Viral Exanthems Flashcards

1
Q

What is the etiology, taxonomy, genome, and morphology of rubeola?

A

measles virus, paramyxoviridae, morbillivirus, RNA single strand (-) sense, enveloped

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2
Q

what are the three major membrane associated proteins of rubeola? RNA associated?

A

F (fusion) H (Hemagglutinin), M (Matrix), N (Nucleoprotein), P (Phosphoprotein), and L (Large protein)

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3
Q

What are the features of F protein in rubeola?

A

surface glycoprotein, allows viral envelope to fuse with cell membrane, responsible for giant cell (syncitia formation),

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4
Q

What are the features of H protein in rubeola?

A

surface projection glycoprotein, hemagglutinin inhibition assay

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5
Q

What are the features of M protein in rubeola?

A

inner surface membrane, non-glycosylated, required for proper assembly of nucleocapsids and progeny release

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6
Q

What are the features of N protein in rubeola?

A

protects viral RNA

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7
Q

What are the features of P protein in rubeola?

A

replication of viral genome, RNA-dependent RNA polymerase

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8
Q

What are the features of L protein in rubeola?

A

not bale to classify well, possibly part of transcription complex

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9
Q

what are the physical properties of rubeola?

A

extremely liable, sensitive to: heat, UV, ether, and trypsin

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10
Q

How is rubeola transmitted?

A

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

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11
Q

what is the incubation period and most infectious period for classic rubeola?

A

“classic measles”, incubation- 7-21 days from exposure to onset of fever, contagious- 4 days before rash to 4 days after appearance of rash

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12
Q

What are the signs and symptoms of classic rubeola?

A

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)

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13
Q

Who is likely to get modified rubeola? How does it differ from classic?

A

pts who have been passively immunized (Ig), infants with maternal Ab; disease milder and shorter duration

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14
Q

What childhood exanthema disease was declared eliminated in US only to rise again due to antivaccination? Which one is eliminated globally?

A

rubeola; small pox

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15
Q

What are some complications seen with rubeola?

A

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)

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16
Q

What type of immunity is seen with rubeola?

A

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)

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17
Q

What labs are used to diagnose rubeola?

A

PCR, serology (single IgM= acute, 4x rise in IgG titer w/ convalescent- 28d later), detect virus in resp or urine culture

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18
Q

What is the therapy for rubeola? prevention?

A

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)

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19
Q

What is the etiology, taxonomy, genome and morphology or Rubella?

A

rubella virus (German measles), togaviridae, rubivirus, (+) single strand RNA, spherical, enveloped (lipid bilayer)

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20
Q

What are the important viral proteins in Rubella?

A

membrane glycoproteins E1 (hemagglutinin, surface projection), and E2 (membrane), nonmembrane protein C

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21
Q

What are the physical properties of Rubella?

A

relatively labile, sensitive to: heat, UV, Lipid solvents

22
Q

How is postnatal Rubella infection spread? Prenatally?

A

droplets from respiratory secretions, prenatally infected cases multiple cases multiple tissues are persistently infected and serve as foci for transmission (urine)

23
Q

What is the clinical course of Rubella?

A

incubation 12-23d, infectious 7d before and 7d after rash onset

24
Q

what are the signs and symptoms of Rubella?

A

fever (normal or mild elevation), lymphadenopathy (begin 5-10d before rash, occipital, post-auricular, cervical chains), leukopenia and rash

25
Q

What are the features of rash with Rubella?

A

maculopapular, 3 day rash, begins on face and spreads down, gone by 3rd day (comes on and resolves quicker than Rubella)

26
Q

what are the complications of postnatal Rubella infection?

A

arthralgia/arthritis (kids rare, female adults up to 70%), Thrombocytopenia (1:3K), enceohalitis (1:5K), neuritis (r), and orchitis (r)

27
Q

What is infected with congenital/prenatal Rubella?

A

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)

28
Q

What are the signs and symptoms (or lasting effects) of congenital Rubella?

A

growth retardation, cataracts, glaucoma, retinopathy, micropthalmia, deafness, Cardiac (PDA, VSD, PS), psychomotor retardation, microcephaly, spastic quadriplegia, MR, bone lessions, hepatomgaly, hepatitis, splenomegaly, and thrombocytopenia

29
Q

What does the immune response look like for postnatal Rubella?

A

humoral- IgM tends to be short lived, no more than 8 weeks, IgG continues to be present; cell mediated- CD4+ and CD8+

30
Q

What does the immune response look like for congenital Rubella?

A

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

31
Q

How is Rubella diagnosed? Prevented?

A

viral isolation in culture, PCR and serology (acute and convalescent); active immunization (contraindicated in pregnancy and sever immunodeficiency- some HIV kids ok)

32
Q

What is the etiology, taxonomy, genome, and morphology of varicella?

A

“chickenpox”; varicella-zoster (HHV3), herpesviridae, dsDNA, enveloped

33
Q

What is the mechanism of transmission of varicella?

A

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

34
Q

What are the clinical manifestations of varicella?

A

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

35
Q

How is varicella treated? prevented?

A

acyclovir (for severe or immune compromised); passive- VZIG, active- live, attenuated vaccine (Varivax), conatrindicated if pregnant, immmunodefficiency, some HIV kids ok, paired w/ MMR

36
Q

What are some complications with varicella?

A

B superinfection (staph or strep, bulous varicells, cellulitis, sepsis) pneumonia, encephalitis, hemorrhagic, death (rare in kids, increased for adults and immune comp.)

37
Q

What is the virus and mechanism behind zoster?

A

shingles, reactivation of latent HHV3 from sensory ganglion, pain generally precedes vesicular rash which is dermatomally restricted

38
Q

What is the etiology, taxonomy, genome and morphology of roseola?

A

HHV6, herpesviridae, HHV6a and b, dsDNA, enveloped

39
Q

How is roseola transmitted? Epidemiology?

A

respiratory droplets and salivary secretions; nearly 100% newborns gave maternal Ab wane by 6 mo, 90% seropositive by 2 and ~100% by 3

40
Q

what is the incubation period and clinical disease features of roseola?

A

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!)

41
Q

What are the complications seen with Roseola?

A

febrile seizures 10-15%, encephalitis (more severe and very rare)

42
Q

What are the viral features, transmission and epidemiology of fifth disease (Parvovirus)?

A

human parvovirus B19- non-enveloped, icosahedral, small (22nm), ssDNA; respiratory droplet; late winter-spring, age 2-12 (peak @ 7y)

43
Q

What is the incubation period and symptoms with 5th disease (parvovirus)?

A

6-14 days; mild or no systemic symptoms- most infectious prior to rash, rash- “slapped cheeks”, cephalocaudal spread, maculopapular

44
Q

What are some complications seen with 5th disease (parvovirus)?

A

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)

45
Q

what is the disease, family, genus, genome, morphology and replicative place of Variola?

A

small pox; poxvirus; orthopoxvirus (variola, vaccinia- cow or monkey); dsDNA linear; brick shaped; cytoplasm

46
Q

What is the clinical manifestation of small pox?

A

incubation 7-17d, prodrome 2-3d w/ fever spike in middle;

47
Q

What is the pathogenic course of small pox?

A

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

48
Q

What are the phases of the exanthem associated with small pox?

A

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

49
Q

What are some additional clinical manifestations of small pox?

A

panopthalmitis-1%, keratitis-1%, arthritis-2% of kids, Encephalitis-<1%, 2ndary B infection, and pockmarks- 65-80%

50
Q

What are the 5 classifications of spall pox (WHO) an differences?

A

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%)