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Microbiology > Exam #8: Viral infections of the skin, soft tissue, bone, muscle, & joints I & II > Flashcards

Exam #8: Viral infections of the skin, soft tissue, bone, muscle, & joints I & II Flashcards

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Biology 101 flashcards
1
Q

How viruses get into the skin?

A

1) Direct infection via disrupted skin or mucosa

2) Other tissues e.g. spread from the lung

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2
Q

Once the virus is in the skin, what are the two possible outcomes?

A

1) Replication in the skin & infective skin lesions

2) Immune response to virus–>lesion without infectivity

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3
Q

Define papilloma.

A

Benign growth on the surface of the skin or mucous membrane

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4
Q

Define macule.

A

Small discolored patch of skin that forms an area distinct from the normal surrounding surface

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5
Q

Define papule.

A

A small, circumscribed, raised portion of the skin

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6
Q

Define vesicle.

A

Small pouch on the surface of the skin filled with clear liquid; blister

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7
Q

Define pustule.

A

Small circumscribed, raised portion of the skin filled with purulent material

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8
Q

What are the shared features of warts?

A
  • Hyperkeratotic
  • Painless
  • Koilocytes
  • Lump, papilloma, nodule
  • Caused by HPV
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9
Q

What is the same of the common wart? Where is it most commonly found?

A

Verruca valgaris

- Hands

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10
Q

What is the technical name for warts on the soles of the feet?

A

Verruca plantaris

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11
Q

What are flat warts called?

A

Verruca plana

*Note that these most commonly occur on the face, hands, and neck of children

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12
Q

What are the black dots in warts?

A

Punctate hemorrhages

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13
Q

List the characteristics of HPV.

A

Papoviridae
Small
Nonenveloped
dsDNA genome

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14
Q

How is the replication of HPV closely tied to the differentiation status of the tissue it infects?

A
  • The layers of the skin are listed below from superficial to deep:
    1) Suprabasal
    2) Basal
    3) Basement membrane
    4) Dermis
  • Infection occurs in the basal layer
  • E6 & E7 promote proliferation by inactivating p53 & Rb
  • The infected epithelial cell differentiates and moves toward the surface of the skin, where late genes are expressed & virions are assembled

*Thus, production of NEW PHV virions occurs in the most superficial layer, the suprabasal layer

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15
Q

Review the roles of HPV E7 & E6.

A

HPV E7= Inhibits Rb

HPV E6= Inhibits p53

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16
Q

How are the 100 different serotypes of HPV classified? Specifically, how are the cutaneous warts classified?

A 
Common= HPV 2, 3, 10 
Plantar= HPV 1 & 4
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17
Q

How is HPV transmitted?

A

Direct contact with wart or contaminated surface (non-slip shower/pool)

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18
Q

How long is the incubation period for warts?

A

4 months

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19
Q

How are warts diagnosed?

A

1) Clinical appearance
2) Hyperkeratosis
3) Koilodal cells

*Note that PCR can be used to distinguish between high and low-risk HPV

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20
Q

Describe the apperance of a Koilodal cell.

A

Large nucleus

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21
Q

How are common and plantar warts treated?

A

1) Cryotherapy
2) Cytotoxic chemicals
3) Surgical removal

*Note that common and plantar warts usually spontaneously regress after a few months- 2 years

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22
Q

How are warts prevented?

A

Flip-flops for plantar warts

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23
Q

Will the HPV vaccine help with common and plantar warts?

A

NO–different serotypes

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24
Q

What is Molluscum Contagiosum? What are the manifestations?

A
  • Painless lesion
  • “Pearly umbilicated nodules in the epidermis”
  • Purulent material can sometimes be expressed from the lesions

Young children= anywhere
Adult= genital

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25
Q

List the characteristics of the virus that causes Molluscum Contagiosum.

A

Poxviridae family
Large dsDNA genome
Replicates in cytoplasm

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26
Q

What are molluscum bodies?

A

Large eosinophilic cytoplasmic inclusions

*Note that these are present in the purulent material that is expressed from these lesions

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27
Q

How is What is Molluscum Contagiosum transmitted?

A

Direct contact with lesions

Fomites

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28
Q

How is What is Molluscum Contagiosum treated?

A
  • Surgery
  • Cryotherapy

*Will spontaneously resolve in 2-12 months

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29
Q

What is Herpes Labialis?

A

Cold Sores

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30
Q

What causes Herpes labialis?

A

Reactivation of HSV infection

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31
Q

How do primary HSV infections compare to Herpes labialis?

A

Primary= worse= primary herpetic gingivostomatitis

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32
Q

Aside from Herpes labialis, what else can HSV cause?

A

1) Herpes Simplex Keratitis (leading cause of infectious blindness in the US)
2) Herpes Simplex Encephalitis (most common cause of infectious encephalitis in the US)
3) Herpetic Whitlow
4) Neonate HSV infection

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33
Q

List the characteristics of HSV.

