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Microbiology Exam V > Zoonotic/Exotic Viruses > Flashcards

Zoonotic/Exotic Viruses Flashcards

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1
Q

Zoonoses

A

Diseases of vertebrate animals that can be transmitted to man; either directly or indirectly through an insect vector (i.e. an Arboviral disease)

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2
Q

Flaviviruses

A

West Nile Virus
Dengue
Yellow Fever Virus
St. Louis Encephalitis Virus

All are transmitted by MOSQUITOES

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3
Q

West Nile Virus (Life Cycle)

A

Humans and horses are Incidental/Accidental Hosts
-Do not develop infectious-level (for mosquitoes) viremias
“Dead End Hosts”

BIRDS are the main reservoir hosts and MOSQUITOES act as the vector

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4
Q

West Nile Virus (Transmission)

A

NO evidence of infection from handling live/dead birds

NO evidence of person-to-person or animal-to-person transmission

  • Except from transfusions/organ transplants
  • Breastfeeding
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5
Q

West Nile Virus (Clinical Disease)

A
  • Most WNV infections are mild and clinically unapparent
  • 20% of those infected develop a mild illness (West Nile Fever) –> incubation period of 3 to 14 days with symptoms lasting 3 to 6 days
  • A sudden onset of febrile illness (accompanied by malaise, anorexia, nausea, vomiting, headache (eye pain), myalgia, rash, and lymphadenopathy
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6
Q

West Nile Virus (Severe Disease)

A

1 in 150 infections will result in severe neurological disease

  • Primarily in the ELDERLY
  • Encephalitis (mostly) and meningitis
  • Fever, headache, weakness, and GI disturbance may accompany the change in mental status
  • Ataxia, seizures, disorientation, visual disturbances
  • May progress to coma and paralysis
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7
Q

What is the greatest risk for developing neuroinvasive West Nile Virus?

A

Age (older you are, higher the risk)

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8
Q

West Nile Virus (Diagnosis and Treatment)

A

Diagnosis:

  • Should be strongly considered in adults > 50 years old who develop unexplained encephalitis or meningitis in summer or early fall*
  • Clinical suspicion, Serology, and CSF fluid

Treatment:
SUPPORTIVE

Vaccine for horses but NOT humans

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9
Q

St. Louis Encephalitis Virus (SLE)

A

MAJOR cause of Arbovirus Encephalitis in the U.S.

Was the big virus before WNV

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10
Q

St. Louis Encephalitis Virus (SLE) (Transmission)

A

Transmitted to humans by CULEX MOSQUITOES
Mosquitoes acquire virus from infected BIRDS
Horses can serve as reservoirs
Virus levels in humans do not reach levels to support human-to-human transmission via mosquitoes

In temperate areas in the U.S., SLE cases primarily occur in LATE SUMMER/EARLY FALL

In southern U.S., cases can occur year round

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11
Q

St. Louis Encephalitis Virus (SLE) (Disease)

A

5 to 15 day incubation period
Sudden onset of symptoms
Mild disease
-Fever with headache
Severe disease
-Headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions (especially in infants) and spastic paralysis
-Fatality rates range from 3% to 30% (highest in aged)
-Neurological sequelae in 10% of infected patients

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12
Q

St. Louis Encephalitis Virus (SLE) (Diagnosis and Treatment)

A

NO vaccine

Treatment: Supportive Therapy

95% of severe disease (encephalitis) requires hospitalization

Confirmation of infection is through serological testing

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13
Q

Japanese Encephalitis Virus

A

Leading cause of viral encephalitis in Asia
BIRDS and LIVESTOCK serve as reservoirs

Up to 70% of individuals from endemic regions are SEROPOSITIVE (with most infections being clinically inapparent)
Symptoms: similar to other Arboviral encephalitis
Fatality rate: as high as 30%

30 to 40% of survivors are left with lifelong neurological sequlae

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14
Q

Togaviruses (Alphaviruses) (Transmission and Reservoirs)

A

Transmission: infected MOSQUITOES

Virus maintained in the wild primarily by infected RODENTS and BIRDS

Major Reservoir: HORSES

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15
Q

Togaviruses (Alphaviruses)

A

Eastern, Western, and Venezuelan Equine Encephalitis (EEE, WEE, and VEE)

EEE and WEE are significant causes of vector borne viral encephalitis in the U.S.

VEE primarily occurs in South and Central America, as well as sporadically in the U.S.

