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Microbiology Unit 3 > 3 Viral Skin Infections > Flashcards

3 Viral Skin Infections Flashcards

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
Eye defects associated with congenital rubella
Cataracts Glaucoma (led to initial recognition of congenital defects with infection)
26
Other than cardiac and eye defects, what other complications of congenital rubella are common?
Hearing loss - may be profound CNS involvement
27
________ of infection is critical element in outcome of congenital rubella
Timing Early in pregnancy is the worst - 50% risk if in the first month, exceedingly low after fourth month
28
What is the best way to prevent congenital rubella?
VACCINE But avoid giving MMR during the first trimester of pregnancy (duh)
29
What can you provide prophylactically to non-immune pregnant women with documented exposure to rubella?
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)
30
What two unique properties influence the disease capacity of HSV?
Capacity to invade and replicate in the CNS Ability to establish latent infections
31
After resolution of primary HSV infection, what happens?
Primary infection resolves and HSV establishes a quasi-stable state of latency subject to deactivation (recrudescence)
32
Clinical manifestations of HSV infection
Production of shallow vesicles on an erythematous base Ballooning pathology - vesicles crust over (painful)
33
How does HSV establish latency?
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
What is recrudescence?
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
Probability of HSV recrudescence is greater in...
Individuals with larger and more extensive initial outbreaks
36
_______ are the only reservoir for HSV
Humans Spread by contact with vesicular fluid, saliva, and secretions ASYMPTOMATIC SHEDDING possible
37
What is the difference between HSV-1 and HSV-2
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
Dendritic corneal lesion
HSV
39
Whitlow lesions on hands
HSV - wear gloves
40
90% of oral HSV is...
HSV-1
41
90% of genital herpes is ...
HSV-2
42
How is neonatal HSV acquired?
In uterine or during birth canal passage
43
How is HSV diagnosed?
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
Treatment of HSV
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
Varicella-zoster virus (VZV) causes both...
Chicken pox and shingles It’s a herpesvirus (aka Herpes zoster)
46
Asymmetrical vesicular rash in a dermatomal pattern
VZV Lesions are pruritic, often secondarily infected Also get fever, malaise, HA, neuralgia
47
How does VZV infection occur?
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
_____ are the only known reservior for VZV
Humans Seasonal occurrence (peak during Winter-Spring)
49
What is the highest incident age group for VZV?
5-9 years (>90% of all cases in ages 1-14) Remains a common US childhood exanthem despite being vaccine-preventable
50
How long is the incubation period for VZV?
15 days Patient is most contagious 1-2 days before appearance of lesions and 4-5 days after
51
How is presentation of VZV different in older children/adults vs younger children?
Includes prodromal symptoms (fever, malaise, HA, myalgia, anorexia)
52
How is Chickenpox diagnosed?
Clinical findings Rash and fever May be difficult to distinguish from HSV in immunocompromised and neonates Excoriated lesions may look like insect bites
53
How is chickenpox treated?
No specific therapy needed in normal patient Aspirin not recommended Lotions to control itching Can also use Acyclovir or immune serum VariZig
54
Lots of facial lesions with chickenpox indicates...
Patient is not fighting the virus well
55
Why should you not give aspirin for at least 28 days after chicken pox vaccine?
Risk of Reyes syndrome
56
What is the chickenpox vaccine?
Varivax - live attenuated virus Breakthrough cases no recognized - may eventually recommend additional boosters
57
Congenital/neonatal VZV
Infection during pregnancy can produce significant disease damage
58
What should you give to high risk persons who have been exposed to chickenpox?
Immune globulin (VariZig)
59
Shingles is...
Recrudescence of VZV Half of all individuals living to age 85 will experience at least one outbreak of shingles
60
How do shingles lesions present?
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
Where does the term zoster come from?
Refers to belt or stripe Shingles lesions appear in unilateral dermatomal distributions with sharp limits
62
10% of shingles patients have involvement of...
Ophthalmic branch of the the fifth cranial nerve 20% will have ocular involvement
63
How do you treat shingles?
Disease is self-limited but painful - take steps to control pain Postherpetic neuralgia is the most common complication - pain may persist for months
64
Absolute prerequisite for shingles infection?
A previous case of chickenpox or varivax vaccination Shingles is not directly transmissible
65
How do you prevent shingles?
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
Sequence of fever followed by a rose-colored rash
Exanthem subitum aka Roseola Infantum aka 6th Disease Caused by Human Herpes Virus 6 (HHV6)
67
Clinical manifestations of HHV6 infections
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
How is HHV6 diagnosed?
Detection of antibody by EIA DNA sequence detection by PCR
69
Do you need to treat HHV6
Nope No isolation necessary No antiviral therapy No primary preventative measures
70
What is “Fifth Disease”
Erythema infectiosum Caused by Parvovirus B19
71
“Slapped cheek” rash
Fifth Disease or Erythema Infectiosum
72
Clinical manifestations of Erythema Infectiosum
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
Connective tissue manifestations of fifth disease
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
When do parvovirus infections typically occur?
Epidemics in late winter and spring Worldwide distribution Highest incidence of infection is in school age children
75
How is Fifth Disease diagnosed
Facial rash helpful Detection of anti-B19 IgM antibody Epidemic outbreaks aid diagnosis
76
Do you need to treat Fifth Disease?
Most patients make a rapid and full recovery Just treat for relief of symptoms - NSAID Immunoglobulin available for anemic patients
77
Which types of HPV cause anogenital warts?
HPV 6 and 11
78
Which types of HPV cause cervical dysplasia and cancer?
HPV 16 and 18
79
How do you prevent HPV?
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

Microbiology Unit 3 (10 decks)

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