1- Infections of the Oral Mucosa
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Transcript of 1- Infections of the Oral Mucosa
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7/30/2019 1- Infections of the Oral Mucosa
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Dr. Tahani Abualteen
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Infections of the Oral Mucosa I
Common oral mucosal infections: Viral infections Bacterial infections Fungal infections HIV infection and AIDS
Viral infections: The following viruses may cause oral infections or oral manifestations:
1. Herpes viradae (family) orHuman Herpes viruses:o Generally speaking, these viruses tend to produce an initial primary infection, get latent
somewhere in the body and then they may be reactivated for a reason or another to cause
recurrent or secondary infections
oThese viruses include: Herpes Simplex (HSV) type 1 causing herpetic stomatitis (primary/recurrent) Herpes Simplex (HSV) type 2 causing herpetic stomatitis (primary/recurrent) Varicella Zoster (VZV) causing chickenpox (primary) & shingles"herpes zoster"
(recurrent)
Epstein-Barr virus (EBV) causing infectious mononucleosis "glandular fever" andhairy leukoplakia
Cytomegalovirus (HHV5) causing cytomegalovirus infection Human Herpes Virus 6 (HHV6) not common Human Herpes Virus 7(HHV7) not common Human Herpes Virus 8(HHV8) thought to be associated with Kaposis sarcoma
2. Coxsackie A virus causing Herpangina and hand, foot & mouth disease3. Paramyxovirus causing measles and mumps (may be associated with non-specific stomatitis)4. Human Papilloma Virus (HPV) causing warts/epithelial hyperplasias5. Human Immunodeficiency Virus (HIV)6. Influenza Viruscausing influenza (may be associated with non-specific stomatitis)
Lesions may be termed according to their size (depending on the 5mm or the 1 cm rule)
Papule vs. nodule:
Elevated Solid lesionsPapule: small (< 5mm or 1 cm in diameter)
Nodule: large (> 5mm or 1 cm in diameter)
Macule vs. plaque:Represent areas distinguishable from surrounding tissue by color change, usually flatbut may be slightly
elevated
Macule: small (< 5mm or 1 cm in diameter)
Plaque: is larger (> 5mm or 1 cm in diameter)
Vesicle vs. bulla:
Elevated fluid-filled lesionsVesicle: small ( 5mm or 1 cm in diameter)
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Herpes simplex virus (HSV): The most frequent cause of viral infections of the mouth There are two types of herpes simplex virus with serological, biological and clinical differences but
they share the same histopathological features:
oType 1: is frequently associated with infections of the skin and oral mucosa
o Type 2: is frequently associated with infections of the genitalia Primary Infection of HSV Type 1 (Acute Herpetic Gingivostomatitis):
o Common infectiono Occurs predominantly in young children (about 6 years of age)o Transmitted by droplet spread orcontact with the lesiono The majority of cases are subclinical (causing no symptoms or just mild Pharyngitis)o However in some patients it presents as primary herpetic Gingivostomatitis (acute stomatitis
with vesicles and ulcers)
o The usual course of HSV Type 1 infection: 5 days incubation period, then: 2 days of Prodromal symptoms (acute onset of malaise, fever and lymphadenopathy) the
disease process may stop here (subclinical case) or it may continue to result in:
Multiple small vesicles (which can occur on any partof the oral mucosa andlips"keratinized & non-
keratinized") with
widespread gingival
inflammation (which is
erythematous and
edematous) Vesicles soon ulcerate
and may become
secondarily infected
Circumoral crustinglesions on the lips may occurwhen the exudates (from ruptured vesicles) start to dry
Extraoral lesions may also be present, particularly inchildren (for example: vesicles may occur on skin of
chin as a result of drooling of saliva and on nail bedof
fingers "herpetic whitlow" as a result of sucking, andon eyes as a result of rubbing)
This infection is a self-limiting infection that usually takes 10-14 days to resolve (even if the
patient has been given antibiotics)
Herpes virus may be transmitted
to fingers causing a primary
infection which is extremely
painfulknown as Herpetic
whitlow this may arise in the
same patient or in another
person contacting the patient
Mild Circumoral crusting
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o Following the primary infection, immunity to HSV develops but it does not fully protectagainst recurrent infections (but symptoms may be absent/minimal)
However if the immunity is deficient, infections tend to occurmore frequently and to be more
pronounced and persistent
o Microscopic features of HSV infection: Shows an infection of epithelial cells Shows an intraepithelial vesicle (within the
thickness of epithelium NOT subepithelial)
that contains fluid and cellular debris
The vesicle results from degeneration andrupture of the virally infected epithelial
cells by intracellular edema and the
coalescence of disrupted cells
The rupture of infected cells release new viralparticles to infect adjacent cells
A characteristic finding in herpeticinfections (particularly herpes simplex and
Varicella zoster) is the ballooning
