VIRAL INFECTIONS OF THE ORAL CAVITY IN IMMUNOCOMPETENT CHILDREN

Dr. Yulia Iriani, SpA

Subbag Infeksi & Pediatri Tropis IKA RSMH FK UNSRI

VIRAL INFECTIONS
Many different viruses can be found in various intraoral lesions and tissues, including malignancies; It is not always clear if and when a virus is a direct causative agent, plays an adjuvant role, or is an innocent bystander. The clinical expression, as well as treatment for viral diseases, may differ greatly between immunocompetent and immunodeficient individuals.

VIRAL INFECTIONS
Some viral diseases, such as HIV, not directly associated with causative relationship to specific oral lesion, but rather indirectly responsible for development of oral lesions secondary to immune suppression. Other viral diseases, such as hand-foot-mouth disease, are directly responsible for ulcerations of oral mucosa. This possible viral origin of oral mucosal conditions in immunocompetent individuals (Table 1) .

Herpes Virus Infections

Eight different herpes viruses are known to cause disease in humans; at least six of these viruses have been associated with oral lesions.

Transmission
A. a.

Common Intraoral Site

Oral Manifestation

Herpes viruses Herpes simplex virus type 1 and herpes simplex virus type 2 Saliva; direct contact with active lesions (oral, perioral, genital) Saliva; direct contact with active lesions (oral, perioral, genital) Saliva; direct contact with active lesions (oral, perioral, genital) Attached gingiva, hard palate, tongue, lips Vesicles, ulcerations covered with yellowish exudate, gingival enlargement Vesicles, ulcerations, and crusting Vesicles, ulcerations

Primary gingivostomatitis

Herpes labialis

Lips

Recurrent intraoral herpes

Attached gingiva, hard palate

Erythema multiforme

HSV reactivation

Buccal and labial mucosa, tongue, lips

Erythematous macules, vesicles, ulcerations

Transmission
b.Varicella

Common Intraoral Site

Oral Manifestation

zoster virus (VZV) Saliva; direct contact with active lesions Saliva; direct contact with active lesions Hard and soft palate, buccal mucosa, tongue, lips Palate, lips, tongue, buccal mucosa, gingiva Vesicles, ulcerations

Chickenpox

Herpes zoster

Unilateral vesicles, ulcerations, bone necrosis, tooth exfoliation; pain along a trigeminal branch

Transmission
c.

Common Intraoral Site

Oral Manifestation

Epstein-Barr virus Saliva Hard and soft palate, gingiva Lymphadenopathy, palatal petechiae, gingival necrosis and ulcerations, edematous uvula Vertical white, hyperkeratotic lesions Tumors, loosening and displacement of teeth

Infectious mononucleosis

Oral hairy leukoplakia Burkitt's lymphoma

Established EBV infection Not known

Lateral borders of the tongue Maxilla, molar-premolar area

Nasopharyngeal carcinoma

Not known

Nasopharynx

Keratinizing squamous carcinoma (WHO type I); nonkeratinizing squamous carcinoma (WHO type II); undifferentiated carcinoma (WHO type II)

Transmission
d.

Common Intraoral Site Teeth

Oral Manifestation Enamel hypoplasia, attrition, discoloration

Cytomegalovirus

Congenital; breast feeding; saliva

e.

Human herpesvirus-8 Coxsackievirus

Possibly sexually

Hard and soft palate

Kaposi's sarcoma

B.

Hand-foot-mouth disease

Saliva

Buccal and labial mucosa, tongue Soft palate

Vesicles, ulcerations

Herpangina

Saliva

Vesicles, ulcerations

Transmission
C.

Common Intraoral Site

Oral Manifestation

Human papillomaviruses Condyloma acuminata Focal epithelial hyperplasia (Heck's disease) Squamous cell papilloma Verrucae vulgaris Direct contact with lesions Direct contact with lesions; self-inoculation Direct contact with lesions; self-inoculation Direct contact with lesions; self-inoculation Tongue, gingiva, labial mucosa, palate Alveolar mucosa, lips Soft, broad-based papules with a pebble-like surface Soft, flat, nonpedunculated papules, usually with a pebblelike surface Soft, pedunculated, exophytic papules with a cauliflower-like surface Firm, broad-based elevated papules with a cauliflowerlike surface

a.

b.

c.

