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Oral and Maxillofacial Pathology > Chapter 7: Viral Infections > Flashcards

Chapter 7: Viral Infections Flashcards

1
Q

___ comes from the Greek word meaning “to creep or crawl”

A

herpes

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2
Q

___ are the only reservoir for HHV

A

humans

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3
Q

what are the 8 human herpes viruses (HHVs)?

A
  • HSV-1 or HHV-1 - herpes simplex virus, type 1
  • HSV-2 or HHV-2 - herpes simplex virus, type 2
  • VZV or HHV-3 - varicella-zoster virus
  • EBV or HHV-4 - epstein-barr virus
  • CMV or HHV-5 - cytomegalovirus
  • HHV-6
  • HHV-7
  • KSHV or HHV-8 - kaposi’s sarcoma herpesvirus
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4
Q

how does HSV-1 spread?

A

primarily through saliva or active perioral lesions

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5
Q

HSV-1 is best adapted to what locations?

A

above the waist

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6
Q

___ exposure has been the only condition to unequivocally induce HSV-1 lesions experimentally

A

UV light

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7
Q

in the case of HSV-1 symptomatic primary infections, ___ affects clinical presentation. how?

A

age

  • younger = gingivostomatitis
  • 18+ = pharyngotonsillitis
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8
Q

how does HSV-2 spread?

A

primarily through sexual contact

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9
Q

HSV-2 is best adapted to ___ locations

A

below the waist

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10
Q

clinical lesions produced by what herpes viruses are identical?

A

HSV-1 and HSV-2

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11
Q

in the initial exposure (aka primary infection) or HSV-2, is it primarily in old or young patients, and what percent are asymptomatic?

A

young, 80%

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12
Q

after initial HSV-2 exposure, the virus is taken up by ___ and transported to associated ___. which viral state does this describe?

A
  • sensory nerves
  • sensory ganglia
  • at this point, the virus would be in the latent state
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13
Q

what is the most common site of HSV-2 latency?

A

trigeminal ganglion

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14
Q

what is the most common site of recurrence of HSV-1? what are other locations where recurrent lesions can occur?

A
  • vermillion border and adjacent skin of the lips: herpes labialis, “cold sore”, “fever blisters”
  • can also occur on the nose, chin, and cheek
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15
Q

___% of the US population have a history of herpes labialis

A

40%

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16
Q

HSV lesions appear as multiple, small, erythematous papules. describe them.

A
  • papules form clusters of fluid-filled vesicles
  • vesicles rupture and crust within 2 days
  • heals without scarring in 7-10 days
  • symptoms are most severe in the first 8 hours
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17
Q

the majority of people with HSV-1 or 2 will have how many outbreaks annually?

A

2

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18
Q

active viral replication of HSV-1 and 2 is complete within how many days?

A

2

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19
Q

what can result in the spreading of HSV-1 and 2 lesions?

A

mechanical rupture of intact vesicles releases the virus and can result in spreading of the lesions

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20
Q

recurrent intraoral herpes simplex lesions occur almost always on what type of tissue?

A

almost always on keratinized, bound mucosa (palate and attached gingiva)

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21
Q

describe the clinical presentation of recurrent intraoral herpes simplex lesions

A
  • lesions begin as 1-3mm vesicles
  • rapidly collapse to form a cluster or erythematous macules that coalesce and slightly enlarge
  • damaged epithelium is lost
  • central, yellowish area of ulceration
  • heals in 7-10 days
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22
Q

primary HSV-1 infection is called ___

A

acute herpetic gingivostomatitis

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23
Q

what is the most common pattern of symptomatic primary HSV infection?

A

acute herpetic gingivostomatitis

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24
Q

most cases of acute herpetic gingivostomatitis occur before what age?

