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I & I Part II > Zoonotic Viruses > Flashcards

Zoonotic Viruses Flashcards

1
Q

Zoonotic Viruses

A
  • Arthropod Borne (Arbovirus)
  • Non Arthropod Borne (Hemorrhagic Fever and Encephalitis Viruses)
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2
Q

Zoonotic Viruses Reservoirs

A

Reservoir in lower vertebrates or insects.

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3
Q

Arthropod Borne (Arboviruses)

A
  1. Togaviruses
  2. Bunyaviruses
  3. Flaviviruses
  4. Reoviruses
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4
Q

Non Arthropd Borne

A
  1. Rhabdoviruses
  2. Arenaviruses
  3. Filoviruses
  4. Hantavirus (Bunyavirus)
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5
Q

Arbovirus Transmission

A
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6
Q

3 Major Manifestations of Arbovirus Disease

A

•Viral tropisms for human organs play important roles.

  1. CNS is primarily affected leading to aseptic meningitis or encephalitis.
  2. The second syndrome involves many major organs with particular damage to liver as in yellow fever.
  3. The third is manifested by hemorrhagic fever with damage to small blood vessels and intestinal and other hemorrhages.
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7
Q

Arbovirus Immunity

A
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8
Q

Togavirus and Flavivirus

A
  • ( + ) ss RNA icosohedral enveloped
  • Envelope contains hemagglutinin and lipoproteins
  • Alphavirus of the family Togaviridae and flavivirus of the family Flaviviridae include most of the arthropod borne viruses
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9
Q

Togavirus and Flavivirus Structure

A
  • Single stranded, positive sense RNA viruses
  • Enveloped virions, 40 to 70nm in external diameter
  • Envelope contains hemagglutinin and lipoproteins
  • Alphavirus of the family Togaviridae and flavivirus of the family Flaviviridae include most of the arthropod borne viruses
  • Each genus possesses its own unique structure of RNA genome
  • Replication can occur in cells of infected arthropods and vertebrate hosts
  • Viruses within these genera are frequently serologically related to one another
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10
Q

Western Equine Encephalitis

A
  • caused by Alphavirus
  • Western U.S.
  • Horses and Humans = blind hosts
  • more severe in children
  • Mild nonspecific febrile illness to aseptic meningitis, severe and overwhelming encephalitis.
  • Mortality estimated at 5% for cases of encephalitis.
  • Serious disease in infants below 1 yr of age;60% of survivors have permanent neurologic impairment
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11
Q

Eastern Equine Encephalitis

A
  • caused by Alphavirus
  • New England to South AMerica
  • usually animals, sometimes human outbreak
  • virus can cause severe encephalitis
  • highest attack rate –> infants and children
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12
Q

St. Louis Encephalitis

A
  • caused by Flavivirus
  • Major cause of arbovirus encephalitis in the United States
  • Mosquito vector: Culex tarsalis
  • Disease spectrum similar to western equine encephalitis virus; mild nonspecific febrile illness to aseptic meningitis, severe and overwhelming encephalitis
  • Major morbidity and mortality as well as highest attack rates among adults more than 40 years of age
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13
Q

Yellow Fever

A
  • caused by Flavivirus
  • Caribbean, Central America and South America.
  • Potential threat to the southeastern and southwestern United States because of presence of mosquito vector (Aedes aegypti)
  • abrupt onset of fever, chills, headache and hemorrhage
  • May progress to severe vomiting (sometimes with gastric hemorrhage), bradycardia (slowness of heart beat), jaundice and shock
  • Live attenuated yellow fever virus vaccine (17-D strain) recommended for endemic areas
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14
Q

Dengue

A
  • caused by Flavivirus
  • Distributed throughout the world, particularly in the Middle East, Africa, India, the Far East, and the Caribbean Islands.
  • Domestic vector: Aedes aegypti (mosquito).
  • Transmission cycle: human-mosquito-human, a sylvatic cycle involving monkeys may exist.
  • Clinical illness usually results in fever, an erythematous rash, severe pain in the back, hand, muscles and joints.
  • A severe form is characterized by shock, pleural effusion (liquid in lungs lining), and hemorrhage often followed by death.
  • Risk in Southeast/west U.S. because of the vector
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15
Q

Dengue Immunity

A
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16
Q

Japanese B. Encephalitis

A
  • caused by Flavivirus
  • Prevalent on Eastern coast of Asia, on its offshore islands (Japan, Taiwan and Indonesia) and in India.
  • Transmission cycle: mosquito, similar to St. Louis encephalitis and Western equine encephalitis viruses
  • High proportion of human infections are subclinical: especially in children
  • Development of encephalitis is severe and often fatal
  • Inactivated Japanese encephalitis (JE) vaccine (IXIARO) is licensed in the U.S. for use in 2 months and older
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17
Q

