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Oral Medicine > Recurrent herpes simplex (w2) > Flashcards

Recurrent herpes simplex (w2) Flashcards

1
Q

Recurrent Herpes Simplex Lesions are Due to …

A

reactivation of latent virus after a previous primary attack (not a re-infection)

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2
Q

What are the types of herpes simplex?

A

A) Recurrent Herpes Labialis

B) Recurrent Intraoral Herpes

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3
Q

What is the percentage of patients who’s subjected to virus reactivation?

A

20 - 30%

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4
Q

What are the factors that trigger recurrent herpes labialis?

A
  1. common cold
  2. febrile infections
  3. exposure to strong sunshine
  4. menstruation
  5. emotional upsets
  6. local irritation (dental treatment)
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5
Q

Describe the prodrome of recurrent herpes labialis

A
  1. parasthesia (burning sensations)
  2. erythema
  3. Vesicles form after an hour or two in clusters along the mucocutaneous junction of the lips but can extend onto the adjacent skin.
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6
Q

What is the pathogenesis of herpes labialis?

A
  1. The vesicles enlarge, coalesce and weep exudates.
  2. After two or three days they rupture and crust over but new vesicles frequently appear for a day or two only to scab over
  3. they heal, usually without scarring.
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7
Q

How long does a cycle of herpes labialis take?

A

The whole cycle may take up to 10 days.

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8
Q

What changes herpes labialis vesicles to pustules?

A

Secondary bacterial infection

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9
Q

What is the treatment of herpes labialis?

A

1-Sun block and avoid exposure to sunlight if it is the predisposing factor.

2- When viral damage is seen, treatment must start as soon as the primary (premonitory) sensations are felt.

  • Acyclovir cream 5 times daily for 5 days should be started within 24 hours.
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10
Q

What is the pathogenesis of recurrent intraoral herpes?

A
  1. Clusters of small vesicles that break into ulcers, 1-2 mm in diameter
  2. appear MAINLY ON KERATINIZED oral mucosa (gingival, hard palate,…).
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11
Q

What is the treatment of recurrent intraoral herpes?

A

Tetracycline mouth bath/ wash after meals and before bedtime.

(antibiotic that treats side effects)

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12
Q

What is chronic Herpes Simplex Lesions?

A
  1. It is a variant of recurrent herpes simplex lesion
  2. occurring in immune compromised patients (AIDS, immunosuppressive therapy, leukemia, lymphoma, …..)
  3. Lesions appear on skin or mucosal surfaces as an ordinary recurrent herpetic lesion
  4. remain for weeks or months
  5. develop into large, deep, painful ulcers (up to several centimeters in diameter).
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13
Q

What is the treatment of chronic Herpes Simplex Lesions?

A
  1. Systemically administered acyclovir

2. doubling the dose; i.e. 400 mg 5 times/day, till healing takes place.

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14
Q

What is herpetic whitlow?

A

It is a cross infection of fingers after manipulation of herpetic lesions

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15
Q

Who is subjected to herpetic whitlows?

A
  1. dental surgeons and their assistants.
  2. patients themselves
  3. Mothers applying antiherpetic drugs to children’s lesions should wear gloves.
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16
Q

How can herpetic whitlows be prevented?

A

By using gloves when giving dental treatment

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17
Q

When is herpetic whitlows dangerous?

A

In immunodeficient patients

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18
Q

How is herpetic whitlows treated in In immunodeficient patients?

A

acyclovir doubling the dose 400 mg 5 times per day till healing

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19
Q

What is Zoster (shingles) characterized by?

A
  1. pain
  2. vesicular rash
  3. stomatitis in the related dermatome.
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20
Q

What is the virus that causes chicken pox and zoster? And what does it do?

A

The varicella zoster virus (VZV) causes:

  1. chickenpox in the non-immune (mainly children),
  2. reactivation of the latent virus causes zoster, mainly in the elderly.
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21
Q

How frequent is the reactivation of zoster?

A

very rare

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22
Q

when does zoster reoccur?

A

When there is an underlying immunodeficiency:

  1. in organ transplant patients
  2. can be an early complication of some tumors, (Hodgkin’s disease, AIDS.)
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23
Q

What is the pathogenesis of herpes zoster?

A
  1. May involve one of the divisions of trigeminal nerve.
  2. produces similar epithelial lesions to those of herpes simplex
  3. inflammation of the related posterior root ganglion.
    (later it becomes latent in nerve ganglion and it is called neurotoropic virus)
  4. Vesicles, often confluent, form on one side of the face and in the mouth up to the midline. Vesicles contain clear fluid but after few days may become purulent; they rupture forming ulcers and turn to crust in 1 week.
  5. Mixed skin lesions can develop on the same skin area such as papules, vesicles, pustules and crusts.
  6. The regional lymph nodes are enlarged and tender. The acute phase usually lasts about a week.
  7. Pain preceeds rash until the lesions crust over and start to heal (severe neuralgic pain), but secondary infection may cause suppuration and scarring of the skin. Malaise and fever are usually associated.
  8. Lesions are localized to one side (absolutely unilateral), within the distribution of any of the divisions of the trigeminal nerve
  9. Patients are sometimes unable to distinguish the pain of trigeminal zoster from severe toothache, this has sometimes led to unnecessary dental extraction. Also, sometimes pain occurs without rash or oral lesions, (herpes sine eruption) which leads to problems in diagnosis.
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24
Q

What happens when herpes zoster affect ophthalmic nerve?