A

5

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25
Q

describe the clinical presentation of acute herpetic gingivostomatitis

A
  • affected mucosa develops numerous pinhead vesicles
  • both movable and attached oral mucosa can be affected
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26
Q

self-inoculation of fingers, eyes, and genitals can occur with ___

A

acute herpetic gingivostomatitis

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27
Q

what are the initial symptoms of pharyntotonsillitis (form primary herpes)

A
  • sore throat
  • fever
  • headache
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28
Q

what is herpetic whitlow?

A
  • aka herpetic paronychia
  • less common presentation of HSV-1
  • infection of the thumb or fingers
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29
Q

what is herpes gladiatorum?

A
  • aka scrumpox
  • less common presentation of HSV-1
  • herpetic infection found in wrestlers or rugby players with contaminated abrasions
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30
Q

what is herpes barbae?

A
  • less common presentation of HSV-1
  • herpes over the bearded region of the face into minor injuries created by daily shaving
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31
Q

describe ocular involvement of HSV-1

A
  • less common presentation of HSV-1
  • leading infectious cause of blindness in the US
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32
Q

what is eczema herpeticum?

A
  • aka kaposi’s varicelliform eruption
  • less common presentation of HSV-1
  • diffuse, life-threatening infection that can occur in patients with chronic skin conditions
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33
Q

how can newborns be infected with HSV, and what is the mortality rate without treatment?

A
  • via an infected birth canal (usually HSV-2)
  • 50% mortality rate without treatment
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34
Q

what are some histologic features of HSV?

A
  • multinucleation
  • ballooning degeneration
    • acantholysis
    • nuclear clearing
    • nuclear enlargement
  • tzanck cells
    • free floating epithelial cells in an intraepithelial vesicle
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35
Q

what are some ways that HSV can be diagnosed?

A
  • strong presumptive diagnosis from clinical presentation
  • cytologic smear
  • tissue biopsy
  • serologic testing is positive 4-8 days after initial exposure
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36
Q

what is the general treatment of HSV?

A

antivirals, like acyclovir

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37
Q

what is the treatment for primary herpetic gingivostomatitis (HSV)?

A
  • antivirals introduced early can reduce severity and frequency of recurrent infection
  • antivirals introduced within 3 days can greatly accelerate clinical resolution
  • once therapy is initiated, no new lesions develop
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38
Q

what is the primary varicella zoster (VZV) infection?

A

chickenpox represents the primary infection

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39
Q

how does VZV spread?

A

through air droplets or direct contact with active lesions

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40
Q

most cases of primary VZV infections occur in what age patients?

A

5-10

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41
Q

after initial VZV infection, where does the virus establish latency?

A

in dorsal spinal ganglia

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42
Q

what is shingles?

A
  • reactivation VZV infection (single recurrence)
  • occurs in 20% of patients
  • prevalence increases with age
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43
Q

what are predisposing factors for reactivation of VZV?

A
  • immunosuppression/immunosuppressive drugs
  • radiation
  • malignancies
  • increasing age
  • alcohol abuse
  • emotional or physical stress
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44
Q

describe recurrent VZV oral lesions (shingles)

A
  • occur with trigeminal nerve involvement
  • present on movable or bound tissue (different from HSV)
  • lesions tend to follow the path of the affected nerve and terminate at the midline; patient usually has accompanying skin lesions
  • lesions are 1-4mm, white, opaque vesicles that rupture to form shallow ulcerations
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45
Q

describe ocular involvement of recurrent VZV (shingles)

A
  • may cause significant morbidity (permanent blindness)
  • if the tip of the nose is involved, it is a sign ocular infection may occur
  • referral to ophthalmologist is mandatory if the patient experiences these lesions
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46
Q

what is ramsay hunt syndrome?

A
  • cutaneous lesions of the external auditory canal as a result of recurrent VZV (shingles)
  • involvement of ipsilateral face and auditory nerves
  • facial paralysis
  • hearing deficits
  • vertigo
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47
Q

___ is the most common disease resulting from EBV exposure

A

infectious mononucleosis (kissing disease)

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48
Q

what are other lesions that demonstrate EBV?

