

How is equine herpes virus transmitted? how long is incubation period?

A

Transmission: aerosols, direct contact, vertical (trans-placental) – shed nasally from 0-7d
* Incubation = 1-10d

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4
Q

What is a notable outbreak of equine herpes virus and why did it occur

A

Outbreaks:
* National cutting horse event in Utah causing EHV type 1 associated myeloencephalopathy and neurotropic herpes
* Many horses transported long distances = stress
* Latent herpes re-activated and caused productive/shedding infection = infect others

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5
Q

What is the pathogenesis of equine herpes virus? How does this relate to the clinical signs

A

Pathogenesis
1. Ciliated respiratory epithelium – virus replication
a. Respiratory disease
2. Immune response and immune cell recruitment (mainly monocyte/macrophages)
3. Virus can be transmitted in leukocytes and spread via hematogenous (viremia) or in lymph
a. Leukocyte trafficking in monocytes and CD4 cells
4. Virus can then end up in placenta (if pregnant) or in CNS (only certain type of virus cause CNS lesions)
a. Thrombo-ischemic necrosis in placenta
b. Vasculitis, hemorrhage, and thrombo-ischemic necrosis in CNS
5. Establish latency in trigeminal ganglion

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6
Q

What are the target cells of equine herpes virus

A

Target cells; placental cells, endothelial cells, monocytes, CD4+, epithelial cells, neurons

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7
Q

What are the clinical signs of equine herpes virus

A

Clinically
* Biphasic fever: 0-4d and 6-10d (coincide with viremia)
* Respiratory (main)
* Abortion storms: if infected late term (7-11mo) = foal with pneumonia and death within hr-d
o Abortion within 2-12wk
o Due to thrombus and ischemia or infection of fetus
* Neurological: depends on specific variant that affects CNS
o Paralysis/paraplegia/recumbency/behavioural changes/head pressing/ataxia/loss of bladder function

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8
Q

What is the histo lesions of equine herpes virus

A

Histo: viral proteins in endothelial cells and perivascular cuffing + occlusion of lumen of blood vessels (thrombus)
* Eosinophilic intranuclear inclusions

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9
Q

How to diagnose equine herpes virus? What tests will determine active viral replication

A
  • Sample: nasopharyngeal swab
    o PCR/virus isolation
  • Sample: blood (unclotted blood – use EDTA tubes) because buffy coat contains the virus
    o PCR
    o Virus isolation
  • Sample: aborted fetus tissue
    o Histo/immunostaining – can determine active viral replication (identify viral proteins)
  • PCR is more sensitive – can identify virus for up to 2 weeks – but does not differentiate active or inactive viral replication
  • Virus isolation will give false negative from 7-14d – can determine active viral replication
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10
Q

What is the neurologic form of EHV associated with?

A
  • 10% of EHV1 is neurovirulent
  • Due to faster replication in lymphocytes = higher viremia and vasculitis
  • Associated with point mutation in viral polymerase gene
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11
Q

What are the types of pathogens that can induce Equine Neurological Disease

A

Equine Neurological Disease
* EHV type 1
* WNV
* Rabies
* Venezuelan, eastern, and western encephalitis viruses (eastern is most prevelant)
* Equine protozoal encephalomyelitis
* Bacterial myeloencephalitis (botulism/staphylococcus/listeria)

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12
Q

What vaccines are there to protect against equine herpes virus? What are the differences between the vaccines? What is thee vaccination schedule and how does it differ for deals and mares?

A
  • Attenuated: protect against resp dz
    o Not abortion, neuro, shedding, viremia
  • Inactivated: protect against resp dz and abortion
    o Not neuro, shedding, viremia
  • Vector vaccine: canarypox, vaccinia: experimental/non licensed
  • Short lived immunity: vaccinate at 5, 7 , 9mo of gestation
    o Foal: 4-6mo then 4-6wk after + 10-12mo and then every 6mo
  • Combined EHV 1 and 4
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13
Q

Is the equine herpes virus vaccine effective? why?

A

yes

  • Vaccine induce neutralizing Ig (IgG4 and 7) + cell mediated immune response = neutralize incoming viruses and prevent entry into respiratory tract/blood infection
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14
Q

What are the viral features of Equine Infectious Anemia/Swamp Fever

A
  • Retrovirus, rtRNA
  • Susceptible to detergent - enveloped
  • Retroviridae (subfamily, orthoretroviridae + genus, lentivirus)
  • Lifelong infection
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15
Q

Compare EHV and Equine Infectious Anemia/Swamp Fever

A

both
- enveloped (susceptible to detergents)
- establish lifelong infection (different mechanisms)

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16
Q

What species and where does Equine Infectious Anemia/Swamp Fever affect**

A

Target: all Equidae
* Clinical disease in horse/pony, subclinical in donkeys
* CA: more prevalent in AB

17
Q

How is Equine Infectious Anemia transmitted

A

Transmission: vector
* Mechanical: mouthparts of biting insects (horse fly/stable fly/deer fly)
* Fomite: needle, sx instruments, floats
* In utero/milk/venereal/aerosol

