Oral Manifestations of Viral Infections
Oral Manifestations of Viral Infections
Viruses cause a plethora of symptomatic or asymptomatic infections
in the oral cavity, with clinical manifestations ranging
from no change to epithelial ulcerations, benign soft tissue
growths, and malignancy
Ulcerative manifestations of various viral infections are
often difficult to discern from each other and from clinically
similar conditions of different etiology.
we will reviews
presentation, diagnosis, and the management approach for
major viral conditions of oral cavity
Herpes simplex type
Description
The herpesviridae group of viruses includes more than 80
herpesviruses; for 8 viruses, people are the natural host. All
human herpes viruses (HHVs) have a double-stranded DNA core
within a protein capsid, enclosed by a tegument and an envelope,
and are capable of causing life-long latency. Herpes
simplex virus (HSV) has 2 serotypes, HSV1 and HSV2, which are
partially homologous in their DNA core but have different
antigenic properties.
Although HSV1 and HSV2 primarily infect orofacial and
genital regions, respectively, sexual practices could result in
cross-over infections. Herpes simplex viruses are highly transmissible
through contact with oral or genital secretions of individuals
with active lesions as well as asymptomatic shedding
Primary oral herpes
Primary herpetic gingivostomatitis (PHGS) develops when a
nonimmune individual is exposed to HSV-1 for the first time.
Clinical presentation and differential diagnosis
Most cases affect children 1 to 5 years of age and are often
subclinical. Symptomatic patients present with lymphadenopathy,
fever, sore throat, and vesiculo-ulcerative lesions
affecting the oral and perioral regions Both movable
and nonmovable oral mucosa may be affected, and acute onset
of generalized gingival inflammation and pain is a classic
feature
Differential diagnosis includes herpangina, erythema multiforme,
allergic stomatitis, acute necrotizing ulcerative
gingivitis, and acute eruptions of vesiculobullous diseases.
Management
The condition is self-limiting in healthy individuals. When
oral pain and dysphagia pose risk of dehydration and poor
nutritional intake, palliation and off-label antiviral therapy
with acyclovir or valacyclovir may be indicated.
Antipyetics such as acetaminophen may be used to treat
fever, and anesthetic rinses may be used for palliation. Hydration
and a bland, soft diet should also be encouraged. Patients
should be educated about the contagious nature of the
virus and potential for spread of infection to others or autoinoculation
to other body sites.
Secondary oral herpes
HSV 1 establishes life-long latency in trigeminal ganglion. Internal
and external triggers such as stress, fatigue, fever,
menstruation, immunosuppression, and exposure to heat, cold,
or sunlight could cause viral reactivation. Viral reactivation
may occur in up to 40% of individuals testing positive for HSV1
antibodies and lead to asymptomatic viral shedding (recurrence)
or clinical disease (recrudescence).
Clinical presentation
Recrudescence may affect mucocutaneous junction of the lips
or keratinized intraoral tissues .
Unlike PHGS, there are no systemic symptoms with recrudescence.
However, onset of HSL is often preceded by a local
prodrome of tingling, burning, or itching. Recrudescent
intraoral herpes (RIH) is less common than herpes simplex
labialis (HSL), and in the immunocompetent host, it affects
keratinized tissues such as gingiva and palate
Management
In the immunocompetent host, HSL heals within 7 to 14 days
without scarring. Frequent or disfiguring recurrences of HSL
and severe or chronic HSV outbreaks in the immunosuppressed
host may require antiviral therapy. US Food and Drug Administration
(FDA)-approved medications for HSL include topical
deconasol and penciclovir, as well as systemic valacyclovir.
Maximal therapeutic efficacy requires early recognition of signs
and symptoms of an outbreak and initiation of antiviral therapy
during the prodrome
Varicella-zoster virus
Varicella zoster (chicken pox)
Description
Varicella zoster virus (VZV) is one of human herpes group of
viruses capable of developing primary and secondary disease.
Primary exposure to VZV in a nonimmunized person results in
an acute disease known as chicken pox. The main route of viral
transmission is through respiratory tracts or conjunctiva.
Clinical presentation and management
A prodrome may precede development of a generalized, pruritic
skin rash, which spread centripetally. Fever and malaise
may also be present. Lesions progress through macular to
papular, vesicular, pustular, and crusted stages. Although
mouth and oropharynx may be affected, intraoral lesions are
minimally symptomatic.
In healthy individuals, recovery is uneventful and leads to
life-long immunity. Condition is highly contagious and measures
to prevent transmission to other should be considered.