A
  • oral hairy leukoplakia
  • lymphomas/lymphoproliferative disorders
    • notably african’s burkitt’s lymphoma
  • nasopharyngeal carcinoma
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49
Q

up to ___% of adults are infected with infectious mononucleosis

A

95%

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50
Q

how does infectious mononucleosis spread?

A

by intimate contact

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51
Q

how is infectious mononucleosis diagnosed?

A

presence of paul-bunnell heterophil antibodies

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52
Q

what is the treatment for infectious mononucleosis?

A
  • most cases resove in 4-6 weeks
  • NSAIDs can be given
  • patients should avoid contact sports
  • no steroids or antibiotics due to possible complications
  • antivirals do not have clinical benefit
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53
Q

where can CMV reside?

A

in salivary gland cells, endothelium, macrophages, and lymphocytes

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54
Q

almost ___% of CMV infections are asymptomatic; of the ones that are symptomatic, what are the symptoms?

A
  • 90%
  • most common symptoms include fever, joint and muscle pain, shivering, etc.
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55
Q

CMV is common in patients with what disease?

A

AIDS

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56
Q

most individuals affected by CMV have ___

A

chronic mucosal ulcerations

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57
Q

what is the histology of CMV?

A

“owls eye” cell

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58
Q

enteroviruses are classified into what 3 categories?

A
  • echoviruses
  • coxsackievirus
  • poliovirus
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59
Q

how many types of enteroviruses have been discovered up to this point? of those, how many cause symptomatic infections associated with rashes?

A
  • about 60
  • 30
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60
Q

what are the three enteroviruses that are important to oral health care professionals, and what subgroup of enteroviruses are they produced by?

A
  • herpangina
  • hand-foot-and-mouth disease
  • acute lymphonodular pharyngitis
  • all three are produced by the coxsackievirus
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61
Q

what is the incubation period for enterovirus?

A

4-7 days

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62
Q

___ and ___ promote the spread of enteroviruses

A

crowding and poor hygiene

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63
Q

what is the major path of transmission of enteroviruses?

A

fecal-oral route

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64
Q

during the acute phase, enterovirus can be transmitted via ___ or ___

A

saliva or respiratory droplets

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65
Q

what does infection to one enterovirus strain confer?

A

immunity to other enteroviruses

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66
Q

nearly half of reported cases of enterovirus infection occur in what age patient?

A

infants younger than 1 year

85% of all reported cases occur in patients younger than 20

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67
Q

what is the annual incidence of enterovirus in the US?

A

between 10-15 million symptomatic infections

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68
Q

how does herpangina present clinically?

A
  • skin rash
  • 2-6 oral lesions in the posterior mouth
    • soft palate, tonsillar pillars
  • begin as red macules and form fragile vesicles that rapidly ulcerate
  • ulcerations are 3mm in diameter
  • resolve within 10 days
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69
Q

what are symptoms of herpangina?

A

sore throat, fever, and dypshagia

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70
Q

with hand-foot-and-mouth disease, skin rash and oral lesions are associated with ___

A

flu-like symptoms

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71
Q

what lesions are almost always present with hand-foot-and-mouth disease?

A

hand and oral lesions

72
Q

describe the oral lesions present with hand-foot-and-mouth disease

A
  • arise first and without prodrome
    • resemble those of herpangina, but larger and more numerous
    • up to 30 lesions, up to 1cm in diameter
    • affect buccal mucosa, labial mucosa, and tongue most commonly
73
Q

describe the cutaneous lesions associated with hand-foot-and-mouth disease

A
  • borders of palms and soles
  • ventral surfaces and sides of fingers and toes
  • erythematous macules that develop central vesicles
  • heal without crusting
74
Q

acute lymphonodular pharyngitis is characterized by what 3 symptoms?

A

sore throat, fever, mild headache

75
Q

how does acute lymphonodular pharyngitis present clinically? when does it resolve?

