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Viral Diseases Affecting the Oral Cavity Flashcards

1
Q

Vaccine preventable diseases include:

A
  1. Diphtheria
  2. Haemophilus influenzae type b (Hib)
  3. Hepatitis A
  4. Hepatitis B
  5. Influenza
  6. Measles
  7. Meningococcal
  8. Mumps
  9. Pertussis (whooping cough)
  10. Pneucoccal disease
  11. Polio
  12. Rotavirus (severe diarrhea)
  13. Rubella (German measles)
  14. Tetanus (lockjaw)
  15. Varicella (chickenpox)

Note: MMRV = measles, mumps, rubella, varicella

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2
Q

Neurotropic (affects nervous system preferentially) herpes viruses

A
  • HSV-1
  • HSV-2
  • VZV
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3
Q

Lymphotropic herpes viruses

A
  • EBV
  • CMV
  • HHV-8
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4
Q

Causes primary infection that are asymptomatic or symptomatic

A

Herpes viruses

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5
Q

Remain latent in specific cell types for host’s life

A

Herpes viruses

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6
Q

Can undergo reactivation after latent period to cause recurrent infections that are asymptomatic or non-symptomatic.

A

Herpes viruses

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7
Q

How are herpes viruses spread?

A

Viruses shed in secretions –> spread to new hosts

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8
Q

Initial contact of HSV-1 in lower s-eco groups early in life results in…

A

primary herpetic gingivostomatitis

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9
Q

Initial contact of HSV-1 in wealthier individuals occur later. Disease that results is…

A

pharyngotonsillitis

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10
Q

Most primary HSV-1 infections in previously seronegative individuals are from contact with infected person…

A
  • Infected saliva

* Active lesions

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11
Q

Three possible consequences of initial HSV-1 contact with oral tissues of seronegative individuals…

A
  1. Minority of children develop primary herpetic gingivostomatitis
  2. A few young adults develop pharyngotonsillitis
    a. Repeated autoinoculation of eyes may –> blindness
  3. Most individuals: effects are subclinical
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12
Q

Where does HSV-1 migrate to remain latent or dormant?

A

Trigeminal nerve ganglion

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13
Q

Cause of viral reactivation (HSV-1)

A

May be due to reduced local or systemic host resistance:

• Results in 2nd disease, which usually subsides without treatment and is often recurrent.

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14
Q

Clinical features of primary herpetic gingivostomatitis

A

• Abrupt onset
• Malaise, fever, nausea
• Cervical lymphadenopathy
• Vesicles throughout mouth and vermilion; rupture rapidly
- Numerous pinhead vesicles –> ulcers (fibrin-covered)
• Lesions extend onto vermilion and perioral skin
• Severe edematous, enlarged, very erythematous painful gingivitis
- Punched out erosions along midfacial free gingival margins

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15
Q

How long does primary herpetic gingivostomatitis last?

A

lasts 5-14 days

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16
Q

How long is the incubation period of primary herpetic gingivostomatitis?

A

3 to 9 days

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17
Q

Demography of primary herpetic gingivostomatitis

A
  • Initial exposure in absence of antibodies (usually children)
  • Most cases 6 months to 5 years of age
  • Maternal antibodies before 6 months.
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18
Q

What is herpetic pharyngotonsillitis?

A
  • Primary infection in adults
  • Sore throat, fever, malaise, headache
  • Tonsils and posterior pharynx: vescles –> ulcers
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19
Q

Viral cytopathy of HHV-1, HSV-1, and herpes simplex vius…

A

• Ballooning degeneration
- enlarged, vacuolated nucleus and cytoplasm
• Acantholysis –> Tzanck cells
- free-floating epithelial cells in intraepithelial vesicle
• Cowdry inclusions – uniform glassy appearance
- Surrounded by nuclear clear zone (halo)
• Chromatin condensed around nuclear margin
• Epithelial cells fuse –> multinucleated

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20
Q

Distinct clinical presentation:
• Vesicles throughout mouth and vermilion; rupture rapidly
• Numerous pinhead vesicles –> ulcers (fibrin-covered)
• Lesions extend onto vermilion and perioral skin

A

primary herpetic gingivostomatitis

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21
Q

How is the gingiva affected in primary herpetic gingivostomatitis?

A
  • Severe edematous, erythematous gingivitis
  • Gingiva enlarged, painful, and very erythematous
  • Punched out erosion along midfacial free gingival margins
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22
Q

What happens in recurrent (reactivation) / secondary HSV-1 infection?

A
  • Latent virus in ganglia
  • Reactivation follows exposure to: sunlight, cold, trauma, stress, immunosuppression, UV light

** Note: only UV light definitely induces lesions

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23
Q

Where do symptomatic lesions in secondary (recurrent) HSV-1 infection occur?

A

Symptomatic lesions at site of primary inoculation or adjacent areas of epithelium supplied by involved ganglion

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24
Q

What percentage of the population has antibdies to HSV? What percentage may develop 2nd herpes?

A

• Up to 90% of population has antibodies to HSV

- Up to 40% of this group may develop 2nd herpes

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25
Q

Shedding occurs in what percentage of secondary (recurrent) HSV-1 infection?

A

Shedding in 2-10%

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26
Q

Describe how secondary (recurrent) HSV-1 infection can spread?

