Other viral diseases Flashcards

1
Q

What are the two major subtypes of molluscipox virus?

A

MCV-1 and MCV-2

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2
Q

What molluscum virus is more common in HIV + patients?

A

MCV-2

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3
Q

What type of virus is molluscum?

A

Poxvirus (large double-stranded DNA virus)

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4
Q

What cutaneous diseases are associated with poxvirus?

A

Molluscum, smallpox, Orf, MIlker’s nodules

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5
Q

What are the major DNA viruses that cause cutaneous diseases?

A

Herpes virus (HSV, VZV, CMV, EBV); hepadnavirus (Hep B); Papovavirus (HPV); Parvovirus (erythema infectionsum); Poxvirus (molluscum, smallpox, orf, milker’s nodules)

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6
Q

What must be done if molluscum lesions are restricted to the genital area in a child?

A

Sexual abuse must be considered

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7
Q

What is the most common clinical presentation of molluscum?

A

Umbilicated, pink, pearly papule

  • distribution: intertriginous areas, torso, lower extremities and buttocks
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8
Q

What patients are at risk of widespread molluscum infection?

A

Patients with impaired skin barrier (AD or ichthyosis) or immunodeficiency

Patients with HIV/immunosuppression may get giant molluscum

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9
Q

Histology of molluscum?

A
  • Acanthosis and cup-shaped
  • Eosinophilic and later basophilic inclusion bodies in the prickle cell layer (Henderson-Patterson bodies)
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10
Q

Treatments for molluscum?

A

Topical tretinoin or imiquimod

Extraction

Light cryotherapy

Cantharadin

Surgical tape

Curettage

Podophyllotoxin

Subcutaneous IFN-alpha

5-FU

HAART for AIDS patients

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11
Q

What virus causes monkeypox?

A

Orthopox virus

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12
Q

Who generally gets monkeypox?

A

90% of cases occur in children <15 y/o

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13
Q

Where is monkeypox usually found?

A

Usually in Central/western African, but there was an outbreak in the US from prairie dogs

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14
Q

What is the clinical of monkeypox? prognosis?

A

The disease is similar to smallpox but there are fewer lesions. Lesions tend to favor the face and extremities (esp palms and soles) with centrifugal spread. These lesions may be present in various stages.

  • May have systemic sx’s: respiratory, fever, and LAD in 67%
  • Fatality rate of 11%
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15
Q

Can monkeypox be passed from human to human?

A

Yes, initial dz usually following contact with wildlife sources

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16
Q

What virus causes smallpox?

A

Variola virus, orthopox genus

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17
Q

How does infection of smallpox spread?

A

Infection occurs via respiratory tract (incubation period = 7-17 days).

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18
Q

Clinical of small pox?

A

Prodrome with fever, headache, myalgias, and malaise, then centrifugal spread of race (face/arms/legs/trunk).

  • The rash is vesiculpustular and may involve hands/feet.

One key is that lesions in a site will be of the same stage and the pt w/ be toxic appearing

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19
Q

How long is a patient with smallpox infectious?

A

Patients are infectious from eruption onset til 7-10 days post-eruption

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20
Q

What are some complications of smallpox and what is its prognosis?

A

Complications: blindness, encephalitis, toxemia, hypotension, pneumonitis, arthritis, and osteitis

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21
Q

What type of vaccine is the smallpox vaccine and what are some potential side effects?

A

Live vaccine: vaccinia virus is used for live vaccine

Complications: LAD, ocular vaccinia, generalized vaccinia, eruptions, eczema vaccinator, EM, postvaccinial CNS dz, and progressive vaccinia (immunocompromised pts)

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22
Q

What virus causes cowpox?

A

Cowpox virus, genus orthopox virus

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23
Q

What animal usually causes cowpox?

A

Cats

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24
Q

Clinical progression of cowpox?

A

Europe and Asia

  • Spread is via cutaneous contact (usually hands or face) with an infected animal
  • Incubates for 7 days and then a painful red papule at the site of contact forms –> vesicular –> pustular –> hemorrhagic ulcer w/ eschar
  • Lesions usually solitary and located on hands/fingers
  • Can cause fever/systemic sx’s
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25
Q

What virus causes Orf?

