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x virology term 2 quiz 4 > arboviruses, rubella, and parvovirus B-19 > Flashcards

arboviruses, rubella, and parvovirus B-19 Flashcards

1
Q

what is phenotypic mixing of virions?
(when does it occur, how does it occur, how does it affect the phenotype and genotype of virions, and does the anomaly persist?)

A

occurs when two viruses infect the same cell
the genome of one parent may be enclosed by a coat determined, at least in part, by the genome of the other parent
phenotype may not correspond to genotype
disappears after one cycle of growth if further mixed infections are avoided

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2
Q

in which viruses does phenotypic mixing occur?

A

arboviruses
polioviruses
-myxoviruses
some other viruses

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3
Q

what is arbovirus short for?

how are they usually named?

A

arthropod-borne virus - epideiological subset of viruses

typically named for the disease they cause or where they were first identified

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4
Q

what are two taxonomic groups of arbovirus?

A

togavirus and flavivirus (there are others, but these are the only two we’re learning about)
will mention bunyaviruses (california encephalitis)

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5
Q

what qualities do togaviruses and flaviviruses share? (summary card)

A

1: small, enveloped
2: icosahedral nucleocapsid with single molecule of plus-stranded RNA - serves first as mRNA upon entry into the cell
3: most are arboviruses (transmitted by an infected blood-sucking arthropod vector) but this isn’t true of rubella or hep C

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6
Q

are togaviruses and flaviviruses enveloped?

A

yes, and are also small

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7
Q

what is the virion structure of togaviruses and flaviviruses?

A

icosahedral

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8
Q

what is the genetic structure of togaviruses and flaviviruses?

A

single molecule of plus-stranded RNA that serves first as mRNA upon entry into the cell

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9
Q

how are most arboviruses transmitted? which two are exceptions to this?

A

most are transmitted by an infected blood-sucking arthropod vector
not true of rubella (togavirus) or hep C (flavivirus)

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10
Q

describe the incubation of arboviruses (summary card)

A

requires multiplication in the arthropod host, so there are two incubation periods

1st: intrinsic incubation period - in humans - about a week, occasionally longer
2nd: extrinsic incubation period in mosquito or other arthropod - about 14 days - mosquito can’t transmit the virus for 14 days after biting the viremic animal - mosquito then infectious for life and not harmed by the virus

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11
Q

what is the intrinsic incubation period of arboviruses? (in what species does it occur and how long does it last?)

A

in humans

lasts about a week, occasionally longer

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12
Q

what is the extrinsic incubation period of an arbovirus? in what species does it occur? how long does it last?

A

when the arbovirus is multiplying in the arthropod after the arthropod bites and infected human
usually lasts about 14 days - can’t infect until incubation period complete

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13
Q

how many variations of arboviruses are known? what causes the variation?

A

hundreds are known
antigenic cross-reaction, genome sequences and other shared characteristics result in several taxonomic groups (including togaviruses and flaviviruses)

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14
Q

in what region are most arboviruses found?

A

most are tropical

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15
Q

what diseases and arboviruses can be found in the US? where would you find certain ones (rural versus urban)?

A

the only serious disease is encephalitis, caused by eastern equine encephalitis virus, western equine encephalitis virus, west nile virus, and the california group of encephalitis virus (the venezuelan encephalitis virus is occasionally seen in texas)
equine encephalituses usually occur in rural areas, st. louis in urban areas because mosquitoes that carry it like to breed in stagnant wastewater

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16
Q

can arboviruses be spread by human-to-human transmission?

A

no, with the rare exception of blood transfusions

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17
Q

how quickly does viremia occur in arboviral encephalitis?

A

since the arthropod vector introduces the virus into the blood, the viremia occurs quickly

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18
Q

what will increase viremia of arboviruses?

A

multiplication of the virus in the vascular endothelium

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19
Q

what is the disease course of arboviruses?

A

brief febrile malaise followed by encephalitis with paralysis, coma, and death

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20
Q

how are arboviruses treated?

A

no specific treatment is available

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21
Q

what type of virus are eastern and western equine encephalitis?

A

both are togaviruses

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22
Q

what is the most deadly arboviral encephalitis in the US?

A

eastern equine encephalitis

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23
Q

in what populations would you expect to see infections with eastern equine encephalitis?

A

mostly in children but also in adults living in swampy and wetland areas with high fatality

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24
Q

what does it mean for a species to be a “dead-end host” for a virus? give an example of when this occurs (species and virus).

