3 Viral Skin Infections Flashcards

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1
Q

In what patients can measles be severe?

A

Malnourished and/or vitamin A deficient persons

“Tropic Measles” worse b/c of malnourishment

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2
Q

What is the incubation period for measles?

A

10-14 days

Multiplication in respiratory epithelium and lymph nodes

Waves of VIREMIA, dissemination to other tissues by monocytes

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3
Q

What are the “Three C’s” of measles?

A

Coryza, persistent Cough, Conjunctivitis

Will see during the prodromal stage

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4
Q

What are the signs of measles prodromal stage?

A

1-12 days post infection

HIGH fever

Coryza, cough, conjunctivitis (three Cs)

KOPLIK’S SPOTS***** on buccal mucosa

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5
Q

Pathognomic sign of measles during the prodromal stage

A

KOPLIK’S SPOTS on buccal mucosa

Will precede rash and persist for a few days after rash

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6
Q

When does the measles rash appear?

A

3-4 days after prodromal initiates

Time of highest fever (sickest patient)

Begins below ears, spreads —> very extensive, lesions may become merged

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7
Q

What accounts for the most measles deaths?

A

Pneumonia - malnourished and aged at greatest risk

Can also get other bacterial superinfections

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8
Q

What measles complication is especially common in younger patients?

A

Diarrhea

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9
Q

What CNS complications can occur with measles?

A

Acute symptomatic encephalitis - high fatality rate in affected population

Measles used to be #1 cause of viral encephalitis. Not anymore. Thanks, vaccines!

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10
Q

What is sub acute sclerosis panencephalitis?

A

Kids who recover from measles but later have lots of problems (very rare in the US now)

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11
Q

What are the only known hosts of measles?

A

Humans and monkeys

No healthy carrier state is known

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12
Q

Measles is primarily a disease of …

A

Children

Most immune by age 10

Rare in infants under 6 months b/c of maternal immunity

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13
Q

How is measles transmitted?

A

Respiratory droplets - agent is highly contagious

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14
Q

How is measles diagnosed?

A

Presence of rash or KOPLIK’S spots

Serology

Fluorescent antibody test from buccal swab —> MULTINUCLEATED GIANT CELLS

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15
Q

How do we prevent measles?

A

Through use of MMR (Measles, Mumps, and Rubella) vaccine x2 (15 months and 4-6 years)

Immune globulin (BayGam) for exposed non-immune subjects (within 6 days)

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16
Q

When should the first dose of MMR be given?

A

At 15 months

May vaccinate children under 15 months with mono alert measles vaccine if exposure is deemed likely (but revaccinate at 15 months)

2nd dose before school entry

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17
Q

Which measles vaccine do we use in the US?

A

MMR2 - has a different Mumps component

More $$$ and more labor intensive to make

Live, attenuated vaccine, so not suitable for immunocompromised patients

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18
Q

_____% of the population must be vaccinated to halt measles persistence in the population

A

95%

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19
Q

Recent measles outbreaks in the US have mostly involved…

A

Non-vaccinated persons and air travel to foreign locations

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20
Q

Which component of the MMR vaccine is the weakest?

A

Mumps

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21
Q

Rubella is also called…

A

German Measles

“Little Red”

Mild exanthematous disease that resembles measles superficially

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22
Q

How do you get infected with Rubella?

A

Close and prolonged contact needed

Children often escape infection

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23
Q

Rubella infection during the first trimester of pregnancy can result in…

A

Congenital Rubella Syndrome

Maternal infection —> placental infection —> fetal infection

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24
Q

Cardiac defects associated with congenital rubella

A

Pulmonary artery stenosis

Patent ductus arteriosis

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25
Q

Eye defects associated with congenital rubella

A

Cataracts

Glaucoma (led to initial recognition of congenital defects with infection)

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26
Q

Other than cardiac and eye defects, what other complications of congenital rubella are common?

A

Hearing loss - may be profound

CNS involvement

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27
Q

________ of infection is critical element in outcome of congenital rubella

A

Timing

Early in pregnancy is the worst - 50% risk if in the first month, exceedingly low after fourth month

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28
Q

What is the best way to prevent congenital rubella?