A
  • Virus may spread to other sensory ganglia

* Both asymptomatic shedding and symptomatic active lesions can spread to uninfected hosts

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27
Q

Locations involved in secondary (recurrent) HSV-1 infection

A
  • Herpes labialis: “cold sores”, “fever blisters”

* Intraoral: keratinized mucosa

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28
Q

Relation of erythema multiforme and secondary (recurrent) HSV-1 infection

A

> 15% of erythema multiforme cases proceeded by 2nd HSV

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29
Q

Most common site for recurrent HSV-1 infection…

A

Vermilion and adjacent skin of lips (herpes labialis)

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30
Q

Percent of US population affected by herpes labialis?

A

15-45% of US population

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31
Q

Clinical features of herpes labialis

A

• Prodrome 6-24 hours before lesions
- Burning, tingling, itching, erythema
• Multiple small red papules
• Clustered fluid-filled vesicles

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32
Q

What presents as clustered fluid filled vesicles, which rupture & crust in 2 days?

A

Herpes labialis

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33
Q

Resolution of herpes labialis

A
  • Clustered fluid-filled vesicles
  • Rupture & crust in 2 days
  • Healing 7 to 10 days
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34
Q

What is recurrent intraoral HSV infection?

A

Secondary HSV-1 infection within oral cavity; less common than herpes labialis

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35
Q

Location of recurrent intraoral HSV-1 infection

A

In otherwise healthy people, clustered vesicles on keratinized mucosa (mucoperiosteum)
• Hard palate and attached gingiva

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36
Q

What is herpetic whitlow (herpetic paronychia)?

A

• Primary or secondary HSV infection localized to hands or fingers

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37
Q

How is herpetic whitlow (herpetic paronychia) acquired?

A

Acquired by direct contact with active lesion:
• Dentists, etc.
• Self-inoculation in children with orofacial herpes

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38
Q

Clinical features of herpetic whitlow…

A
  • Seronegative: Infection –> vesiculoulcerative eruption with signs and symptoms of primary systemic disease
  • Pain (often throbbing) and redness
  • Vesicles or pustules break to form ulcers
  • High fever
  • Regional lymphadenopathy
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39
Q

Can people who are seropositive (HSV history) contract herpetic whitlow?

A

Seropositive (HSV history): whitlow less likely

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40
Q

Resolution of herpetic paronychia (whitlow)

A
  • Lasts 4-6 weeks

* May –> paresthesia and permanent scarring

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41
Q

Where can herpetic paronychia (whitlow) recur?

A

May recur on fingers

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42
Q

Clinical presentation of herpes simplex virus infection in IMMUNOCOMPROMISED hosts

A
  • Oral lesions at any site usually with herpes labialis

* Enlarging lesion has central necrosis with raised yellow border (zone of active viral destruction)

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43
Q

Diagnosis of oral herpes simplex virus infection

A
  • Often made clinically

* Lab tests

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44
Q

What lab tests are done to diagnose oral herpes simplex virus infection?

A
  • Cytologic smear or tissue biopsy of active lesion
  • Serology in primary HSV
  • Culture
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45
Q

Results of culture lab test in the diagnosis of oral herpes simplex virus infection

A
  • Requires intact vesicle, rare intraorally

* Up to 2 weeks for definitive result

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46
Q

Results of serology lab test in the diagnosis of oral simplex virus infection

A

Serology in primary HSV:

• Igs positive in 4-8 days

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47
Q

Results of cytologic smear in the diagnosis of oral simplex virus infection

A

Cytologic smear or tissue biopsy of active lesion:
• Viral cytopathy
• Fluorescent monoclonal antibody to rule out HZV

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48
Q

How do you rule out HZV in lab tests done to diagnose oral herpes simplex infection?

A

In cytologic smear or tissue biopsy of active lesion, do fluorescent monoclonal antibody to rule out HZV.

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49
Q

Treatment for healthy patients with oral herpes simplex virus infection

A

• Mild cases don’t require treatment
• Symptomatic treatment:
- NSAIDs
- Topical dyclonine hydrochloride spray
- SPF 15 sunscreen for herpes labialis
• Early antiviral agents

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50
Q

Treatment for immunocompromised patients with oral herpes simplex virus infection

A

Oral and IV antiviral agents

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51
Q

Primary ____ infection in children is varicella

A

HHV-3

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52
Q

HSV-1 causes…

A
  • Primary herpes gingivostomatitis

* Secondary herpes infections

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53
Q

HSV-2 causes…

A

Genital herpes

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54
Q

Varicella-zoster causes…

A
  • Varicella (chickenpox)

* Zoster (shingles_

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55
Q

Epstein-Barr causes…

A
  • Mononucleosis
  • Burkitt’s lymphoma
  • Nasopharngeal carcinoma
  • Hairy leukoplakia
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56
Q

Cytomegalovirus causes…

A

Salivary gland inclusion disease

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57
Q

HHV-6 causes…

A

Roseola infantum

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58
Q

HHV-8 causes…

A

Kaposi’s sarcoma

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59
Q

Papillomaviruses causes…

A
  • Oral papillomas/warts
  • Condyloma acuminatum
  • Focal epithelial hyperplasia
  • Some carcinomas
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60
Q

Coxsackieviruses causes…

A
  • Herpangina

* Hand-foot-mouth disease

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61
Q

Path of virus during varicella active disease…

A
  • The virus follows along sensory nerve to sensory ganglia

* Resides there in latent form

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62
Q

Recurrent HZV infection is called…

A

Zoster/Shingles

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63
Q

How is varicella spread?

