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Microbiology test 3 > Viral Skin Infections (session 21) > Flashcards

Viral Skin Infections (session 21) Flashcards

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1
Q

Measles aka/overview

A

Rubeola
a classic childhood exanthema (skin eruptions)
can be severe in malnourished and/or vit A deficient ppl.

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2
Q

Measles phases

A

(measles=rubeola)

  1. incubation period (10-14 days): multiplication in resp epithelium & lymph nodes, viremea, 2ndary viremia
  2. prodromal stage: 1-12 days post infection, high fever, coryza, persistent cough, conjunctivitis (the 3 Cs), KOPLIK’S SPOTS on bucal mucosa (diagnost)
  3. Rash: begins 3-4 days post-prodrome, highest fever (sickes patient), begins below ears, spreads
  4. Resolution: risk in antibody titres, viremia stops, rash fades in same order it appears
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3
Q

Koplik’s spots: what, where

A

on buccal mucosa are diagnostic for Rubeola (measles)

-occur during the prodromal stage

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4
Q

Measles complications

A

pneumonia (accounts for most measles deaths; malnourished & aged at greatest risk, bacterial superinfection common)
diarrhea
CNS involvement: acute symptomatic encephalitis (15% fatality, .5% encephalitis, SSPE:subacute sclerosing panencephalitis very rare in US)

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5
Q

Measles Hosts & Epidemiology

A

humans & monkeys=only known hosts
no healthy carrier state is known
primarily a dz of kids (most immune by age 10, rare in infants under 6 mos-maternal immunity)
transmission by respiratory droplets (highly contagious)

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6
Q

Measles dx

A

rash &/or Koplik’s spots
serology
FA test on cells obtained from swabs of pharynx, nasal & buccal cavities-multinucleated giant cells

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7
Q

Measles prevention

A 
MMR vaccine (measles [rubeola], mumps & rubella)
since vaccine, 99% reduction in US
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8
Q

MMR vaccine schedule

A

initiation before school entry
15 mos: first dose
4-5 yrs: second dose
may vaccinate kids under 15 mos w/monovalent measles vaccine if exposure deemed likely (revaccinate at 15 mos)
recent outbreaks may lead to routine 3rd application of vaccine (booster)

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9
Q

Are all MMR vaccines the same?

A

NO, US uses MMRII

live, attenuated vaccine NOT suitable for all patients

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10
Q

Measles outbreaks in the US

A

most involved non-vaccinated persons & air travel to foreign locations
UK measles outbreak 2013: acceptance rate for vaccine had fallen
-large scale epidemic emergency; Andrew Wakefield

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11
Q

German Measles aka & description

A

Rubella=”little red”
mild exanthematous dz that resembles measles superficially
close & prolonged contact probably needed for infection
Kids often escaped infection

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12
Q

Rubella Complications

A

Congenital Rubella Syndrome (CRS)-maternal infection (viremia) may lead placental infection & fetal infection
Substantial risk to fetus: cardiac defects, eye defects, hearing loss (may be profound CNS involvement)

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13
Q

Outcome of CRS is affected by what?

A

timing of infection is critical element in outcome (early in pregnancy is worst)
1st mo: 50% risk of CRS
2nd mo: 30%
3rd mo: 20%
4th mo: exceedingly los
vaccination has nearly eliminated CRS in US

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14
Q

Rubella tx & prevention

A

symptomatic relief
prevention-MMR vaccine:
live virus vaccine
avoid infection in pregnancy first trimester
do not administer vaccine to pregnant pts

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15
Q

Herpes simplex virus (HSV) unique props

A

2 unique props infl. dz capacity of HSV:

  1. capacity to invade & replicate in CNS
  2. ability to establish latent infections (they are permanent)
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16
Q

HSV clinical manifestations

A

HSV causes primary infection (may be asymptomatic) that will resolve and establish quasi-stable state of latency subject to reactivation (recrudescence)
SHALLOW VESSELS ON AN ERYTHEMATOUS BASE
BALLOONING PATHOLOGY, VESICLES CRUST OVER (painful)

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17
Q

how does HSV become latent, what is latency like?