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16
Q

Eastern Equine Encephalitis (EEE) Virus

A

Infections occur: Eastern seaboard, Gulf Coast, and some areas of the Midwest

Outbreaks occur primarily in the SUMMER and FALL

Equine (Horse) epidemics are a more common occurrence and usually precede human infections

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17
Q

Eastern Equine Encephalitis (EEE) Virus (Disease)

A
  • Incubation of 4-10 days
  • Sudden onset of fever, general muscle pains, and a headache of increasing severity
  • Many individuals will progress to more severe symptoms such as seizures and coma
  • 1/3 of people with clinical encephalitis will die
  • Many will suffer PERMANENT BRAIN DAMAGE
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18
Q

Western Equine Encephalitis (WEE) Virus

A

Infections occur: mainly in western parts of the USA and Canada

***Similar to the EEE virus

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19
Q

Western Equine Encephalitis (WEE) Virus (Disease)

A

Usually first seen in June or July

Most infections are ASYMPTOMATIC or MILD

Clinically apparent illness presents with a sudden onset of fever, headache, nausea, vomiting, anorexia, and malaise, followed by altered mental status, weakness, and signs of meningeal irritation

CHILDREN are affected more severely than adults and may be left with PERMANENT NEUROLOGICAL SEQUELAE (5 to 30%)

20
Q

Venezuelan Equine Encephalitis (VEE) Virus

A

Acute viral disease (fevers, chills, headache, nausea, vomiting, lumbosacral pain, and myalgia)
-May progress to encephalitis

LARGE EPIDEMICS

A disease predominantly found in South and Central America

21
Q

Venezuelan Equine Encephalitis (VEE) Virus (Disease)

A
  • Most infections ARE symptomatic
  • Initially present with symptoms typical of the flu
  • Children are more likely to have CNS involvement
  • Symptoms include disorientation, nuchal rigidity, convulsions, paralysis, coma, and death
  • The overall fatality rate is less than 1%
  • Neurological manifestations occur at a rate of 4-14% in children (< 1% in adults), with a case fatality rate of 20%
22
Q

Bunyaviruses

A

Hantaviruses
-Spread by inhalation of dried feces and urine from infected rodents

LaCrosse (California) Encephalitis Virus

  • Arbovirus
  • Transmitted by the bite of infected mosquitoes
23
Q

LaCrosse (California) Encephalitis Virus (Epidemiology and Transmission)

A

Infections primarily occur in Midwestern and Mid-Atlantic states

Mostly in CHILDREN

Virus maintained in CHIPMUNKS and SQUIRRELS

Transmitted by MOSQUITOES

24
Q

LaCrosse (California) Encephalitis Virus (Disease)

A
  • LAC encephalitis initially presents as a non-specific summertime illness (fever, headache, nausea, vomiting, and lethargy)
  • Severe disease (about 50% of cases) occurs most commonly in children (seizures, coma, paralysis, neurological sequelae after recovery)
  • Fatal in less than 1% of clinical cases
25
Q

Rhabdoviruses - Rabies (Lyssavirus)

A

Worldwide distribution (except Australia, Great Britain, and Hawaii)

Effects humans and other mammals (dogs, cats, raccoons, bats)

26
Q

Rhabdoviruses - Rabies (Lyssavirus) (Transmission)

A
  • INFECTED SALIVA*
  • Bites
  • Contamination of mucous membranes (i.e. eyes, nose, mouth)
  • Aerosol transmission
  • Corneal transplantations
  • Most infections are transmitted by exposure to infected DOGS or BATS

15 to 40,000 individuals receive post-exposure prophylaxis in the U.S. annually

27
Q

Rhabdoviruses - Rabies (Lyssavirus) (Clinical Disease)

A
  • Following inoculation the virus proliferates locally
  • Virus enters peripheral nerves and is transported to the central nervous system (CNS) (Sensory and Motor Nerves) Retrograde transport
  • Incubation period of a few days to more than a month
  • Non-specific flu-like signs

Virus rapidly disseminates within the CNS and spreads to peripheral nerves

28
Q

Rhabdoviruses - Rabies (Lyssavirus) (Signs and Symptoms)

A
  • During period of cerebral infection BEHAVIORAL CHANGES develop (confusion, hallucinations, insomnia)
  • HYDROPHOBIA (fear of water) is a classic sign of rabies and occurs in approximately 50% of cases
  • End result is COMA and DEATH
  • Once clinical signs of rabies appear, the disease is nearly ALWAYS FATAL (within 2 weeks) and treatment is typically SUPPORTIVE
29
Q

Rhabdoviruses - Rabies (Lyssavirus) (Prevention and Treatment)

A

Prevention:
-Vaccination of animals and high risk individuals

Treatment:
-1 dose of immune globulin and 5 doses of vaccine over a 28-day period
(Immune globulin and 1st dose of vaccine should be given ASAP; additional doses given on days 3, 7, 14, and 28)

30
Q

Rhabdoviruses - Rabies (Lyssavirus) (Diagnosis)

A

Virus isolation or Serology

Disease in animals may be confirmed post-mortem by the presence of NEGRI BODIES (distinct intracytoplasmic inclusions) in infected neurons, as well as through serology and viral identification

31
Q

Lymphocytic Choriomeningitis Virus (LCMV) (Arenavirus)

A
  • Rodent-borne virus which cause aseptic meningitis, encephalitis, or meningoencephalitis
  • Most infections are asymptomatic or produce a mild febrile illness
  • Pregnancy-related infection has been associated with abortion and neurological deficits
32
Q

Lymphocytic Choriomeningitis Virus (LCMV) (Transmission)

A

Humans become infected by INHALING INFECTIOUS AEROSOLIZED PARTICLES OF RODENT URINE, FECES, OR SALIVA or by ingesting food contaminated with virus