A
  • 1-5 yellow to dark pink nodules on the soft apalte or tonsillar pillars
  • represent hyperplastic lymphoid aggregates
  • resolves within 10 days without vesiculation or ulceration
76
Q

the diagnosis of enteroviruses can be made from ___ manifestations, and the infection is ___

A
  • clinical manifestations
  • self-limiting
77
Q

rubeola (measles) is caused by ___

A

a paramyxovirus

78
Q

is there a vaccine for rubeola (measles)?

A

yes, it has been available since 1963 and is 95% effective (probably don’t need to know these specifics)

79
Q

most cases of rubeola (measles) arise in what season?

A

winter

80
Q

how does rubeola (measles) spread?

A

through respiratory droplets

81
Q

the incubation period for rubeola is ___

A

10-12 days

82
Q

rubeola is infectious how long before symptoms and how longer after the rash appears? what is responsible for the rash?

A
  • 2 days before symptoms
  • 4 days after rash appears
  • vasculitis is responsible for the rash
83
Q

rubeola is associated with significant ___

A

lymphoid hyperplasia

84
Q

which disease lasts 9 days, with 3 stages that are 3 days each?

A

rubeola

termed nine-day measles

85
Q

what is the first stage of rubeola?

A
  • 3 C’s + fever
  • cyroza, conjunctivitis, cough
  • koplik’s spots
86
Q

describe koplik’s spots

A
  • multiple areas of mucosal erythema with numerous, small, blue-white macules (“grains of salt” on a red background)
  • pathognomonic
  • represent foci of epithelial necrosis
87
Q

describe the second stage of rubeola

A
  • fever continues
  • koplik’s spots fade
  • maculopapular and erythematous (morbilliform) rash begins
    • face first
    • downward spread from trunk extremities
    • blanches on pressure
88
Q

describe the 3rd stage of rubeola

A
  • fever ends
  • rash fades in similar downward progression
  • replaced by brown pigmentary staining
89
Q

rubella is caused by ___

A

togavirus

90
Q

what is the greatest importance of rubella?

A

capacity to induce birth defects (congenital rubella syndrome)

91
Q

what is the incubation time of rubella?

A

2-3 weeks

92
Q

when are patients infected with rubella contagious?

A

from 1 week before rash to 5 days after its development

93
Q

what are the vaccine contraindications for the rubella vaccine?

A
  • pregnancy
  • immunodeficiency
  • acute febrile illnesses
  • allergy to vaccine components
94
Q

how long does rubella last? what are the symptoms?

A
  • 3 days
  • mild symptoms
95
Q

arthritis is the most common complaint of ___

A

rubella

96
Q

what are the oral lesions of rubella?

A
  • forchhemier’s sign
    • 20%
    • small, discrete, dark-red papules on the palate
97
Q

describe congenital rubella syndrome

A
  • frequency of transmission from infected mother during first trimester is 80%
  • triad: deafness (80%), heart disease, cataracts
98
Q

the rubella vaccine is ___ preventative

A

95%

99
Q

mumps is also called ___

A

epidemic parotitis

100
Q

mumps are a disease of ___

A

exocrine glands

salivary glands are best known sites of involvement

101
Q

in mumps, the involved glands exhibit ___ and ___

A

edema and lymphocytic infiltration

102
Q

what is the incubation period of mumps?

A

2-4 weeks

103
Q

when are mumps cantagious?

A

from 1 day before clinical appearance to 2 weeks after resolution

104
Q

30% of mumps infections are ___

A

subclinical

105
Q

with the onset of mumps, there will be a nonspecific ___ followed by significant ___ changes. what are the changes?

A
  • prodrome
  • salivary gland
    • discomfort and swelling
    • saliva stimulation increases pain
106
Q

25% of postpubertal males with mumps will experiencee ___, characterized as swelling of the testicles (up to 4x the size), followed by atrophy

A

epididymorchitis

107
Q

25% of first-trimester women with ___ will experience spontaneous abortions

A

mumps

108
Q

what is the treatment of mumps?