A

Spread by air droplets or direct contact with active lesions

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64
Q

Demography of varicella

A

Most cases ages 5 to 9

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65
Q

Incubation period of varicella

A

Incubation 10-21 days

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66
Q

Clinical features of of varicella

A 
• Start: malaise, pharyngitis, rhinitis
• Then rash:
     - Intensely pruritic exanthem
     - Starts on face and trunk
     - Then extremities
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67
Q

Describe the rash in Varicella

A
  • Pruritic rash: red macules –> vesicles –> pustules –> crusting
  • Successive crops (so see all stages at any one time)
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68
Q

Duration of varicella

A
  • New lesions appear for 4-7 days
  • Lasts several weeks
  • Self-limiting
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69
Q

“Dewdrop on rose petal” is classic in this…

A

Varicella

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70
Q

Occurrence of oral lesions in varicella?

A
  • Oral and perioral lesions may precede skin
  • Vermilion, hard palate, etc.
  • Usually few oral lesions (2 or 3 ulcers) that heal in 3 days
  • Many lesions in severe cases
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71
Q

What do oral lesions in varicella resemble?

A

• Occasionally gingival lesions resemble primary HSV, but less pain

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72
Q

Diagnosis of varicella involves: history of exposure within past __ weeks

A

history of exposure within past 3 weeks

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73
Q

Viral cytopathy for varicella reveals…

A

Viral cytopathy in Tzanck cells (same as HSV)

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74
Q

Rapid diagnosis of varicella involves…

A

Rapid diagnosis by fluorescent-conjugated monoclonal antibodies on smear or biopsy (separates HZV from HSV)

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75
Q

Serum samples in acute stage of varicella shows….

A

Should show 4x increase in antibody titers to VZV

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76
Q

Tissue culture diagnosis of varicella…

A

Viral isolation in tissue culture

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77
Q

Management of varicella…

A

HZV vaccination (Varivax):
• Most children in USA are vaccinated
• But efficacy diminishes over time

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78
Q

Management of varicella in immunosuppressed children

A

• Peroral antiviral meds in immunosuppression
- Acyclovir, valacyclovir, famciclovir
- Reduce duration and severity
• Purified V-Z immune globulin

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79
Q

Varicella complications in childhood…

A
  • 2nd skin infections
  • Encephalitis
  • Reye’s syndrome
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80
Q

Varicella complications in adults…

A
  • Varicella pneumonitis
  • Encephalitis
  • Potentially fatal
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81
Q

Varicella complications in immune-compromised…

A
  • Extensive cutaneous involvement
  • High fever
  • Hepatitis
  • Pneumonitis
  • ~ 7% mortality before there was effective antiviral treatment
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82
Q

10-20% of pregnant women who get VZV get…

A

pneumonia

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83
Q

Women who get varicella in early pregnancy…

A
  • Small chance (0.4-2.0%) baby could be born with “congenital varicella syndrome”
  • Low birthweight, scarring of skin, and problems with arms, legs, brain, and eyes
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84
Q

Women with varicella rash from 5 days before to 2 days after delivery…

A
  • Babies at risk for chickenpox shortly after birth

* Chance of death <30%

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85
Q

Herpes zoster is…

A

reactivated HHV-3

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86
Q

How many episodes occur in herpes zoster (reactivated HHV-3)?

A

• Recurrent HZV but usually only ONE episode

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87
Q

In what percentage of people does reactivated HHV-3 occur?

A

10-20% of people

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88
Q

Predisposing factors for herpes zoster (reactivated HHV-3)

A
  • Immunosuppression
  • Maliganancies
  • Dental treatment
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89
Q

Herpes zoster goes through stages. What is it called, and what are the stages?

A

“Immunosenescence”
• Prodrome
• Acute phase
• Chronic phase

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90
Q

What is zoster sine herpete?

A

Zoster without rash

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91
Q

What happens in the prodrome phase of herpes zoster?

A
  • Initial viral replication in sensory trigeminal ganglion

* Ganglionitis –> neuronal necrosis & severe neuralgia

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92
Q

Path of pain in herpes zoster (prodrome phase)?

A

Pain in area of epithelium innervated by the affected sensory nerve

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93
Q

Timing of onset of pain in herpes zoster (prodrome)…

A

Pain 1-4 days before mucosal or skin lesions

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94
Q

Clinical symptoms of herpes zoster in prodrome phase

A
  • Sensitive teeth, etc.

* Fever, malaise, headache

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95
Q

UNILATERAL lesions in epithelium innervated by affected sensory nerve occurs in…

A

Herpes zoster - acute phase

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96
Q

Occurrence of rash in herpes zoster acute phase…

A
  • Erythematous macular-papular rash –> clusters of vesicles
  • Vesicles –> pustular and ulcerate in 3-4 days –> crusting in 7-10 days
  • On keratinized or non-keratinized mucosa or skin
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97
Q

Oral lesions occur in herpes zoster acute phase with…

A

Oral lesions occur with trigeminal nerve involvement

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98
Q

Ocular (V1) involvement in herpes zoster acute phase results in….

