Viral Exanthems Flashcards
What is the etiology, taxonomy, genome, and morphology of rubeola?
measles virus, paramyxoviridae, morbillivirus, RNA single strand (-) sense, enveloped
what are the three major membrane associated proteins of rubeola? RNA associated?
F (fusion) H (Hemagglutinin), M (Matrix), N (Nucleoprotein), P (Phosphoprotein), and L (Large protein)
What are the features of F protein in rubeola?
surface glycoprotein, allows viral envelope to fuse with cell membrane, responsible for giant cell (syncitia formation),
What are the features of H protein in rubeola?
surface projection glycoprotein, hemagglutinin inhibition assay
What are the features of M protein in rubeola?
inner surface membrane, non-glycosylated, required for proper assembly of nucleocapsids and progeny release
What are the features of N protein in rubeola?
protects viral RNA
What are the features of P protein in rubeola?
replication of viral genome, RNA-dependent RNA polymerase
What are the features of L protein in rubeola?
not bale to classify well, possibly part of transcription complex
what are the physical properties of rubeola?
extremely liable, sensitive to: heat, UV, ether, and trypsin
How is rubeola transmitted?
airborne droplets from respiratory secretions (contact epithelium of nasopharynx or conjunctivae, stay suspended in air 2 hours), one of most communicable diseases, most infectious in late prodrome
what is the incubation period and most infectious period for classic rubeola?
“classic measles”, incubation- 7-21 days from exposure to onset of fever, contagious- 4 days before rash to 4 days after appearance of rash
What are the signs and symptoms of classic rubeola?
fever (crescendo, pk 5-6d), coryza (w/in 24 hr fever, sneeze, mucopurulent nasal drain), conjunctivitis, cough, koplik’s spots (2d b4 rash, oral mucosa by molars), rash (3-4d after illness onset, start hairline, spread down, feet= 3d, fade head to toe)
Who is likely to get modified rubeola? How does it differ from classic?
pts who have been passively immunized (Ig), infants with maternal Ab; disease milder and shorter duration
What childhood exanthema disease was declared eliminated in US only to rise again due to antivaccination? Which one is eliminated globally?
rubeola; small pox
What are some complications seen with rubeola?
otitis media, pneumonia, acute encephalitis (0.1%), subacute sclerosing panencephalitis (1:100K, progressive personality change, irreversible and fatal, CNS can’t clear due to M protein not expressed, see 7-10y after measles)
What type of immunity is seen with rubeola?
humoral response (IgG and IgA produced due to infection, long term protection) and cell mediated (T cell, major importance in recovery from acute, lack or poor T cell= persistent infection and often death)
What labs are used to diagnose rubeola?
PCR, serology (single IgM= acute, 4x rise in IgG titer w/ convalescent- 28d later), detect virus in resp or urine culture
What is the therapy for rubeola? prevention?
supportive and Vit A (50% reduction in mortality and morbidity i.e. blindness); passive Ig after exposure, active measles vaccine (live- not in pregnancy and severe immunodefficient, some HIV kids ok)
What is the etiology, taxonomy, genome and morphology or Rubella?
rubella virus (German measles), togaviridae, rubivirus, (+) single strand RNA, spherical, enveloped (lipid bilayer)
What are the important viral proteins in Rubella?
membrane glycoproteins E1 (hemagglutinin, surface projection), and E2 (membrane), nonmembrane protein C
What are the physical properties of Rubella?
relatively labile, sensitive to: heat, UV, Lipid solvents
How is postnatal Rubella infection spread? Prenatally?
droplets from respiratory secretions, prenatally infected cases multiple cases multiple tissues are persistently infected and serve as foci for transmission (urine)
What is the clinical course of Rubella?
incubation 12-23d, infectious 7d before and 7d after rash onset
what are the signs and symptoms of Rubella?
fever (normal or mild elevation), lymphadenopathy (begin 5-10d before rash, occipital, post-auricular, cervical chains), leukopenia and rash
What are the features of rash with Rubella?
maculopapular, 3 day rash, begins on face and spreads down, gone by 3rd day (comes on and resolves quicker than Rubella)
what are the complications of postnatal Rubella infection?
arthralgia/arthritis (kids rare, female adults up to 70%), Thrombocytopenia (1:3K), enceohalitis (1:5K), neuritis (r), and orchitis (r)
What is infected with congenital/prenatal Rubella?
serious damage to fetus, greater risk earlier in pregnancy (0-2wk 80%, by 14wk 6-10%, 20-30% overall), all germ layers affected (2ndary to cell necrosis, gen. vascular damage, chromos. aberrations, noncytolytic infection- virus persists)
What are the signs and symptoms (or lasting effects) of congenital Rubella?
growth retardation, cataracts, glaucoma, retinopathy, micropthalmia, deafness, Cardiac (PDA, VSD, PS), psychomotor retardation, microcephaly, spastic quadriplegia, MR, bone lessions, hepatomgaly, hepatitis, splenomegaly, and thrombocytopenia
What does the immune response look like for postnatal Rubella?
humoral- IgM tends to be short lived, no more than 8 weeks, IgG continues to be present; cell mediated- CD4+ and CD8+
What does the immune response look like for congenital Rubella?
humoral- both transplacentally acquired from mom and made by fetus, IgG (B), IgM (F), IgA (F), IgM prolonged up to up to 6 mo (most) or 2 yr (few) due to latent infection; Cell mediated- decrease rubella specific response
How is Rubella diagnosed? Prevented?
viral isolation in culture, PCR and serology (acute and convalescent); active immunization (contraindicated in pregnancy and sever immunodeficiency- some HIV kids ok)
What is the etiology, taxonomy, genome, and morphology of varicella?