A
  • palliative treatment
  • 99% decrease since MMR vaccine
109
Q

when were the first cases of HIV/AIDS in the US documented?

A

1981

110
Q

where is the HIV virus found?

A

in bodily fluids

111
Q

what are the most frequent routes of transmission of HIV/AIDS?

A
  • sexual contact
  • parenteral exposure to blood
  • transmission from mother to fetus
112
Q

what is the target cell of HIV/AIDS?

A
  • CD4+ helper T lymphocyte
  • when T-helper cells are destroyed, immune function is lost
113
Q

what are the 3 stages of HIV/AIDS?

A
  • acute self-limited viral syndrome
  • asymptomatic period
  • final symptomatic period
114
Q

what are the 5 oral manifestations most strongly associated with HIV infection?

A
  • oral hairy leukoplakia (EBV)
  • candidiasis
  • non-hodgkins lymphoma
  • kaposi’s sarcoma (HHV-8)
  • periodontal disease
115
Q

oral candidiasis is present in ___ of HIV patients and ___ of AIDS patients

A
  • 1/3
  • 90%
116
Q

what is the treatment for oral candidiasis associated with HIV/AIDS?

A
  • treatment is difficult - skip nystatin and prescribe topical clotrimazole
  • systemic fluconazole is given if:
    • patient is not on HAART
    • patients CD4+ count is <50
    • patient has a high viral load
    • there is esophageal involvement
117
Q

oral hairy leukoplakia present in HIV/AIDS patients is a sign of what?

A

severe immune depression and advanced disease

118
Q

oral hairy leukoplakia rarely occurs in any other form of immune suppression other than ___

A

HIV/AIDS

its presence in the absence of known immunosuppresion mandates HIV testing

119
Q

___ is the most common EBV-related lesion in AIDS patients

A

oral hairy leukoplakia

120
Q

how does oral hairy leukoplakia in HIV/AIDS patients present clinically? how is it diagnosed? what is the treatment?

A
  • white mucosal plaque that does not rub off, usually occurs on the lateral border of the tongue
  • clinical diagnosis can be made
  • no treatment necessary
121
Q

___ is present in up to 20% of AIDS patients and is characterized by multifocal neoplasm of vascular endothelial cell origin

A

kaposi’s sarcoma (HHV-8)

122
Q

with kaposi’s sarcoma in HIV/AIDS patients, the ___ may represent the predominant reservoir of the infectious virus

A

oral cavity

123
Q

___% of HIV/AIDS patients with kaposi’s sarcoma have oral lesions

A

70%

124
Q

in 20% of HIV/AIDS patients, where is the primary site of involvement of kaposi’s sarcoma?

A

the oral cavity

125
Q

what 3 areas of the oral cavity are commonly affected by kaposi’s sarcoma?

A

hard palate, gingiva, and tongue

126
Q

how is kaposi’s sarcoma in HIV/AIDS patients diagnosed?

A

biopsy is required

127
Q

up to ___% of HIV-infected patients will have non-hodgkins lymphoma

A

5%

128
Q

how does non-hodgkin’s lymphoma in the HIV/AIDS patient present?

A

high-grade and aggressive disease

129
Q

what is non-hodgkin’s lymphoma in the HIV/AIDS patient associated with?

A

widespread involvement and short survival times

130
Q

a large number of non-hodgkin’s lymphoma in the HIV/AIDS patient cases have a relationship with what other virus?

A

EBV

131
Q

what are the 3 atypical patterns of periodontal disease associated with HIV?

