#11 Emerging Childhood Disease Flashcards
Viruses: Measles, Mumps, Rubella, Parvovirus B19, Varicell zoster, Human Herpes 6
Respiratory Trnasmission→
Replication in URT→ Viremia→ Target organs and Symtpoms
Measles, mumps, rubella→ viruses are controlled by
vaccines: each will typically cause disese in children and see seriousl sequelle in small number of individuals
Immunizations for MMR:
natural infections protects against re-infection and disease, each has only a single antigenic type—key to vaccine effectiveness!!!!
For MMR: -each virus has______ prior to infecting target organ where symptoms develop
systemic repication phase
MMR—______ develop as result of immunization can limit or block virus at this stage prior to infection of target organ
antibodies
-Humans are the only known host
MMR
Pathology of Measels
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
How do we get lifelong immunity to Measles
when virus infects endothelial cells and T cells
Measle life cycle
Paramyxovirade family- 1 segment virus, with fusion protein for fusion to endocytic vesicle, and HN in same protein
Vaccine status for measles:
Live attenuated vaccine- effective for single antigenic type, only host is human, Ab stop infection target organ (act during systemic replication)
typical Measles presentation
See MACULOPAPULAR rash, cough, conjunctivitis, coryza, photophobia, KOPLIK spots (white on inside of cheek)
Complications: otitis media, croup, *pneumonia, blind, encephalitis
see maculopapular rash + kolpick spots
typical measles
Atypical Measles
More intense rash, most prominent in distal areas, see vesciles; petechiae, purpura or uticaria
More intense rash, most prominent in distal areas, see vesciles; petechiae, purpura or uticaria
atypical measeles
Acute onset of headache, confusion, vomit, possible coma after rash dissipates
Postmeasles encephalitis
Subacute sclerosing panencephalitis
CNS manifestations (e.g personality, behavior, memory changes; myocolonic jerks; spasticity; and blindness)
________is our highest cause of death d/t measles
OR **more intense rash d/t previous immune response
Pneumonia
Virus for measesls
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
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
strong, long-lasting antiB response
Mumps clincal syndromes
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
see bilateral severly swollen parotics and fever
mumps
Vaccine status for mumps
Live attenuated vaccine- effective for single antigenic type, only host is human, Ab stop infection target organ (act during systemic replication)
Mumps
virus
genome
Paramyxovius, -ssRNA, via respoiratory secrations
Often Assymptomatic, Cause Parotitis (bilateral and with fever), orchritis, oophoritis, mastitis, pancreatitis, throiditis, mild meningitis
Mumps
paramyxovirius
-ssRNA
Infection path of mumps (paramyxo -ssRNA)
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)
Togavirus…. Only infects humans…has only 1 serotype… does not cause readily detctable
Rubella (German Measles)
Rubella family
genome
infection
Togavirus
RNA
via respiratory
(wear a ruby toga)
Route of rubella
URT (reticuloendothelial system cells)–> prinmary viremia to amplify the virus then secondary viremia, transmissino to other organs (skin/tissue) can go to fetus
Rubella goes to URT and organs to ______ then to ______ and can cross placenta to infect fetuc
primary viremia
secondary viremia
rubella pathology in
children:
adults:
mild rash
adults is worse: mild rash + arthrisi/arthrlagia
adult comes in with mild rash and joint pain… test for
rubella, kid may have mild rash too
Rubella pahtology in neonate under 20 weeks
Congenital rubella syndrome
cataracts/ocular/heart defects/ deafness/ mortality/ fail to thrive
Baby born with cataracts, microencephaly, heart issues and mental retardation… likely cause
Rubella~ toga virus
Pr and convrol of Rubella/togavirus
live attentuate vaccine
-ssDNA, Icosahedral, non-enveloped and replicated in nucleus. Depends on host DNA replication functions
Parvovirus B19
Parvovirus B19
genome
enveloped?
where does it replicate?
-ssDNA, Icosahedral, non-enveloped and replicated in nucleus. Depends on host DNA replication functions
Parvovirus infects:
rapidly replicating RBC progenitors in bone marrow (viremia)~ where most patho happens
Parvovirus has specific receptor:
-receptor is blood group P antiG (globoside) that’s expressed on mature erythrocytes, erythroid progenitors, megakaryocytes, endothelial cells, placenta, fetal liver and fetal heart
What phase must cel be in for parvovirus B19 to infect
- requires host cells to be in S phase for replication
- use cellular DNA polymerase to replicate
How is parvovirus spread in body
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
Can cause anemia for reduces hemoglobin…in chronic hemolytic anemia cause aplastic crisis
Parvovirus B19
Pathology of Parvovirus B19
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
Whats so tricky about Parvovirus B19
we see the lytic infection befrore or bright red rash appears
‘slapped cheek’ virus
Slap cheeked virus
maculopapular rash
lacy looking rash
dt Parvovirus B19
When Parvoviris is clinically apparent its callled
Fifth disease or eythema infectiosum
What do circularing immune complexes resopnding to Parvovirus B19 do
don’t fix complement… the cause rash, arthralgia and arthrisis
Big complication of ParvoB19
anemia d/t reduced cell number and hB lelffes
in chronic hemolytic pts get aplastic anemia d/t destruction of red blood cell progenitors
Inucbation of Parvo B19
For 7 days, inoculation of URT
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
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
Parvovirus B19 Transmited to fetus (vertically):
are there congentical defects?
cause still births, generatlized edema, anemia, CHF and is assoicated with fetal death but NOT congenital abnormatilies