A

the viremia rarely reaches the level required to infect mosquitoes and so it doesn’t continue to be transmitted via infected people
this is the case in humans and horses infected by eastern and western equine encephalitis

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25
Q

what species maintain the eastern and western equine encephalitis viruses?

A

birds and mosquitoes (both largely unaffected by the infection)
allows infection to survive despite the fact that horses and humans are dead-end hosts

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26
Q

what occurences preceed and may indicated an upcoming epidemic of eastern or western equine encephalitis?

A

excessive rainfall
abnormally high mosquito populations
best warning from high prevalence of virus in mosquitoes (discovered via PCR)

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27
Q

what are the standard control measures used to prevent an epidemic of eastern and western equine encephalitis?

A

1: reduction of mosquito population
2: avoidance of mosquitoes during epidemic

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28
Q

how are st. louis encephalitis and west nile virus similar? (summary card)

A

both are flaviviruses
antigenically related to each other
both cause encephalitis - fatal cases mostly in elderly
both maintained by bird–>mosquito–> bird cycles - humans are dead-end hosts

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29
Q

what kind of viruses are st. louis encephalitis virus and west nile virus?

A

arboviruses; flaviviruses

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30
Q

what virus is st. louis encephalitis antigenically related to?

A

west nile virus

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31
Q

how are st. louis encephalitis virus and west nile virus maintained (think species)?

A

by bird–>mosquito—>bird cycles

humans are dead-end hosts

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32
Q

where is St. Louis encephalitis virus indigenous to?

A

north america

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33
Q

where is west nile virus found?

A

native to north africa and the middle east - was recently imported to northeastern US and has rapidly spread throughout the US - now most common arbovirus infection in the US

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34
Q

what is the most common arbovirus infection in the US?

A

west nile virus

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35
Q

what causes the most common arboviral encephalitis world-wide?

A

japanese encephalitis virus (found in Japan and SE asia)

vaccine recommended for travelers

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36
Q

when do arboviruses epidemics occur?

A

in temperate zones, focal epidemics of short duration are seen
conditions must be just right for transmission (they don’t tell us what these conditions are)

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37
Q

what other patterns of disease due to arboviruses are seen outside of the US?

A

severe systemic liver degeneration (yellow fever)

non-fatal systemic disease with muscle pain and rash (classical form of dengue fever)

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38
Q

what type of virus causes dengue?

A

a flavivirus (arbovirus)

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39
Q

where is dengue fever found?

A

the tropics and subtropics, especially SE asian and the caribbean islands

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40
Q

what is the incubation period of dengue?

A

about 1 week

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41
Q

what are the symptoms of classic dengue fever?

A

fever, severe headache (retro orbital) muscle and joint pains, rash
sudden fever, malaise, cough, headache
severe pains in muscles and joints
enlarged lymph nodes, maculopapular rash, and leukopenia common
symptoms regress after week or so but weakness may persist

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42
Q

which two arboviruses share a pattern of transmission?

A

dengue and yellow fever

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43
Q

how many antigenic types of dengue virus are there?

A

there are 4 cross-reacting antigenic types (types 1,2,3,4)

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44
Q

for which viruses are humans not dead-end hosts?

A

dengue virus and yellow fever

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45
Q

what is dengue hemorrhagic fever? (where is it seen, symptoms, populations it affects)

A

a more severe, fatal form of dengue that has been in SE asia since the 1950s and has more recently appeared in the Caribbean
characterized by hemorrhage, vomiting, blood and shock
seen primarily in the native population - most visitors get the classical mild disease

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46
Q

what is the most likely theory to explain the occurrence of dengue hemorrhagic fever?

A

seen only in persons who have sequential infections with two different antigenically cross-reacting dengue viruses
in the second infection, the non-neutralizing but cross-reacting antibodies from the first infection bind teh virions to macrophages through the Fc receptor and promote macrophage infection
massive macrophage infection results in overproduction of lymphokines and cytokines
results in increased vascular permeability and hemorrhage

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47
Q

what type of virus is yellow fever?

A

flavivirus (arbovirus)

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48
Q

what is the incubation period of yellow fever?

A

about 7 days

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49
Q

where does yellow fever virus multiply?

A

multiplies first in the vascular endothelial cells

resultant viremia infects liver and other organs including spleen and kidney

50
Q

what are the symptoms associated with yellow fever?