A
  • linear gingival erythema
  • necrotizing ulcerative gingivitis
  • necrotizing ulcerative periodontitis
132
Q

describe linear gingival erythema associated with periodontal disease in the HIV patient

A
  • linear gingival erythema diagnosis is reserved for gingivitis that doesn’t respond to improved plaque control and has a greater degree of erythema than would be expected
  • distinguishes from marginal gingivitis
133
Q

describe necrotizing ulcerative gingivitis associated with periodontal disease in the HIV patient

A

ulceration and necrosis of interdental papillae with no attachment loss

134
Q

describe necrotizing ulcerative periodontitis associated with periodontal disease in the HIV patient

A

ulceration and necrosis with rapidly progressing attachment loss

135
Q

what is the treatment for linear gingival erythema associated with periodontal disease in the HIV patient?

A

systemic antifungals

136
Q

what is the treatment for NUG and NUP associated with periodontal disease in the HIV patient?

A

debridement, antimicrobials, immediate follow up, long term maintenance

137
Q

___ can occur if periodontal disease in the HIV/AIDS patient is left untreated

A

necrotizing stomatitis

138
Q

___ altered the course of the HIV/AIDS epidemic

A

highly active antiretroviral therapy (HAART)

139
Q

how has the risk of seroconversion after exposure to HIV-contaminated blood been altered as a result of HAART?

A
  • percutaneous exposure = 0.3%
  • mucous membrane exposure = 0.09%
  • non-intact skin exposure = lower than 0.09%
140
Q

in addition to HAART, the risk of seroconversion after exposure to HIV-contaminated blood is reduced by 75% via ___

A

prophylaxis with antiretrovirals

must take within 24 hours and for 4 weeks

141
Q
A

HSV-1

younger patient, so this is gingivostomatitis

142
Q
A

HSV-1

older patient, so this is pharyngotonsilitis

143
Q
A

acute herpetic gingivostomatitis

90% from HSV-1

144
Q
A

acute herpetic gingivostomatitis

90% from HSV-1

145
Q
A

acute herpetic gingivostomatitis

146
Q
A

pharyngotonstilitis

can be HSV-1 or 2

147
Q
A

recurrent herpes simplex

148
Q
A

recurrent intraoral herpes simplex

149
Q
A

recurrent intraoral herpes simplex

150
Q
A

recurrent intraoral herpes simplex

151
Q
A

HSV-1 - herpetic whitlow

152
Q
A

HSV-1 - herpes gladiatorum aka scrumpox

153
Q
A

HSV-1 - herpes barbae

154
Q
A

HSV-1 - eczema herpeticum aka kaposi’s varicelliform

155
Q
A

VZV - chicken pox

156
Q
A

VZV - chicken pox

157
Q
A

VZV - shingles

158
Q
A

ramsay hunt syndrome (VZV)

characterized by cutaneous lesions of the external auditory canal, involvement of ipsilateral face and auditory nerves, and facial paralysis, hearing deficits, and vertigo

159
Q
A

VZV herpes zoster oral lesions

160
Q
A

VZV herpes zoster oral lesions

161
Q
A

VZV - herpes zoster oral lesions

162
Q
A

infectious mononucleosis (EBV)

163
Q
A

cytomegalovirus

notice the “owl eyes” cells

164
Q
A

herpangina (coxsackie virus, enterovirus)

165
Q
A

hand foot and mouth disease

166
Q
A

Rubeola - characterized by koplik’s spots

167
Q
A

Rubeola

168
Q
A

rubella

169
Q
A

rubella - characterized by forchheimer’s sign

170
Q
A

mumps aka epidemic parotitis

171
Q

HIV+

A

HIV-associated candidiasis

172
Q

HIV+

A

HIV-associated oral hairy leukoplakia

173
Q

HIV+

A

HIV-associated kaposi’s sarcoma (HHV-8)

174
Q

HIV+

A

HIV-associated kaposi’s sarcoma (HHV-8)

175
Q

HIV+

A

HIV-associated kaposi’s sarcoma (HHV-8)

176
Q

HIV+

A

HIV-associated kaposi’s sarcoma (HHV-8)

177
Q

HIV+

A

HIV-associated kaposi’s sarcoma (HHV-8)

Oral and Maxillofacial Pathology (45 decks)

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