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Immunology 3 > #11 Emerging Childhood Disease > Flashcards

#11 Emerging Childhood Disease Flashcards

1
Q

Viruses: Measles, Mumps, Rubella, Parvovirus B19, Varicell zoster, Human Herpes 6
Respiratory Trnasmission→

A

Replication in URT→ Viremia→ Target organs and Symtpoms

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2
Q

Measles, mumps, rubella→ viruses are controlled by

A

vaccines: each will typically cause disese in children and see seriousl sequelle in small number of individuals

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3
Q

Immunizations for MMR:

A

natural infections protects against re-infection and disease, each has only a single antigenic type—key to vaccine effectiveness!!!!

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4
Q

For MMR: -each virus has______ prior to infecting target organ where symptoms develop

A

systemic repication phase

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5
Q

MMR—______ develop as result of immunization can limit or block virus at this stage prior to infection of target organ

A

antibodies

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6
Q

-Humans are the only known host

A

MMR

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7
Q

Pathology of Measels

A

Inoculation→ local replication in respiratory tract→ lymphatic spread→ viremia → wide dissemination→ conjuctivae/respiratory tract/urinary tract/small blood vessels/lymphatics/CNS→virus infected endothelial cells + immune T cells (this is where we get the rash AND lifelong immunity)→ RASH can cause

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8
Q

How do we get lifelong immunity to Measles

A

when virus infects endothelial cells and T cells

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9
Q

Measle life cycle

A

Paramyxovirade family- 1 segment virus, with fusion protein for fusion to endocytic vesicle, and HN in same protein

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10
Q

Vaccine status for measles:

A

Live attenuated vaccine- effective for single antigenic type, only host is human, Ab stop infection target organ (act during systemic replication)

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11
Q

typical Measles presentation

A

See MACULOPAPULAR rash, cough, conjunctivitis, coryza, photophobia, KOPLIK spots (white on inside of cheek)
Complications: otitis media, croup, *pneumonia, blind, encephalitis

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12
Q

see maculopapular rash + kolpick spots

A

typical measles

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13
Q

Atypical Measles

A

More intense rash, most prominent in distal areas, see vesciles; petechiae, purpura or uticaria

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14
Q

More intense rash, most prominent in distal areas, see vesciles; petechiae, purpura or uticaria

A

atypical measeles

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15
Q

Acute onset of headache, confusion, vomit, possible coma after rash dissipates

A

Postmeasles encephalitis

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16
Q

Subacute sclerosing panencephalitis

A

CNS manifestations (e.g personality, behavior, memory changes; myocolonic jerks; spasticity; and blindness)

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17
Q

________is our highest cause of death d/t measles

OR **more intense rash d/t previous immune response

A

Pneumonia

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18
Q

Virus for measesls

A

Live attenuated viruses given as combination→ 12-15 months and 4-6 yrs
→induce strong, long-lasting antiB response
→vaccine-induced immunity and blocks virus during system stage and prevents infection of target organs

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19
Q

Measles virus
: Live attenuated viruses given as combination→ 12-15 months and 4-6 yrs
→induce_________
→vaccine-induced immunity and blocks virus during system stage and prevents infection of target organs

A

strong, long-lasting antiB response

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20
Q

Mumps clincal syndromes

A

Infections are often asymptomatic such as Parotitis—almost always bilateral and accompanied by fever
Swelling of other glands: orchitis (can cause sterility), oophoritis, mastitis, pancreatitis, throiditis, CNS, mild meningitis, and rearely encephallits

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21
Q

see bilateral severly swollen parotics and fever

A

mumps

22
Q

Vaccine status for mumps

A

Live attenuated vaccine- effective for single antigenic type, only host is human, Ab stop infection target organ (act during systemic replication)

23
Q

Mumps
virus
genome

A

Paramyxovius, -ssRNA, via respoiratory secrations

24
Q

Often Assymptomatic, Cause Parotitis (bilateral and with fever), orchritis, oophoritis, mastitis, pancreatitis, throiditis, mild meningitis

A

Mumps
paramyxovirius
-ssRNA

25
Q

Infection path of mumps (paramyxo -ssRNA)

A

srtrats in URT (epithelial cells)–> then viremia–> infect parotid gland, testes, CNS, Eye, Inner Ear, Peripheral nerves, Ovaries, and Pancreas(may cause juvenile onset diabetes)

