DD vesicular lesions.ppt

Vesicular lesions

1. PRATHIMA SHETTY

2. Format
oIntroduction & terminologies
oClassifications
oViral infections
HSV infections
Varicella zoster infections
Varicella
Herpes zoster
Hand-foot-and mouth disease
Hoof-and-mouth disease
Herpangina
Small pox

3. Format
Immunological diseases
mucus membrane Pemphigoid
Dermatitis herpetiformis
Dyskeratosis congenita
Acrodermatitis enteropathica
Pemphigus
Erythema multiformae
Miscellaneous
Allergic contact stomatitis
Impetigo

4. Introduction

5. Terminologies
Macule:well-circumscribed, flat lesions that are
noticeable because of their change from normal skin
colour.
Papule: solid lesion raised above the skin surface
that are smaller than 1 cm in diameter.
Plaque:solid raised lesions that are over 1 cm in
diameter.
Nodule:lesions present deep in the dermis, and the
dermis can be easily moved over them.
Vesicle: elevated blisters containing clear fluid that
are under 1 cm in diameter.

6. Bullae:elevated blister like lesions containing clear
fluid that are over 1 cm in diameter
Erosion:moist red lesion often caused by the
rupture of vesicle or bullae as well as trauma.
Pustule:raised lesions containing purulent
material.
Ulcer: A defect in the epithelium; it is a well-
circumscribed depressed lesion over which the
epidermal layer has been lost.
Crust: accumulation on the skin of dried body
secretions like blood, pus or serum.

7. Scales:horny mass flaking from the outer part of
the skin.
Scar:morphological connective tissue replacement
of normal structures of skin or mucosa.
Autoimmune:failure of an organism to recognize
its own constituent parts as "self", which results in
an immune response against its own cells and
tissues.
Eczema:is broadly applied to a range of persistent
or recurring skin rashes characterized by redness,
skin edema, itching and dryness, with possible
crusting, flaking, blistering, cracking, oozing, or
bleeding.

8. Classifications
A] Congenital & inherited disorders
-Epidermolysis bullosa
-Hailey-hailey disease
-Relapsing linear acantholytic dermatolysis
B] Immmunological disorders
1)Intra epidermal
-Pemphigus
2) Subepidermal
-Bullous pemphigoid
-Cicatricial pemphigoid
-Pemphigoid gestationis
-Linear IgA disease
-Epidermolysis bullosa acquisita
-Bullous SLE
-Dermatitis herpetiformis

9. C] Miscellaneous disorders of unknown etiology
-Sub corneal pustulardermatosis
-Intercellular IgAdermatoses
-Acantholyticdermatoses
-Bullaein renal disease
-Diabetic bullae
(Text book of dermatology by Rook, Wilkinson,Ebling)

10. Classification
Intra epithelial vesiculobullouslesions
A) Acantholyticlesions
-Pemphigus vulgaris
-Paraneoplasticpemphigus
-Darrier’sdisease
B)Non-acantholyticlesions
-viral infections
Subepithelialvesiculobullouslesions
-Erethemamultiforme
-Pemphigoid
-Dermatitis herpetiformis & linear IgAdisease
-Epidermolysis bullosa
-Angina bullosahemorrhagica
-Bullous lichen planus
-(Oral pathology by J.V Soames, J.C.Southam)

11. Classification
Viral diseases
•Herpes simplex infections
•V-Z infections
•Hand-foot-and-mouth disease
•Herpangina
•Measles
Associated with Immunological defects
•Pemphigus vulgaris
•Cicatricialpemphigoid
•Bullous pemphigoid
•Dermatitis herpetiformis
Hereditary diseases
•Epidermolysis bullosa
•(Oral pathology by Regezi& Sciubba& Jordan))

12. Classification
The patients with acute multiple lesions
Herpes virus infections
Primary herpes simplex virus infections
Coxsacki virus infections
Varicella-zoster infections
Erythema multiforme
Contact allergic stomatitis
The patient with recurring oral ulcers
Recurrent herpes simplex virus infections
The patient with chronic multiple lesions
Pemphigus
Sub epithelial bullous dermatoses
Herpes simplex virus infection in immunosuppressed patients
(Burkit’s10
th
edition)

13. Herpes simplex virus infections
Human herpes virus
Herpeto viridae
HSV1, HSV2
Other members
Natural reservoir & all HSVs have the ability to reside
within the infected host

14. Vesicular eruptions
two forms
systemic or primary & may be localized or secondary in
nature
HSV1, HSV2 & Varicella-Zoster
Cytomegalovirus –oral ulcerations, salivary gland
disease

15. 4 layers

16. pathogenesis
Physical contact
Heparin sulphate, followed by the activation of specific
genes
Only a small % of individuals shows clinical signs &
symptoms
several days to 2 weeks
Primary lesions-vesicular eruption
After resolution, the virus migrate through unknown
mechanism to trigeminal ganglion