A

blindness

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99
Q

Describe osteonecrosis in the acute phase of herpes zoster

A

Osteonecrosis with loss of devitalized teeth:
• Inflammation in nerves extends to adjacent vessels that supply alveolar ridges and teeth
• Vessel damage –> necrosis

100
Q

Describe the chronic phase of herpes zoster

A
  • Postherpetic neuralgia: pain+++ for one to mainy months after rash
  • Burning sensation with episodic “stabbing” pain
  • “Tactile allodynia”: even light touch causes pain
  • Due to chronic VZV ganglionitis
101
Q

Management of herpes zoster

A
  • Live attenuated HZV vaccine for all people over 60 years olf
  • Early use of antiviral meds
  • PHN
102
Q

Discuss the vaccine for herpes zoster..

A
  • Live attenuated HZV vaccine for all > 60 years

* 14x more powerful than childhood vaccine

103
Q

Discuss the early use of antiviral meds for the management of herpes zoster.

A
  • Accelerate healing of skin lesions

* Acyclovir, valacyclovir, famciclovir

104
Q

Discuss PHN in the management of herpes zoster

A

• Many methods (topical and systemic)
• Topical capsaicin (red pepper origin)
- takes 2 weeks
- too irritating for oral mucosa or open lesions

105
Q

What is Ramsay Hunt Syndrome?

A

HZV cutaneous lesions of external auditory canal or face

106
Q

What nerves are involved in Ramsay Hunt Syndrome?

A

Involvement of ipsilateral VII and VIII nerves, as well as V

107
Q

Ramsay Hunt Syndrome causes…

A
  • Facial paralysis
  • Hearing deficits
  • Vertigo
108
Q

Research has not yet produced a vaccine for….

A

EBV (HHV-4)

109
Q

What does EBV bind to and infect?

A

EBV binds to and infects nasopharyngeal epithelial cells –> B cells

110
Q

EBV is “linked” to:

A
  • Infectious mononucleosis
  • Oral hair leukoplakia
  • Nasopharyngeal carcinoma
  • Burkitt’s lymphoma
  • Hodgkin disease
111
Q

Herpes virus (HHV-4/EBV) is tropic for …

A

Herpes virus is tropic for human B lymphocytes

• Target cell receptors on their surface

112
Q

What percent of the population harbors EBV?

A

~ 90% of the population

113
Q

How is EBV transmitted?

A
  • EBV shed from epithelial cells and transmitted via saliva

* Because it is shed into saliva, contacts are frequent

114
Q

Describe infection of EBV in childhood…

A

Initial infection in childhood is mild, often subclinical

115
Q

Describe the infection of EBV in adults…

A

Adults have higher risk for disease (infectious mononucleosis) than children

116
Q

Infectious mononucleosis is synonymous with…

A

“Kissing Disease”

117
Q

EBV infection in young adults results in…

A

EBV –> infectious mononucleosis if initial infection occurs in young adults

118
Q

Percentage of people entering college that are EBV negative…

A
  • In US, 50% entering college are EBV negative

* 10-15%/year then become positive

119
Q

In adults afflicted with infectious mononucleosis prodrome occurs…

A

Prodrome up to 2 weeks before fever:

• fatigue, malaise

120
Q

Clinical feature pf infectious mononucleosis (in adults)

A 
• Fever  90% of cases
• Tonsils enlarged in > 80% of cases
     - Exudate +/- abscess
     - Enlarged lingual tonsils
• Pharyngitis, tonsillitis
     - Rare respiratory obstruction
121
Q

Symptoms less common in infectious mononucleosis includes….

A
  • Hepatosplenomegaly
  • Rash
  • Thrombocytopenia
  • Palatal petechiae for 2 days
  • NUG
122
Q

Diagnosis of infectious mononucleosis

A
  • Rising titer of antibodies specific for EBV antigens
  • Positive heterophil reaction (Monospot test)
  • Lymphocytosis with mononucleosis cells (atypical lymphocytes) in peripheral blood
123
Q

What does a positive heterophile reaction entail (infectious mononucleosis)?

A

Positive heterophile reaction (Monospot test):
• Heterophile antibody is a byproduct of rapid increase in B lymphocytes
• IgM binds to and agglutinates Paul-Bunnell antigen of sheep and bovine red blood cells

124
Q

Prognosis for infectious mononucleosis

A

• Most resolve in 4-6 weeks

- but some symptoms for 6 months

125
Q

Complications of infectious mononucleosis includes…

A
  • Splenic rupture
  • Chronic fatigue syndrome
  • Bell’s palsy
126
Q

Complications of infectious mononucleosis in immunocompromised…

A

Potentially fatal polyclonal B-lymphocyte proliferation

127
Q

Cytomegalovirus is also…

128
Q

What percent of the US population has been exposed to cytomegalovirus?

A

At least 60% of U.S. population has been exposed to CMV

129
Q

How is CMV spread?

A
  • Person to person contact in saliva, urine, etc
  • Sexual transmission
  • Transplacenal and perinatal transmission
130
Q

What percentage of CMV infections are asymptomatic?

A
  • ~90% CMV infections are asymptomatic

* Infection is nearly always asymptomatic in healthy people

131
Q

Cytomegalovirus inclusion disease from primary CMV infection _____ occurs.