Uvula, hard and soft palate, tongue, frena, lips, buccal mucosa, gingiva Lips, tongue, labial mucosa, gingiva

d.

Transmission
D.

Common Intraoral Site Lip Buccal and labial mucosa; teeth

Oral Manifestation Waxy, dome-shaped papules Bluish-white macules surrounded by erythemata (Koplik's spots); pitted enamel Swelling of salivary glands, erythema and edema of Wharton's and Stensen's duct openings, oral dryness Petechiae; small dark-red papules (Forchheimer's sign) Lichen planus

Molluscum contagiosum Measles

Direct contact with lesion Saliva, respiratory droplets

E.

F.

Mumps

Saliva, respiratory droplets

Salivary glands

G.

Rubella

Saliva, respiratory droplets

Hard and soft palate

H.

Hepatitis C virus

Herpes Simplex Virus Infections

Herpes simplex viruses the most recognized viralassociated oral lesion. Herpes simplex virus type 1 (HSV-1) & herpes simplex virus type 2 (HSV-2) associated with oral & genital manifestations. HSV-1 and/or HSV-2
Primary Infection Secondary Infection

Herpes Simplex Virus Infections

HSV-1 inf: commonly manifested as herpetic gingivostomatitis 5 stages of infection:
Primary mucocutaneous inf Acute infection of ganglia Establishment of latency Reactivation Recurrent infection

Herpes Simplex Virus Infections

Primary infection direct contact:
People + draining lession Asymptomatic carrier

Primary inf incidence

2 4 yrs Infant protected by maternal Ab Series 19000 children + gingivostomatitis by Jauretic: (-) in < 6 months Male = female

Herpes Simplex Virus Infections

Primary Infection
Herpetic gingivostomatitis Younger patients Often asymptomatic May be associated with fever, chills, malaise Vesicles-ulcers-crusting Anywhere in the oral cavity

Herpes Simplex Virus Infections

Incubation period: 6 days Clin manifestation:

Herpes Simplex Virus Infections

Clin manifestation:
Most HSV-1 inf localized to mouth & oropharynx 10 30% perioral HSV-1 inf: symptomatic Clin finding in children: high fever, extensive oral mucosal eruption + tender submandibullar lymphadenopathy & irritability Intraoral lesion: vesicular or ulcerative lesion on lips, gingivae, tongue, buccal mucosa, & palate. Vesicle shallow ulecer on erythematous base, intraoral edema & pain prevent drinking dehydration

Herpes Simplex Virus Infections

Secondary transmission face, conjunctivae, & hands Healing: 1 2 weeks (crusting re-epithelialization)

Secondary Infection
Reactivation of latent virus Not associated with systemic symptoms Small vesicles Occur only on the hard palate and gingiva Prodromal signs

Herpes Simplex Virus Infections

Latency:
Continue throughout life Reactivation various times Trigger: actinic radiation, emotional or physiccal stress Recurrent disease:
1/3 clin orolabial HSV-1 inf vesicles at mucocutaneous border / outer edge if vermilion border of the lips (painful for 2 days) crusting & complete healing in 7 8 days.

Herpes Simplex Virus Infections

Therapy: Acylovir
May be effective in severe gingivostomatitis Marginally effective in recurrent disease Oral prophylaxis maybe useful for frequent recurrences

 Herpes labialis

Gingivostomatitis

Herpes fasialis

Varicella Zoster Virus Infection

Varicella zoster virus (HHV-3)
Latent infection Oral ulcers Dermatomal distribution

VZV inf
Primary infection: varicella / chickenpox Latency reactivation: herpes zoster / shingles

Varicella:
Endemic disease Highest prevalence: 4 10 yrs old age group Highly communicable, attack rate 90%

Varicella Zoster Virus Infection

Incubation period: 14 21 days Presents fever, lymphadadenopathy. a widespread vesicular rash. Rash characterized by
(1) a rapid evolution of macule to papule to vesicle to pustule to crust, (2) a central distribution of lesions that appear in crops, (3) intense itching, and (4) the presence of lesions in all stages in any one anatomic area.