17. Reactivation -exposure to sunlight, to cold, trauma,
stress or immunosuppression
Travels by the way of trigeminl nerve to the originally
infected epithelial surface where replication occurs
The viruses returns to the trigeminal ganglion
Orofacial herpetic lesions

18. Primary herpes simplex virus infections
Children
Vesicular eruption
May appear on any mucosal surface
5-7 days, may range from 2-12 days
Generalized Prodromal symptoms
that precede the local lesions by 1-2 days

19. Small vesicles appear on oral mucosa; Thin walled small
vesicles
As the disease progress, several lesions may coalesce
forming larger irregular lesions
Gingiva –enlarged, painful & erythematous, acute
marginal gingivitis.
Posterior pharynx
After the systemic primary infection
runs its course of about 1 week to
10 days

20. Secondary or recurrent herpes simplex virus
Reactivation of latent virus
Up to 90% have antibodies to HSV & up to 40% of this
group
Prodromalsyndromes in the site in which lesions will
appear
Within a hours, multiple, fragile & short lived vesicles
appear
Unroofed & coalesce to form Map like superficial ulcers

21. Heal without scaring in 1-2 weeks rarely become
secondarily infected
Recurrence is variable
Decline with age with each individual
Typically occur at or near the same site
Herpes labialis
Hard palate & gingiva
1-3mm , with the size of cluster ranging from 1-2cm
Causing discomfort & disfigurement

22. Immune deficiency
Significant pain & discomfort as well as predisposition
to secondary bacterial & fungal infections
A typical, chronic or destructive.
Not site restricted
Larger lesions are more common

23. Herpetic whitlow
HSV infection involving the finger
Medical & dental personnel could infect their digits
Pain, redness & swelling
Vesicles or pustules
4 to 6weeks

24. Diagnosis
Usually made on clinical basis
Confirmation by laboratory methods
Expensive & time consuming

25. H/F
Intra epithelial blister filled with fluid
Swollen & have pale eosinophelic cytoplasm
Ballooning degeneration
Lipschutz bodies
Eosinophilic, ovoid, homogeneous structures within
the nucleus, chromatin peripherally
Vesicles containing exudates, inflammatory cells

26. Cytology
Giemsa, wright’sor papanicolaou’sstain
Multinucleated giant cells, syncytium& ballooning
degeneration of the nucleus
Fluorescent staining of cytology smears are has been
shown more senstive(83%) compared with routine
cytology (54%)
Multinucleated Giant cells

27. i
HSV Isolation
Isolation & neutralization of a virus in tissue culture is
the most +ve method of identification
Antibody titers
Testing for Complement –fixing or neutralizing
antibody in acute & convalescent sera
Rarely necessary in routine clinical situations

28. D/D
Primary herpes simplex virus infections
Streptococcal pharyngitis
Hand-foot-& mouth disease
Erythema multiforme
ANUG or Vincent's infection
Herpengina
Food or drug allergy
Secondary herpes virus infections
Herpes zoster
Pemphigus
Benign mucus membrane pempigoid
Apthous stomatitis
Chelitis granulomatosis

29. Management
Supportive treatment
Oral rehydration –Electrolytic Balance
Fever
Dyclonine hydrochloride 0.5%, if not available dypin
hydramine hydrochloride5mg/ml mixed with magnesia
Infants
Oral hygiene Maintenance
Chlorhexidine mouth wash

30. Curative Treatment
Timing is important
Acyclovir and its analogs
Inhibits DNA replication, decreases days of fever, pain,
lesions & viral shedding
Antiviral treatment
Axovir200mg 1-1-1-1-1 x 5 days
(Acyclovir)
Valacyclovir250mgtwice daily & Famciclovir250mg for
preventing genital recurrences
HIV +vepatients
Corticosteroids are CI

31. Preventive treatment
Patient should be isolated
If affected child has multiple siblings
Utensils should be kept separate
HSV vaccine
Live vaccines
Inactivated vaccines (Lupidon)
Nucleic acid based vaccines(DNA vaccine)

32. HSV vaccines
Should be given early in life
Prevent productive infection does not prevent latent infection
Importantly, recent epidemiological data indicate that HSV
infection increases the rate of HIV transmission twofold.
Current Herpes Simplex Virus Vaccine Approaches—A Short Reviewa report
byE l i z a b e t h E B r i t t l e and Har vey M Friedman Division of Infectious
Diseases, University of Pennsylvania

33. Herpvac vaccine
Preventing HSV-2 infection
The vaccine has only been shown to be effective for women
who have never been exposed to HSV-1.
BioVex, are involved in immune evasion and reduction of
immunogenicity
Current Herpes Simplex Virus Vaccine Approaches—A Short Reviewa
report byE l i z a b e t h E B r i t t l e and Har vey M Friedman
Division of Infectious Diseases, University of Pennsylvania

