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IHO Week 5 > PBL Measles > Flashcards

PBL Measles Flashcards

1
Q

measles DNA and structure (Diebel classification)

A 
ssRNA(-) (Group V)
Nonsegmented
Helical Nucleocapsid 
Enveloped 
Paramyxovirus
Morbillivirus
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2
Q

Route of entry

A

upper respiratory endothelium (maybe conjunctiva)

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3
Q

tropisms

A

lymphocytes

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4
Q

where does measles virus replicate

A

conjunctiva, respiratory tract, urinary tract, lymphatic system, blood vessels, central nervous system

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5
Q

measles incubation

A

10-12 days (10-14?)

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6
Q

replication cycle measles

A

-ssRNA –> +ssRNA = mRNA
this can be translated into capsomere proteins, and or used to replicate more -ssRNA (DNA of measles), then assembled inot virions which are released

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7
Q

proteins on measles that help it infect cells

A

hemogluttinin and fusion proteins (also what we make Ab to)

H mediates receptor attachment (to CD46, SLAM, or nectin-4) and fusion helps cause membrane fusion

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8
Q

what TLR recognizes measles

A

endosomal TLR7/7 (ssRNA)

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9
Q

what is measles transported through (ie air, fluids, blood)

A

respiratory droplets

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10
Q

measles AKA

A

rubeola

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11
Q

when is measles contagious

A

5th day of incubation to 2-3 days of rash

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12
Q

diagnostic features of measles

A

rash, Koplic spots, conjunctivitis, dry cough, serology

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13
Q

treatment measles

A

symptomatic
? Vitamin A? (third world countries)
treat secondary infections d/t immunosuppression

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14
Q

vaccination for measles

A

live, attenuated

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15
Q

human cell receptors that mediate measles infection of cells

A

CD46 - on all nucleated cells (cofactor in proteolytic inactivation of C3b and C4b)
SLAM - thymocytes, activated lymphocytes, mature dendritic cells, macrophages, and platelets. Absent from monocytes, NK cells, granulocytes (explains tropism).
Human nectin-4 - placenta cells, trachea cells (lesser degree)

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16
Q

Prodrome

A

10-14 days after exposure, lasts 2-4 days
Fever, cough, fatigue, decreased appetite, red watery eyes, runny nose (vomiting, diarrhea, sore throat, swollen glands/spleen), Koplik spots
Lasts 2-3 days, ends with onset of rash

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17
Q

Rash in measles

A

Around 14 days after exposure, after 2-4 days of prodrome
Starts on face, spreads to neck, trunk, arms and legs
Feel better about 2 days into rash, fades within 3-4 days
May be some fine peeling

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18
Q

Primary site of infection

A

respiratory epithelium of nasopharynx

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19
Q

When does primary viremia occur

A

2-3 days after invasion and replication in respiratory epithelium and regional lymph nodes

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20
Q

After primary viremia, what becomes infected

A

reticuloendothelial system (mononuclear phagocyte system (MPS) is a part of the immune system that consists of the phagocytic cells located in reticular connective tissue)

21
Q

Second viremia when

A

5-7 days after initial infection

22
Q

what becomes infected with second viremia

A

respiratory tract and other organs

23
Q

beneficence and measles vaccination

A

Do what is good for the patient (is protecting a child from a future measles infection doing good? Or is allowing them to not get the vaccine, preventing any adverse events, doing good?)

24
Q

non-maleficence and measles

A

Do no harm

Is vaccination harm (a shot, adverse event, etc.)? Is NOT vaccinating doing them harm (act of omission)?

25
Q

autonomy and measles vaccination

A

patient or guardian are only people who can make decision to vaccinate
Must have informed consent (Dr. provide accurate and complete information, no coercion)

26
Q

justice and measles vaccine

A

fairness of distribution (vaccinations accessible to all school-age children), also should people who ride on herd immunity be allowed to not vaccinate?

27
Q

warthin finkeldey cells

A

giant cells with inclusion bodies - present in measles, may be the infected cells that set off inflammatory measures leading to symptoms like conjunctivitis and cough (body trying to get rid of these cells?)