degeneration which is acantholysis in the
prickle cell layer due to viral infection and
which result in the formation of Tzanck
cells which are large swollen infected cells
that have eosinophilic cytoplasm and large
pale vesicular nuclei (nuclei with thin anddispersed chromatin)
Enlarged, multinucleated epithelial cellsmay result from fusion of cytoplasm of
infected cells
The virus also gain access to the sensoryaxons of the trigeminal nerve and remain latent there (its DNA transcription is blocked),
andthis usually happens after reaching a balance between the virus and the immune system
(cell-mediated immunity)
Any factor that may disturb the immunity may reactivate the virusand induce viralreplication and then viral particles start to travel down the nerve axons or branches to
nerve endings where they may be shed asymptomatically into the mouth or re-infect the
epithelial cells
o Treatment: Supportive/symptomatic:
Analgesics to relieve pain (e.g. Paracetamol) Mouthwashes may be given to prevent secondary infections It is a viral condition so antibiotics wont help
Antiviral agent (e.g. Acyclovir) may be given in extreme cases
Tzanck cells
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o Prognosis: Self-limited infection Resolves in 10-14 days
Secondary infection of HSV Type 1(Recurrent Herpetic Stomatitis/ herpes labialis):o About one in three of those who have had a primary infection (either clinical or subclinical) later
develop recurrent HSV infection
o This is due to reactivation of the virus which, following the primary infection, has remainedlatent in the sensory ganglion of trigeminal nerve
** Latency is a characteristic property of the herpes viruses
** Herpes simplex in most of the cases prefers to stay in the sensory ganglion of trigeminal
nerve, and usually doesnt affect the geniculate ganglion of facial nerve
o Recurrence (viral reactivation) may be brought by a number of predisposing factors: Factors that may alter or suppress immunity (e.g. Menstruation, old age, stress, febrile
illness "common cold", immunosuppressive drugs, AIDS ) Factors that damage epithelial cells (e.g. mechanical trauma, UV light )
o Systemic symptoms are usually absent in recurrent infectionsbecause of the immunity acquired at the primary infection
and thus recurrent infections may result in asymptomatic
shedding of HSV into the oral cavity or in local Prodromal
symptomsprior to vesicles eruption (e.g. tingling, itching,
burning, or paresthesia)
o After that patients develop clusters of vesicles and ulcerso Vesicles soon rupture and become crusted, and they usually
heal within a week
o Herpes labialis is the most frequent type of recurrentinfection and appears as clusters of vesicles on the lips and
adjacent skin a few hours afterlocal Prodromal symptoms
of itching or tingling
** Herpes labialis is usually unilateral; however it may be
bilateral and more severe especially in immune-
compromised patients
** If the patient recognizes the recurrent herpes labialis in the
Prodromal stage (at the period of tingling and burning
sensation prior to vesicles eruption), then he may benefit
from topical application of alcohol, ice , or acyclovir as it is
thought that these agents may lessen symptoms or they may
shorten the infection period
o Recurrent intraoral lesions occur occasionally, almost alwayson the hard palate or gingiva (keratinized areas) and
usually unilateral
Summary:- When a patient acquires HSV, in most of the cases infection goes subclinical; however some maydevelop the symptomatic primary herpetic Gingivostomatitis
- After primary infection, virus remains latent in the sensory ganglion of trigeminal nerve- Recurrent/secondary infection results from reactivation of the virus particularly following
immunosuppression or epithelial cells damage
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Varicella zoster virus (VZV): Primary Infection of VZV (Varicella or Chickenpox
" "):o The lesions of chicken pox may be found on the oral
mucosa especially thesoft palate and may precede
the characteristic skin rash
o Lesions present as macules, papules, vesicles, orulcerson skin and oral mucosa
o Prodromal symptoms may arise (acute onset ofmalaise, fever and lymphadenopathy)
o Skin lesions are pruritic & usually start in the trunko Oral lesions are usually asymptomatico Microscopic features of VZV:
Identical to HSV Shows an infection of epithelial cells Shows an intraepithelial vesicle The vesicle results from degeneration and
rupture of the virally infected epithelial cells
The rupture of infected cells release new viralparticles to infect adjacent cells
A characteristic finding is the ballooningdegeneration which is acantholysis in the
prickle cell layer due to viral infection and which
result in the formation of Tzanck cells which
are large swollen infected cells that have
eosinophilic cytoplasm and large pale vesicular
nuclei
Enlarged, multinucleated epithelial cells mayresult from fusion of cytoplasm of infected cells
The virus also gain access to the sensory axonsof the trigeminal nerve and remain latent there(its DNA transcription is blocked) probably for
the reminder of the life of the host
Reactivation of the virus to cause zoster is