A

fever, nausea, jaundice (from viral damage to liver cells), hemorrhage (black vomit)
starts with sudden onset of fever, headache, myalgias, and photophobia
progress to liver, kidneys and heart
prostration and shock occur
upper GI tract hemorrhage with hematemesis (black vomit)

51
Q

where is yellow fever found?

A

rural tropical africa and south america - endemic in both locations

52
Q

what is the mortality rate of yellow fever? can there be subclinical infections?

A

mortality rate is high but there can be occasional subclinical infections

53
Q

what is the pattern of transmission for urban yellow fever and dengue virus?

A

mosquito (aedes aegypti) –> humans –> mosquito (aedes aegypti) –> humans

54
Q

what is the cycle of transmission for jungle yellow fever?

A

in tropical forests:

monkey –> tree mosquito –> monkey –> tree mosquito –> humans –> aedes aegypti (mosquito) –> humans

55
Q

is there a vaccine for yellow fever? if so, what kind of vaccine and for how long is it effective?

A

live-attenuated (17-D vaccine)

give long-term protection

56
Q

how do yellow fever epidemic occur? where is there danger of epidemics?

A

there is danger of epidemics wherever aedes aegypti (strain of mosquito) is found
if an unvaccinated person enters during the incubation period the virus may spread to mosquitoes and then to the susceptible population
currently the situation in southeastern USA

57
Q

what are vertical infections?

A

neonatal infections acquired from the mother

other infection types are called horizontal

58
Q

what two pathways can lead to vertical infections? (list)

A

1: perinatal pathway
2: transplacental pathway

59
Q

what is the perinatal pathway of infection? how do infections caused by this pathway compare to horizontal pediatric infections?

A

neonate is infected during birth by contact with maternal blood or other fluids
infections generally resemble horizontal pediatric infections of the same virus

60
Q

what are some examples of perinatally acquired viruses?

A

HBV
HIV
herpes simplex type 2

61
Q

what is the transplacental pathway of infection? how do infections caused by this pathway compare to horizontal pediatric infections?

A

virus crosses placenta to invade the developing fetus

disease often different from horizontally acquired pediatric disease

62
Q

what are some examples of viruses spread by the transplacental pathway?

A

parvovirus B-19
rubella virus
cytomegalovirus
lymphocytic choriomeningitis virus

63
Q

how do viruses cross the placental barrier?

A

the placental barrier is impermeable to particles the size of the smallest viruses
some can penetrate barrier by replicating in placental tissue

64
Q

what are the defense mechanisms to viruses that the fetus has (4)?

A

1: maternal IgG
2: fetal antibody after fourth month (IgM)
3: interferon (probably adequate after 4th month)
4: cell mediated immunity?

65
Q

are parvoviruses enveloped?

A

no

66
Q

describe the virion structure of parvovirus B-19

A

icosahedral

67
Q

describe the genetic material of parvovirus B-19

A

linear, single-stranded DNA

68
Q

how is parvovirus B-19 transmitted?

A
  • -inhalation of respiratory aerosol from respiratory tract of an infected person
  • -Transplacental
69
Q

how common is parvovirus B-19 infection?

A

about 50% of adults are seropositive

70
Q

what is the normal course of infection by parvovirus B-19? (incubation period, symptoms)

A

14-day incubation period
asymptomatic or causes fever, malaise, and rash after the incubation period
rash = erythema infectiosum aka fifth disease or slapped cheek disease

71
Q

what is erythema infectiosum? what virus causes it? how?

A

aka fifth disease or “slapped cheek disease”
caused by parvovirus B-19
likely due to immune complexes (virions plus antivirion antibody) deposited in capillaries

72
Q

what type of tissue does parvovirus B-19 infect? what is the effect of infection of this tissue type?

A

has a tropism for erythroid precursors (RBC precursors)

as a result, infection inhibits RBC production for about a week

73
Q

in which patients does parvovirus B-19 cause transient aplastic crisis?

A

in patients with a pre-existing deficit in RBC production or with a pre-existing abnormally high rate of RBC destruction (eg sickle cell anemia)

74
Q

what will parvovirus B-19 cause in patients with immunological defects? how can this be treated?

A

can cause prolonged anemia since they cannot eradicate the infection
passive immunization with pooled human gamma globulin can cure these patients

75
Q

what is the most common symptom of infection with parvovirus B-19?

A

most often asymptomatic - the rash rarely seen or escapes notice
most commonly get acute and transient arthritis (lasts a few weeks or months)

76
Q

how can parvovirus B-19 be transmitted vertically?