34. Varicella-zoster infection
Varicella or chicken pox
Herpes zoster or shingles
Pathogenesis
The inhalation of contaminated droplets
Contagious
Virus proliferates within macrophages, with subsequent
viremia & dissemination to the skin & other organs
Host defense mechanisms of nonspecific interferon
production
As the viremia overwhelms body defenses, systemic signs &
symptoms develop

35. Primary diseases or chicken pox
Self limiting, common in children
Vesicular eruption (in crops)
Fever, malaise, pharyngitis & rhinitis etc
Face & trunk, followed by involvement of extremities
Erythema, vesicles, pustules & hardened crust

36. Early vesicular stage
Surrounded by a zone of erythema & has been described
as “ a due drop on a rose petal.”
Contagious
Oral lesions are fairly common & may precede the skin
lesions
Most frequently involve sites
Occasionally there are gingival lesions

37. Complications
More frequent in in adult patient
Pnemonitis, encephalitis & inflammation of other organs
Fetal abnormalities may occur
Typically Ataxia but may result in head aches, drowsiness,
convulsions or coma
Dry cough & chest pain
Congenital or neonatal chicken pox
Spontaneous abortion or congenital defects

38. H/F
Identical to HSV
Acantholysis , with formation of numerous free-floating
Tzanck cells, which exhibit nuclear margination of
chromatin & occasional multinucleation
D/D
HSV
Herpengina
HFM disease

39. Diagnosis
History of exposure & by the type & distribution of lesions
Cytologic changes are identical HSV.
Virus antigen typing using laboratory immunologic tests (
eg ; immunohistochemistry or DNA in situ hybridization)
Treatment & prognosis
Supportive therapy
In immunocompromised patients more substantial
measures are warranted
Virus –specific drugs
Acyclovir, vidarabine & human leukcyte interferon

40. Herpes zoster
Older adult population & who have compromised immune
responses
Transported to sensory nerves & establish latency in dorsal
spinal ganglia
Occurs after reactivation of virus
Uncommon, immunosuppressive states,
drug administration or HIV infection.
Radiation or surgery of spinal cord or local trauma

41. Prodromal symptoms
Vesicular skin eruption
Lasts several weeks & may be followed by post herpetic
neuralgia, local hyper pigmentation
The sensory nerves are commonly effected
Unilateral oral facial or ocular lesions
Ramsay hunt syndrome

42. Prodromal pain is present 1 to 4 days before the
development of cutaneous or oral lesions
Cluster of vesicles with erythematous base within 3-4days
vesicles beome pustular & ulcerate with crust developing
after 7-10 days
Scarring is not un common

43. Follow the path of the affected nerve & terminate at the
midline
Post herpeuticneuralgia
Ocular involvement is usual
Oral lesions occur with trigeminal nerve involvement
Lesion often extend the midline
Individual lesion present as 1-4mm white opaque vesicles
Involvement of maxilla
Significant bone necrosis with loss of teeth

44. H/F
Microscopically identical to those seen in primary
infections varicella
D/D
Recurrent HSV infections
HFM disease

45. Diagnosis
Viral cultures
Cytologic smears demonstrate viral cytopatologic effects
Use of direct staining of cytologic smears with fluorescent
monoclonal antibodies for VZV

46. ```````````````
Treatment
Shortening the course of the disease, preventing
posttherepetic neuralgia & preventing dissemination
Acyclovir or newer anti herpes drugs accelerate healing &
reduce acute pain
Effective therapy includes application of capsaicin
Topical capsaicin
Tricyclic antidepressant or gaba pentin
Chemical or surgical neurolysis may be necessary in
refractory cases
Oral corticosteroids provide symptomatic relief but do not
reduce the risk of post herpetic neuralgia

47. Varicella –zoster vaccines
There are two types of varicella vaccines:
chickenpox vaccine
shingles vaccine
[A vaccine (Proquad) for children ages 1 -12 years now
combines measles, mumps, rubella, and varicella in one
product.]

48. Recommendations for the Chickenpox Vaccine in Adults
Those with high risk of exposure or transmission
People in contact with those who have compromised immune
systems
Nonpregnant women of childbearing age
International travellers
Shingles Vaccine
The zoster vaccine (Zostavax) is a stronger version of the
chickenpox vaccine

49. Varicella-Zoster Immune Globulin
Pregnant women
Newborn infants
Premature infants
Immunocompromised children and adults with no
antibodies to VZV
bone-marrow transplants
debilitating disease

50. Hand –foot –and-mouth disease
Picorna virus is the coxsackie group
Certain coxsackie subtypes cause oral vesicular eruptions:
Highly contagious, coxsackie type A16 less frequently by
types A5, A6 & occasionally even by B2, B5 or entero virus 71
Air born spread or fecal-oral contamination with subsequent
viremia
Common sites