  • Similar to BLV transmission (many ways to transmit)
18
Q

What is the pathogenesis for Equine Infectious Anemia

A

Pathogenesis: immune response is responsible for clinical disease
* Circulating immune complexes (systemic HS3) = vasculitis and glomerulonephritis
* Infection and destruction of macrophages
* Upregulate TNFa, IL6, IL1 = fever, lethargy, inappetence, reduced platelet + RBC production in bone marrow = thrombocytopenia/anemia
* Complement (C3b) coated RBC + Ig coated platelet (due to attachment of virus) = phagocytosis or agglutination (IgM binding) = thrombocytopenia/anemia
o Membrane attack complex (MAC) can also destroy RBC
o RBC lifespan reduced
o Reduced erythropoiesis
o Impaired flow of Fe from macrophages to plasma

19
Q

What are the methods of diagnosing EIV

A
  • Serology
    o Agar gel immunodiffusion test/Coggins test: high false negative (better for positive samples)
     Lines connecting = positive, if not connected = negative
    o ELISA: high false positive (better for negative samples)
    o Both of these are tested for and if they disagree the sample must be tested for via an immunoblot
  • PCR: sensitive but does not differentiate carriers
20
Q

How to control EIV

A

Immunity and Control
* Adaptive immunity required – develops around 2-4wks
* Recurrent episodes of viremia and clinical disease occur even if neutralizing Ig and cytotoxic lymphocyte response
* First Ig fails to bind viral antigen butt avidity of Ig increases by 1-3mo
* Variants are common and immune response can be challenged
Control
* Reportable disease
* No vaccine or tx
* If infected = kill or lifelong quarantine

21
Q

What are the viral features of west nile virus

A

Virus
* Enveloped, Flaviviridae, (+)ssRNA
* In CA: AB is the most

22
Q

How is WNV transmitted and who does it target

A

Transmit: vector (Culex and Aedes mosquites)
Target: >300 spp. Birds (crow, magpie, jays = high viral titres with high mortality)

Enzootic Cycle
* Culex transmit to birds (corvids can develop high titre and die)
* Aedes can transmit from birds to dead end hosts (horse/human)

23
Q

What is the pathological mechanism of WNV

A

Pathology: neurological disease
* Travel to CNS
1. Retrograde transport in neurons
2. Blood
a. Cross BBB via trojan horse model (intracellular transport in macrophage/neutrophil) or loss of integrity (cytokine TNFa mediated/matrix metalloproteinase disruption of tight junction/basement membranes

24
Q

What cells are targeted by WNV

A
  • Infect neutrophils and monocytes, endothelial cells, neurons
25
Q

What is the timeline of WNV and what are the clinical signs

A

Clinically: from 6-14d
* Stumbling/ataxia/paresis/paralyss/myoclonus/death
* Fever in <1/4 all cases
* Viremia 2-6d – viremia before clinical signs
* Ig response persist for months

26
Q

What are the histo signs of WNV

A

Histo: encephalitis
* Direct (virus iinduced) and indirect (immune mediated) mechanisms
* Glial proliferation
* Non-suppurative vasculitis – leukocytes associated (CD3 B cells,

27
Q

how to control WNV

A

Control: reduce mosquito
* Vaccines induce good immune response
o Canarypox vectored vaccine
o Live attenuated/inactivated WNV yellow fever virus chimera

28
Q

Equine herpesvirus (EHV)1 and 4 are different since
A EHV1 induces no clinical signs and EHV4 induces
encephalomyelitis
B EHV4 induces no clinical signs and EHV4 induces coital
exanthema
C EHV1 establishes lifelong infection whereas EHV4 is cleared in
7-10 days
D EHV1 induces no clinical signs and EHV4 induces
keratoconjunctivitis
E Seroprevalence of EHV1 is lower than that of EHV4

A

E

29
Q

A common outcome of equine herpesvirus (EHV)1 and West
Nile virus (WNV) infection is
A Colic
B Anemia
C Reproductive failure
D Swollen limbs
E Infection of leukocytes

A

E

30
Q

What is the possible clinical sign of equine infectious
anemia virus (EIAV) infection? Please mark the WRONG
answer.
A Recurring episodes of disease
B Colic
C Fever
D Depression
E Nasal discharge

A

B

31
Q

Viremia of EHV1
A Follows lytic viral replication in trigeminal ganglion
B Occurs after infection with neuropathogenic but not with non-
neuropathogenic strains
C Is mostly cell-associated
D Is not involved in viral dissemination in the body
E Is not evident in this infection

A

C

32
Q

Anemia due to equine infectious anemia (EIA) virus infection is
A Due to increased erythrocyte life-span
B Not related to compromised erythropoiesis
C Due to destruction of erythroblasts
D Non-immune mediated
E Due to impaired flow of iron from macrophage to plasma

A

E

VETM 422 Virology (16 decks)

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