A 
CID from primary infection rarely occurs.  CID includes:
• Congenital & perinatal CMV infection
• CMV mononucleosis
• CMV in Immunosuppressed individuals:
     - Transplants
     - HIV infection
132
Q

Latency and CMV

A

Infection followed by latency:

• In glands, endothelium, macrophages, lymphocytes

133
Q

Reactivation of CMV linked to…

A

Reactivation linked to reduced host resistance:

• Immunosuppression including AIDS

134
Q

Histologic appearance of CMV

A

• Very large cells
- Epithelium of glands
- Neurons
- Alveolar macrophages, epithelium and endothelium
- Kidney tubular epithelium and glomerular endothelium
• Single dark basophilic nuclear inclusion with peripheral halo
• Multiple indistinct cytoplasmic basophilic inclusions

135
Q

What is CMV (heterophil-negative) mononucleosis?

A
  • Mononucleosis-like infection in healthy individuals

* Clinically like infectious mononucleosis but heterophil antibody negative

136
Q

Symptoms of CMV mononucleosis

A
  • Fever
  • Lymphadenopathy
  • Atypical lymphocytosis
  • Hepatomegaly
  • Rarely acute salivary sialadenitis w/ xerostomia
137
Q

Prognosis of CMV mononucleosis

A

Most recover without sequelae, but excretion of virus via body fluids may occur for months or years

138
Q

Congenital CMV infection?

A
  • 95% in utero CMV infections asymptomatic
  • CID when mother has primary infection
  • Some surviving infants: permanent mental retardation, hearing loss, etc.
  • Most with mild CID recover but may have later delayed-onset mental retardation with hearing deficits
139
Q

Consequences of congenital CMV infection when mother has primary infection…

A
  • Intrauterine growth retardation
  • Profound illness
  • Jaundice
  • Hepatosplenomegaly, anemia, thrombocytopenia –> bleeding
  • Encephalitis
  • Enamel hypoplasia
140
Q

CMV in AIDS occurs as a result of…

A
  • Reactivation of latent infection

* Also infection by sex partners

141
Q

Most common opportunistic viral pathogen in AIDS

142
Q

Oral manifestation of CMV in AIDS

A

Oral: chronic ulcers

143
Q

CMV in AIDS causes serious life-threatening disseminated infections including…

A
  • Pneumonitis can –> ARDS
  • Colitis: debilitating diarrhea due to intestine necrosis and ulceration
  • Retinitis: most common form of opportunistic CMV disease. May –> blindness
144
Q

Most common form of opportunistic CMV disease…

A

Retinitis (may cause blindness)

145
Q

Diagnosis of CMV infections involves…

A 
• Biopsy: morphology of viral cytopathy
     - Electronmicroscopy
• Viral culture
• Rising Ig titer
     - ELISA (serology)
146
Q

How are CMV antigens detected?

A
  • IHC
  • In situ hybridization
  • PCR
147
Q

Treatment for CMV infections, particularly infectious mononucleosis-like cases

A

Most infectious mononucleosis-like cases resolve spontaneously

148
Q

Treatment for CMV infections in immunocompetent

A

Immunocompetency:
• NSAIDS
• Corticosteroids
• IV gammaglobulins

149
Q

Treatment for CMV infections in immunosuppressed

A

Immunosuppression:
• Antivirals
• Improve immune status

150
Q

Demographic of coxsackievirus infections

A

Infections occur mostly in infants or young children

151
Q

Coxsackie viruses have 3 clinical patterns closely related and not separate infections…

A
  • Herpangina
  • HFM
  • Acute lymphonodular pharyngitis
152
Q

Coxsackie viruses involved in herpangina…

A

A1 to A6, A8, A10, A22 and others

153
Q

Coxsackie viruses involved in HFM

A

A16 and others

154
Q

Coxsackie viruses involved in acute lymphonodular pharyngitis

A

A10 in some cases

155
Q

Incubation period for Coxsackie viruses

A

4 to 7 days

156
Q

Most coxsackievirus infections occur during this time…

A

Most in summer or early fall

157
Q

How does coxsackievirus infections spread?

A
  • Crowding and poor hygiene aid spread

* Fecal-oral route or saliva or respiratory droplets

158
Q

Describe the severity in the 3 patterns of coxsackievirus infections…

A

In all 3 patterns, severity varies:
• Most strains cause self-limiting disease
• Occasional epidemics, even mortalities

159
Q

Diagnosis of coxsackievirus infections involves…

A
  • Usually by clinical criteria
  • Culture or PCR
  • Serology: rising antibody titers
160
Q

What is herpangina?

A

Coxsackie childhood infection. Usually subclinical or mild.

161
Q

Clinical presentation of herpangina…

A

• Lesions occur on soft palate and oropharynx
• Red macules –> fragile vesicles –> soon ulcerate
- 2 to 6 vesiculo-ulcers
• Acute flulike onset: sore throat, dysphagia, fever

162
Q

Prognosis of herpangina

A
  • Self-limited

* Heal 7-10 days

163
Q

Acute flulike onset, such as sore throat, dysphagia, and fever, are associated with this…

A

Herpangina

164
Q

This disease presents with oral lesions like herpangina…

A

Hand, foot, & mouth disease

165
Q

Oral lesions in hand, foot, and mouth disease…

A
  • Precede skin lesions

* More extensive than herpangina

166
Q

Appearance of oral lesions in HFM disease

A
  • Vesicles –> ulcers
  • Most ulcers small, but may > 1 cm
  • Resolve in one week
167
Q

