Vesiculo bullous I

Vesiculo-Bullous Diseases
Aiman A. Ali DDS, PhD.

Vesiculo-Bullous Diseases




Viral
Associated with immunologic defects
Hereditary


Viral infections of significance
to clinical dentistry


Viral infections of significance
to clinical dentistry
 Herpes

Simplex Virus (HSV)
infection
 Varicella-Zoster infections
 Hand, Foot, and Mouth Disease
 Herpangina
 Measles (Rubeola)


Herpes Simplex Virus (HSV) infection
Pathogenesis
 DNA

virus.
 Two types HSV1 & HSV2
 Transmitted by physical contact with an infected
person
 Travel through the trigeminal nerve to the t. ganglion
 Become latent in the neural tissue
 With reactivation it travels to the epithelial surface
 Reactivation by exposure to sunlight [fever blister] or
exposure to cold [cold blister] or other factors.

Precipitating Factors

Stress
Nutrition
Trauma
Hormonal
Diet
Immunologic

Clinical features (Primary)
 Primary herpetic gigivostomatitis
 Usually affects children
 Vesicular eruption may appear on the
skin vermilion
 In the oral cavity, lesions may appear
on any part of the oral mucosa
 Viremia symptoms: fever, arthralgia,
malaise, headache and cervical
lymphadenopathy
 After 7 to 10 days the lesions heal
without scar

Clinical features (Secondary)
• Usually on the lip and rarely on gingiva
or palate
• Prodromal symptoms

• Within hours multiple fragile vesicles
appear
• Lesions ulcerate and coalesce
• Lesions heal without scaring in 1 to 2
weeks
• Rarely become secondarily infected
• Recurrence vary from 1 per year to 1
per month

Clinical features (Whitlow)







Typically occur in dental
practitioners who don’t use
gloves
and had physical contact
with
infected individuals
Either primary or secondary HSVI
involving the fingers
Recurrent lesions if occurred, would
be expected on fingers
Pain, redness, vesicles that break to
become ulcers
Duration vary from 4 to 6 weeks

Histopathology
 Vesicles are intraepithelial
 Some virus-infected epithelial cells
are seen
 After several days these features
disappear


Differential Diagnosis
 Primary HSV infection
 Streptococcal pharyngitis
 Erythema multiform
 ANUG
 Secondary HSV infection
 Recurrent aphthous stomatitis


 Virus culture, monoclonal antibodies
or DNA hybridization

RIH

RAS

Appearance of primary
lesion

vesicle

ulcer

Appearance of mature
lesion

shallow, punctate ulcers

ulcer (with erythematous halo)

Common location

attached gingiva, hard
palate,vermillion border

buccal mucosa, floor of mouth, oropharynx,
vestibule, tongue

Number

few to several

one to few

Lesion duration

1-3 weeks

1-2 weeks

Etiology

Viral

Unclear; immunologically mediated

Prevalence (by
adulthood)

70-80% (HSV-1)

Possibly up to 66%

Treatment
 Time

is very important

 Acyclovir
• Oint 5% 5t. daily when symptoms first appear
• Tab 200 to 400 mg 5t daily is effective

 Vidarabine

or Idoxuridine are effective on
ocular HS but not LHS.

 Primary

HSV infection is best managed
with supportive therapy [fluid, rest, oral
lavage and antipyretics]

Varicella-Zoster Infection
Etiology & Pathogenesis
 VZV

is one of the herpes virus

 Cause

primary infection (varicella or
chickenpox) and secondary disease
(herpes zoster or shingles)

 After

primary infection, virus remain latent
in a sensory ganglia

 Reactivation

of latent VZV usually follows
immunosuppressive status, drug
administration, irritation or local trauma

Clinical features (Varicella)
 Common
 Fever,

among children

chills, malaise and headache

 Rash

involves the trunk, head & neck
including oral mucosa

 It

develops into vesicles
ulcerations

 Lesions

pustular

heal after several weeks

 Secondary

infection is common


Clinical features (Herpes Zoster)
• Involvement of 5th nerve result in unilateral oral, facial,
and ocular lesions
• Prodromal symptoms of pain or paresthesia
maculo-papular rash
vesiculo-bullae
Ulcerations
heal after several weeks
• Complications include
• secondary infection
• Post-herpetic neuralgia
• Motor paralysis
• Ocular inflammation