West Nile Virus

A
  • caused by Flavivirus
  • Epidemiology: Distributed throughout Africa, the Middle East, parts of Europe, the USSR, India and Indonesia

-West Nile infection has been appearing in the United States since 1999 and in Arizona from 2003

•Vector: mosquito

  • Principal vertebrate host: Bird
  • Transmission may be via transplanted organs or blood transfusion
  • During pregnancy, breast feeding
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18
Q

WNV Incubation

A

•2-14 days (average 2-6)

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19
Q

WNV Infection

A
  1. Asymptomatic
  2. West Nile Fever
  3. Severe West Nile Disease
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20
Q

WNV Asymptomatic

A

•About 80% of WNV-infected people do not get any symptoms.

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21
Q

WNV West Nile Fever

A
  • 20% infected people develop West Nile Fever
  • Typical case is mild characterized by fever, headache, backache, generalized myalgia
  • Rash appears in half of the cases, involving the chest, back and upper extremities
  • Generalized lymphadenopathy is a common finding
  • Pharyngitis and gastrointestinal symptoms (nausea, vomiting, abdominal pain) may occur
  • The disease runs its course 3 to 6 days, followed by recovery for several weeks
  • Children experience milder illness than adults
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22
Q

WNV Severe

A
  • 1 in 150 infected persons develop severe disease
  • WNV invades the nervous system causing aseptic meningitis, meningo-encephalitis, encephalitis, or West Nile poliomyelitis, especially in the elderly, and some cases result in death
  • Symptoms of severe disease include headache, fever, stiff neck, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. Severe disease may last for weeks and cause permanent injury or, in some cases, death.
  • Serious illness can occur in people of over age 50 and immunocompromised
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23
Q

WNV Lab Findings

A

•leukopenia CNS infection: CSF pleocytosis and elevated protein

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24
Q

[] chemokine receptor provides resistance to West Nile Virus infection.

A

CCR5 chemokine receptor provides resistance to West Nile Virus infection.

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25
Q

[] homozygosity is significantly associated with severe outcome.

A

Δ32CCR5 homozygosity is significantly associated with severe outcome.

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26
Q

WNV Diagnosis

A

•Serology, Confirmed by PCR

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27
Q

WNV Treatment

A

•supportive

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28
Q

WNV Prevention

A

•Antiviral and vaccine research underway

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29
Q

Zika Virus

A

•caused by Flavivirus

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30
Q

Zika Virus Epidemiology

A
  • South America, Africa, Southeast Asia, Puerto Rico
  • Cases now reported in the United States (Florida)
31
Q

Zika Virus Transmission

A

•Mosquitoes (Aedes agypti), mother-tochild (during pregnancy), sexual, blood transfusion

32
Q

Zika Virus Incubation

A

•2-14 days

33
Q

Zika Virus Symptoms

A

•Many people don’t have any symptoms. Most common symptoms include: fever, rash, joint pain, muscle pain, headache, conjunctivitis, which last for several days to a week (2-7 days).

34
Q

Zika Virus Severity

A

•infection during pregnancy can cause brain microcephaly and other brain defects, defects of the eye, ear and growth.

-Infants with microcephaly have several problems such as seizures, developmental delay, intellectual disability, problems with movement and balance, feeding problems, hearing loss, visual problems.

•In adults, Zika infection may also cause Guillain-Barre syndrome (GBS).

35
Q

Zika Virus Pathogenesis

A

•Not known, may involve innate and adaptive immunity, viral factors

36
Q

Zika Virus Diagnosis

A

•RT-PCR (blood and bodily secretions),IgM

37
Q

Zika Virus Treatment

A

•Supportive, No aspirin unless Dengue ruled out

38
Q

Chikungunya Fever

A
  • caused by Alphavirus
  • Transmitted by mosquitoes mainly in Asia, Africa, Southern Europe
  • Abrupt fever, excruciating myalgia and polyarthritis
  • Symptoms last for 1 week, musculoskeletal complaints persist for months
39
Q

Powassan Virus

A
  • caused by Flavivirus
  • The only known tick-borne Flavivirus
  • Species of North America
  • Isolated in Ontario from fatal human case of encephalitis
  • Not significantly related to humans
40
Q