uncommonbut may occurspontaneously or when the host defenses are depressed
o Treatment: Supportive/symptomatic:
Antihistamines, topical lotions (e.g. calomine lotion) It is a viral condition so antibiotics wont help Vaccine is available
Antiviral agent (e.g. Acyclovir) may be given in immune-compromised patients
A patient with herpetic infection (either primary or secondary) can transmit the virus to another
one and cause primary infection if the recipient has never been exposed to the virus before
This recipient can't develop secondary infection immediately because secondary infection needs
the virus to be already latent there and then reactivated
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o Prognosis: In children, it is a mild condition but in adults it may cause some complications
Secondary infection of VZV (Shingles or Zoster (:"" o Multiple recurrence is rare (repeated attacks of
Zoster are unusual since they require much more
powerful predisposing factors compared to those needed
for HSV recurrent infections)
o Same latent state as HSV, in sensory ganglia oftrigeminal nerve
o Recurrence (viral reactivation) may be brought by anumber of predisposing factors:
Decreased immune-competence: Elderly patients Immunosuppressive drugs
o Prodromal symptoms ofpain and paresthesiamay arise forup to 2 weekso Characterized by unilateral vesicular eruptionsextending over one or more branches of
trigeminal nerve (lesions are restricted to one side and may end sharply at the midline)
o Shingles is an extremely painful conditiono Trigeminal Nerve involvement:
Ophthalmic division is most frequently involved Involvement of the maxillary or mandibular
divisions results in facial and dental pain
Intra, extra oral lesions or botho Lesions usually run a course of about 14 dayso Complications of shingles/zoster:
Post herpetic neuralgia (due to fibrosis around thenerves) so that pain will continue even after lesions
subside Ramsay Hunt syndrome due to involvement of geniculate ganglion of facial nerve and
subsequent facial paralysis Coxsackievirus (Enteroviradae):
RNA virus which has over 30 types Infections worth mentioning are caused by group A Coxsackievirus:
o Herpanginao Hand-foot and moutho Acute lymphonodular Pharyngitis
Herpangina:o Caused by Coxsackie Viruses, Group A, RNAo Seen most commonly in children
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o Sudden onset of mild illness with fever, sore throat, dysphasia, anorexia, nausea, vomiting,diarrhea and lymphadenopathy
o Vesicles and ulcersinposterior oral cavity (tonsils, soft palate, and uvula)o Self-limiting, symptoms persist for2-3 days onlyo
Differential diagnosis: primary herpes (howeverherpes is a Gingivostomatitis, whereasHerpangina is an oropharyngitis)
o Treatment is supportive/symptomatic Hand-foot and mouth:
o Caused by Coxsackie viruses, group A, especially type16, RNA
o Occurs predominantly in childreno Spread by close association e.g. in householdso Oral lesions almost always present, characterized by
shallow painful ulcers, they may resemble Herpanginabut can be larger
o The disease may be distinguished by the presence of handand foot lesions
o Self-limiting, usually lasts for7-10 days Epstein-Barr virus (EBV):
Infectious Mononucleosis (glandular fever):o Affects young adultso Transmitted by salivao Clinically: Pharyngitis, lymph nodes enlargement, Fever,
prolonged malaise (maybe be for months or more)
o Oral lesions are non specific with ulceration orinflammation of the oral mucosa
o Petecheial hemorrhages may be seen at the junction ofhard and soft palate
** Petechia = small red spot on the body caused by minor
hemorrhage (broken capillary)
o Serology: atypical peripheral lymphocytes becauseEBV get latent in B-lymphocytes
o Recall EBV is also associated with : Nasopharyngeal carcinoma Hairy leukoplakia Burkitts lymphoma Oral Sequamous cell carcinoma? (questionable role)
Paramyxovirus: Measles (Rubella):
o Occurs predominantly in childreno Prodromal symptoms may resemble common cold
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o Koplik spots on the oral mucosapin-point bluishwhite spots/macules against an erythematous
background mostly seen on the buccal mucosa opposite
to molar teeth
They usually disappear as skin rash starts so they maybe overlooked or passed unnoticed
o Skin rash (start on face, then go to trunk)o Complications of Measles:
Otitis media, pneumonia, encephalitis, braindamage
Noma may be a complication in malnourished patients** Noma = gangrenous disease leading to tissue destruction of the face especially mouth and
cheeks
o The disease is now rare thanks to vaccines Cytomegalovirus:
Rarely causes disease in immune-competent patients, howeverSubclinical infection is commonaffecting 40-80% of population
Often affects immune-compromised individuals (e.g. AIDS patients, Neonates, patients withtransplant, patients on immunosuppressant )
It tends to infect endothelial and epithelial cells It also commonly affects salivary glandsasymptomatically, or causing Xerostomia especially in
AIDS
Oral lesions are non specific with ulceration of the oral mucosa Serology: Atypical peripheral lymphocytes might be one of the microscopic features