MMR (RNA Viruses) Flashcards

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1
Q

How is the measles virus different from the other Paramyxoviruses?

A

It lacks a neuraminidase activity (has an H protein rather than an HN) and it forms intracellular inclusion bodies.

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2
Q

What phase of life is Measles associated with and how is it spread?

A

Childhood; respiratory route

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3
Q

What is the latent period of Measles?

A

10-14 days

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4
Q

What are the symptoms of Measles?

A

2-3 prodrome of fever, cough, and conjunctivitis followed by a characteristic maculopapular rash

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5
Q

What does the rash coincide with in Measles?

A

T-Cell response (CD8) and virus clearance

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6
Q

What is the clinical definition of Measles?

A

Generalized rash (>3 days), Temperature >38.3 C, Cough, +/- Rhinorrhea, +/- conjunctivitis

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7
Q

Where is replication of Measles initially limited to? Where does it spread to after that?

A

Initially in trachea and bronchial epithelium, after 2-4 days to lymph nodes

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8
Q

What does replication of Measles in lymphoid tissue result in?

A

The appearance of lymphoid or reticuloendothelial giant cells (Warthin-Finkeldey Cells)

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9
Q

When do symptoms occur in Measles?

A

Soon after the onset of viremia

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10
Q

When is the patient infectious in Measles?

A

1-2 days BEFORE symptoms occur (10-20 days post exposure)

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11
Q

What are the two characteristic symptoms of Measles?

A

Maculopapular (morbilliform) rash and Koplik spots

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12
Q

What is the adverse effect that occurs during a Measles virus infection that will lead to suppression of delayed type HS skin test responses? What else is impaired?

A

Immunosuppression; Ab and cellular immune responses to new antigens

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13
Q

According to the timeframe given in the handout, what is the first Measles complication and when does it occur?

A

Acute disseminated encephalomyelitis (ADEM) or postinfectious encephalomyelitis (PIE); Occurs about 10-30 days after an infection.

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14
Q

What is ADEM/PIE? (no…. not just what does it stand for…) What does it do to you?

A

It is a autoimmune demyelinating disease associated with an immune response to myelin basic protein. Induction is unknown and not restricted to measles. Good prognosis

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15
Q

According to the timeframe in the handout, what is the second Measles complication and when does it occur?

A

Measles Inclusion Body Encephalitis (MIBE); occurs 1-9 months post infection

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16
Q

According to the timeframe in the handout, what is the third Measles complication and when does it occur?

A

Subacute Sclerosing Panencephaliits (SSPE); occurs 3-12 years after (more detailed chart says 6-10 years)

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17
Q

What are MIBE and SSPE resultant from?

A

Result from the establishment of persistent infections of the brain; mechanism of entry to CNS unknown, are fatal within years

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18
Q

What is the main method of prevention of Measles?

A

MMR; live-attenuated measles vaccine is effective and safe; administered in the trivalent (with mumps and rubella) at 12-15 mo. and again at 4-6 years

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19
Q

Why are both mumps and measles so easy to vaccinate against?

A

They both are antigenically stable monotype viruses; so once someone recovers they are immune for life

20
Q

Are there different strains of measles and mumps? Does it matter?

A

Yes there are, defined by AA differences in H and HN proteins but it doesn’t matter because neutralizing Ab to one protects against all known strains

21
Q

Why are Measles and Mumps good candidates for “eradication”

A

Only one serotype, most cases clinically identifiable, no animal reservoir, and “herd immunity” (98%) can be achieved with vaccine

22
Q

What are the factors limiting the MMR vaccine?

A

Pregnancy and Immune status

23
Q

What genus is Measles a part of?

A

morbillivirus genus of Paramyxoviridae

24
Q

What genus is Mumps a part of?

A

Rubalavirus genus of parayxoviridae

25
Q

What do the mumps initially infect? what is its incubation peroid? where does it spread? and where is it shed from for how long?

A

Nasal mucosa and URT epithelium; incubated for 18 days; spreads to draining lymph nodes; shed in saliva for 6 days before clinical disease

26
Q

What are the first clinical signs of the mumps?

A

Infection of the parotid gland (95% of cases)

27
Q

What are the complications of the mumps?

A

CNS involvement = aseptic meningitis and deafness

28
Q

What are some other mumps complications?

A

Symptomatic gonad involvement in post-pubertal men; correlation with T1 insulin dependent diabetes; myocardial invasion (rather frequently); and fetal wastage = spontaneous abortion in first trimester

29
Q

What are the prevention and control measures of Mumps?

A

Usually directed at prevention; live attenuated vaccine is safe and effective

30
Q

What type of virus is Rubella virus?

A

Small, enveloped, non segmented, + strand RNA’ member of Togaviridae

31
Q

How is Rubella virus (Ribiviruses) distinguished from Alphavirus?

A

Limited host range (humans)

32
Q

How does the rubella virus enter the host?

A

Via receptor-mediated endocytosis, viral envelopes fuse via pH dependent mechanism

33
Q

The genome of Rubella serves as what in translation of viral polymerase?

A

mRNA

34
Q

The polymerase of Rubella synthesizes what?

A
  • sense strand antigenome
35
Q

What does the antigenome of Rubella do?

A

Template for synthesis of subgenomic mRNA for viral capsid and envelope and more full length strand genomic RNA

36
Q

How is Rubella transmitted and where does it replicate?

A

Aerosols and in the mucosa of URT/Nasopharyngeal lymph nodes

37
Q

What does Rubella cause (disease wise)?

A

A mild disease with low grade fever, occasional conjunctivitis, sore throat, lymphadenopathy, and morbilliform rash that starts on face and spreads to body

38
Q

What is the incubation period for Rubella?

A

7-9 days before virus in serum

39
Q

Where can rubella virus be shed from and isolated?

A

Nasopharynx and isolated from nasopharynx and stool

40
Q

When does the rash of rubella start?

A

Day 16-21 post exposure

41
Q

How long can the Rubella virus continue to be shed after rash disappears?

A

Up to a month post exposure

42
Q

What are the most devastating effects of rubella?

A

In fetuses = congenital defects (Congenital rubella syndrome)

43
Q

When is the highest risk of pregnancy in regards to rubella?

A

first and second trimseter (typically 3rd is fine)

44
Q

What does infection with rubella during the first month of pregnancy usually result in? What happens if the baby makes it to term?

A

Spontaneous abortion; mental retardation, motor disabilities, hearing loss, congenital heart disease, cataracts

45
Q

What has the goal of the Rubella vaccine been?

A

To protect fetuses from infection

46
Q

What is the antiviral treatment for Rubella?

A

There is none, actual disease is mild; incidence low since vaccine in 1969