“chickenpox”; varicella-zoster (HHV3), herpesviridae, dsDNA, enveloped
What is the mechanism of transmission of varicella?
airborne from respiratory secretion or aerosols from disrupted lesions, or direct contact with lesions (one of most communicable), contagious 1-2d before rash until lesions dry
What are the clinical manifestations of varicella?
incubation:10-21d (may be 10-28d if VZIG given), fever, central rash- starts on trunk moves to extremities, lesions in all stages or crops, macular -> papular -> vesicular -> pustular
How is varicella treated? prevented?
acyclovir (for severe or immune compromised); passive- VZIG, active- live, attenuated vaccine (Varivax), conatrindicated if pregnant, immmunodefficiency, some HIV kids ok, paired w/ MMR
What are some complications with varicella?
B superinfection (staph or strep, bulous varicells, cellulitis, sepsis) pneumonia, encephalitis, hemorrhagic, death (rare in kids, increased for adults and immune comp.)
What is the virus and mechanism behind zoster?
shingles, reactivation of latent HHV3 from sensory ganglion, pain generally precedes vesicular rash which is dermatomally restricted
What is the etiology, taxonomy, genome and morphology of roseola?
HHV6, herpesviridae, HHV6a and b, dsDNA, enveloped
How is roseola transmitted? Epidemiology?
respiratory droplets and salivary secretions; nearly 100% newborns gave maternal Ab wane by 6 mo, 90% seropositive by 2 and ~100% by 3
what is the incubation period and clinical disease features of roseola?
approx. 9-10d; fever- abrupt onset, very high, continuous 3-4d, exanthema- appearance corresponds with fever subsidence, macules or maculopapules (rose-pink), trunk-> neck-> upper extreme> face and lower extreme (Fever, Fever, Fever Rash!)
What are the complications seen with Roseola?
febrile seizures 10-15%, encephalitis (more severe and very rare)
What are the viral features, transmission and epidemiology of fifth disease (Parvovirus)?
human parvovirus B19- non-enveloped, icosahedral, small (22nm), ssDNA; respiratory droplet; late winter-spring, age 2-12 (peak @ 7y)
What is the incubation period and symptoms with 5th disease (parvovirus)?
6-14 days; mild or no systemic symptoms- most infectious prior to rash, rash- “slapped cheeks”, cephalocaudal spread, maculopapular
What are some complications seen with 5th disease (parvovirus)?
aplastic crisis (pt w/ hemaglobinopathy [sickle cell] @ increased risk), arthritis- poyarthropathy, most common in adult females (70%), and intrauterine infection- non-immune hydrops (severe anemia, can lead to miscarriage, serial ultrasounds)
what is the disease, family, genus, genome, morphology and replicative place of Variola?
small pox; poxvirus; orthopoxvirus (variola, vaccinia- cow or monkey); dsDNA linear; brick shaped; cytoplasm
What is the clinical manifestation of small pox?
incubation 7-17d, prodrome 2-3d w/ fever spike in middle;
What is the pathogenic course of small pox?
Infection 3d- nose, mouth pharyngeal mucosa-> regional lymph node then Latent period 4-14d, viremia, spread to spleen, liver and reticuloendothelial system finally prodromal 2-3d viremia to dermis, abrupt onset of headache (severe), backache, fever 40C, enanthema- change in mouth, tongue and oropharynx
What are the phases of the exanthem associated with small pox?
follows prodrome; eruption maccules 1-2d, papules 1-2d, vesicles 2-3d, pustules 5-8d, crusts 5-7d, and desquamation weeks; lesions all evolve together
What are some additional clinical manifestations of small pox?
panopthalmitis-1%, keratitis-1%, arthritis-2% of kids, Encephalitis-<1%, 2ndary B infection, and pockmarks- 65-80%
What are the 5 classifications of spall pox (WHO) an differences?
Variola- most common, 30% mortality; Modified- milder, 25% vaccinated individuals, rarely fatal; Hemorrhagic- <1%, difficult to diagnose, presumed to be related to immune status of host, always fatal; Variola sine eruption- previously vaccinated, infants w/ maternal Ab, transmission not documented; and Flat- flater lessions, evolve slow, coalesce, large areas desquamation, 7% unvaccinated, very high mortality (90-97%)