A

blindness due to corneal scarring may occur.

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25
Q

What happens when herpes zoster affect 2nd (maxillary) and 3rd (mandibular) divisions?

A

Oral lesions are seen

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26
Q

What is Chicken Pox characterized by?

A

It is a childhood disease :

• Mild systemic symptoms.

  • Generalized pruritic eruption
  • of maculopapular lesions
  • that rapidly develop into vesicles (tear drops)
  • on erythematous base.
  • Oral vesicles that rapidly rupture giving ulcers.
  • Successive crops of rashes continue to appear for 3-6 days due to repeated waves of viremia
  • intraorally: pseudomembrane
  • extraorally: crust

But: Oral lesions are not an important problem regarding symptoms, diagnosis or management.

27
Q

What is the prodrome of Herpes Zoster?

A
  1. 2-4 days of sharp shooting pain
  2. paresthesia
  3. burning and tenderness along the course of affected nerve.
28
Q

Why is there a mixed skin lesion in chicken pox or zoster?

A

due to different times of virus entry.

vesicle: early
bulla: later
ulcer: late

29
Q

What is the treatment of chickenpox?

A 
acyclovir (antiviral)
calamine lotion (to treat erythema and pruritic lesions)
30
Q

What is the treatment of herpes zoster?

A
  1. According to the severity of the attack oral acyclovir (800 mg five times daily, for 7 days) should be given at the earliest possible moment
  2. analgesics.
  3. prednisolone (corticosteroids) may
    a. accelerate relief of pain and healing
    b. prevent post-herpetic neuralgia in elderly patients.
  4. In immune deficient patients, intravenous acyclovir is required and may also be justified for the elderly in whom this infection is debilitating.
31
Q

What are the complications of herpes zoster?

A
  1. Post-herpetic neuralgia which mainly affects the elderly and is difficult to relieve.
  2. Can be life-threatening in immune compromised patients.
  3. Secondary infection may cause suppuration and scarring of the skin.
  4. When the ophthalmic division is involved, blindness due to corneal scarring may occur
32
Q

What is Ramsay Hunt Syndrome?

A

It is Herpes zoster of the geniculate ganglion

affecting the facial nerve which contains both motor and sensory fibers) (rare

33
Q

What are the characteristics of Ramasy Hunt Syndrome?

A
  1. Prodrome of facial pain which may radiate to the jaws and be misdiagnosed as tooth ache.
  2. Bell’s palsy.
  3. Unilateral vesicles of external ear (herpetic oticus)
  4. Unilateral vesicles of oral mucosa which soon turn into ulcers, on erythematous base.
    - The areas affected are the anterior 2/3 of the tongue and soft palate on the same side (distribution of chorda tympani “responsible for taste sensation”).
34
Q

What are the complications of herpes zoster?

A
  1. Permanent facial paralysis.
  2. Post-herpetic neuralgia
  3. Deafness
35
Q

What is the management/ treatment of herpes zoster?

A
  1. Corticosteroids or ACTH

2. Antiviral drugs (acyclovir) (to avoid permanent fibrosis of the facial nerve.)

36
Q

What is Hand-foot-and-mouth Disease?

A

This common mild viral infection which often causes minor epidemics among school children as it is highly infectious. it can even infect teachers and parents>

37
Q

What are the characteristics of hand-foot and mouth disease?

A
  1. ulceration of the mouth

2. vesicular rash on the extremities.

38
Q

What is the causative agent of hand-foot and mouth disease?

A

Strains of Coxsackie A virus

39
Q

How long is the incubation period of hands-foot and mouth disease?

A

between 3-10 days.

40
Q

Which age is most commonly affected by hands-foot and mouth disease?

A

3-10 years

41
Q

What are the clinical features of hands-foot and mouth disease?

A
  1. The small scattered oral ulcers usually cause little pain.
  2. Intact vesicles are rarely seen and gingivitis is not a feature.
  3. Regional lymph nodes are not usually enlarged and systemic upset is mild or absent.
  4. The rash consists of vesicles, sometimes deep-seated, or occasionally bullae, mainly seen around the base of fingers or toes, but any part of the limbs may be affected.
  5. In some outbreaks either the mouth or the extremities alone may be affected.
42
Q

What is the treatment for hands-foot and mouth disease?

A

No specific treatment available or needed.

43
Q

What is the causative agent of herpangina?

A

Coxsackie virus A infection (usually A4).

44
Q

Which age is most commonly affected by herpangina?

A

3-10 years (but other ages are possible)

-occurs in epidemics

45
Q

What are the clinical features of herpangina?

