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Flashcards in export_cns zoonotic viruses Deck (42):
1

Zoonoses

Diseases of invertebrate animals that can be transmitted to man

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Arboviral disease

Involves an insect vector for transmission

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Arbovirus examples

Flaviviruses - West Nile, St. Louis and Japanese encephalitis
Togaviruses - Eastern, Western, Venezuelan equine encephalitis

Bunyaviruses - LaCrosse encephalitis

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Viruses transmitted to humans directly from other mammals

Rhabdoviruses - rabies
Arenaviruses - lymphocytic choriomeningitis

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Flaviviruses transmission

All by mosquitos

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West Nile Virus (WNV) reservoirs

Birds serve as reservoirs

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WNV symptoms

Most infections are mild and clinically unapparent
Some develop West Nile fever (3-6 days of symptoms)

Sudden onset of febrile illness (malaise, nausea, vomiting, rash)

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WNV in the CNS

Primarily affect elderly
Encephalitis and meningitis

Fever, headache, weakness, GI disturbances, may progress to coma and paralysis

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Diagnose WNV

Adults >50 years old who suddenly develop encephalitis or meningitis in summer/early fall

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WNV treatment

Supportive

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St. Louis encephalitis virus (SLE) disease

Major cause of arbovirus encephalitis

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SLE transmission

Birds are reservoir
Humans get it from Culex mosquitoes

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SLE symptoms

Sudden onset
Fever with headache (mild)

Headaches, high fever, stiff neck, coma, tremors, spastic paralysis (severe)

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SLE diagnosis

Confirmed via serology

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SLE treatment

Supportive

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Japanese encephalitis virus disease

Leading cause of viral encephalitis in Asia
Birds and livestock are reservoirs

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Togaviruses transmission

Horses are a major reservoir
Transmitted via mosquito bite

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Togaviruses diseases

Eastern equine encephalitis (EEE)
Western equine encephalitis (WEE)

Venezuelan equine encephalitis (VEE)

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EEE symptoms

Sudden onset of fever, muscle pain, and headache
Many progress to seizures/coma

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WEE symptoms

Most people are asymptomatic or mild
May have sudden onset fever, headache, nausea, vomiting, malaise

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VEE symptoms

Most infections are symptomatic
Fever, chills, headache, nausea, vomiting, may progress to encephalitis

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LaCrosse encephalitis (LAC) virus transmission

Arbovirus
Transmitted by the bite of infected mosquitoes

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LAC symptoms

Fever, headache, nausea, vomiting
Severe disease can lead to seizures, coma, paralysis

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Rhabdovirus transmission

Through infected saliva via bites (dogs, bats)

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Rabies lifecycle

Inoculation, local proliferation, enters PNS, travels to CNS, dissemination

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Rabies symptoms

During cerebral infection, behavioral changes occur (anxiety, confusion, agitation, hallucination)
Hydrophobia is a classic sign

Coma and death

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Rabies prevention

Vaccination of animals and high risk individuals

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Rabies diagnosis

Disease in animals can be confirmed post-mortem by the presence of Negri bodies

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Arenavirus CNS disease

Lymphocytic choriomeningitis virus (LCMV)

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LCMV reservoirs

Rodent-borne virus

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LCMV symptoms

Most infections are asymptomatic or produce a mild febrile illness
Can cause aseptic meningitis, encephalitis, or meningoencephalitis

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LCMV transmission

Inhaling infectious aerosolized particles of rodent urine, feces, or saliva
Most common is the common house mouse

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LCMV symptoms

Febrile illness
Biphasic - 1 week of fever, malaise, headache, nausea, vomiting, remission for a few days, then second phase of disease (meningitis or encephalitis)

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Prions diseases

Slow developing neurodegenerative diseases, thought to be caused by a family of viruses known as "slow viruses"

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Human spongiform encephalopathis

Kuru
CJD

GSS

FFI

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Prion features

Lack nucleic acid
Consists of protease, heat and chemically resistant hydrophobic glycoprotein (PrP)

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PrPc

Normal cellular prion-related protein
Extended conformation containing numerous alpha-helices

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PrPSc

Infectious form of PrPc
Globular conformation with beta-pleated sheets

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Theory for Prion replication

PrPSc binds to PrPc on cell surface
Induces conversion to PrPSc

Cycle repeats

Aggregates form, internalized by neurons

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Symptoms of Prion infiltration to CNS

Neuronal vacuolization
Astrocyte and glial cell proliferation

Amyloid plaques

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Prions clincal syndromes

Slow, progressive neurological degeneration
Very long incubation period

Death ensues rapidly (months)

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Prion diagnosis

Postmortem histological examination