A

Herpesviridae family
Enveloped
dsDNA genome
Latent & lytic cycles

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34
Q

What are the two different serotypes of HSV?

A

HSV-1 & HSV-2

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35
Q

Which serotype of HSV typically causes oral lesions?

A 
HSV-1 = oral 
HSV-2= genital

*Remember 1 mouth, 2 testicles

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36
Q

How are HSV oral lesions transmitted?

A

1) Direct contact with lesions

2) Saliva

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37
Q

Describe the mechanism of action of Acyclovir.

A

Acyclovir= nucleotide analog that must be phosphorylated by VIRAL ENZYMES to be activated

1) Activated by viral thymidine kinase enzyme
2) Acyclovir monophosphate–>Acyclovir triphosphate
3) Acyclovir triphosphate= active form that inhibits viral DNA polymerase & can incorporate into viral DNA to cause chain termination

*Note that Foscarnet is the second line treatment for HSV. it does NOT require the action of thymidine kinase & is associated with higher toxicity.

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38
Q

What is the technical name for chickenpox?

A

Varicella

39
Q

What virus causes Varicella?

A

Varicella Zoster Virus (VZV)

40
Q

What are the symptoms of Varicella?

A
  • Mixture of evolutionary lesions that are most prevalent on trunk, face, and scalp
  • Fever lasts ~5 days & preceeds lesions by ~2 days
41
Q

Describe the evolution of lesions in chicken pox.

A

Vesicles–>pustules–>scabs

*Lesions are often found in multiple evolutionary stages in a single area of the body, called “crops of lesions”

42
Q

Where do lesions in chicken pox most often appear? Where do they NOT appear?

A

Prevalent on: trunk, face, scalp

*NOT observed on the palms or soles

43
Q

What are the complications of varicella?

A

1) Bacterial infection of lesions
2) Pneumonia
3) Neonatal complications
4) Shingles (Herpes Zoster)

44
Q

What causes the neonatal complications of VZV?

A

Maternal infection during the first 20 weeks of gestation

45
Q

What are the neonatal complications of VZV?

A 
Low birth weight 
Skin scarring 
Encephalitis 
Chorioretinits
Microcephaly
46
Q

In what patient population is Shingles most commonly seen?

A

Elderly

Immunosuppressed

47
Q

What are the symptoms of shingles?

A
  • Paresthesia prodrome
  • Vesicular lesions on trunk (dermatomal pattern)
  • Fever & malaise
  • Postherpetic neuralgia
48
Q

What pattern does Shingles follow?

A

Dermatomal pattern

49
Q

List the characteristics of VZV.

A

Herpesviridae
Enveloped
dsDNA

50
Q

How is VZV transmitted?

A

Respiratory secretions
Saliva
Contact with lesions

51
Q

How is VZV diagnosed?

A
  • Chickenpox and Shingles are diagnosed clinically
  • Tzanck smear
  • Serological testing: ELISA & Latex Agglutination
52
Q

How is VZV prevented?

A

Varicella Vaccine, which has been approved for use in the US in persons 12 & older

53
Q

What is the VZV vaccine?

A
  • Live attenuated VZV virus that is given with mumps, measles, and rubella vaccines
  • MMRV
54
Q

What is the Zoster Vaccine?

A

Same live attenuated strain as varicella vaccine
- Higher varicella titer

*Recommended for all adults that are 60 & older

55
Q

What is given to individuals at risk for VZV complications?

A

Passive immunization with VZV antibodies

56
Q

What is used to treat VZV?

A

Acyclovir

*Note that this is not as effective as with HSV

57
Q

What are the symptoms of smallpox?

A
  • Abrupt onset fever
  • Malaise
  • Headache
  • Muscle pain
  • Nausea
  • Lesions
58
Q

Describe the lesions associated with smallpox.

A
  • Mouth (enanthem)
  • Skin (exanthem)

Usually on the face & extremities (centrifugal distribution)
Common on palms of hands and soles of feet
Synchronous evolution

59
Q

What virus causes smallpox? List the characteristics of the virus.

A

Variola virus:

Poxviridae
dsDNA
Replicates in cytoplasm
Strictly human

60
Q

How is smallpox transmitted?

A
  • Contact with virus in lesions
  • Fomite transmission
  • Air in enclosed spaces
61
Q

How long are individuals considered contagious with smallpox?

A

Until all scabs have separated from lesions (21-28 days)

62
Q

What complications are associated with smallpox?

A
  • Bacterial infection of skin lesions
  • Arthritis
  • Respiratory tract infections
  • Encephalitis

*Note that there is a higher mortality rate with hemorrhagic & flat forms of smallpox

63
Q

What is the vaccine for smallpox?

A
  • Live strain of vaccinia virus, which is another virus in the poxvirus family but NOT variola virus
  • Cross-protection mechanism
64
Q

What is eczema vaccinatum?

A

Complication of smallpox vaccination

65
Q

Compare and contrast smallpox and chickenpox.