Skin rash associated with flulike symptoms are associated with this disease…

A

Hand, Foot, and Mouth disease

168
Q

Skin rash associated with flulike symptoms in HFM disease occurs on…

A

Palms, soles, fingers and toes, etc…

169
Q

Appearance and quantity of skin rashes in HFM disease…

A
  • Few to dozens of lesions

* Red macules –> vesicles –> ulcers

170
Q

Histology of HFM disease and herpangina…

A

• Epithelium
- Intracellular and intercellular edema
- Spongiosis
- Intraepithelial vesicle
- Vesicles enlarges & ruptures through basal layer
• So subepithelial vesicle is formed
• Epithelial necrosis –> ulceration

171
Q

Hyperplastic lymphoid aggregates occurs in…

A

Acute lymphonodular pharyngitis

172
Q

Clinical features of acute lymphonodular pharyngitis

A
  • Sore throat, fever, headache lasts 4-14 days
  • 1-5 yellow to pink nodules on soft palate or tonsils
  • No clinical vesicles or ulcers
  • Hyperplastic lymphoid aggregates
173
Q

Resolution of acute lymphonodular pharyngitis…

A

Resolves in 10 days

174
Q

Rubeola is synonymous with…

A
  • Measles

* “Nine day measles”

175
Q

Worldwide statistics for Rubeola (Measles)

A

Worldwide: ~20 million cases and 164 thousand deaths each year
• Encephalitis in 1 in 1,000
• Subacute sclerosing panencephalitis in 1 in 100,000 as late as 11 years later

176
Q

Severe disease in immunosuppression (e.g. HIV)

A

Rubeola (measles)

177
Q

Vaccine for this disease was introduced in the US in 1963

A

Rubeola (measles):

• Vaccine led to dramatic decreased incidence

178
Q

Rubeola (measles) is in this family and genus of viruses…

A
  • Family: paramyxovirus

* Genus: Morbillivirus

179
Q

Rubeola is transmitted via…

A
  • Highly contagious

* Virus spreads via respiratory droplets

180
Q

Incubation period of rubeola

A

7 to 12 days

181
Q

How rubeola spreads…

A
  • First multiples within upper respiratory tract epithelial cells
  • Spreads to lymphoid tissues (where it replicates in mononuclear cells)
  • Then spreads via blood throughout body
182
Q

Oral manifestations of Rubeola include..

A
  • Koplik’s spots
  • Candidiasis
  • NUG
  • Can affect odontogenesis – enamel hypoplasia in primary teeth
183
Q

Describe the first stage of rubeola

A
  • 3 Cs: coryza (runny nose), cough, conjunctivitis
  • Fever
  • Koplik’s spots on oral mucosa
  • Lymphoid organ hyperplasia
184
Q

What are the 3 Cs observed in the first stage of rubeola?

A
  • Coryza (runny nose)
  • Cough
  • Conjunctivitis
185
Q

Describe the second stage of rubeola

A
  • Rash: vasculitis of small vessels in skin
  • T lymphocytes act on virally infected vascular endothelium
  • Erythematous macular-papular rash spreads from face to runk and extremities
186
Q

Describe the third stage of rubeola

A

Rash fades with desquamation

187
Q

When are Koplik’s spots observed?

A

First stage of Rubeola

188
Q

What are Koplik’s spots?

A
  • Areas of erythema on buccal and labial mucosa, etc.
  • Small blue-white macules within these areas
  • Due to foci of epithelial necrosis
  • As spot ages, neutrophil exocytosis into epithelium leads to microabscess formation, necrosis, ulceration
189
Q

Effect of rubeola/measles on lymphoid organs

A
  • Marked follicular hyperplasia with large germinal centers
  • Virus –> fusion of infected lymphocytes
  • Warthin-Finkeldey cells (multinucleated lymphocytes)
190
Q

What are Warthin-Finkeldey cells (multinucleated lymphocytes)…

A

Multinucleated lymphocytes observed in measles/rubeola:
• Up to 100 nuclei
• Intranuclear & intracytoplasmic eosinophilic inclusions

191
Q

Rubella is also known as…

A
  • German measles

* “Three day measles”

192
Q

Virus responsible for rubella…

A
  • Togavirus

* Genus: Rubivirus

193
Q

Prognosis of rubella…

A

Mild disease, but can cause congenital rubella syndrome

• If primary infection in early pregnancy

194
Q

Vaccination for rubella…

A

Vaccine (MMRV) needs boosters:
• Rubella - 2 dose vaccine
• 2004: no longer endemic in U.S.

195
Q

Clinical presentation of rubella…

A

Symptoms often mild (< 50% infections subclinical):
• Rash: discrete pink macules –> papules –> fade
• Lymphadenopathy
• low-grade fever
• Malaise

196
Q

Oral manifestations of rubella include…

A
  • Forchheimer’s sign in 20% of cases

* Confused with palatal petechiae

197
Q

Infected (rubella) adults often have…

A

Transient arthralgia or arthritis

198
Q

What is Forchheimer’s sign?

A
  • Small discrete dark red papules on soft palate and may extend to hard palate.
  • Arises simultaneous with rash and lasts only 14 hours

Note: observed in rubella

199
Q

How is HIV transmitted?

