B3 measles Flashcards

(44 cards)

1
Q

What happens in an acute symptomatic infection?

A

→ Infection of a small number of cells, followed by multiple cycles of viral replication.

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2
Q

How does an acute infection spread?

A

It can stay local or spread systemically.

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3
Q

What are the outcomes of an acute symptomatic infection?

A

Clearance by the immune response and recovery, or progression to chronic/latent infection or death.

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4
Q

What is the typical duration of an acute symptomatic infection?

A

Days to weeks.

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5
Q

How contagious is measles?

A

One of the most contagious diseases.

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6
Q

What is the mortality rate of measles in developed countries?

A

→ 0.1%.

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7
Q

What is the mortality rate of measles in developing countries?

A

→ 5-10%.

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8
Q

How are paramyxoviruses transmitted?

A

Readily via the respiratory route.

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9
Q

What are the two patterns of infection caused by paramyxoviruses?

A
  1. Localised respiratory infections (e.g., RSV, hMPV). 2. Systemic infections (e.g., measles, mumps).
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10
Q

Why are paramyxoviruses dangerous for infants?

A

Localised respiratory infections are trivial in adults but can be severe in infants and children.

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11
Q

How is measles transmitted?

A

Aerosol droplets.

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12
Q

Where does measles initially replicate?

A

Upper respiratory tract epithelium.

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13
Q

What happens in primary viraemia?

A

Virus is mainly associated with lymphocytes and macrophages, with little free virus in the blood.

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14
Q

Where does measles replicate after primary viraemia?

A

Lymphoid tissues (spleen, lymph nodes, appendix, tonsils).

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15
Q

What happens in secondary viraemia?

A

Virus spreads to organs such as skin, conjunctiva, liver, kidney, lungs, and gut.

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16
Q

What causes the characteristic measles rash?

A

Immune response to virus-infected endothelial cells.

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17
Q

What are the main symptoms of measles?

A

Fever, cough, runny nose (coryza), conjunctivitis, maculopapular rash.

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18
Q

What are Koplik’s spots?

A

White spots inside the mouth, a hallmark of measles.

19
Q

What is giant cell pneumonia?

A

Severe pneumonia caused by syncytia formation, often fatal in immunocompromised patients.

20
Q

How does measles suppress the immune system?

A

Infects and depletes memory B and T cells, causing “immune amnesia” and increased risk of secondary infections.

21
Q

What bacterial infections are common after measles?

A

Otitis media (ear infection) and pneumonia (~15% of cases).

22
Q

What is the leading cause of measles-related deaths?

A

Pneumonia (60% of deaths).

23
Q

What is measles encephalitis?

A

Inflammation of the brain, occurring in 1 in 1000 cases, often causing neural damage.

24
Q

What is SSPE?

A

A rare, fatal, slow-progressing CNS disease occurring years after measles infection.

25
Who is at highest risk of SSPE?
Males and those infected with measles under 2 years old.
26
What causes SSPE?
Persistent defective (non-infectious) measles virus in the brain, triggering a hyperimmune response.
27
What type of genome does measles have?
Negative-sense single-stranded RNA (-ve ssRNA).
28
What proteins are important for measles virus entry?
H protein (docking) and F protein (fusion).
29
What cellular receptors does measles target?
CD46/CD150 on lymphocytes and epithelial cells.
30
What is the function of RdRp in measles?
Transcribes the genome into mRNA and replicates it into a full-length positive-sense copy.
31
How does measles virus assemble and release?
F & H proteins move to the cell membrane, M protein associates with RNP, leading to viral release.
32
What is syncytia formation, and why is it important?
Measles virus induces fusion of infected cells, forming multinucleated giant cells.
33
What is more important for clearing measles: T cells or antibodies?
→ T cells.
34
What causes the symptoms of measles?
Immune response rather than direct viral damage (e.g., cytokines cause fever, T cells attack infected endothelial cells causing rash).
35
Why is the absence of a rash a bad sign in measles?
→ Indicates poor T cell response and poor prognosis.
36
What is required for lifelong immunity to measles?
A strong antibody response (IgG) prevents reinfection.
37
Why is measles vaccine effective?
Only one serotype, live attenuated vaccine, induces a strong immune response.
38
What does the MMR vaccine protect against?
Measles, mumps, and rubella.
39
hy are two doses of measles vaccine given?
First dose may be neutralised by maternal antibodies; second dose ensures full immunity.
40
Why is high vaccine uptake essential?
To achieve herd immunity and break the chain of transmission.
41
What are examples of localised acute infections caused by paramyxoviruses?
Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV).
42
Why does measles have little free virus in the blood during primary viraemia?
The virus is mostly associated with immune cells like lymphocytes and macrophages.
43
What does “gradient of transcripts” mean in measles virus transcription?
RdRp transcribes genes in a sequential manner, leading to higher levels of 5’ genes and lower levels of 3’ genes.
44