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Herpes simplex
Introduction It is a DNA virus and a member of human herpes virus family, herpetoviridae Types Clinical manifestations Oral manifestations Differential diagnosis Treatment and prognosis

Types
Herpes simplex type I(orofacial type) Herpes simplex type II(Genital type) Human herpes virus III(Varicella zoster) Human herpes virus IV(epstein barr virus) Human herpes virusV(cytomegalovirus virus) Human herpes virusVI(Betavirus) Human herpes virus VII(R.K virus) Human herpes virusVIII(kaposi sarcoma)

Herpes simplex type 1

Clinical features
90% results of HSV I causes acute herpetic gingivostomatitis
Seen during teething age 6months to 5 years and old age 60 years of age Affects movable and attached oral mucosa Gingiva is enlarged,painful and erythematous Punched out erosions along free gingival margins

Mild cases resolve in 5 to 7 days while severe cases in 2 weeks

Symptomatic present pharyngotonsillitis,present on tonsils and posterior pharynx A diffuse, exudate over ulcer occur anterior to waldeyers ring occur in 10%

In young adults herpes simplex virus manifests as pharyngotonsilitis

Type I causes herpes labialis in 15 to 45% cases in USA also known as cold sores/fever blisters
Multiple small erythematous papules develop and vesicle rupture in 2 days,healing in 7 to 10 days Recurrence is bound as erythematous macules on attached gingiva and hard palate.

Herpes simplex type I


Infection of thumbs or finger is known as herpetic whitlow(herpetic paronchynia) results in paraesthesia and scarring.

50 % mortality rate in newborn as infected after delivery through birth canal

Wrestlers and rugby players also may contaminate infection known as herpes gladitorum or scrumpox.

Reccurence is seen in immunocomprised hosts

Other features like geometric glossitis which is herpes on dorsal surface of tongue and appears as a deep midline fissure that typically exhibits multiple peripheral branches.

Histopathology features
Epithelium exhibits multinucleated cells known as tzanck cells and nucleolar fragmentation occurs

Intraepithelial vesicle develops due to intracellular edema

Ballooning degeneration of cells contain intranuclear inclusions called lipschutz bodies

eosinophilic, ovoid structures within nucleus and displace nucleolus and chromatin peripherally.

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Investigations
Serological tests are positive within 4 to 8 days after initial exposure Oral cavity has rare intact vesicles Asymptomatic oral HSV shedding happens in 9% cases and 38% prevalance in immunocomprised patients Cytology and biopsy if possible is taken

Immunofluroscene exhibit fluroscent monoclonal antibodies

Management
Acyclovir suspension during first 3 days
Associated symptoms eating,drinking,pain,healing,fever are shortened. Topical rinsing with0.5% dyclonine hydrochloride Ibuprofen to alleviate discomfort Valacylovir and famciclovir are more convenient in acylovir resistant cases.

Acyclovir ointment in polyethylene glycol in herpes labialis in imunocomprised patients

Dimethyl carbonal for herpes labialis is marketed.

A 10%n-docosanol cream shortens healing by 3 days.

Differential diagnosis

Herpangina

Hand,foot and mouth disease

Varicella zoster

Measles

Herpangina
Also known as apthous pharyngitis,vesicular pharyngitis Caused by coxsackie group A viruses INCUBATION PERIOD IS 2-10 days
It begins as sore throat,cough,rhinorrhea,low grade fever,headache and abdominal pain. Small vesicle rupture to form ulcer showing gray base involving tongue,hard and soft palate,buccal mucosa

Hand ,foot and mouth disease


Epidemic infection,first reported by Robinson in 1958 and caused by coxsackie virus.

Affects young children,betweeen six months to five years

A refusal to eat bcoz of sore throat

The most common site are hard palate,tongue and buccal mucosa is due to small,multiple vesicular and ulcerative oral lesions.

Measles
Acute,contagious, dermatropic viral infection affecting children Caused by paramyxoviridae,which is RNA VIRUS. Spread by direct contamination. Face is involved first, with spread to trunk and diffuse erythematous maculopapular eruptions are formed.

Lesions known as kopliks spots are common in buccal mucosa. foci of epithelial necrosis described as grains of salt on red background. Candidiasis, necrotising ulcerative gingivitis and necrositing stomatitis may be present in oral cavity bcoz of malnutrition Enlargement of lymphoid tissues is also present.

Histopathological features

Focal hyperparakeratosis in which spongiosis,intracelluar edema,dyskeratosis and giant cells are present.

Warthin-Finkeldey giant cells are multinucleated cells and specific for measles.

Diagnosis

detection of antibodies in the blood or, less commonly, the detection of the mumps or measles virus in a culture. Real-time polymerase chain reaction (RT-PCR) testing may be performed to confirm and investigate the source of measles infections.

Management

Routine vaccination for all children between ages of 12 and15 months, second dose administered between 4to 6 years.

Herpes zoster(shingles)
Clinically, the infection is manifested by burning, itching and pain, accompanied by grouped blisters, which proceed to crust and are distributed over one side of the body. The most frequent sites of involvement are the trunk and head.

Herpes zoster (shingles) is caused by the same virus that produces chicken pox. It may occur in childhood, but it is seen most frequently in adults. It is extremely rare to have recurrent infections with this virus.

The most common places of involvement include the thoracolumbar and facial dermatomes.

Affects 10%to20% of individuals


Clinical features can be grouped into prodome, acute and chronic Active ganglionitis with neuronal necrosis and neuralgia One sensory dermatome is affected ,as virus travels it causes prodomal symptoms Pain in form of otitis media, migrane,headache,myocardial infection,appendicitis depending on which dermatome is affected.

Acute phase

In 3to 4 days vesicles

Pustules ulcerate with crust within 2to 3weeks healing with hypopigmentation.

Oral lesions
Lesions extend to midline Skin affecting that quadrant is present Bone necrosis with loss of teeth Involves fifth cranial nerve
Nasocilliary ,ocular branches of fifth nerve is involved Ramsay Hunt sydrome causes hearing defects,facial paralysis,vertigo and auditory symptoms

Diagnosis
Molecular techniques such as dot-blot hybridization and polymerase chain reaction

Cowdry bodies are eosinophilic nuclear inclusions composed of nucleic acid and protein seen in cells infected with Herpes simplex virus, Varicella-zoster virus, and Cytomegalovirus.

Management
Zoster infection by antiviral agents within 72 hrs of onset Acyclovir(I.V) immunosuppresants Oral- bioavaliability10 to 30% 800mg for 7-10 days Valacylovir-1gm 3 times daily for 7days Famciclovir-500mg 3times daily Oral corticosteroids as adjuvant.
Main goal in post herpetic neuralgia 1) Alleviating pain 2) Improving quality of life 3) To maintain sleep 4) Physical activity 5) Nutrition

References
Nevelli,oral and maxillofacial pathology,2nd edition,664-666 Sapp ,oral and maxillofacial pathology, 2nd edition,268 www.emedicine.com Shafer,Hine,Levy.dermatological skin lesions,shafers textbook of oral pathology 2006;668