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Oral ulcers; herpes simplex virus type 3, Varicella Zoster Virus, Chicken pox

Chapter · November 2017

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Diaa M. Zahran
Future University in Egypt
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 HSV 3: Varicella Zoster Virus
DNA Virus
Primary infection: Chicken pox
Secondary infection (Reactivation): Herpes Zoster (Shingles)

Chicken pox
Age: usually common in young age
Transmission: by droplets or direct contact with skin lesions
Incubation period: 2-3 weeks
Virus proliferation: in Macrophages  they don’t release the virus in one shot but in waves
- More common in Winter and Spring.
- Prodrome (systemic manifestations): fever, malaise, headache, fatigue…etc.
Then the lesions appear as skin rash on successive waves that turn into vesicles (tear drop)
containing clear fluid then turns into turbid\cloudy pustules (as they contain pus) 
rupture giving crusted ulcers.
 Mixed lesion due to the release on successive waves from macrophages  rash, vesicles,
pustules and crusted lesions exist together.
Ulcers  Painless ulcer ( as in 1ry extraoral syphilis -chancer- and tertiary syphilis -
Gumma- )
Treatment:
1. Healthy patient  self-limiting  bed rest, good diet, antipyretic and analgesic)
2. Immunocompromised pateints Acyclovir
 Older than 12 years old  10 mg/kg every 8 hours for 7 days
 Younger than 12 years old  5 mg/kg every 8 hours for 7 days
o Passive immunization: injection of a preformed Varicella Zoster Immunoglobulins-Ig

Herpes Zoster (Shingles)

2ry infection (reactivation) of VZ virus
Etiology: reactivation of a latent virus in trigeminal ganglion by
1. Trauma
2. Surgery
3. Irradiation
4. Malignancy
5. Immunosuppression
 May affect any nerve

Age: adults and old age

Period: 3-4 weeks
 May manifest prodrome in the form of pain along the nerve as tenderness that turns into
severe neuralgic pain
 The lesion is related to the nerve as the pain is unilateral neuralgic.
 Then the lesion appears as typical viral skin lesion (ulcer):
Erythema vesicles clear vesicles that turns cloudy  rupture  skin ulcer
 The ulcers appear along the distribution of the nerve (areas supplied by the nerve) e.g. if it
affects the ophthalmic nerve, ulcers appear on areas supplied by the ophthalmic nerve;
similar with maxillary or mandibular nerves.
 Unilateral lesion.
 Vesicles eventually turns into crust
 Mixed lesion due to successive waves
 Healing within 3-4 weeks
Rarely without scar formation which is only in case of no secondary bacterial infection
Usually heals by scar  the patient either loses sensation over the affected region or has
severe pain Post Herpetic Neuralgia
There may be increase of tongue coating as the patient eats on one side because of the pain on
the affected side
- If the virus affects the mandibular nerve the lesions are on: Tongue, Buccal mucosa, lower
vestibule and skin of the chin
- If the virus affects the maxillary nerve the lesions are on: soft and hard palate, upper
vestibule, lateral skin of the nose and the cheek
- If the virus affects the ophthalmic nerve the lesions are on: eye lid, cornea and forehead
- Bilateral lesions are rare but may occur in case of viremia due to decrease in immunity.
Diagnosis:
1. History  contacting a lesion, prodrome, visiting another patient
2. Mixed lesion  erythema, papules, vesicles, pustules and crusted ulcers
** Herpes sine herpes (Zoster sine eruption)
 Pain due to VZ but with no clinical lesions yet
 Misdiagnosed as abscess or pulpitis or appendicitis (when lesions are on the
trunk)
 Antibody titre should be made first
Complications:
1. Post Herpetic Neuralgia  pain persists after healing of the lesions up to 3-4 months due
to inflammation and fibrosis of the nerve
o Scar
o Pain is severe that some patients may commit suicide
o Prescribe Antidepressants as Carbamazepine (Tegretol)
o Persistence may be 1 or 2 months or reach 1 year
2. Generalized herpes zoster (viremia)
 Lung, liver, cerebrospinal fluid affecting spinal cord, brain and meningitis; causing
pneumonia, hepatitis …etc.
3. In motor nerves  paralysis
4. Secondary infection  healing by scar
5. In Eye  ulcer in Cornea  blindness
Management:
1. Healthy patient:
i. Mild or moderate cases: Symptomatic ttt
Fever antipyretic, pain  analgesic
Bed rest
Chlorhexidine mouth wash to avoid 2ry infection
Proper oral hygiene
Topical Acyclovir  in Eye and Skin lesions
ii. Severe cases:
Oral Acyclovir 800 mg 5 times/day for 7-10 days
2. Immunocompromised patients or viremia disseminated VZ:
IV 10 mg/kg every 8 hours for 10 days
3. Elderly patients:
Acyclovir + Prednisone (cortisone) to avoid post herpetic neuralgia

