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ULCERATIVE AND INFECTIVE
VESICULOBULLOUS LESIONS
PRESENTERS:
SSEMAGANDA ADDINAN
RAJAB CHAKA TUI
NAMUWAYA SUMAYA
Learning Objectives
Definition
Classification
Etiology
Clinical manifestation, differential diagnoses and
management
CLASSIFICATION OF INFECTIVE
VESICULLOBULLOUS LESIONS
 Based on etiology – viral, fungal and bacterial
Viral – Herpes simplex 1,cytomegalo virus, varicella zoster,
coxsackie virus, hand-foot-and-mouth disease,
herpangina and NUG & NUP. Also (acute and multiple)
Bacterial- syphilis, tuberclosis
Fungal- histoplasmosis, blastomycoses, mucomycoses
(Also they are single
single ulcers)
 Based on the length of time - Acute or Chronic
 Based on number of lesions – Single or Multiple
 Recurent – herpes labialis infection
VIRAL INFECTIOUS LESION
 Herpes simplex virus (HSV) infection
 Etiology - HSV 1 (lesions above the waist) and 2 (below the waist).
 Transmission - contact of the virus through secretions from mucosa, skin and eyes.
 Age – common children 6mon-5years.
 Pathogenesis - travels through sensory nerve and axons up to sensory ganglion where it
establishes chronic latent infection.
In case of recrudescent HSV on the lips is called recurrent
herpes labialis.
 Clinical manifestation – normally it is self limiting, resolves
in 10-14 days.
CONT …
Early symptoms of fever, headache, myalgia and loss of appetite.
 Oral findings
Primary gingivostomatitis
Pharyngotonsolitis
Erythema and clusters of vesicles
Later ulcers appear on keratinized mucosa(hard palate, gingiva and dorsum
of the tongue) non keratinized mucosa (buccal, labial and ventral of the
tongue)
 Differentials- cosaxkie virus and necrotizing ulcerative gingivitis.
 Lab test- HSV culture, PCR, direct fluorescent antigen
 Management- control pain, supportive care and antivirals (acyclovir)
Fungal Infectious Lesions
 HISTOPLASMOSIS.
 Etiology and Pathogenesis - Fungus Histoplasma capsulatum, a dimorphic fungus that grows in
yeast form in infected tissue. The infection results from inhaling dust contaminated with infected
bats or birds.
 Clinical manifestation – it’s a self limiting pulmonary disease primarily
In progressive disease, it results in cavitation
and dissemination
Mostly common in HIV/AIDs patients
CONT …
 Oral Findings.
 Begin as an area of erythema that forms a papule and
eventually form a painful granulomatous lesion.
 Cervical lymphnodes are alyways enlarged and firm
 Differential Diagnosis
 TB lesions
 Squamous cell carcinoma
 Lymphoma
CONT …
 Smear
 Culture
 PCR and DNA Probes
 Management
 Supportive, definitive treatment
Blastomycosis
 Etiology and Pathogenesis
Caused by Blastomyces dermatitidis. Found in soil mostly affects agricultural and
construction workers. It begins by inhalation of fungus then later primary pulmonary
infection that’s self limiting
 Clinical manifestations
The primary infection is always asymptomatic, always follows a chronic course with mild
symptoms like malaise, low grade fever and mild cough
If untreated, it can worsen to shortness of breath, blood sputum and weight loss. Can
metastatise through the lymphatic system.
 Oral findings
Non specific painless verricous ulcers with indulated boarders
Hard nodules and radioluscent jaw lesions
CONT …
 Investigations
Culture, serology basing on enzyme immune assay
 Management
Drugs like ketoconazole, fluconazole or itraconazole for mild
disease and amphotericin B in severe cases
Mucormycosis
Etiology and pathogenesis
 An infection of a saprophytic fungus that occurs in soil or as a mold on decaying
food
 Its an opportunistic infection and rarely a pathogen
 Clinical manifestations
 It occurs in patients with decreased host resistance
 In rhinomaxillary form of the fungus is inhaled and invades the arteries and
cause damage due to thrombosis.
 Oral findings
 Ulceration of d palate, gingiva, lip alveolar ridge
 The lesion is large and deep causing denudation of the underlying bone.
 Necrosis and occlusion of vessels.
CONT…
 Investigations
Culture
Biopsy
 Management
Debridement of the infected area and systemic administration of amphotericin b
for 3 months
Proper management of the underlying disorder.
Palatal Mucormycosis
Oral candidiasis
 Etiology and pathogenesis
 3 pieces c albicans ctropicalis c glabrata
 Most common cause is Candida albicans
 Microorganism must adhere to the epithelial surfaces then penetrate by their produced lipases
 Local Predisposing conditions
 Denture wearing
 Smoking
 Inhalation steroid
 Topical steroids
 quality and quantity of saliva
General predisposing factors
 Immunosuppressive disease
 Impaired health status
 Chemotherapy
 Endocrine disorders
 Classification of oral candidiasis
 Erythematous candidiasis
 It applies to patchy red mucosal macules due to c albicans infection in HIV
 Mostly affects the hard palate, dorsum of the tongue and soft palate
 Pseudomembranous candidiasis
 Common in infants and HIV infected
Thrush
 Thrush forms soft friable and creamy coloured plaques of mucosa.
 They can easily be wipped off and at times cause bleeding
 Mostly common in HIV pts and those on steroid inhalers
 Management
 Control the local cause
 Nystatin lozenges
 Fluconazole to the immune suppressed
Denture induced stomatitis
 Denture induced stomatitis
 Candidal infection caused by well fitting denture
 Enclosed mucosa is cut off of salivary protection mucosal
erythema is restricted to areas covered by the denture.
