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OPath Block 2 > 6. Viral Infection II > Flashcards

6. Viral Infection II Flashcards

1
Q

What is the most common clinical presentation for patients that develop symptoms from primary herpes?

A

Primary herpetic gingivostomatitis

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2
Q

What population does primary herpetic gingivostomatitis tend to affect?

A

Children

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3
Q

What are the clinical presentations of gingivostomatitis?

A

Vesiculo-ulcerative eruptions (not limited to bone-bound mucosa)

numerous pin head vesicles which quickly ulcerate and merge

gingiva is always involved, extremely erythematous

May involve vermillion and perioral tissue

Older pts develop vesicles in pharynx and mimics pharyngostonsillitis

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4
Q

What are the systemic symptoms of primary herpetic gingivostomatitis?

A

fever

malaise

headache

cervical lymphadenopathy

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5
Q

How does primary herpetic gingivostomatitis resolve?

A

Heals in a week as virus migrates to trigeminal ganglion (latnecy)

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6
Q

What allows a secondary/recurrent HSV to occur?

A

A breakdown in local immunosurveillance allows the virus to reactivate

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7
Q

What kind of symptoms occur at the site where secondary HSV lesions will appear?

A

Prodromal symptoms (pain or tingling)

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8
Q

S/S of 2nd HSV infection

A

Vesiculo-ulcerative process

clusters of pin head vesicles that rupture quickly

In oral cavity, limited to mucosa that is bound to bone (hard palate and gingiva)

Vermillion and surrounding skin can have lesions (esp commissure area): herpes labialis

No systemic symptoms

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9
Q

How does secondary HSV infection resolve?

A

Selt-limited

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10
Q

How does secondary HSV infection affect immunodeficient pts?

A

Atypical presentation

lesions not limited to bound muscoa (will see on tongue)

vesicles are bigger, chronic and destructive

Presdisposes pt to bacteria infection andusually con-infected with CMV

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11
Q

What is herpetic whitlow?

A

infection of the finger by the HSV

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12
Q

S/S of herpetic whitlow

A

Vesiculo-ulcerative eruptions

very painful and lasts for 4-6 weeks

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13
Q

Do herpetic whitlow lesions occur in primary or secondary infection?

A

both

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14
Q

What population was once often affected by herpetic whitlow?

A

dentists before use of gloves

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15
Q

What are other conditoins that must be listed as a DDH when thinking about primary oral HSV infection? What differentiates each condition from primary HSV?

A

Erythema multiforme

  • spares gingiva whereas gingivostomatitis always involves gingiva

Acute necrotizing ulcerative gingivitis

  • no vesicles whereas gingivostomatitis has vesicles
  • do not involve other mucosa whereas gingivostomatitis can involve palate, tongue, etc
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16
Q

What are other conditions that must be considered for an secondary oral HSV infection? How do they differ from secondary oral HSV?

A

Apthous ulcers

  • movable ulcers
  • non-keratinized mucosa
  • no vesicles

Traumatic ulcers

  • one single large lesion whereas HSV tends to be multiple small vesicles
  • no vesicles
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17
Q

Dx for oral HSV infection

A

Clinical symptoms unless for atypical or immunocompromised pts

Culture is difficult for herpes

Serology only works for primary HSV infection

Cytology smear or biopsy:

  • Ballooning degeneration
    • acantholysis
    • Tzanck cells
    • intraepithelial vesicles
  • Cytopathologic effects on virus infection
    • herpes infection causes keratinocytes to fuse resulting in below features
    • multinucleation
    • margination of chromatin
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18
Q

Tx for oral HSV infection

A

Ideal treat within 48 hours fro monset of symptoms

Normal pts don;t need any antiviral drugs. Just supportive treatment

Immunodeficient pts always need antiviral treatment

Primary

  • supportive therapy w/o antiviral agents

Secondary

  • Normal pts usually dont need tx
  • prophylactic Tx is reserved for problematic cases
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19
Q

What are the general clinical features of varicella-zoster virus?

A

Vesiculoulcerative eruption on skin and mucosa

Self-limiting in immunocompetent patients

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20
Q

What are the two classifications of varical-zoster virus infections?

A

Primary infection = Varicella (chickenpox)

Secondary/recurrent infection = Herpes zoster (shingles)

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21
Q

How does chickenpox differ in adults vs children?

A

adults usually suffer from severe symptom and may develop complications

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22
Q

how is chickenpox transmitted?

A

Inhalation of contaminated droplets, readily spread from child to child

Pts are very contagious, readily spread from child to child

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23
Q

Clinical features of varicella?

A

Rash + systemic symptoms (fever + malaise)

Generalized eruption of vesicles

Start as skin rash, progress to vesicles and pustules that rupture and ulcer

For about a week, a mixture of lesions at various stages of development and resolution is present

Oral invovlement is common but minor

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24
Q

Varicella Dx

A

Based on clinical presentation

25
Q

Varicella complications

A

Secondary skin infections, encephalitis, pneumonia

infection during pregnancy may result in spontaneous abortion or congenital defects

Most common in adults

Prevention is the best Tx, get vaccinated

26
Q

What populatin does herpes zoster (shingles) affect?