A

VACCINE

But avoid giving MMR during the first trimester of pregnancy (duh)

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29
Q

What can you provide prophylactically to non-immune pregnant women with documented exposure to rubella?

A

Intravenous immunoglobulin (IVIG)

But it’s a last ditch effort to avoid CRS - may or may not work (not as effective as BayGam for measles)

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30
Q

What two unique properties influence the disease capacity of HSV?

A

Capacity to invade and replicate in the CNS

Ability to establish latent infections

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31
Q

After resolution of primary HSV infection, what happens?

A

Primary infection resolves and HSV establishes a quasi-stable state of latency subject to deactivation (recrudescence)

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32
Q

Clinical manifestations of HSV infection

A

Production of shallow vesicles on an erythematous base

Ballooning pathology - vesicles crust over (painful)

33
Q

How does HSV establish latency?

A

Retrograde transport of virus through sensory neurons and ultimate infection of the dorsal root ganglia

Latency life long

May reactivate with sunlight, stress, menses, nutrition

34
Q

What is recrudescence?

A

Deactivation of latent HSV - will occur even in the presence of active humoral and cellular immunity (“cold sores”, “fever blisters” on vermillion border of lips)

35
Q

Probability of HSV recrudescence is greater in…

A

Individuals with larger and more extensive initial outbreaks

36
Q

_______ are the only reservoir for HSV

A

Humans

Spread by contact with vesicular fluid, saliva, and secretions

ASYMPTOMATIC SHEDDING possible

37
Q

What is the difference between HSV-1 and HSV-2

A

HSV-1 infection is common and occurs early in life (>90% seropositive)

HSV-2 infection tends to occur later and correlates with sexual activity

38
Q

Dendritic corneal lesion

A

HSV

39
Q

Whitlow lesions on hands

A

HSV - wear gloves

40
Q

90% of oral HSV is…

A

HSV-1

41
Q

90% of genital herpes is …

A

HSV-2

42
Q

How is neonatal HSV acquired?

A

In uterine or during birth canal passage

43
Q

How is HSV diagnosed?

A

Ballooning pathology

Presence of ENLARGED AND FUSED GIANT CELLS ON TZANCK SMEAR

FA assay for viral antigens

Culture in HeLa, Hep-2 cell lines

PCR

Antibody tests

44
Q

Treatment of HSV

A

Acyclovir or Valacyclovir - viral enzyme thymidine kinase phosphorylates ACV, will halt viral DNA replication b/c it can’t incorporate into host DNA

Can be used to suppress HSV recrudescence

Alt - Famciclovir

45
Q

Varicella-zoster virus (VZV) causes both…

A

Chicken pox and shingles

It’s a herpesvirus (aka Herpes zoster)

46
Q

Asymmetrical vesicular rash in a dermatomal pattern

A

VZV

Lesions are pruritic, often secondarily infected

Also get fever, malaise, HA, neuralgia

47
Q

How does VZV infection occur?

A

Virus infects through conjuctiva or respiratory tract mucosa

Replicates in regional lymph nodes, primary viremia 4-6 days after infection

Virus replicates in liver and spleen —> secondary viremia (coincident with rash) 10-14 days after infection

48
Q

_____ are the only known reservior for VZV

A

Humans

Seasonal occurrence (peak during Winter-Spring)

49
Q

What is the highest incident age group for VZV?

A

5-9 years (>90% of all cases in ages 1-14)

Remains a common US childhood exanthem despite being vaccine-preventable

50
Q

How long is the incubation period for VZV?

A

15 days

Patient is most contagious 1-2 days before appearance of lesions and 4-5 days after

51
Q

How is presentation of VZV different in older children/adults vs younger children?

A

Includes prodromal symptoms (fever, malaise, HA, myalgia, anorexia)

52
Q

How is Chickenpox diagnosed?

A

Clinical findings

Rash and fever

May be difficult to distinguish from HSV in immunocompromised and neonates

Excoriated lesions may look like insect bites

53
Q

How is chickenpox treated?