51. C/F
Young children
Mucopapular, exanthematous & vesicular lesions of the
skin
Hands, feet, legs, arms etc
Common manifestations

52. O/M
A sore mouth & refusal to eat
Small, multiple vesicles & ulcerative oral lesions
Hard palate, tongue & buccal mucosa
Lips, gingiva & pharynx including the tonsils
Vesicular state & eventually become ulcerated & encrusted

53. Laboratory findings
Intra cytoplasmic viral inclusions
In addition, viral isolates may usually be obtained from
throat swabs from vesicular fluid it self
Remarkable rise in acute or convalescent serum antibody
titer to coxsackie A16

54. D/D
Primary herpetic gingivostomatitis
Varicella
Treatment
Symptomatic treatment, bland mouth rinses such as
sodium bicarbonate in warm water

55. Foot & mouth disease
( Apthous fever, hoof –and –mouth disease, epizootic -
stomatitis)
Rarely affects man
Contact with infected animals
C/F
Fever, nausea, vomiting, malaise & appearance of ulcerative
lesions
Vesicles on the skin also occurs in some cases, most
commonly on the palm & soles

56. O/M
Any site, more chiefly affected areas
Begin as small vesicles, which rapidly rupture, but heal
usually within two weeks
D/D
HFMD
Treatment

57. Herpangina
(Apthous pharyngitis, vesicular pharyngitis )
Another coxsackietype A( type A1-6 , A8,A10, A22,B3 & possibly
others)
Contaminated saliva
C/F
Frequently occurs in sporadic outbreaks
2-10 days
Young children
Chiefly a summer disease
Comparatively mild & of short duration

58. Sore throat, cough, rhinorhea, low grade fever, headache,
sometimes vomiting, abdominal pain
Vesicles ,rupture to form crops of ulcers
Grey base & inflamed periphery
Vesicles preceding the ulcers are small & of short duration
Not extremely painful
Heal within 7-10 days

59. D/D
Historical & clinical
Herpetic gingivostomatitis, HFM disease & varicella
Apthous stomatitis
Lympho nodular pharyngitis
Treatment

60. Small pox ( variola)
Was epidemic in nature & accounted for literally millions
of death
C/F
After incubation period, manifests high fever, nausea,
vomiting, chills & headache
Skin lesions first appear on the face, but rapidly spread to
cover much of the body surface
Papule –vesicles –pustule
Small, elevated, & yellowish green with an inflamed border
Secondarily infected

61. O/M
Ulceration
Multiple vesicles
Tongue swollen & painful
D/D
Chicken pox
Drug eruptions
Complications
Secondary infections. Abscesses formation, septicemia , as
well as respiratory infection & infections of eye & ear

62. Comparison b/w vesicular viral lesions
Disease Area involved prodroml
symptoms
Incubation Treatment
Primary herpes
virus infection
Face ,lips,
gingivitis,
upper body
skin
precede local
lesions by 1-2
days
5-7days,
ranging from2-
12days
Self limiting
heal within1
week
Secondary
herpes
infection
Perioral skin,
lips, gingiva
,palate
Pain ,tingling,
burning
precede lesion
by 1hr
Possible control
with Acyclovir
Varicella Head ,trunk ,
face& neck in
crops
Fever , malaise,
pharyngitis &
rhinitis
2 weeks symptomatic
Herpes zosterUnilateral
distribution
Pain &
paresthesia of
involved nerve
site
Anti herpes
drugs, useof
corticosteroid
is controversial

63. Comparison b/w vesicular viral lesions
Hand foot
mouth disease
Hands,feet ,
legs, arms
Anorexia , low
grade fever,
coryza,
diarrhea,
lymphdenopat
hy
Symptomatic
Hoof & mouth
disease
Lips, tongue,
palate,
oropharynx&
skin in some
cases
Fever, nausea,
vomiting &
malaise
Self limiting
Herpangina Anterior faucial
pillars,
sometimes on
hard palate
Sore throat,
cough
rhinohorhea,
abdominal pain
2-10 days Not required
Small pox Oral mucosa&
pharynx
trachea,
esophagus ete
Fever ,nausea
vomiting ,chills
& head ache
7-10 days Self limiting

64. END OF PART 1

65. REFERENCES
Differential diagnosis of oral & maxillofacial
lesions, NORMAN K WOOD & PAUL W . GOAZ
Burket’s oral medicine (10
th
addition )
Oral and maxilofacialpathology (Neville, Damm, Allen)
Text book of dermatology by Rook, Wilkinson,Ebling
Oral pathology by J.V Soames, J.C.Southam
Shafer’s text book of oral pathology (5
th
adition)
Oral pathology by Regezi& Scuiubba