A

elderly and immunocompromised

27
Q

S/S of shingles

A

Prodromal: pain or paresthesia in the affected dermatome

Develop unilateral rash along the nerve distribution and terminate at the midline (coalescence of the vesicles followed by crusting)

Vesicles develop in one dermatome - waistline = common location

Postherpetic neuralgia (15%) - resolves in a year and uncomon in young pts

Trigeminal ganglia presence:

  • Oral lesions
    • both movable and bound mucosa, terminate at the midline
    • skin overlying the affected quadrant is affected
  • Ocular involvement may result in blindness
28
Q

Herpes Sozter Dx

A

Clinical presentation

Unilateral lesions along dermatome of the peripheral nerves

Lab tests are req’d for atypical presentation:

  • Immunocompromised pts wide spread and chornic lesions that cross the midline with severe complications
  • histopathology is the same as HSV
29
Q

Tx for Zoster

A

normal patients only need symptomatic and supportive treatment

immunocompromised pts need antivirals (acyclovir and analogs)

Vaccine for shingles is available and recommended for elderly but not 100% effective

30
Q

What diseases are caused by EBV?

A

Infectious mononucleosis

Oral hairy leukoplakia

Lymphoproliferative disorders (NHL, African Burkitt lymphoma)

Nasopharyngeal carcinoma

Chronic fatigue syndrome

31
Q

How is CMV transmitted?

A

Exchange of body fluid

organ transplant

32
Q

S/S of CMV infection in normal pts

A

almost everyone is infected by CMV

asymptomative in healthy individuals

33
Q

S/S of CMV in immunocompromised pts

A

Affects many organs

Oral manifestations:

  • chronic oral ulcer: often co-infect with HSV
  • CMV sialadenitis (salivary gland enlargement)
34
Q

CMV Dx

A

Clinical + lab test

Histopathology:

  • CMV infected cells are HUGE
  • Cells have owl eye presentation
  • Cells contain intranuclear and cytoplasmic inclusions
35
Q

Tx for CMV

A

Only necessary for immunocompromised pts

36
Q

Which enterovirus causes head and neck conditions?

A

Coxsackie virus

37
Q

How is coxsackie virus transmitted?

A

Inhalation of resp droplets

Fecal-oral route

38
Q

Population most affected by coxsackie?

A

Children

39
Q

3 diseases caused by coxsackie

A

Herpangina

Hand,foot, mouth dz

Acute lymphonodular pharyngitis

40
Q

Dx for coxsackie infection?

A

Clinically

Specific lab tests are available

41
Q

S/S of herpangina

A

sore throat

dysphagia

mild flu-like symptom

small number of vesicles develop in oropharynx area

vesicles ulcerate very quickly

self-limiting process with recovery in 1 week

42
Q

S/S of hand-foot-mouth disease

A

skin rash (eruption of small vesicles on the hands and the feet, including fingers and toes)

oral lesions (oral vesicles and uclers on any mucosa)

flu-like smyptom

43
Q

S/S of acute lymphnodular pharyngitis

A

No vesicles or ulcers

Low number of yellow nodules develop in oropharynx area (nodules caused by lymphoid hyperplasia)

sore throat

flu like symptoms

Usually recover in 1 week without Tx

44
Q

How are rubeola, rubella and mumps transmitted?

A

respiratory droplets, highly contagious

45
Q

S/S of rubeola infectoin (measles)

A

Koplik’s spots (clusters of tiny white papules; preceed the skin rash and are pathognomonic)

Skin rash: spread from face to trunk and extremities

Rash fades and followed by desquamation

pt feels very sick

Self limiting but can be complicated by significant morbidity and mortality

46
Q

Rubeola (measles) Dx

A

clinical and confirm with lab tests such as serology

47
Q

Rubella (german measles) S/S

A

Similar to measles but milder and shorter

Skin rash all over body that fades in ~3 days

low fever

mild symptoms (pt doesnt feel sick)

48
Q

What is congenital rubela syndrome?

A

Rubella infects fetus and induces birth defects

49
Q

What happens to most fetus that contract a rubella infection?

A

spontaneous abortion

50
Q

How to prevent congenital rubella syndrome

A

80% transmission from mother to child in first trimester

Check mother’s immunity to ensure she’s immune bc vaccine does not provide lifetime protection

51
Q

Rubella Dx

A

Clinicaland confirmed by lab tests

52
Q

What structure does mumps attack?

A

Excorine glands esp salivary glands (parotid gland = #1 target)

53
Q

S/S of parotid gland infection by mumps

A

Swelling

pain

discomfort

mostly bilateral

54
Q

What population often only has salivary gland involvement in mumps infection?

A

Children

55
Q

What occurs in mumps infection of postpubertal males?

A

Epididymis and testis involvement (epididymo-orchitis)

Swelling, pain, atrophy on affected testes

Permanent sterility is rare

56
Q

Tx for mumps?

A

self limited dz

control symptoms with pain meds

57
Q

Oophoritis?

A

Ovary affected by mumps

58
Q

Mastitis?

A

Breast affected by mumps

59
Q

What does the MMR vaccine protect from?

A

Measles (98%)

Mumps (95%)

Rubella (protection doesnt last as long as other two)

OPath Block 2 (10 decks)

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