A

No specific therapy needed in normal patient

Aspirin not recommended

Lotions to control itching

Can also use Acyclovir or immune serum VariZig

54
Q

Lots of facial lesions with chickenpox indicates…

A

Patient is not fighting the virus well

55
Q

Why should you not give aspirin for at least 28 days after chicken pox vaccine?

A

Risk of Reyes syndrome

56
Q

What is the chickenpox vaccine?

A

Varivax - live attenuated virus

Breakthrough cases no recognized - may eventually recommend additional boosters

57
Q

Congenital/neonatal VZV

A

Infection during pregnancy can produce significant disease damage

58
Q

What should you give to high risk persons who have been exposed to chickenpox?

A

Immune globulin (VariZig)

59
Q

Shingles is…

A

Recrudescence of VZV

Half of all individuals living to age 85 will experience at least one outbreak of shingles

60
Q

How do shingles lesions present?

A

PAINFUL - “searing, burning, stabbing”

Pain may precede rash by days to weeks

Area of redness evolves to papules to vesicles in 24 hour period

Low grade fevers, anorexia

61
Q

Where does the term zoster come from?

A

Refers to belt or stripe

Shingles lesions appear in unilateral dermatomal distributions with sharp limits

62
Q

10% of shingles patients have involvement of…

A

Ophthalmic branch of the the fifth cranial nerve

20% will have ocular involvement

63
Q

How do you treat shingles?

A

Disease is self-limited but painful - take steps to control pain

Postherpetic neuralgia is the most common complication - pain may persist for months

64
Q

Absolute prerequisite for shingles infection?

A

A previous case of chickenpox or varivax vaccination

Shingles is not directly transmissible

65
Q

How do you prevent shingles?

A

Zostavax - for patients over 50, high potency VZV vaccination to boost immunity; same virus used in varivax but much higher potency

Shingrix - adjuvanted, recombinant
Recommended for prior zostavax recipients, may replace zostavax

66
Q

Sequence of fever followed by a rose-colored rash

A

Exanthem subitum aka Roseola Infantum aka 6th Disease

Caused by Human Herpes Virus 6 (HHV6)

67
Q

Clinical manifestations of HHV6 infections

A

Sustained fever for 2-5 days (but kid doesn’t look sick)

Then bright red rash

One of the most regularly acquired viral infections of childhood - 30% of all children 6 months to 3 years

68
Q

How is HHV6 diagnosed?

A

Detection of antibody by EIA

DNA sequence detection by PCR

69
Q

Do you need to treat HHV6

A

Nope

No isolation necessary

No antiviral therapy

No primary preventative measures

70
Q

What is “Fifth Disease”

A

Erythema infectiosum

Caused by Parvovirus B19

71
Q

“Slapped cheek” rash

A

Fifth Disease or Erythema Infectiosum

72
Q

Clinical manifestations of Erythema Infectiosum

A

Prodromal illness of several days (mild)

Prodrome followed by skin rash with slapped cheek appearance, circumpolar sparing

Maculopapular rash may also involve limbs/trunk

Resolves in 1-2 weeks

73
Q

Connective tissue manifestations of fifth disease

A

Arthralgia and/or arthritis may follow skin eruptions - involves hands, wrists, knees, ankles and feet

May be quite severe

Many adults have arthritis or arthralgia alone without any preceding or concurrent symptoms

74
Q

When do parvovirus infections typically occur?

A

Epidemics in late winter and spring

Worldwide distribution

Highest incidence of infection is in school age children

75
Q

How is Fifth Disease diagnosed

A

Facial rash helpful

Detection of anti-B19 IgM antibody

Epidemic outbreaks aid diagnosis

76
Q

Do you need to treat Fifth Disease?

A

Most patients make a rapid and full recovery

Just treat for relief of symptoms - NSAID

Immunoglobulin available for anemic patients

77
Q

Which types of HPV cause anogenital warts?

A

HPV 6 and 11

78
Q

Which types of HPV cause cervical dysplasia and cancer?

A

HPV 16 and 18

79
Q

How do you prevent HPV?

A

Vaccines available to prevent HPV STIs

Gardasil 9 includes HPV 6, 11, 16, 18, and 5 others

Indicated for males and females ages 9-45