A

Orf virus, genus parapox

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26
Q

How is Orf spread?

A

Contact with infected animals

  • Most common: sheep, goats, or reindeer
  • Usually from contact with udder or perioral areas of ewes
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27
Q

Clinical of Orf?

A

One to few lesions usually develops at the site of inoculation (often on hands).

Lesions go through 6 stages: maculopapular (umbilicated) –>targetoid –>acute (weeping nodule –>regenerative nodule w/ thin crust and black dots –>papillomatous–>regressive (curst overlying)

self resolves, no tx needed

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28
Q

What virus causes Milker’s nodule?

A

Pseudocowpox, Paravaccinia virus, genus = paradox

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29
Q

What is Milker’s nodule?

A

Papules at the site of contact (usually muzzles of calves and teats of cows)

  • Usually singular lesion that looks like Orf. Most common in farmers/ranchers, veterinarians, and butchers

dx via histology or PCR

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30
Q

What type of virus causes hand foot and mouth dz?

A

Picornavirus –> coxsackieviruses, echoviruses, and enterovirus type 71

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31
Q

What group of coxsackie viruses cause herpangina?

A

Group A coxsackievirus

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32
Q

Clinical presentation of herpangina?

A

Acute onset of fever, headache, cervical lymphadenopathy, sore throat, dysphagia, anorexia, and sometimes a stiff neck

Yellowish white, vesicles in the throat, surrounded by an intense areola

Most frequently on the anterior faucial pillars, tonsils, uvula, or soft palate

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33
Q

What is the progression of hand foot and mouth disease?

A

Infection begins with fevers and sore mouth (90% have oral involvement). Oral lesions are small rapidly ulcerating vesicles sounded by red areola

  • Lesions on the hands and feet run parallel to skin lines. These are initially red papules that turn to gray football-shaped vesicles surrounded by a red halo
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34
Q

What is the timecourse of hand foot and mouth disease?

A

Typically lasts less than a week. Treatment is supportive.

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35
Q

What virus is most commonly implicated in hand foot and mouth disease?

A

Coxsackievirus A-16>>Coxsackie A-6 and enterovirus 71

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36
Q

When can children with hand foot and mouth disease go back to school?

A

There is no evidence for reducing spread by keeping children from going back to school. They are contagious before the emergence of the lesions and for many weeks after via shedding in stool. Can return when the fever has resolved and the child feels up to it.

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37
Q

What clinical presentation does coxsackie A6 tend to be associated with?

A

Is thought to cause a more widespread and severe vesiculobullous eruption and is associated with atypical presentations including eczema coxsackium (in atopic patients), gionotti-crosti-like eruptions, purpuric eruptions, and onychomadesis (nail matrix arrests at time of acute infection)

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38
Q

What is the risk of CNS disease in coxsackie A-16 infection? What HFMD-causing virus has the highest risk of CNS involvement?

A

No CNS disease reported in coxsackie A-16

  • Enterovirus 71 has the highest risk of CNS involvement
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39
Q

What is eruptive pseudoangiomatosis?

A

Happens in young children immediately after a viral illness. They develop blanchabel red papules that resemble angiomas.

  • Resolves spontaneously in 10 days

*Most common on trunk and extremities

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40
Q

What viruses are associated with eruptive pseudoangiomatosis?

A

Echoviruses 25 and 32 have been implicated and more recently EBV

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41
Q

How is HFMD transmitted?

A

Fecal oral route and respiratory route.

Incubation time is 3-6 days –>prodrome of fever and malaise followed by a cutaneous eruption

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42
Q

What type of virus causes measles?

A

paramyxovirus (RNA)

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43
Q

Clinical of cutaneous measles?

A

A macular or maculopapular eruption appears after 1-7 days. Often starts on the anterior scalp line and behind the ears

  • Quickly spreads over the face and involves the entire body by day 3
  • Purpura may be present

Koplik’s spots are pathognomonic, appear during the prodrome. Appear first on the buccal mucosa nearest to the lower molars as 1mm white papules on an erythematous base.

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44
Q

Complications of measles?