28
Q

pathogenesis conjunctivitis

A

after second viremia, infect cells of conjunctiva. CD8+ T cells attack these cells –> inflammation. Also macrophages release inflammatory cytokines.
Mast cells degranulate –> histamine, PGE2, LTD4

29
Q

inflammatory cytokines (released by macrophages)

A

TNF-a and IL-1 - induce local inflammation

30
Q

what does histamine do

A

increase vascular permeability

31
Q

PGE2 does

A

vasodilation and increased vascular permeability

32
Q

LTD4 does

A

increased vascular permeability

33
Q

pathogenesis fever

A

Macrophages encounter viral antigen –> release IL-1, TNF-a –> go to increase COX activity –> increased PGE2 in preoptic area –> shivering and increased metabolic rate –> body temp rises = set point of hypothalamus is raised

34
Q

pathogenesis rash

A

2 ways:
Type III HS (immune complex) - IgG binds antigen, complex binds FcgR on mast cells and PMNs causing degranulation
Type IV HS (cell-mediated) - T cells attack infected epithelial cells, release inflammatory cytokines (CD8+ kill infected stratum granulosum)–> rash
also C5a opsonization to mast cell degranulation

35
Q

CD8+ ways of killing infected cells

A

release perforin
Granzymes,
FasL
TNF production

36
Q

Pathogenesis loss of appetite and nausea

A

Infected enterochromaffin cells in GI tract –> release of serotonin –> vagal to solitary nucleus –> nausea and loss of appetite

37
Q

Pathogenesis vomiting

A

Infected enterochromaffin cells in GI tract –> release of serotonin –> vagal to solitary nucleus –> nausea and loss of appetite –> vagal motor efferent –> emesis

38
Q

Diarrhea

A

Possibly due to immunosuppression (from decreased IL-12), get secondary infection –> diarrhea
Or infected enterochromaffin cells –> release serotonin –> gastroenteritis, diarrhea
OR cell mediated toxicity of infected GI cells –> destroy villi –> diarrhea

39
Q

MHC Class I and Cell mediated toxicity

A

Virally infected cells present antigen via MHC Class I to CD8 T cells

40
Q

CD8+ response to infected cells

A 
Note: Activated by Th1
Sense intracellular pathogen on MHC class I, with CD8+ coreceptor. CD80/86 (B7) on infected cell = costimulatory signal. Binding through ICAM/LFA-3. Cell killing through perforins, granzymes, Fas-L, and TNF.
41
Q

Role of CD4 Th1 cells in combating measles

A

Recognize antigen on APC MHC class II –> costimulatory signals. IL-12 to polarize and proliferate into Th1 –> Th1 secretes IFN-g and TNF-a –> angry M1 macrophages, also license APC to show on MHC class I for CD8

42
Q

Role of CD4+ Th2 cells in combating measles

A

Activated closer to end of response (stimulated by IL-4)

Stimulate M2 healing macrophages (release IL-4, IL-5, IL-13), limit other immune responses

43
Q

CD8+ role in combating measles

A

Kill virally infected cells - activated following interaction iwth CD4+ and cross presentation of Ag to DC cells (licensed). Perforins, granzymes, Fas-L

44
Q

role of humoral immunity in measles

A

CD8+ cell mediated toxicity is more important in recovery from initial measles infection (hypogammaglobulinemia can still be vaccinated, live from measles)
Ab memory more important in re-exposure, to quickly shut down new infection (memory T cells take more time to proliferate)

45
Q

4 immunological functions of antibodies

A

complement fixation
agglutination
opsinization
toxin neutralization

46
Q

IgM and IgG roles in measles infection

A

IgM increase around day 10, first ig to help with initial infection, then clonal switching to IgG which there is way more of (peak around 25 days) and is the humoral memory

47
Q

Herd Immunity

A

More people who get vaccinated in a population, more protected those who cannot be (IC, young, old) will be d/t cannot contract and spread disease.

48
Q

Measles epidemiology

A

One of leading causes of death worldwide, despite safe and cheap vaccine
115000 deaths globally in 2014, mostly kids under 5
85% vaccination globally in 2014 (1 dose), want over 95%

IHO Week 5 (3 decks)

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