A

Smallpox=

  • centrifugal (face & extremities)
  • palms & soles
  • synchronous lesion evolution

Chickenpox=

  • centripetal (trunk & face)
  • rarely on palms and soles
  • asynchronous lesion evolution
66
Q

What is the postexposure protocol for smallpox?

A
  • Prophylaxis with vaccine within 3 days of exposure

* Note that a vaccine within 4-7 days of exposure will provide partial protection or lessening degree of disease

67
Q

List the classic childhood exanthems.

A

1) Measles (Rubeola)
2) Scarlet fever
3) German Measles
4) Atypical Scarlet Fever
5) Erythema Infectiosum
6) Roseola

68
Q

What are the symptoms of the measles?

A
  • Prodrome for 2-4 days, then

- Maculopapular rash that begins in the hairline and spreads downward for 5-6 days

69
Q

What are the 3 C’s of the measles prodrome?

A

Cough
Coryza
Conjunctivitis

*Coryza= catarrhal inflammation of the mucous membrane in the nose, caused especially by a cold or by hay fever.

70
Q

What causes Measles?

A

“Measles Virus”

Paramyxovirus
ssRNA
Enveloped

71
Q

What are the important parts of the Measles virus envelope?

A
  • F gene that is important for fusion

- HA protein that is important for attachment

72
Q

How is Measles transmitted?

A
  • Respiratory
  • Highly contagious–90% secondary attack rate

*Note that an infected individual is contagious from prodrome to 3-4 days following onset of rash

73
Q

Why is the Measles so infective?

A

Infectious for up to 2x hours in the air

74
Q

What are Koplik spots?

A
  • Small white spots with red border opposite of the molars

- Pathognomonic for Measles

75
Q

How is measles diagnosed?

A
  • Clinical diagnosis

- Confirmed w/ lab

76
Q

What are the complications of Measles?

A

Complications occur in ~30% of cases:

  • Diarrhea
  • Otitis Media
  • Pneumonia (due directly to Measles in adults & bacterial superinfection in children)
  • Encephalitis
  • Seizures
  • Death
77
Q

How is Measles prevented?

A

*Vaccination

  • Infected patients should limit contact with susceptible individuals
  • Passive immunoprophylaxis for exposed contacts

*Note that Measles is a reportable disease

78
Q

Who is resistant to Measles?

A

1) Documented receipt of 2x doses of Measles vaccine
2) Lab evidence of immunity (titer)
3) Documentation of physician diagnosed Measles
4) Birth before 1957

79
Q

Describe the Measles vaccine.

A
  • Live attenuated virus
  • Prepped in chicken embryo fibroblasts
  • MMR or MMRV
80
Q

What are the vaccination recommendations for Measles?

A

Children:
- 1st dose @ 12-15 months & 2nd @ 4-6 years

Adults

  • One dose for those born after 1957
  • 2nd dose for international travelers, post high-school students, & healthcare workers
81
Q

How is a Measles outbreak defined?

A

Three or more cases linked in time or place

82
Q

What are the symptoms of German Measles? How is this different from Measles?

A
  • Maculopapular rash that appears on the face and spreads downward
  • Fainter than measles
  • Less severe prodrome
  • Arthralgia and arthritis
83
Q

What causes German Measles?

A

Rubella virus

84
Q

What is Congenital Rubella Syndrome?

A

Mother gets Rubella during 1st trimester

  • Deafness
  • Cataracts
  • Congenital glaucoma
  • Pigmentary retinopathy
  • Congenital heart disease
85
Q

List the characteristics of Rubella virus.

A

Togaviridae
Eveloped
+ssRNA

86
Q

How is Rubella transmitted?

A

Respiratory route

87
Q

How is Rubella diagnosed?

A
  • Direct culture of virus from patient samples
  • RTPCR
  • Serology
88
Q

Describe the Rubella vaccine.

A

Live attenuated vaccine
MMRV

  • Vaccinating one generation to prevent disease in another
89
Q

What is 5th Disease/ Erythema Infectiosum ?

A

“Slap Cheek”

  • Fever
  • Rash beginning on cheeks & spreads to the rest of the body
90
Q

What causes 5th disease?

A

B19 virus

  • Parvoviridae
  • ssDNA
  • grows exclusively in mitotically active cells i.e. hematopoietic cells in bone marrow
91
Q

Aside from 5th disease, what are the disease manifestations caused by B19 virus?

A
  • Aplastic crisis
  • Arthralgia & Arthritis
  • Pregnancy complications
92
Q

What is Roseola Infantum?

A
  • High fever that lasts 4 day
  • Maculopapular rash follows fever resolution
  • Rash lasts 24-48 hours & then resolves spontaneously
93
Q

What causes Roseola?

A

HHV-6 & HHV-7

  • Herpesviridae
  • dsDNA
  • Enveloped
  • Replicates in T, B, or oral pharyneal cells
  • Latent infection in T-cells
94
Q

How does HHV-7 differ from HHV-6?

A

Present more predominantly in CD4+ T cells; later infection

Microbiology (49 decks)

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