A

• HIV in most bodily fluids
- but transmission by oral fluids is rare
• Sexual contact/venereal
- male to male
- heterosexual contact with high risk group
• Parenteral exposure to contaminated blood
- Tranfusion
- IV drug use
• Organ transplant
• Mother-to-fetus
• Breast-feeding

200
Q

Rubella infection in pregnant women, especially during the first trimester can result in…

A
  • Miscarriages

* Stillbirths

201
Q

Congenital Rubella Syndrome birth defects often includes:

A
  • Cataracts
  • Hearing loss
  • Mental retardation
  • Congenital heart defects
202
Q

Discuss viral integration of HIV

A

• Virus enters host cell
• Viral RNA uses reverse transcriptase to synthesize proviral DNA using viral RNA as template
- Viral RNA reversed to proviral DNA
• Proviral DNA splices into host genome using viral enzyme, integrase
• Integrated proviral DNA transcribes to RNA which directs host cell to synthesize more HIV virions

203
Q

How does HIV enter the body…

A

HIV enters body through mucosa –> blood

204
Q

___ molecule is a high-affinity receptor for HIV

A

CD4 molecule

205
Q

What cells does HIV first infect?

A

HIV first infects cells with CD4 receptor:
• CD4+ helpter T lymphocyte
• Monocytes/macrophages
• Dendritic cells

206
Q

Where does HIV infection establish itself?

A
  • Infection establishes in lymphoid tissues

* Virus may be latent for long periods

207
Q

How are T-cells depleted in HIV?

A

• Major mechanism of loss of CD4+ T cells is lytic HIV infection of the cell, and cell death during viral replication and production of virions
• Other mechanisms include:
- apoptosis of uninfected cells
- killing of infected cells by cytotoxic T lymphocytes

208
Q

Ratio of CD4+/CD8+ in peripheral blood

A
  • Normal ratio is ~ 2 to 1

* Ratio gradually falls to 0.5 as CD4+ T cells are destroyed

209
Q

CD4+ T cell count

A

• Normal is 500-1000/milli-micro-liter but falls below 200 in AIDS

210
Q

HIV stages

A

• Acute: acute viral syndrome
• Chronic
- Clinically asymptomatic (latent): 8 to 10 years
- Persistent generalized lymphadenopathy
- Minor opportunistic infections
• CRISIS (progression to AIDS)

211
Q

In the acute stage of HIV, HIV infection may be _________ initially

A

Asymptomatic

212
Q

In the acute stage of HIV, ____-_______ illness develops in 50-70% of affected persons _ to _ weeks after infection

A
  • Self-limited

* 3 to 6 weeks

213
Q

Non-specific symptoms or symptoms resembling severe influenza in the acute phase of HIV include…

A
  • Generalized lymphadenopathy
  • Sore throat
  • Myalgia
  • Fever
  • Rash
  • Fatigue
  • Diarrhea
  • Photophobia
  • Peripheral neuropathy
  • Weight loss
  • (sometimes) aseptic meningitis
214
Q

Resolution of acute viral syndrome (acute phase of HIV)

A

Acute viral syndrome clears spontaneously in a few weeks

215
Q

Oral manifestations in acute phase of HIV

A

Oral mucosa erythema and focal ulcers

216
Q

Virus production in the acute phase of HIV …

A
  • Seroconversion 3 to 17 weeks after exposure with development of virus specific CD8+ CTLs (cytotoxic lymphocytes)
  • High level of virus production, viremia, and widespread seeding of lymphoid tissues with modest reduction in CD4+ T cells
217
Q

Chronic phase of HIV entails…

A

• Most newly infected individuals enter latent period with slow immune system decline
• Average of ~10 years before serious immune compromise develop
- Viral replication continues but is restrained by immune reaction
• Viral replication almost always begins to increase with decrease in CD4+ T cells
- Minor opportunistic infections
- Thrombocytopenia (in some cases)
- Persistent generalized lymphadenopathy
• Concurrent fever, rash, and fatigue
• Signals immune breakdown and abrupt increased viral replication

218
Q

What does the Crisis phase of HIV entail?

A 
• Progression to AIDS
• Increasing viremia
• Breakdown of host defenses
• Clinical disease
     - Long-lasting fever, fatigue, weight loss, diarrhea
219
Q

AIDS indicator diseases include

A 
• Opportunistic infections
    - ~ 80% of deaths
• Opportunistic neoplasms
     - Kaposi sarcoma
     - Non Hodgkin lymphoma
     - Neurologic dysfunction
220
Q

HIV testing can be done using…

A
  • Antibody tests
  • Antigen tests
  • PCR test
  • Viral load test
  • CD4 cell count
  • Home testing kits
  • HIV-1/2 Ag/Ab Combo test
221
Q

Antibody tests are the most common HIV tests to look for HIV antibodies, and they include…

A
  • ELISA or EIA (enzyme-linked immunosorbent assay or enzyme immunoassay) tests detect HIV antibodies in blood, oral fluid, or urine as early as 3 weeks after exposure. Results for these tests can take up to two weeks.
  • Rapid HIV antibody tests also use blood, oral fluid, or urine to detect HIV antibodies. Results for these test can take 10-20 minutes.
  • A positive result from either of these tests requires a Western blood to confirm that result. It can take up to two weeks to confirm a positive result.
222
Q

Antigen tests in HIV testing are…

A
  • Not as common as antibody tests, but they can be used to diagnose HIV infection earlier (from 103 weeks after intial infection with HIV).
  • Antigen tests require a blood sample.
223
Q

In HIV testing, PCR (polymerase chain reaction test) detects…

A
  • Detects the genetic material of HIV itself

* Can identify HIV in the blood within 2-3 weeks of infection

224
Q

Viral load test for HIV testing determines….