A

Otitis media, gastrointestinal symptoms, encephalitis, myocarditis, and subacute sclerosing panencephalitis

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45
Q

What treatment should be given to pediatric patients with measles?

A

Vitamin A supplementation: For those from communities w/ vitamin A deficiency, those aged 6months to 2yrs of age that are hospitalized and those > 6 with risk factors

46
Q

What is the vaccine schedule for measles?

A

First dose at 12-15 months and the second dose at age 4-6 years

47
Q

Diagnosis of measles?

A

IgM may be initially negative for 3 days after rash onset. IgG should increase 4-fold, PCR from nasopharyngeal swab or urine is another option

48
Q

What virus (what type of virus) causes rubella?

A

RNA virus, togaviridae, rubella virus

49
Q

How is rubella transmitted?

A

Respiratory droplets

50
Q

What is the principle concern with rubella?

A

Rubella is nicknamed the “3 day measles” as the course is shorter and milder. However, important to avoid in pregnancy as it is a TORCH organism

51
Q

What is the clinical of the cutaneous reaction?

A

Morbilliform rash that starts on head/neck (like measles) and spreads in cephalocaudal fashion

Enanthem: Forchheimer’s spots (palatal petechiae)

LAD typically generalized/painful w/ involvement of suboccipital/postauricular/anterior and posterior cervical lymph nodes

52
Q

Complications from Rubella?

A

arthritis, arthralgias, hemolytic anemia, hepatitis, myocarditis, pericarditis, thrombocytopenia, and encephalitis

53
Q

What virus causes erythema infectiosum (“Fifth disease”)?

A

Parvovirus B19 (single stranded DNA virus)

54
Q

How is parvovirus transmitted?

A

Respiratory secretions, blood, or vertically from mother to fetus

55
Q

What can occur with hemoglobin counts in parvovirus infection?

A

Hgb counts can go down, the parvovirus B19 grows in the bone marrow and replicates in erythroid precursors (binds to globoside blood group P antigen) –> transient decreases in hemoglobin

56
Q

Is a patient contagious with the rash of parvovirus B19?

A

No, infectious during prodrome consisting of fevers, myalgias, and headache. Exanthem appears 1-1.5 weeks later

57
Q

Appearance of the rash in parvovirus B19?

A

“Slapped cheek” erythema sparing the central face. This rash is more common in children and may not occur in adults. This progresses to a maculopapular eruption with “lacy reticulated” patter favoring the extremities.

58
Q

What can occur with fetal infection of parvovirus B19?

A

Highest risk if acquired before 20 weeks gestation

  • Fetal loss rate highest in the second trimester
  • Fetal effects: anemia, high-output congestive heart failure, hydrops fetalis, and intrauterine fetal demise
59
Q

What are some blood sequelae that can occur with parvovirus B19 infection and what are some predisposing factors?

A

Aplastic crisis and pancytopenia

  • predisposing factors: sickle cell anemia and other hemoglobinopathies
60
Q

What rash involving the hands and feet can occur with Parvovirus B19?

A

Papular purpuric gloves and socks syndrome: Young adults, symmetric edema and erythema of palms/soles, may extend to the dorsal surface.

  • Associated petechiae and purpura with sharp demarcation at the wrists and ankles
61
Q

Are patients infectious with the papular purpuric gloves and socks syndrome rash?

A

Yes, unlike the “slapped cheek” and maculopapular rash of parvo B19 usually the papular purpuric gloves and socks syndrome rash occurs during viremia and the patients are infectious.

62
Q

What type of viruses causes hand foot and mouth disease?

A

Picornaviruses (Coxsackievirus, echovirus, and enterovirus type 71 cause skin dz).

  • these are single-stranded RNA viruses
63
Q

What virus most often causes hand foot and mouth disease?

A

Coxsackie A16>A6>Enterovirus 71

64
Q

Transmission pattern for hand foot and mouth disease?

A

Fecal-oral and respiratory routes

65
Q

Clinical progression of hand foot and mouth disease?

A

The incubation period for 3-6 days with a prodrome of fever and malaise followed by a cutaneous eruption

  • They are most contagious during the prodrome
66
Q

Lesions of hand foot and mouth disease?