Varicella Zoster Virus Infection

Herpes Zoster:
Sporadic Affect a single dermatome of skin Occur at any age; majority: > 50 years of age. The latent virus reactivates in a sensory ganglion and tracks down the sensory nerve to the appropriate segment. A characteristic eruption of vesicles in the dermatome: often accompanied by intensive pain which may last for months (postherpetic neuralgia)

Varicella Zoster Virus Infection

Varicella Zoster Virus Infection

Epstein-Barr Virus
Developed countries: 2 peaks of infection:
1st in very young preschool children aged 1 - 6 & 2nd in adolescents & young adults aged 14 20 Eventually 80-90% of adults are infected

Developing countries: occures earlier by the age of two, 90% children are seropositive. Disease association:
Infectious Mononucleosis Burkitt's lymphoma Nasopharyngeal carcinoma Lymphoproliferative disease and lymphoma in the immunosuppressed. X-linked lymphoproliferative syndrome Chronic infectious mononucleosis Oral leukoplakia in AIDS patients Chronic interstitial pneumonitis in AIDS patients.

Epstein-Barr Virus

HFMD
Usually caused by coxsackie A virus (A16), but may be caused less commonly by other group A and group B coxsackie viruses and enterovirus 71 (EV71). Incubation period: 36 days Clin Manifestation:
Syndrome characterised by vesicular stomatitis and cutaneous lesions of the distal extremities.

HFMD
Usually begins with a prodrome of fever, sore throat & anorexia. 1 or 2 days after fever begins vesicles on cheeks, gums and sides of tongue, begin as small red spots that blister and often become ulcers. Skin rash develops over 12 days with papulovesicular lesions occurring in 75% of cases. These appear on the palms, fingers, toes, soles, buttocks (common), genitals and limbs. Lesions not itchy. The illness usually lasts 710 days.7

Management: symptomatic

HFMD

Herpangina
NOT caused by Herpesvirus Coxsackie A virus Children < 10 years of age Common in summer and fall Often subclinical presentation Headache/Abdominal pain 48hrs prior to papulovesicular lesions on tonsils and uvula. Sore throat

Herpangina

Measles
Rare in countries with high levels of immunization. Characteristic features of measles:
35 days of prodromal features of fever, malaise, conjunctivitis, coryza and cough. High fever, which persists after the rash appears. Downward spread of the rash from the preauriculararea and the face to involve the body. Tendency of the rash to become confluent on the trunk and remain discrete lower down. Tendency of the rash to become brown and then desquamate after 23 days.

Measles

Mumps

Rubella
Clin manifestation:
erythematous, discrete exanthem that is often faint but may be morbilliform (measles-like) and spreads down from the face. Occipital and/or post-auricular lymphadenopathy is typically (but not exclusively) associated, & arthritis and conjunctivitis can occur. Relatively few systemic symptoms in children.

Important to trace & investigate pregnant contacts of a case.

Rubella

Cytomegalovirus
Congenital infection cytomegalic inclusion disease:
CNS abnormalities - microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification. Eye - choroidoretinitis and optic atrophy Ear - sensorineural deafness Liver - hepatosplenomegaly and jaundice which is due to hepatitis. Lung - pneumonitis

Cytomegalovirus
Heart - myocarditis Thrombocytopenic purpura, Haemolytic anaemia Late sequelae in individuals asymptomatic at birth hearing defects and reduced intelligence.

Perinatal infection usually asymptomatic Postnatal infection - usually asymptomatic. In minority cases syndrome of infectious mononucleosis may: fever, lymphadenopathy, and splenomegaly.