A

The amount of HIV-1 in blood plays a role in determining when to start anti-HIV treatment or to change treatment.

225
Q

In HIV testing CD4 cell count is a useful indicator…

A
  • It is a useful indicator for when to start antiretroviral treatment.
  • It can also help predict the risk of complications such as infections.
226
Q

In HIV testing, home testing kits entails…

A
  • HIV antibody tests is not a true HIV testing kit, but a sample-collection kit.
  • A blood sample obtained by sticking a finger with a sterile lancet is put the blood on a special collection card in the kit, and send it back to laboratory for testing.
227
Q

In HIV testing, HIV-1/1 Ag/Ab Combo tests involves…

A
  • Recently approved
  • Detects HIV-1 p24 antigen that can appear just 12-26 days after infection and HIV-1/2 antibodies 20-45 days after infection
  • Results are generated in 20 minutes
  • The antigen test is not definitive
228
Q

What is Truvada?

A

a multidrug antiretroviral medication used in the treatment of HIV

229
Q

Different classes of drugs target distinct steps in the HIV lifecycle, so they are prescribed to be taken in combination…

A
  • Protease inhibitors
  • Entry inhibitors
  • Nucleoside/nucleotide reverse transcriptase inhibitors
  • Non-nucleoside reverse transcriptase inhibitors
230
Q

Effects of treatment in HIV

A 
• Therapies reduce symptoms
• CD4+ count increases
• Reduced viral load
• Reduced oral lesions
• But lymphomas not reduced
• Some reports increased:
     - HPV lesions
     - HIV related salivary gland disease
231
Q

What are the different types of Kaposi Sarcoma?

A
  • Classic
  • Endemic (African)
  • Iatrogenic immunosuppression-associated
  • AIDS-related
232
Q

Etiology of Kaposi Sarcoma

A
  • All caused by HHV8 (KS-associated herpes virus)

* Endothelium is cell of origin

233
Q

Clinical features of Kaposi Sarcoma

A
  • Most common tumor in HIV infection
  • Highest frequency in men who have sex with men (in U.S.)
  • Often appear first in mouth
  • Usually multiple lesions
  • Palate and gingivae are most common sites
234
Q

Stages of Kaposi Sarcoma

A
  • Patch (macular). Early stages flat & slightly discolored
  • Plaque
  • Papules and nodules
  • Enlarge, darken, hemorrhagic, and painful
235
Q

Histology of the patch stage of Kaposi Sarcoma…

A
  • Resembles granulation tissue or capillary hemangioma

* Bizarre-shaped vessels

236
Q

Histology of plaque stage of Kaposi Sarcoma…

A
  • Proliferation of vessels
  • Spindle cell component
  • Bland cytology
237
Q

Histology of nodular stage of Kaposi Sarcoma…

A
  • Fascicles of malignant spindle cells compress extravasated erythrocytes with release of hemosiderin
  • Positive for CD34 antigen immunoreactivity
238
Q

Management of Kaposi Sarcoma includes…

A 
• HIV therapy
• Chemotherapy
     - Deoxyrubicin
     - Paclitaxel
• Surgery
• Cryotherapy
• Intralesional
     - Chemotherapy
     - Sclerosing agent
239
Q

Oral hair leukoplakia occurs in vast majority in immunosuppression including…

A
  • HIV infection
  • Transplant patients
  • Rarely in immunocompetent people
240
Q

Characteristics of oral hairy leukoplakia…

A
  • White adherent lesions
  • Most on lateral borders of tongue (often bilateral)
  • Occasionally other sites
  • Surface typically corrugated
241
Q

Definitive diagnosis of oral hairy leukoplakia must…

A

Definitive diagnosis must show EBV within lesion by in situ hybridization, PCR, or EM

242
Q

Histology of oral hairy leukoplakia…

A
  • Thickened parakeratin surface projections
  • Epithelium is acanthotic with bandlike zone of lightly stained cells with abundant cytoplasm (“balloon cells”) in upper spinous layer
  • Nuclear beading
  • No dysplasia
  • Heavy candida without normal inflammatory reaction
243
Q

What is nuclear beading, and when is it examined?

A
  • Nuclear beading: scattered cells with nuclear clearing and peripheral margination of chromatin
  • Oral hairy leukoplakia
244
Q

Management of oral hairy leukoplakia…

A
  • Treatment is not needed (unless there is discomfort or esthetic problem)
  • Systemic antiherpesviral drugs produce rapid resolution but recurs when treatment stops
  • Surgery
  • Cryotherapy
  • HAART reduces OHL
245
Q

What is hyperpigmentation in HIV?

A

Macules in skin and mucosa

246
Q

Why does hyperpigmentation in HIV occur?

A

Due to:
• AIDS meds
• Infectious destruction of adrenal cortex
• Idiopathic

247
Q

Histology of hyperpigmentation in HIV…

A
  • Histology: focal melanosis

* Increased melanin in basal cell layer

Oral Pathology (9 decks)

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