A

via transplacental transmission

77
Q

what are the affects of fetal infection with parvovirus B-19?

A

primary B-19 virus infection during pregnancy can lead to fetal death no matter when in gestation
if during the 1st or 2nd trimester: some fetal deaths associated with hydrops fetalis (severe edema)
in 3rd trimester: intra-uterine fetal death but no hydrops

78
Q

what kind of virus is rubella virus?

A

a togavirus but not an arbovirus (because no arthropod transmission, though it has the same structure and pattern of multiplication as other togaviruses)

79
Q

how is rubella transmitted?

A

by respiratory aerosols from the respiratory tract of an infected person

80
Q

where does rubella virus multiply?

what happens after infection (replication cycle)? (lev)

A

in the respiratory epithelium
penetrates cell and uncoats
plus-strand RNA translated into several nonstructural and structural proteins
has RNA-dependent RNA polymerase, replicates genome by making a minus-strand template and then using that to make a plus-stranded progeny

81
Q

what is the course of infection of rubella virus?

A

multiplies in respiratory epithelium
followed by viremia
rash that lasts for about 3 days with fever and lymphadenopathy
rash starts on the face and progresses downward to involve extremities

82
Q

how does the structure and pattern of replication of rubella virus compare to other togaviruses?

A

the structure and pattern of replication are the same but rubella does not have an arthropod transmission step

83
Q

what diseases does rubella virus cause? (ie what are the common names?)

A

german measles aka the childhood rash

84
Q

what is the incubation period of rubella virus

A

18 days

85
Q

when is rubella virus excreted?

A

excreted from the respiratory tract one week before and after the rash

86
Q

why can rubella diagnosis be difficult?

A

sometimes subclinical

even with rash, is sometimes difficult to diagnose

87
Q

how long are those infected with rubella immune?

A

even subclinical infections produce lifelong immunity

88
Q

is there a vaccine for rubella? if so, what type? how is it administered?

A

there a live-attenuated vaccine

administered as part of the pediatric MMR vaccine

89
Q

how can rubella be vertically transmitted? what does this cause?

A

via transplacental transmission during the first trimester

causes congenital rubella syndrome

90
Q

what are the possible congenital abnormalities due to congenital rubella syndrome? (list - 5)

A

1: spontaneous abortion
2: cataracts
3: heart defects, especially patent ductus areteriosus
4: deafness
5: retardation
note: some of these, particularly deafness, may not be obvious at birth but become progressively worse in the early years of life

91
Q

what are the mechanisms of rubella virus action on the fetus (2)?

A

1: when used to infect tissue culture cells, many infected cells just grow more slowly and show no other cytopathic efect
2: in aborted infected fetuses only a small portion of fetal cells are infected - these cells are concentrated at a site of malnutrition

92
Q

what is the likelihood of malformation due to congenital rubella syndrome based on the timing of infection?

A

first month of gestation: 50% malformation
second month: 25%
third month: 9%
fourth month: 4%
risk is first trimester - if infection occurs after first trimester really not of clinical concern

93
Q

how long will rubella virus occur in individuals infected via transplacental transmission?

A

virus production through gestation

gradually decreases through first two years of life (mostly in urine)

94
Q

what is the fetus’s immune response to rubella virus infection?

A

fetal IgM rubella antibody is made
after birth, IgG antibody to rubella is also made
tolerance is not developed, despite the continued production of virus

95
Q

what is the main goal of administration of the rubella vaccine (what is it trying to prevent)? how is this accomplished?
how long does protection from the vaccine last?

A

the goal of the vaccine is to prevent congenital rubella
do so by interrupting the natural pattern of rubella epidemics by immunizing schoolchildren to provide herd immunity for non-immune pregnant women
to accomplish this:
1: nearly all children must be immunized
2: individual immunity must be maintained through the child-bearing years to reduce the number of susceptible pregnant women

immunity lasts at least 10 years

96
Q

what is done for seronegative women of child-bearing age to prevent congenital rubella?

A

these women are vaccinated but should avoid pregnancy for two months after vaccination
note, though, that no transpacental infection or congenital anomalies have been seen in about 100 accidentally vaccinated pregnant women, so the risk is only theoretical

97
Q

what are the major concerns regarding the spread of rubella?

A

1: children whose parents don’t allow for immunization
2: rubella cases in immigrant children
3: sero-negative immigrant women of child-bearing age

98
Q

what is the incidence of rubella in the US currently?