Hunt’s Syndrome
A

special type of herpes zoster
infection with involvement of the
external ear and oral mucosa
(facial and auditory nerves)

Histopathology
 The

same as those seen in HSV

 Virus

infected epithelial cells

 Homogenous
 In

nuclei

uncomplicated cases, epithelium
regenerates with little or no scar


Differential diagnosis

 HSV

infection:

• Clinical features
• Virus antigen typing using
immunologic tests


Treatment
 Varicella:
• Supportive therapy
• In immunocompromised patients more
substantial measures are indicated

 Herpes

zoster:

• The same for HSV but in high dose
• Acyclovir 800 mg x 5 x 7 to 10 days
• Analgesics

 Corticosteroids

are contraindicated

Hand foot & mouth disease
 Coxsackie

virus

• CV type A
• CV type B

 A16,

and occasionally A5, A9, A10, B2
and B5 cause HFM disease
 HFM is a highly contagious infection
 Virus transmission: through airborne
spread or oral-fecal contamination


Clinical Features
• Affect children under the age 5 years (epidemic)
• Resolve spontaneously after 1 to 2 weeks
• Signs and symptoms of viremia (low grade)
• Oral lesions: multiple vesicles
Ulcers
covered by yellow membrane surround by
erythema
• Occur anywhere of the oral cavity
• Hand and feet lesions are maculopapular
with or shortly after the oral lesions
vesicles
ulcers

Histopathology
 Vesicles

are intraepithelial
 The vesicle cavity filled with
proteinaceous debris and
inflammatory cells


 Primary

HSV infection and varicella:

• Milder symptoms
• Cutaneous distribution
• Virus culture or detection of antibodies



Recurrent Aphthous


Treatment

 Symptomatic


therapy

Herpangina

 Coxsackie

type A (A1-6, A8, A10, A22,
B3 and possibly others)
 Transmission through contaminated
saliva


Herpangina
Clinical Features
 Common in summer and in children
 Pain, malaise, fever, dysphasia and sore throat
 Oral vesicular eruption on the soft palate, faucial
pillars and tonsils
 Pharyngitis
 Lesions last less than 1 week

Herpangina
 HSV

infection, HFM and varicella

• Clinically
• Short duration

 Streptococcal

Pharyngitis

• Vesicular eruption
• Summer presentation
• Mild symptoms

 Aphthous

stomatitis

• Systemic symptoms


Herpangina
Treatment

 Treatment

required


is usually not

Measles (Rubeola)

 Highly

contagious
 Measles virus (DNA paramyxovirus)


Measles (Rubeola)
Clinical Features
 Commonly affect children in winter and spring
 incubation period of 7 to 10 days
 Fever, malaise, conjunctivitis and cough
 After 2 days small macules with white necrotic center
(Koplik’s spots) appear in the buccal mucosa
 After 2 days skin rash appear initially on the head and
neck followed by the trunk and then the extremities

Measles (Rubeola)
Histopathology

 Warthin-Frankeldey

giant cells are
seen in lymphoid tissue
 Infected epithelial cells which become
necrotic


Measles (Rubeola)
Diagnosis
 Usually
•
•
•
•

made on:

Clinical signs and symptoms
Prodromal symptoms
Koplik’s spots
If necessary, serologic test for
antibodies to measles virus


Measles (Rubeola)
M. Rubeola

Rubella (German M.)

• Paramyxovirus Family

• Togavirus Family

• Contagious

• Contagious

• (sever) Fever respiratory
symptoms and rash

• (mild) Fever, respiratory
symptoms and rash

• Koplik's spots

• no Koplik's spots

• Does not cause developmental abnormalities in
the fetus

• Cause developmental
abnormalities in the
fetus


Measles (Rubeola)
Treatment


Supportive treatment:
•
•
•
•

Bed rest
Fluids
Adequate diet
Analgesics


Vesiculo bullous I

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