Lecture 16: Equine Viruses 2 Flashcards
(32 cards)
Viral features of equine herpesvirus
- dsDNA, enveloped
- lifelong infection
What are the types of equine herpesvirus? which are relevant and how prevalent are they
- 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
How is equine herpes virus transmitted? how long is incubation period?
Transmission: aerosols, direct contact, vertical (trans-placental) – shed nasally from 0-7d
* Incubation = 1-10d
What is a notable outbreak of equine herpes virus and why did it occur
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
What is the pathogenesis of equine herpes virus? How does this relate to the clinical signs
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
What are the target cells of equine herpes virus
Target cells; placental cells, endothelial cells, monocytes, CD4+, epithelial cells, neurons
What are the clinical signs of equine herpes virus
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
What is the histo lesions of equine herpes virus
Histo: viral proteins in endothelial cells and perivascular cuffing + occlusion of lumen of blood vessels (thrombus)
* Eosinophilic intranuclear inclusions
How to diagnose equine herpes virus? What tests will determine active viral replication
- 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
What is the neurologic form of EHV associated with?
- 10% of EHV1 is neurovirulent
- Due to faster replication in lymphocytes = higher viremia and vasculitis
- Associated with point mutation in viral polymerase gene
What are the types of pathogens that can induce Equine Neurological Disease
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)
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?
- 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
Is the equine herpes virus vaccine effective? why?
yes
- Vaccine induce neutralizing Ig (IgG4 and 7) + cell mediated immune response = neutralize incoming viruses and prevent entry into respiratory tract/blood infection
What are the viral features of Equine Infectious Anemia/Swamp Fever
- Retrovirus, rtRNA
- Susceptible to detergent - enveloped
- Retroviridae (subfamily, orthoretroviridae + genus, lentivirus)
- Lifelong infection
Compare EHV and Equine Infectious Anemia/Swamp Fever
both
- enveloped (susceptible to detergents)
- establish lifelong infection (different mechanisms)
What species and where does Equine Infectious Anemia/Swamp Fever affect**
Target: all Equidae
* Clinical disease in horse/pony, subclinical in donkeys
* CA: more prevalent in AB
How is Equine Infectious Anemia transmitted
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)
What is the pathogenesis for Equine Infectious Anemia
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
What are the methods of diagnosing EIV
- 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
How to control EIV
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
What are the viral features of west nile virus
Virus
* Enveloped, Flaviviridae, (+)ssRNA
* In CA: AB is the most
How is WNV transmitted and who does it target
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)
What is the pathological mechanism of WNV
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
What cells are targeted by WNV
- Infect neutrophils and monocytes, endothelial cells, neurons
