leftover viruses (enteroviruses, mumps, adenoviruses, parovirus B19) Flashcards

1
Q

enteroviruses
enveloped/nonenveloped:
capsid shape:
genome:

A

enteroviruses
enveloped/nonenveloped: nonenveloped
capsid shape: icosahedral
genome: + ssRNA

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2
Q

enterovirus subenera (5)

A

1) polio virus, 1-3
2) Group A coxsackieviruses, 1-24
3) Group B coxsackieviruses, 1-6
4) Echoviruses, 1-34
5) a bunch with no subgenus, but just a type #

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3
Q

transmission of enteroviruses

A

1) fecal oral (like polio)
2) respiratory
3) both
* transmission can be direct or indirect (fomite, water, food)

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4
Q

pathogenesis of enterovirus?

A

1) infect mucosa and associated lymphatic tissue of GI or respiratory route —> minor viremia
2) next infect reticuloendothelial system of liver, spleen, bone marrow —> major viremia
3) spread to other organs —> specific manifestations

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5
Q

The manifestations of enteroviral infections discussed, and the subgenera typically associated with them.

A

1) Polio
2) aseptic (viral) meningitis
3) group A coxsackieviruses: exanthems (rashes) and enanthems (mucosal lesions)
4) group B coxsackieviruses: myocarditis, pericarditis

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6
Q

90% of aseptic (viral) meningitis are caused by?

A

enteroviruses

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7
Q

when does viral meningitis, caused by enterovirus, typically occur?

A

late spring through fall in temperate climates

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8
Q

peak ages for viral meningitis?

A

<1 yo and 5-10 yo

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9
Q

how long does it usually take to recover from aseptic meningitis caused by enterovirus?

A

3-7 days

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10
Q

exanthems (rashes) and enanthems (mucosal lesions) are usually caused by which enterovirus? in who? how long is the recover?

A

group A coxsackieviruses
in children, 3-10 yo
recovery: 7-10 days

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11
Q

manifestations of hand-foot-mouth disease. What causes it?

A

fever and lesions on buccal mucosa, tongue, hands, feet and buttocks
- caused by enteroviruses, especially group A coxsackieviruses

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12
Q

manifestations of herpangina? what causes it?

A

ever, vesicles on fauces and soft palate

- caused by enteroviruses, especially group A coxsackieviruses

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13
Q

which enterovirus causes myocarditis and pericarditis?

A

group B coxsackieviruses (and many other viruses)

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14
Q

manifestations of myocarditis

A

fever, chest pain, dyspnea, arrhythmia, rarely heart failure

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15
Q

pericarditis manifestations

A

sharp stabbing chest pain exacerbated by lying down and deep breathing, fever. Rarely leads to constrictive pericaditis or cardiac tamponade

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16
Q

how is enterovirus diagnosed?

A

usually syndromic diagnosis
if the detection of the virus is important: PCR is the most sensitive and specific, but it’s very expensive. Culturing has generally low sensitivity, and there are no immunoassays

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17
Q

treatment and prevention of enterovirus infections?

A

1) supportive txt– there are no effective antivirals for enterovirus
2) polio is the only enterovirus for which there’s a preventative vaccine

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18
Q

how is mumps transmitted?

A

respiratory droplets/saliva via direct or indirect (fomites) contact

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19
Q

pathogenesis of mumps

A

1) virus replicates in respiratory epithelium, leading to viremia
2) then infects the parotid glands and variable other sites (CNS, testes, ovaries, etc)

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20
Q

salivary glands infected with the mumps show…

A

interstitial edema with a serofibrinous exudate and mononuclear infiltrate

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21
Q

incubation period for mumps

A

16-18 days

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22
Q

manifestation of the mumps

A

nonspecific prodrome w/fever/malaise
pt complains of earache and pain with palpation of parotid gland, followed by swelling of gland and constant pain
- the 2nd parotid gland ins involved in 75% of cases and the submaxillary salivary gland is involved in 10% of cases

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23
Q

how long does it take for mumps to resolve generally?

A

7-10 days

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24
Q

2 more common complications with mumps

A
  1. orchitis in 30-40% of post pubertal men (frequently bilateral, sterility = rare)
  2. aseptic meningitis in 10% of adults (less common in kids)
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25
Q

5 rare complications of mumps

A
  1. hearing loss (children)
  2. encephalitis
  3. fetal loss in 1st trimester
  4. oophoritis
  5. pancreatitis
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26
Q

diagnosis of mumps is made by:

A

symptoms and exposure history. confirmed by serology (IgM or acute and convalescent titers), or detection of virus in saliva by culture or PCR)

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27
Q

is there a vaccine for mumps? if so, what type is it, and how did it change the effects of the disease?