LCMV is naturally spread by the common HOUSE MOUSE, (Mus musculus)

Person-to-person transmission has not been reported; except for vertical transmission from mother to fetus

33
Q

Lymphocytic Choriomeningitis Virus (LCMV) (Disease)

A

Incubation of 1-2 weeks

  • BIPHASIC INFECTION*
  • 1 week of fever, malaise, anorexia, muscle aches, headache, nausea, and vomiting. Remission for a few days, followed by a SECOND PHASE of disease. This consists of symptoms of MENINGITIS or ENCEPHALITIS
34
Q

Lymphocytic Choriomeningitis Virus (LCMV) (Post-Disease)

A

Most patients recover completely
Temporary or permanent neurological damage is possible
Mortality is less than 1%

35
Q

Prions

A

Slowly developing neurodegenerative diseases (SPONGIFORM ENCEPHALOPATHIES), in humans and animals, were thought to be caused by a family of virsues known as SLOW VIRUSES
-Get vacuolization of the neurons

No virus isolated, no nucleic acid (genome) detected and agent found to be resistant to inactivation by chemical and physical methods which typically inactivate viruses

36
Q

Carlton Gajdusek

A

Demonstrated transmission of a human spongiform encephalopathy (Kuru) through the ingestion of contaminated “meat”

37
Q

Stanley Prusiner

A

Identified/implicated PRIONS (a small proteinaceous INFECTIOUS particle as the transmissible agent)

38
Q

Prion Diseases (Human Spongiform Encephalopathies vs Animal Spongiform Encephalopathies)

A

Human Spongiform Encephalopathies:

  • Kuru
  • Creutzfeldt-Jakob Disease (CJD)
  • Gestermann-Straussler-Scheinker Disease (GSS)
  • Fatal Familial Insomnia (FFI)

Animal Spongiform Encephalopathies:

  • Scrapie (sheep and goats)
  • Transmissible mink encephalopathy
  • Bovine spongiform encephalopathy (BSE; “mad cow” disease)
  • Chronic wasting disease (Mule deer, Elk)
39
Q

Nature of Prions

A
  • Lack detectable nucleic acid
  • Consists of aggregates of a protease, heat, and chemically resistant hydrophobic glycoprotein known as PrP (prion protein)
  • Humans possess a protein closely related to the prion protein on many cell surfaces (unknown function)
  • Infectious prion protein is either secreted or found in cytoplasmic aggregates
  • The normal cellular prion-related protein is referred to as PrPC, the infectious form is known as PrPSc (Scrapie prion protein)
40
Q

Nature of Prions (PrPC vs PrPSc)

A

PrPC protein: extended conformation containing numerous alpha-helices

PrPSc protein: globular conformation with beta-pleated sheets

41
Q

Prion Replication - A Theory

A

PrPSc binds to normal PrPC on cell surface –> PrPC is released and converts to PrPSc –> Cycle repeats

Aggregates (fibrils) form and are internalized by neuons

Neurons become vacuolated and amyloid plaques are deposited

42
Q

Prion Transmission

A
  • Not all spongiform encephalopathies are infectious (transmissible); some arise spontaneously or are inherited. This is thought to occur due to mutations in the PrPC gene
  • Following exposure, PrP replicates in the lymphatics and peripheral tissues. The protein is eventually found in the CNS (Neuronal vacuolization and loss, astrocyte and glial cell proliferation, AMYLOID PLAQUES are frequently observed)
43
Q

Prion (Cases)

A

15-20% of all cases are thought to occur through inheritance of mutation of the PrP gene

Remaining cases are thought to occur SPORADICALLY or through the unintentional use of tissues from infected individuals in medical procedures (corneal transplant, pituitary hormone)

Contaminated surgical instruments, etc may also play a role

44
Q

Prions - Mad Cow Disease

A

Prion proteins were (are?) thought to be species specific
-No evidence of transmission from animals to man

The epidemic of “mad cow” disease in England (1986) with a concurrent unusual incidence of CJD in young adults (1996) has led to the speculation that a “NEW VARIANT” of the BSE agent is responsible for causing CJD in humans

45
Q

vCJD

A

It is believed that the person who have developed vCJD became infected through their consumption of cattle products contaminated with the agent of BSE

46
Q

Prion Diseases (Clinical Syndromes)

A
  • Slow, progressive neurological degeneration
  • Incubation period is long (years to decades)
  • Death ensues rapidly (months) once symptoms appear (loss of muscle control, shivering, jerks and tremors, behavioral changes and dementia)
47
Q

Prion Diseases (Diagnosis and Treatment)

A

Diagnosis:

  • Postmortem histological examination of brain tissue
  • Serological tests are being developed for both human and veterinary use
  • Difficulty lies in distinguishing PrPC from PrPSc

Treatment:

  • NO TREATMENT for transmissible spongiform encephalopathies
  • Prolonged autoclaving, as well as concentrated bleach and sodium hydroxide solutions appear to aid in disinfection

Microbiology Exam V (6 decks)

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