A
  1. Incubation period: 2-10 days
  2. Prodrome: sore throat, dysphagia fever, chills, anorexia
  3. Lesions (soft palate, tonsils, pharynx): macules → papules and vesicles → small (1-2 mm) ulcers.
  4. Ulcers heal without treatment in about 7 days.
46
Q

points of comparison between herpangina and primary HSV infection

A
  1. epidemics
    herpangina: yes
    HSV: no
  2. severity
    herpangina: milder
    HSV: sever
  3. distribution
    herpangina: posterior part of mouth
    HSV: anterior part of mouth
  4. gingival involvement
    herpangina: none
    HSV: acute generalized gingivitis
  5. size of ulcer
    herpangina: small
    HSV: large
47
Q

What is tuberculosis?

A
  1. It is a chronic ulcer on the mid-dorsum or tip of the tongue.
  2. It is angular or stellate with over-hanging edges and a pale floor, but can be ragged and irregular.
  3. It is painless in its early stages and painful later
  4. regional lymph nodes are usually unaffected.
48
Q

What is the pathology of tuberculosis?

A

granulomas are seen in the floor of the ulcers.

49
Q

What is the management/ treatment of tuberculosis?

A
  1. Diagnosis is confirmed by biopsy, chest radiography and a specimen of sputum.
  2. Mycobacterial infection is confirmed by culture or PCR.
  3. Oral lesions clear up rapidly if vigorous multi-drug chemotherapy is given for the pulmonary infection.
  4. No local treatment is needed.
50
Q

What is the pathogenesis of primary syphilis?

A
  1. An oral chancre appears 3-4 weeks after infection and may form on the lip, tip of the tongue or rarely, other oral sites.
  2. It consists initially of a firm nodule about a centimeter across.
  3. The surface breaks down after a few days, leaving a rounded ulcer with raised indurated edges.
  4. This may resemble a carcinoma, particularly if on the lip.
  5. A chancre is painless but regional lymph nodes are enlarged, rubbery and discrete.
51
Q

How is syphilis diagnosed?

A
  1. Diagnosis therefore depends on clinical finding because serological reactions are negative at first.
  2. Treponema pallidum can be demonstrated by dark-ground illumination of a smear from the chancre, but they must be distinguished from other oral spirochetes.
52
Q

When is the treatment of syphilis most effective?

A

at the primary stage

53
Q

How does syphilis chancre heal?

A

After 8 or 9 weeks the chancre heals, often without scarring.

54
Q

When does secondary syphilis occur?

A

1-4 months after infection.

55
Q

What does secondary syphilis cause?(prodrome)

A

causes:

  1. mild fever
  2. malaise
  3. headache
  4. sore throat
  5. generalized lymphadenopathy

soon followed by a rash and stomatitis.

56
Q

Describe the rash caused by secondary syphilis.

A

The rash is variable, but typically consists of:
1. asymptomatic pinkish (coppery) macules

  1. symmetrically distributed and starting on the trunk.
  2. It may last for a few hours or weeks
  3. its presence or history is a useful aid to diagnosis.
57
Q

How does the oral lesions look like?

A
  1. They rarely appear without the rash
  2. mainly affect the tonsils, lateral borders of the tongue and lips.
  3. They are usually flat ulcers covered by grayish membrane and may be irregularly linear (snail track ulcers) or coalesce to form well-defined rounded areas (mucous patches).
58
Q

What makes secondary syphilis so infective?

A
  1. Discharge from the ulcers contains many spirochetes

2. saliva is highly infective.

59
Q

How is secondary syphilis diagnosed?

A

Serological reactions are positive and diagnostic at this stage,

but biopsy is unlikely to be informative.

60
Q

What is the pathogenesis of syphilis?

A
  1. Late stage syphilis develops in many patients about three or more years after infection.
  2. The onset is insidious غدار and during the latent period, the patient may appear well.
  3. A characteristic lesion is the gumma.
61
Q

What is the clinical picture of tertiary syphilis?

A
  1. Clinically, a gumma, which may affect the palate, tongue or tonsils
  2. can vary from one to several inches in diameter.
  3. It begins as a swelling, sometimes with a yellowish center which undergoes necrosis, leaving a painless deep ulcer.
  4. The ulcer is solitary, deep, rounded, with soft, punched-out edges.
  5. The floor is depressed and pale (wash-leather) in appearance.
  6. It heals with severe scarring which may distort the soft palate or tongue, perforate the hard palate or destroy the uvula.
62
Q

How can the tertiary syphilis be diagnosed?

A
  1. Serological confirmation of the infection is essential.
  2. Tests are either specific (such as the FTA-ABS) or non-specific as in the VDRL.
  3. The VDRL becomes positive 4-6 weeks after infection and becomes negative only after effective treatment but false positives can result from several other causes.
63
Q

How can the tertiary syphilis be managed?

A
  1. Antibiotics, particularly penicillin, are the mainstay of treatment
  2. but tetracycline and erythromycin are also effective. (+ clindamycin)
  3. Treatment should be by a specialist and must be continued until non-specific serological reactions (VDRL) are persistently negative.

Oral Medicine (3 decks)

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