A

retrograde transport of virus through sensory neurons & ultimate infection of dorsal room ganglia
LATENCY IS LIFE-LONG (reactivation via: sunlight, menses, nutrition, stress)
continued spread is halted by cell & humoral immune processes

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18
Q

HSV: does asymptomatic shedding occur?

A

yes, it is frequent, perhaps up to 2/3 of virus shedding days are asymptomatic & most transmission occurs at these times or from ppl who don’t know they are infected

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19
Q

HSV latency rule of thumb

A

probability of recrudescence is greater in individuals w/larger & more extensive initial outbreaks

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20
Q

HSV latency

A

recrudescence occurs even in the presence of active humoral & cellular immunity (“cold sores”, “fever blisters” on vermillion border of lips)
-lesions generally heal w/out scarring

21
Q

HSV epidemiology

A

humans are the only reservoir
spread by DIRECT CONTACT w/vesicular fluid, saliva & secretions
-ASYMPTOMATIC VIRUS SHEDDING POSSIBLE
HSV-1 infection is common & often occurs early in life, >90% seropositive (rates vary w/SES)
HSV-2 infection tends to occur later & correlate w/sexual activity

22
Q

HSV diseases (3)

A
  1. Oral herpes (90& HSV-1)
  2. Genital herpes (90% HSV-2)
  3. Neonatal HSV infection (infection in utero or MOST COMMONLY during BIRTH CANAL PASSAGE)
23
Q

HSV dx

A
  1. direct samples of lesions for virus or components
  2. ballooning pathology & presence of enlarged & fused cells (Tzanck smear)
  3. FA assay for viral antigens
  4. rapid tests that reveal patient antibodies to HSV, great utility in confirming dx in patients w/sporadic outbreaks or poorly defined lesions
24
Q

HSV tx

A

Acyclovir (ACV)-most prescribed antiherpes agents, may be used to suppress HSV recrudescence
viral enzyme thymidine kinase phosphorylates ACV
-this molecule will halt viral DNA replication b/c it lacks a 3’-OH group & cannot allow the polymerization of more bases

25
Q

Chickenpox: causative agent

A

varicella-zoster virus

26
Q

Varicella-zoster virus causes what?

A

BOTH chickenpox & shingles

VZV is a herpes virus (sometimes known as Herpes zoster)

27
Q

varicella zoster virus clinical manifestations

A
  1. asymmetrical vesicular rash that sometimes follows an obvious dermatomal pattern
  2. fever, malaise, HA, neuralgia w/ PRURITIC lesions that are often secondarily infected
28
Q

How does VCV infect

A

Varicella virus infects through conjunctiva or respiratory tract mucosa

  • replicates in regional lymph nodes, primary viremia 4-6 days after infection
  • replicates in liver & spleen generating a secondary viremia (coincident w/rash) 10-14 days post-infection
29
Q

VZV epidemiology

A
  • HUMANS are the ONLY KNOWN RESERVOIR
  • seasonal occurance (peaks in winter-spring)
  • highest incidence in 5-9 yos (>90% of all cases in ages 1-14 years)
  • most (C) US childhood exanthema-3,000,000 cases/year
  • spreads in resp., conjunctiva, vesicle secretions
  • highly contagious (90% attack rate)
  • incubation period is 15 days
  • pt most contagious 1-2 days before appearance of lesions & 4-5 days after lesions appear
30
Q

Prodromal symptoms of VZV & who exhibits them

A

prodromal sxs in OLDER CHILDREN & ADULTS: fever, malaise, HA, myalgia, anorexia
ABSENT IN YOUNGER KIDS

31
Q

VZV dx

A

clinical findings
rash & fever
may be tricky to distinguish from HSV in immunocomprimised & neonates
excoriated lesions may look like insect bites

32
Q

VZV tx

A

no specific therapy is needed in normal host
ASA is NOT RECOMMENDED->REYE’s SYNDROME RISK)
Acyclovir effective