Ramsay-Hunt Syndrome
Herpes zoster involving Facial nerve
Virus remains latent in Geniculate ganglia
Clinically:
- Prodrome  fever, malaise, headache, fatigue…etc.
- Localized pain in the ear radiating to the jaw.
- Herpetic oticus (vesicles) appear on the external auditory canal, tympanic membrane and
tragus of the ear
- Tinnitus -Vertigo
- May lead to deafness
  Along Facial nerve so the lesions are unilateral
- Loss of high pitched sound  as the nerve to Stapedius muscle is affected
The Ear is supplied by auriculotemporal nerve and the temporal branch from facial nerve.
Oral manifestations:
- Unilateral vesicles  ulcers
- Along the nerve  Soft palate, anterior 2/3 of the tongue and fauces.
Soft palate: as the fibers from motor nucleus of facial nerve are affected as they pass through
the geniculate ganglia
Tongue: as the chorda tympani is affected
- Loss of taste sensation in half of the tongue (chorda tympani)
- Xerostomia (as parotid gland is affected)
- Bell’s Palsy
Treatment:
 Acyclovir + prednisone 60 mg  to decrease nerve inflammation and edema to avoid
permanent damage at the sharply angulated part of the canal leading to paralysis

Coxsackie Virus  Enterovirus

RNA Virus
Coxsackie virus A Coxsackie Virus B
-Herpangina
-Hand, foot and mouth disease HFMD
-Acute lymphonodular pharyngitis
The virus affects the pericardium, myocardium or meninges
Herpangina Hand, foot and mouth disease

Coxsackie virus A Coxsackie virus A

Transmission: Contaminated saliva 1. Air borne
2. Oro-fecal contamination
3.
Age: Children 5m – 6 y
Both are in young age
No reactivation by reinfection (prodrome and systemic manifestations every time)
Clinical Pic.: Sore Throat, headache, dysphagia lymphadenopathy
Extra-Oral: NO extra-oral Papules and vesicle on fingers, hands and feet
manifestations
Intra-Oral: - Vesicles  ulcers: round, - Vesicles: similar
small, shallow surrounded by erythema -
- 1-2 mm (smaller) - 1-10 mm (larger)
- Site: soft palate, uvula, fauces and - Site: hard palate, tongue, cheek mucosa
pharynx
- Pharyngitis and dysphagia - Pharyngitis and dysphagia
 Difference between Herpangina and primary herpetic gingivostomatitis (HSV):
1. Herpangina: Coxsackie virus - 1ry herpetic gingivo.: Herpes Simplex 1
2. Herpangina: mild - 1ry herpetic gingivo. is severe
3. Herpangina: in posterior part of the mouth -1ry herpetic gingivo. affects keratinized and
non-keratinized areas
4. Herpangina: gingiva is free -1ry herpetic gingiva.: marginal gingivitis
5. Herpangina: small ulcers (1-2mm) -1ry herpetic gingiva.: larger ulcers
6. Under microscope: Ballooning degeneration is found in 1ry herpetic gingivostomatitis but
not in Herpangina.

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