A

yes, it’s an ettenuated virus vaccine. before it there were 200,000 cases/yr in the us, not there are a few hundred

28
Q

when is the vaccine for mumps given?

A

at 12-15 months and 4-12 years

29
Q
adenovirus
capside shape:
envelope status:
genome:
serotypes:
A
adenovirus
capside shape: icosahedral
envelope status: nonenveloped
genome: dsDNA
serotypes: 51 (1-51) with 5 subgroups (A-F)
30
Q

adenovirus modes of transmission (3)

A
  1. respiratory
  2. fecal-oral
  3. ocular fluid (fomites)
31
Q

adenovirus pathogenesis

A
  1. initial infection at site of entry often symptomatic
  2. viremia can occur, with manifestations at other sites
  3. clinically latent infection can last for years, the mechanism is unknown, but there’s periodic, asymptomatic shedding, and symptomatic reactivation can occur in immunocomp hosts.
32
Q

what are the 2 problems with clinically latent adenovirus infection?

A

It can last for years, and the mechanism is unknown, but

1) there’s periodic, asymptomatic shedding, 2) symptomatic reactivation can occur in immunocomp hosts.

33
Q

how does adenovirus evade the immune system?

A
  1. It blocks Fas-FasL mediated apoptosis of infected cell by mutiple mechanisms (viral RID induces endocytosis and degredation of FAS)
  2. Reduces class I MHC expression (E1A protein blocks transcription at MHC-1 promoters, and GP19 binds MHC-1 in ER, targets them for recycling and retention)
34
Q

4 manifestations of adenovirus

A
  1. respiratory infections (upper and lower)
  2. Ocular: outbreaks of ocular ifxns, including pharyngoconjunctival fever (pharyngitis and conjunctivitis) and epidemic keratoconjunctivitis
  3. Gastrointestinal- small percentage of diarrheal illnesses (self-limited watery diarrhea)
  4. Immunocompromised Pt:
    - pt undergoing hematopoietic stem cell transplant: virus can cause hemorrhagic cystitis, enteritis, pneumonitis and hepatitis w/in first 100 days of transplant
    - pt undergoing solid organ transplant usually suffer manifestations of adenovirus in the transplanted organ
35
Q
respiratory adenovirus ifxns
where:
manifestations:
resolution period:
what pops:
A

respiratory adenovirus ifxns
where: upper and lower resp. tract
manifestations: no differentiating symptoms from other viral resp ifxns
resolution period: self-limiting, 3- days
what pops: closed pops (like military)

36
Q
pharyngoconjuntival fever
caused by what virus:
manifestations:
where do people get it from:
time to resolution:
A

pharyngoconjuntival fever
caused by what virus: adenovirus
manifestations: follicular conjunctivitis and pharyngitis
where do people get it from: swimming pools, lake outbreaks
time to resolution: self-limited, resolves in 2-3 days

37
Q
epidemic keratoconjunctivitis
caused by what virus:
manifestations:
where do people get it from:
time to resolution:
A

epidemic keratoconjunctivitis
caused by what virus: adenovirus
manifestations: follicular conjunctivitis —-> to corneal subepithelial lymphoid infiltrates.
where do people get it from: outbreaks in military/within ophthalmic practices
time to resolution: It can be severe with persistent corneal opacities

38
Q

gastrointestinal adenovirus ifxns

A

acute, watery diarrhea in infants lasting 8-12 days

39
Q

how does adenovirus affect people who had a hematopoietic stem cell transplantation (HSCT)?

A

virus can cause hemorrhagic cystitis, enteritis, pneumonitis and hepatitis w/in first 100 days of transplant
-viremia is common, so there’s some monitoring of viremia done in pediatric transplant programs

40
Q

how does adenovirus affect people with organ transplants?

A

pt undergoing solid organ transplant usually suffer manifestations of adenovirus in the transplanted organ, with manifestations common to that organ

41
Q

what 3 risk factors increase the likelyhood that people with Hematopoietic stem cell transplants (HSCT) will have symptomatic ifxn with adenovirus?

A
  1. childhood (3x more than adults)– -viremia is common, so there’s some monitoring of viremia done in pediatric transplant programs
  2. t-cell depletion of graft
  3. extent of immunosuppression
42
Q

how is adenovirus diagnosed?