A

Vesicular eruption on the palms, soles, buttocks, and oral cavity

  • erythematous macules and oval, deep-seated erythematous vesical and bullae with a gray center that are often “football-shaped” on these areas.
  • erosive lesions in the oral cavity on the palate/uvula/tongue/buccal mucosa.
67
Q

What type of presentation is coxsackie A6 associated with?

A

More widespread and severe vesiculobullous eruptions and is a/w atypical presentations like:

Eczema coxsackium, Gianotti-Crosti-like eruptions, purpuric eruptions, and onychomadesis

68
Q

What is herpangina?

A

Group A coxsackievirus, headache, fever, cervical lymphadenopathy, sore throat sometimes stiff neck –> yellowish-white vesicles in the throat with intense inflammation.

  • Most commonly on the faucial pillars, tonsils, uvula, or soft palate
69
Q

Progression and treatment of herpangina?

A

Lesions coalesce and ulcerate leaving a shallow crater. These resolve in 5-10 days. Treatment is supportive but topical anesthetics or allopurinol mouthwash can be considered.

70
Q

What is the difference between herpangina and hand foot and mouth disease?

A

In herpangina, it is only in the mouth. If there is the involvement of the skin then it is hand foot and mouth.

71
Q

What hand foot and mouth virus carries a higher risk of CNS disease?

A

Enterovirus 71 is associated with CNS disease in Taiwanese outbreak, no CNS dz in Coxsackie A-16

72
Q

What would we suspect if a child had a sore throat, fever and then developed blanchabel red papules that looked like cherry angiomas on the face, trunk and limbs?

A

Eruptive pseudoangiomatosis

73
Q

What viruses have been implicated in pseudoangiomatosis?

A

Echoviruses 25 and 32 and EBV

74
Q

What should we consider in a child who has a URI/ or GI illness and then gets a largely unilateral exanthem on their trunk?

A

Asymmetric periflexural exanthem of childhood, aka unilateral laterothoracic exanthem

75
Q

What is the rash of asymmetric periflexural exanthem of childhood like?

A

Erythematous papules coalesce to form poorly marginated morbilliform plaques. It can be mildly pruritic.

The contralateral side can be involved in 70% of cases but the rash will still be asymetric

76
Q

What is the “statue of liberty sign”?

A

This is a boards clue for unilateral laterothoracic exanthem. Basically the rash will often begin in the axilla, so the child will have one arm raised to the sky to show the rash on axilla and the lateral trunk

77
Q

Progression and treatment of unilateral laterotheroacic exanthem?

A

Lasts 2-6 weeks on average. There is no tx and topical steroids or oral antibiotics are not beneficial. Can do oral antihistamines if itchy

78
Q

What is the recurrent phase of erythema infectiosum?

A

After parvovirus B19 infection sometimes the eruption can reappear following emotional upset, heat (bathing), exercise, or sunlight for 2-3 weeks after primary exanthem

79
Q

What virus should be checked for if you see papular purpuric stocking and glove syndrome in an adult?

A

HBV

80
Q

What age range is most affected by Gionatti-Crosti?

A

Ages 1-6 (90% younger than 4)

81
Q

What is the most common cause of Gianotti-Crosti in the USA and worldwide?

A

USA= EBV

Worldwide = Hepatitis B

82
Q

What is the rash like in Gianotti-Crosti?

A

Symmetric, monomorphic, skin-colored to erythematous papular eruption with predilection for the face (cheeks), extremities, and buttocks and spares the chest, back and abdomen

83
Q

How long does Gianotti-Crosti last usually?

A

1-2 months

84
Q

What is the arbovirus group?

A

Comprise numerous arthropod-borne RNA viruses

85
Q

What type of virus causes West Nile Fever?

A

Flavivirus, single-stranded RNA virus, endemic to E. Africa but has been in the U.S. since ‘99

86
Q

What is the vector for West Nile Fever?

A

Culex mosquito

image from the creative commons

87
Q

Cutaneous findings in West Nile Fever?

A

Maculopapular eruption accompanied by lymphadenopathy and fever

88
Q

What is sandfly fever?

A

Small pruritic papules that appear after the bite of a sandfly on the face and neck; may appear scarlatiniform in nature.