Herpes zoster (shingles)
Description
Reactivation of VZV dormant in a sensory nerve ganglion results
in herpes zoster (HZ) or shingles in a sensory dermatome
(Fig. 8). Reactivation occurs in 5 out of 1000 individuals testing
seropositive for VZV. Cytotoxic drugs, immunosuppression, internal
malignancies, and aging are among the risk factors for
viral reactivation.
Clinical presentation
Herpes zoster presents with a prodrome of mild fever, malaise
and pain, burning, itching, or paresthesia in the affected area.
This is followed by regional lymphadenopathy and unilateral
vesicular rash in dermatome of a sensory nerve. Involvement of
bilateral or multiple dermatomes is uncommon and should
raise concerns about immunosuppression.
Diagnosis and management
Diagnosis of HZ often relies on history and clinical findings.
However, laboratory investigations such as viral culture, PCR,
or serologic testing and epidemiologic linkage may be used for
confirmation.
Management of HZ depends on the age, immune status,
symptoms, and clinical presentation. Depending on severity,
topical anesthetics, analgesics, anticonvulsants, tricylic antidepressants,
or their combinations may be used to manage
pain and pruritis. When indicated, timely intervention with
high-dose antivirals with or without corticosteroids helps control
symptoms and reduces the likelihood of PHN in susceptible
patients
Herpangina
Herpangina primarily affects young children, causing fever,
malaise, and symptomatic oral lesions. The latter occur in
clusters and progress through macular, popular, and vesicular
stages before diffuse erythema and punctate erosions develop
in posterior oral cavity .
Lesions affect the soft palate, uvula, posterior pharygeal
wall, and tonsils, causing sore throat, odynophagia, dysphagia,
and occasionally throat exudates. Headache, vomiting, and
abdominal pain may also be present.
Herpangina symptoms may overlap with those of streptococcal
pharyngitis and tonsilitis. The latter may be excluded by
a throat culture. Pharyngitis of streptococcal origin does not
present with vesicular lesions seen in herpangina
Hand-foot-mouth disease
HFMD primarily affects children and is highly transmissible.
Patients experience low-grade fever and vesicular sores that
coalesce to form symptomatic oral erosions .
Typical locations include tongue, palate, and buccal mucosa.
Nearly 3/4 of patients will also experience nonpruritic
cuanteous papules and vesicles on dorsal and lateral aspects of
hands and feet . Coxsackievirus A16 is the predominant
serotype in most cases. Severe outbreaks of HFMD often
involve coxsackievirus A6.
Management
No vaccine or specific antibiotic for coxsackievirus infections is
available. Both HFMD and herpangina are generally selflimiting
with good prognosis, and treatment is primarily
supportive.
Antipyetics such as acetaminophen may be used to treat
fever, and anesthetic rinses may be used to alleviate oral
discomfort. Hydration and bland, soft diet should also be
encouraged. Educating patients about hand washing, not
sharing of utensils, and minimizing contact with those affected
are key to preventing transmission.
Human papillomavirus
Description
A group of DNA viruses with predilection for mucocutaneous
tissues. Human papilloma virus (HPV) is most frequently
transmitted through intimate vaginal, anal, or oral contact,
and it is widely distributed throughout the world. Multiple
sexual exposures and immunocompromised status increase
likelihood of HPV infection. There are over 120 types of HPV, of
which 40 types infect mucosal epithelium. Most HPVs are
classified as low risk for malignant epithelial transformation.
Thirteen strains are considered high risk for mucocutaneous
malignancy.
Clinical presentation
Clinical manifestations of HPV include mucocutaneous warts
(oral, anal, genital), respiratory papillomatosis, mucocutaneous
epithelial dysplasia and a variety of epithelial cancers
(cervical, vaginal, vulvar, penile, anal and oropharyngeal). Oral
manifestations of HPV infection includeManagement
Oral warts may be treated by surgical excision, laser ablation
or cryotherapy with liquid nitrogen. There are no approved
medical therapy for oral warts. However, frequent and refractory
lesions in the immunocompromised may improve with
topical application of imiquimod 5% cream, cidofovir gel,
podofilox solution, or intralesional injection of interferon
alpha. Identifying the source of infection (eg, patient’s digital
warts or partner’s genital warts) may help prevent
reinfection.
Oropharyngeal cancer
Persistence of high-risk HPV 16 in the posterior oral cavity
increases the risk of oropharyngeal cancers affecting the base
of tongue, posterior throat, and tonsillar structures. HPV16-
associated cancer in these anatomic sites is the fastest
growing subset of oropharyngeal cancers and frequently affects
white men 35 to 55 years of age who do not smoke or
drink
Management
HPV-associated oral malignancies are treated with surgery,
chemotherapy, and/or radiation. They not only have a better
prognosis than oropharyngeal cancers caused by traditional risk
factors but also lower likelihood of recurrence or second
primaries.
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