A

near-universal use of the rubella vaccine has blocked all childhood disease acquired in the US
congenital rubella syndrome has not been reported in 2005
note: still a major public health problem in developing countries

99
Q

how are roboviruses usually transmitted? (lev)

A

called robo because are usually rodent borne

rodent excrement is inhaled by human lung

100
Q

what are the two classes of togaviruses? (lev)

A

alphaviruses and rubiviruses
only rubivirus is rubella
all others are alpha

101
Q

describe the composition of rubella virus. (lev)

  • genome structure
  • nucleocapsid structure
  • envelope?
A

single-stranded RNA, positive
icosahedral nucleocapsid
lipoprotein envelope

102
Q

how many antigenic types of rubella virus are there? (lev)

A

one

103
Q

what is the difference between translation of rubella virus RNA and togavirus and poliovirus RNA? (lev)

A

rubella translated into several different proteins

other viruses are translated into one long protein that’s cleaved into functional proteins

104
Q

how is rubella virus diagnosed? (lev)

A

can be grown in cell culture but produces little cytopathic effect
usually identified by its ability to interfere with echovirus cytopathic effect
can also be made by observing 4-fold or greater rise in antibody titer between acute-phase and convalescent-phase sera in the hemaggluitination inhibition test or ELISA
also by observing presence of IgM antibody in single acute-phase serum sample
can also use PCR
determine definite fetal infection by amniocentesis - test amniotic fluid

105
Q

what can be done for pregnant women with rubella virus? (lev)

A

can be given immune serum globulins (IG) in first trimester if have been exposed to a known case of rubella
problems = can fail to prevent fetal infection
may confuse interpretation of serologic tests
recommended to terminate pregnancy

106
Q

what are the symptoms/clinical presentation of eastern equine encephalitis? (lev)

A

sudden onset of severe headache
nausea
vomiting
fever
changes in mental status, such as confusion and stupor
nuchal regidity, seizures, coma
usually severe CNS sequelae if patient survives

107
Q

how are eastern and western equine encephalitis diagnosed? (lev)

A

isolating virus or demonstrating a rise in antibody titer

108
Q

what seasons would you expect to see cases of equine encephalitis and st. louis and california encephalitis?

A

not in the winter because there are no mosquitoes - it’s unknown how the virus survives through these months - possibly in birds

109
Q

what is the clinical presentation of west nile virus? what percentage of people have symptomatic disease? (lev)

A

encephalitis with or without signs of meningitis, typically in persons over 60 years
less than 1% of those infected have symptomatic disease

110
Q

how is west nile virus diagnosed? (lev)

A

isolation of virus from brain tissue, blood, or spinal fluid
by detection of antibodies in spinal fluid or blood
PCR based assay

111
Q

how is yellow fever diagnosed? (lev)

A

either by isolating the virus or by detecting a rise in antibody titer

112
Q

what are the symptoms of dengue hemorrhagic fever? (lev)

A

fatality rate approaching 10%
initial clinical presentation same as that of classic dengue fever
then shock and hemorrhage, especially in the GI tract and skin

113
Q

what is the common clinical presentation in all arboviruses?

A

encephalitis
causes destruction that cannot be repaired
week incubation for most infections
paralysis coma and death

114
Q

what age group is preferentially affected by the different arboviruses? (west nile, St. Louis, equine)

A

west nile and St. Louis affect the elderly

equine viruses affect children

115
Q

whats a common pathway in the US to get infected by west nile without a mosquito? why?

A

blood transfusion
7 day window before symptoms appear so that person could donate blood and not know they are infected
surveys don’t catch risk factors
now screen for virus via PCR before transfusion

116
Q

what is often the first symptom of common dengue fever aka bonebreak fever?

A

intense headache behind the eyes

117
Q

why don’t we have malaria and yellow fever in the US?

A

mosquitoes were killed by DDT

118
Q

for which two viruses are humans not dead-end hosts?

A

dengue and yellow fever

119
Q

what phase do cells have to be in for parvovirus B19?

A

only grows in cells in S-phase

results in problems in cells that are turning over frequently, like RBCs

120
Q

how would you treat patients with parvovirus B19 who are immunocompromised?

A

give immunoglobulin from serum of immune patients

121
Q

what causes hydrops faetalis?

A

parvovirus B19

x virology term 2 quiz 4 (6 decks)

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