Bunyaviruses

A

•3 genera are Arboviruses

  • Bunyavirus
  • Phlebovirus
  • Nairovirus

•1 is non-Arbovirus

-Hantavirus

• ( - ) ss RNA helical enveloped segmented

41
Q

Bunyaviruses Structure

A
  • Spherical, enveloped and single stranded negative sense, segmented RNA viruses
  • 90 to 100 nm in external diameter
  • Maturation by budding with smooth surfaced vesicles or near Golgi region of infected cells
  • California virus and hantavirus are the major disease causing bunyaviruses in North America
42
Q

California Virus

A
  • Bunyavirus genus of the Bunyaviridae family
  • Isolated in California
  • Major distribution in Midwest
  • Prevalence of Subtype La Crosse in Wisconsin, Minnesota, Ohio and Indiana.
  • Mosquito vector; Aedes triseriatus
  • Highest attack rates between 5 to 18 years of age.
  • Infection is characterized by abrupt onset of encephalitis and frequently with seizures.
43
Q

Reoviruses

A
  • Reovirus genus of the Reoviridae family
  • Colorado Tick Fever
  • Distributed throughout the Western United States
  • Typical illness occurs 3 to 6 days after the tick bite
  • Characterized by sudden onset with headache, muscle pain, fever and occasionally encephalitis.
  • Leukopenia (reduced leukocytes) is a consistent feature of infection.
  • One clinical illness for every 100 infections
44
Q

Arboviruses Diagnosis

A
  • Virus culture, Viremia in blood, Antibody test
  • Nucleic Acid genome - PCR
  • Detection of IgM antibody within few days of infection
45
Q

Arboviruses Treatment and Prevention

A
  • lSupportive care
  • Prevention: Primarily avoidance of contact with potentially infected arthropods
46
Q

Arboviruses Vaccinations

A
  • Vaccination: Inactivated vaccine for Western, eastern equine encephalitis virus infection for horses, but can be used for laboratory personnel.
  • Vaccine for Yellow Fever: Live attenuated yellow fever virus vaccine (17-D strain). A single subcutaneous dose results in the appearance of antibodies that persist at least 16 to 19 years. Booster doses are given every 10 years if needed.
  • Inactivated Japanese encephalitis (JE) vaccine (IXIARO) is licensed in the U.S. for use in 2 months and older
47
Q

Hantavirus

A
  • non-Arthropod
  • Hantavirus genus of the Bunyaviridae family
  • ( - ) ss RNA helical enveloped segmented
48
Q

Hantavirus Old World

A

•Old world hantavirus (Hantaan virus, Puumala virus, Dobrava virus, Seoul virus, Saaremaa virus) Disease: hemorrhagic fever with renal syndrome (HFRS) found across the world (Asia, Europe, Russia, Balkans, Scandinavia)

49
Q

Hantavirus New World

A

•New world species of hantavirus (Sin Nombre virus), Disease: hantavirus pulmonary syndrome (HPS) found in the United States (Southwest)

50
Q

Hantaviruses: Old World Hemorrhagic Fever with Renal Syndrome (HFRS)

A
  • Cause of hemorrhagic fever during Korean war
  • Detected in lung of wild rodents
  • Transmission by inhalation of infected rodent excreta, by the conjunctival route or by direct contact with skin breaks •Incubation period 1-2 weeks
  • Symptoms are headaches, back and abdominal pain, fever, chills, nausea, and blurred vision. Patients later develop low blood pressure, acute shock, vascular leak-age
  • Complicated by varying degrees of acute renal failure •Fatality rate is 5% to 15% •Diagnosis: IgM, viral antigen, viral RNA (RT-PCR)
  • Treatment: supportive, patient may require dialysis, Ribavirin (iv) may be useful, No vaccine.
51
Q

Hantavirus New World (Sin Nombre virus): Hantavirus Pulmonary Syndrome (HPS) in the United States (Southwest)

A
  • Southwestern (Four corner) outbreak in 1993 related to deer mice, caused by Hantavirus, Sin Nombre virus, caused fulminant respiratory disease with high mortality (56%).
  • Rodents also found in other parts of the United States and Canada.
  • Other species of hantavirus causing HPS found is found in the United States and also in Canada and South America.
  • Transmission by inhalation of infected rodent excreta, by the conjunctival route or by direct contact with skin breaks.
  • No human-to-human transmission reported in the U.S.
  • Incubation period: 1-5 weeks.
52
Q

Hantavirus Pulmonary Syndrome (HPS) Early Symptoms

A

•fever, fatigue, chills, headaches, aches in large muscle group (thighs, hips, back, shoulder), abdominal problems (vomiting, diarrhea)