26
Q

Togavirus…. Only infects humans…has only 1 serotype… does not cause readily detctable

A

Rubella (German Measles)

27
Q

Rubella family
genome
infection

A

Togavirus
RNA
via respiratory
(wear a ruby toga)

28
Q

Route of rubella

A

URT (reticuloendothelial system cells)–> prinmary viremia to amplify the virus then secondary viremia, transmissino to other organs (skin/tissue) can go to fetus

29
Q

Rubella goes to URT and organs to ______ then to ______ and can cross placenta to infect fetuc

A

primary viremia

secondary viremia

30
Q

rubella pathology in
children:
adults:

A

mild rash

adults is worse: mild rash + arthrisi/arthrlagia

31
Q

adult comes in with mild rash and joint pain… test for

A

rubella, kid may have mild rash too

32
Q

Rubella pahtology in neonate under 20 weeks

A

Congenital rubella syndrome

cataracts/ocular/heart defects/ deafness/ mortality/ fail to thrive

33
Q

Baby born with cataracts, microencephaly, heart issues and mental retardation… likely cause

A

Rubella~ toga virus

34
Q

Pr and convrol of Rubella/togavirus

A

live attentuate vaccine

35
Q

-ssDNA, Icosahedral, non-enveloped and replicated in nucleus. Depends on host DNA replication functions

A

Parvovirus B19

36
Q

Parvovirus B19
genome
enveloped?
where does it replicate?

A

-ssDNA, Icosahedral, non-enveloped and replicated in nucleus. Depends on host DNA replication functions

37
Q

Parvovirus infects:

A

rapidly replicating RBC progenitors in bone marrow (viremia)~ where most patho happens

38
Q

Parvovirus has specific receptor:

A

-receptor is blood group P antiG (globoside) that’s expressed on mature erythrocytes, erythroid progenitors, megakaryocytes, endothelial cells, placenta, fetal liver and fetal heart

39
Q

What phase must cel be in for parvovirus B19 to infect

A
  • requires host cells to be in S phase for replication

- use cellular DNA polymerase to replicate

40
Q

How is parvovirus spread in body

A

URT infected then get replication locally or in erythroid precursors in bone marrow go to viremia then replicate in URT or see Rash and arthralgia Due to bone marrow virus see slight drop in Hb levels or life threatening aplastic anemia in those with hemolytic anemia

41
Q

Can cause anemia for reduces hemoglobin…in chronic hemolytic anemia cause aplastic crisis

A

Parvovirus B19

42
Q

Pathology of Parvovirus B19

A

Lytic infection transmitted before rash appears, See bright red cheeks, rash, circulating immune complexes
(IgM then IgG-cause rash, arthralgia, arthritis) If transmitted to fetus- still birth, edema, anemia, CHF, Fetal Death

43
Q

Whats so tricky about Parvovirus B19

A

we see the lytic infection befrore or bright red rash appears
‘slapped cheek’ virus

44
Q

Slap cheeked virus
maculopapular rash
lacy looking rash

A

dt Parvovirus B19

45
Q

When Parvoviris is clinically apparent its callled

A

Fifth disease or eythema infectiosum

46
Q

What do circularing immune complexes resopnding to Parvovirus B19 do

A

don’t fix complement… the cause rash, arthralgia and arthrisis

47
Q

Big complication of ParvoB19

A

anemia d/t reduced cell number and hB lelffes

in chronic hemolytic pts get aplastic anemia d/t destruction of red blood cell progenitors

48
Q

Inucbation of Parvo B19

A

For 7 days, inoculation of URT

49
Q

B19: Inucbation
Lytic, infection phase Noninfectious immunologic phase
For 7 days, inoculation of URT Decreased reticulocyte and HG levels at day 6
See virema and virus in through and nonspecific flulike at day 7 Virus specific IgG antiB~ from lytic to this stage
Rash/arthralgia at day 21

A 
7 days non infectious
inoculate in URT
lowers retics and hemaglobbin by day 6
viremia and virus day 7
virus specific IgG and antiB around day 10
rash at day 21
50
Q

Parvovirus B19 Transmited to fetus (vertically):

are there congentical defects?

A

cause still births, generatlized edema, anemia, CHF and is assoicated with fetal death but NOT congenital abnormatilies

Immunology 3 (20 decks)

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