  • Fever, headache, malaise, nausea, conjunctival inection, stiff neck, and abdominal pains occur.

recovery is slow, recurring fever occurs.
no tx available

89
Q

What type of virus is the dengue virus?

A

Flavivirus (single-stranded RNA virus)

90
Q

What is the vector for dengue fever?

A

Aedes aegypti mosquito

Image from the creative commons: note the white stripes on the abdomen and legs

91
Q

What is the most common presentation of dengue?

A

Asymptomatic (75% of cases)

92
Q

What is the presentation of dengue?

A

Most asymptomatic, mild cases are non-specific viral in nature. But, classic disease = morbilliform/scarlatiniform rash in 50% of cases. Severe headache/myalgia/arthralgia, retroorbital pain, some have petechial mucosal lesions, epistaxis, and gingival bleeding.

One of the classic findings in the dengue rash is white islands of sparing in the rash

93
Q

What patients are most susceptible to dengue hemorrhagic fever?

A

Those who have been infected with one serotype and then get infected with another type.

usually happens in children younger than 15. Look for lethargy/weakness, vomiting, facial flushing, and circumoral pallor.

94
Q

How is the diagnosis of dengue made and what is one way it can be distinguished from the Chikungunya virus?

A

RT-PCR, ELISA during the initial/acute phase, IgM becomes + later in dz.

Neutropenia can occur and can distinguish this from Chikungunya virus

95
Q

What supportive medications should be avoided in dengue?

A

Aspirin and NSAIDs as these can worsen hemorrhagic sequelae

96
Q

What virus causes viral-associated trichodysplasia of immunosuppression?

A

Polyomavirus

97
Q

What patients get viral-associated trichodysplasia of immunosuppression?

A

Organ transplant patients or leukemia/lymphoma patients on chemotherapy

98
Q

What is the clinical of viral-associated trichodysplasia of immunosupression?

A

Pink/flesh-colored spiny papules on face (mid-face), eyebrows, eyelash loss and thickening of facial skin

99
Q

What is the treatment for viral-associated trichodysplasia of immunosuppression?

A

Decrease immunsuppression or topical cidofovir and oral ganciclovir

100
Q

What virus causes Chikungunya?

A

Chikungunya virus, single stranded + sense RNA Togavirus

101
Q

What is the vector for Chikungunya virus?

A

The Aedes aegypti > A. albopictus

Picture from the creative commons

102
Q

What are the clinical symptoms of Chikungunya?

A

Cutaneous: Morbilliform eruption, mucosal apthous-like ulcers, post-inflammatory pigmentation of face/extremities, acral/facial edema, bullous eruptions in infants and ecchymoses.

General: High fever, marked joint sx’s, neuropathic acral findings and headache/nausea/vomiting

103
Q

What type of virus causes Zika?

A

Icosahedral, single-stranded RNA virus in the Flavivirus family

104
Q

What other ways besides mosquito can Zika be passed?

A

Blood transfusions, sexual contact, and vertically from mom to fetus during pregnancy –> microcephaly and other fetal anomalies

105
Q

What long term sequelae are problematic in Zika infections?

A

Has been associated with Guillain-Barré syndrome in adults and also microcephaly during pregnacy

106
Q

Clinical features of Zika?

A

Nonspecific, diffuse, morbilliform/scarlatiniform eruption that begins 3-12 days after the initial infection. It progresses with a cephalocaudal progression. Rash subsites after 3 days and completely resolves in 1 week. Can have petechia and bleeding gums

107
Q

How is the diagnosis of Zika made?

A

RT-PCR or ELASA during initial phase in the first 7 days.

108
Q

Treatment/prevention of Zika?

A

No treatment or vaccine is available as of now. DEET should be used as well as long sleeves/pants in endemic areas. Likewise, pregnant patients should avoid travel to an endemic area

109
Q

What virus group causes Sindbis virus infection and where is it seen?

A

Causes by Alphavirus, seen in Finland

110
Q

Clinical presentation of Sindbis?

A

Multiple erythematous papules with a surrounding halo associated with a fever and prominent arthralgias

  • Symptoms resolve over a few weeks