53
Q

Hantavirus Pulmonary Syndrome (HPS) Second Phase

A

•starts 4 to 10 days after early symptoms that include coughing, shortness of breath, and heaviness around the chest as lungs fill with fluid

54
Q

Hantavirus Pulmonary Syndrome (HPS) Diagnosis

A

•clinical grounds, chest X-ray, IgM/IgG, viral antigen, RT-PCR

55
Q

Hantavirus Pulmonary Syndrome (HPS) Treatment

A
  • no specific treatment, involves respiratory support in intensive care unit
  • No vaccine
56
Q

Arenaviruses

A

• ( - / +) ss RNA helical enveloped segmented

57
Q

Arenaviruses Structure

A
  • Spherical enveloped and single stranded RNA viruses, 50 to 300 nm in diameter
  • Segmented genome [Two segments: ambisense (+/-) RNA], replication in cytoplasm
  • Maturation by budding from host cell.
  • Contain host cell ribosomes in their interior
58
Q

Arenaviruses Transmission

A

•By small rodents in which the virus is sustained for longer periods

-Primary infection of the rodents often results in disease and death, but chronically and perinatally infected rodents have lifelong viremia with no disease

  • Spread to humans by aerosols and close contact. Person-to-person spread by contact with body fluids may occur
  • Most significant infection - hemorrhagic fever
59
Q

Arenaviruses

A
  • Junin virus (Argentinean hemorrhagic fever)
  • Machupo virus (Bolivian)
  • Lassa virus (West Africa)
  • LCMV (Lymphocytic Choriomeningitis virus) of mice can cause infection in humans
60
Q

Arenaviruses Symptoms

A
  • Fever, shock and hemorrhage
  • Hepatitis, myocarditis
  • Viremia may be prolonged
61
Q

Filoviruses

A
  • Ebola and Marburg Viruses genera of the Filioviridae family
  • ( - ) ss RNA helical enveloped filamentous and highly pleomorphic
62
Q

Filoviruses Structure

A
63
Q

Filoviruses Replication

A
  • (-) viral RNA replicates in the cytoplasm
  • overwhelms host synthetic apparatus and defenses
  • rapid packaging and release of virus particles
64
Q

Filoviruses Disease

A

•Marburg and Ebola fever, two highly fatal hemorrhagic fevers

65
Q

Ebola Virus Transmission Cycle

A
  • Primary transmission: from infected animals
  • Natural Hosts: May be fruit bats
  • Person-to-person transmission: through direct contact, broken skin or mucous membrane, with sick person’s blood or bodily fluids(urine, feces, vomit, semen), contaminated needles or objects
66
Q

Ebola Virus Pathogenesis - Main Target Cells

A

•monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical & epithelial cells

67
Q

Ebola Virus Pathogenesis - Cell Entry

A

•macrophages and dendritic cells are probably the first cell type to be infected

68
Q

Ebola Virus Pathogenesis - Incubation Period

A

•2 - 21 days (average 4-10)

69
Q

Ebola Virus Pathogenesis - Initial Presentation

A
  • nonspecific, including flu-like symptoms such as fever (greater than 38.6oC or 101.5oF, myalgia (muscle pain), malaise, weakness, diarrhea, and vomiting, abdominal pain.
  • Further progression exhibits severe bleeding and coagulation abnormalities, GI bleeding, rash
70
Q

Ebola Virus Pathogenesis - Virus Spread in Patients

A

•Following replication in entry cells, the virus spreads to the regional lymph nodes and disseminates to various organs

71
Q

Ebola Virus Pathogenesis - Inflammation

A

•Extensive cytokines release, especially after infection of endothelial cells

72
Q

Ebola Virus Pathogenesis - Damage

A
  • to the liver, combined with massive viremia, leads to disseminated intravascular coagulopathy
  • The virus eventually infects microvascular endothelial cells and compromises vascular integrity.
73
Q

Ebola Virus Pathogenesis - Terminal Stages

A
  • diffuse bleeding and hypotensive shock account for many fatalities
  • Course of infection: 14 to 21 days
74
Q

Ebola Virus Immunity

A
  • Impairment in Adaptive Immunity: Impaired dendritic cell function and T lymphocyte apoptosis allow Ebola to cause severe disease Ø Virus found in several specimens with no evidence of immune response
  • Immunity in survivors: Antibodies against Ebola glycoprotein (GP) detected in recovered patients
  • Antibodies from recovered patients may be used for passive immunization (treatment) but requires scientific evidence for protection

I & I Part II (25 decks)

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