33
Q

VZV prevention

A

vaccines: VARIVAX, MMMRV & VariZIG human immunoglobulin

- live, attenuated virus-may cause mild dz episode in recipients

34
Q

Vaccines for VZV: 3 issues

A
  1. BREAKTHROUGH CASES (mild chickenpox in vaccinated ppl after exposure) are well documented
  2. VZV INFECTION DURING PREGNANCY OR AT TIME OF BIRTH CAN=SIG. CONGENITAL/NEONATAL DZ-healthcare pp. requested to report inadvertent vaccine admin during pregnancy
  3. vaccine DOES NOT guarantee protection from shingles
35
Q

Shingles: how does one acquire this?

A

Recrudescence of a prior VZV (chickenpox infection)

-REQUIRES PRIOR CASE OF CHICKENPOX OR VACCINATION AGAINST CHICKENPOX

36
Q

Shingles: clinical manifestation

A

PAINFUL lesions “searing, burning, stabbing”, pain may precede rash by days to weeks
-areas of redness evolved to papules & vesicles in 24 hour period
low grade fevers, anorexia
UNILATERAL DERMATOMAL DISTRIBUTION (SHARP LIMITS): “zoster”=belt or stripe
10% have involvement of ophthalmic branch of 5th cranial nerve, 20% have ocular involvement

37
Q

Shingles tx

A

self-limited dz, but painful: take steps to control lesion pain
postherpetic neuralgia is most (C) complication, pain may persist for months
SHINGLES IS NOT DIRECTLY TRANSMISSIBLE

38
Q

Shingles prevention

A

Zostavax for pts over age 50
high potency ZVZ vaccination to boost immunity
same virus used in Varivax, BUT MUCH HIGHER POTENCY

39
Q

Human Herpes Virus-6: aka, prevalence, presentation

A

aka Roseola Infantum or 6th dz
VERY PREVALENT, unrecognized until proper culture system available
-EXANTHEM SUBITUM: sequence of fever followed by rose-colored rash

40
Q

HHV-6 clinical manifestion

A

regularly acquired viral infection of childhood: 30% of kids 6 mos to 3 yold
sustained fever 2-5 days, 39-41*C (child often looks remarkable well despite high fever)
ER visits due to high fever w/out obvious source

41
Q

HHV-6 diagnosis

A

detection of antibody by EIA

DNA sequence detection by PCR amplification

42
Q

HHV-6 treatment/prevention

A

DON’T NEED TO isolate
NO antiviral therapy required
NO primary preventative measures exist

43
Q

Parvovirus B19 aka

A

“Fifth disease”

erythema infectiosum

44
Q

Parvovirus B19 clinical manifestation

A

prodrome: several days, mild sxs, fever, HA, malaise, myalgia, resp. sxs, sometimes nausea, vomiting
followed by skin rash: SLAPPED CHEEK APPEARANCE, circumoral sparing, resolves in 1-2 weeks
can see maculopapular rash on limbs & trunk
many adults have ARTHRITIS or ARTHALGIA ALONE w/out and preceding or concurrent sxs

45
Q

Adult w/Parvovirus B19 may present as

A

sudden arthritis or arthralgia along wout any preceding or conceurrent sxs

46
Q

Parvovirus B18 epidemiology

A

epidemics in late winter & spring
worldwide distribution
highest incidence of infection in school age children

47
Q

Parvovirus B19 dx

A

facial rash helpful
detection of anti B19 IgM antibody
epidemic outbreaks aid dx

48
Q

Parvovirus B19 tx & prevention

A

most patients make a rapid & full recovery
relief of sxs: NSAIDs
immunoglobulin available for anemic patients

49
Q

HPV: what is it & how is it tx

A

HPV is an STI
HPV 6 & 11: ano-genital warts
HPV 16 & 18: cervical dysplasia
Gardasil & Cervarix vaccines are now licensed for males & females ages 9-26

Microbiology test 3 (8 decks)

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