A
  1. by detection of virus in specimen from infected site (immunoassays, viral culture or PCR)
43
Q

how is adenovirus treated? (2 mech)

A
  1. cidofovir– a nucleotide analogue that is incorporated into viral DNA by viral DNA polymerase, then it inhibits DNA replication
  2. oral vaccine with un-attenuated types 4 and 7 are used in the us military
44
Q

what is cidofovir and what is it used for?

A

it’s a a nucleotide analogue that is incorporated into viral DNA by viral DNA polymerase, then it inhibits DNA replication
- it’s used to treat adenovirus

45
Q

adenoviruses have been studied to be used for:

A

gene therapy and vaccine development

46
Q

the advantages of using adenoviruses for gene therapy (3)

A
  1. easily produced
  2. infect many cell types
  3. stable incorporation of gene inserts
47
Q

disadvantages of using adenovirus for gene therapy

A
  1. viral dna not incorporated into host DNA
  2. host response —> toxicity
  3. host immunity —> viral neutralization
  4. poorly understod risk of ifxn with HIV following immunization with eperimental vaccine (Ad5 with HIV Ags)
48
Q
parvoviruses
size:
envelop status:
capsid shape:
genome:
A

size: small
envelope status: nonenveloped
capsid shape: icosahedra
genome: ss + or - DNA

49
Q

what is the most important parvovirus infecting human beings

A

Parvovirus B19

50
Q

two type of transmission of Parvovirus B19

A
  1. respiratory

2. vertical (less common)

51
Q

Parvovirus ifxns are common amongst

A

school-age children (50% of 15 yo have been infected– have Abs)

52
Q

what is the primary site of replication of parvovirus B19?

A

human erythroid precursor cells

53
Q

how does Parvovirus 19 get into erythroid precursor cells?

A

it binds to the P Ag on erythroblasts

54
Q

what happens to erythroblasts when they’re infected with parvovirus B19?

A

they become enlarged with nuclear inclusions, die and release the virus

55
Q

how does parvovirus B19 affect immunocompetent people?

A

it temporarily stops erythropoiesis in immunocompetent individuals

56
Q

acute infection with parvovirus B19? the next phase of infection?

A
  1. fever, chills, headache and myalgia

2. rash and arthralgia

57
Q

hematological changes from parvovirus B19?

A

reticulocytes are reduced and then Hemoglobin is reduced. Reticulocytes improve first and go above normal before normalizing.

58
Q

viremia is highest when in the parvovirus B19 ifxn?
Igm?
IgG:

A

viremia: day 7
IgM: about day 14-28
IgG: day 21-forever

59
Q

common manifestations of parvovirus B19 Ifxnsin children

A
  1. 5th disease or erythema infectiosum- childhood viral exanthem
  2. nonspecific prodrome (fever, etc) followed by characteristic “slapped cheek” rash 2-5 days later, variably followed by maculopapular rash on trunk and limbs that becomes lacey as it fades
60
Q

slapped cheek rash is associated with which virus?

A

parvovirus B19

61
Q

how does parvovirus B19 affect joints?

how long does it last? who does it affect?

A

causes arthropathy:
symmetrical swelling and pain of the small joints of the hands and feet
-usually resolves in 1-3 wks, ocassionally persists 1 month
-primarily occurs in adults, more common in women than men

62
Q

how does parvovirus affect the RBCs

A
  1. aplastic crisis in pt with underlying hemolytic disorders (ie sickle cell disease). it’s self-limited and can be severe
  2. Pure red cell aplasia has several causes: a) immunocomp. pt (eg congenital immunodef., AIDS) b) persistent anemia and viremia c) low/no Abs to parvovirus B19
63
Q

usually parvovirus B19 during pregnancy has no consequences for the fetus, but sometimes, there can be 3 adverse outcomes of primary ifxn

A
  1. reduced RBC in fetus
  2. fetal death
  3. fetal hydrops (fluid collections, eg ascites, pleural effusions)
64
Q

diagnosis of parvovirus B19

A
  1. syndromic diagnosis is often adequate
  2. if detection is important, PCR (interpretation of results can be confounded by persistence of low levels of virus following primary ifxn)
65
Q

treatment/prevention of parvovirus B19

A
  1. no antivirals for parvovirus B19, but that’s ok bc 1, most ifxns = self-limited
  2. transient aplastic crisis is treated with RBC transfusions if needed
  3. immunosupporessed pt with persisten ifxn and anemia benefit from iv IgG