 Angular stomatitis frequently associated
 Show gram positive hyphae
 They resolve after elimination of c albicans with antigungal
treatment
CONT …
 Angular stomatitis
 Oral candidiasis associated with HIV
 Most common type is pseudomembranous
candidiasis,erythematous candidiasis angular chelitis and chronic
hyperplastic candidiasis
 Clinical manifestations
 Secondary oral candidiasis accompanied by systemic
mucocutanous candida and other immune deficiencies
 Management
 Identify the predisposing factor and treat
 Use antifungal drugs.
VARICELLA ZOSTER VIRUS (vzv)
INFECTION
 Etiology and pathogenesis
Caused by varicella virus
Primary infection is chicken pox (varicella) and latency reactivation
produces HZI (shingles).
Transmission is through oral route and establishes in the dorsal root
ganglia of cranial nerves (mainly the trigeminal nerve).
 Age – children in varicella
adults and elderly in herpes zoster
For HZI mainly affects the elderly and immunosuppressed.
CONT…
 Clinical features- low grade fever, malaise, intense pruritic
maculopapular rash, early onset of vesicles which rapidly rapture and
leave erosions.
Vesicular eruption follows the distribution of sensory nerves, segmental and
unilateral.
Resolution in 2-4 weeks
If its disseminate- cerebellar ataxia, encephalitis, myocarditis.
In HZI – facial palsy, acute retinal necrosis and postherpetic neuralgia.
Oral findings-
 Differentials- HSV, Pemphigus or Pemphigoid and NUP.
 Investigations- culture, PCR, direct fluorescent antibody
 Management – pain control(ibuprofen), acyclovir and valacyclovir.
CYTOMEGALOVIRUS INFECTION
 Etiology and pathogenesis.
 Transmission- from person to person through intimacy,
blood products and organ transplant.
Establishes latency in connective tissue cells.
 Clinical features
 fever, malaise, myalgia
 Thrombocytopenia, lymphocytosis, meningoencephalitis
 Can be life threatening in children and it’s more common in
AIDS people.
CONT…
 Oral findings
In immunocompromised people – painful single necrotic large ulcer
at any site present for weeks or months.
Mandibular osteomyelitis and exfoliation of teeth.
 Differentials- HSV, VZV, Squamous cell carcinoma
 Investigations- biopsy, PCR, blood culture (systemic infection).
 Management
The infection resolves spontaneously in immunocopetent people.
In immunocompromised-Ganciclovir, valganciclovir
Topical anesthetic for ulcerative lesion pain
COXSACKIEVIRUS(CV)
INFECTIONS.An RNA virus in the family of picornaviridae.
Coxsackie virus A & B
Transmission – fecal-oral.
Virus replicate in the mouth then extend to lower GI where
shedding takes place.
In oral cavity CV infections leads to 3 diseases
 Hand foot and mouth disease(HFM)
 Herpangina
 Lymphonodular pharyngitis
HAND FOOT AND MOUTH
DISEASE(HFM)
Common cause CV-A 16
A common children’s virus causing mouth sores and rashes on
the hands and feet.
Transmission- direct mucous or saliva contact
Clinical features
Low grade fever, skin rash (red macular then becomes
vesicular) on hands, feet and buttocks.
Oral manifestation- sore mouth and throat, vesicles leading to
ulcers on tongue, hard and soft palate and buccal mucosa.
Rashes in Hand foot and Mouth disease
HERPANGINA
Vesicular eruption and throat inflammation
 Etiology-Caused by CV-A(serotypes 1-10,16 & 22), CV-B 1 and
echovirus.
 Age – below 10 yrs
 Clinical features
Fever, headache and myalgia which last for 3 days
 Oral manifestation
Sore throat, pain on swallowing
Erythema of oropharynx and soft palate
Small vesicles rapidly break down to form 2-4mm ulcers
LYMPHONODULAR PHARYNGITIS
A variant of herpangina, associated with CV-A 10
 Clinical features
Sore throat with nodules like vesicles in the oropharynx.
 Differentials for HFM
Primary herpetic gingivostomatitis
Primary HSV
Streptococcal infection
Infectious mononucleosis
CONT…
 Investigations
EV-B culture from throat or fecal matter
Reverse transcriptase PCR
Biopsy
 Management
CV infections are self limiting
Control fever, mouth pain with topical anaesthetics
Non-asprin antipyretics
Bacterial Oral Lesions
TUBERCULOSIS
 Etiology
caused by the acid and acohol bacillus M.Tuberculosis
 Pathogenesis
Typical tuberculous granulomas are seen in the flow of the ulcers. Mycobacteria are rarely identifiable in the
oral lesion
 Age Oral TB is ocassionally seen in immunocompetent persons who are usuall elderly men with pulmonary
infection and a chronic cough that has progressed unrecorgnised or who have neglected treatment.
 Clinical manifestations
Painless lessions in the early stages, lymphnodes usually not affected
 Oral findings
Typical Angular shape or stellate and over hanging edges of the ulcers of the toungue
CONT…
 Diagnosis
Biobsy, chest radiography and specimen of sputum
 Investigations
PCR and culture
 Management
Multi drug chemotherapy for pulmonary infection
TB LESIONS
TB Ulcer on the tip of the toungue
SYPHILS
 Etiology; It is caused by a spirochete bacteria called Treponema pallidum
 Pathogenesis; in primary syphilis, an oral chancre appears 3-4 weeks after infection and
may form on the lip-tip of the tongue or rarely other oral sites.
The secondary stage develops 1-4 months after infection.
Late stage syphilis develops in many patients about 3 or more years after infection.
Age; all age groups but commonly in young adults who are sexually active
 Clinical manifestations; oral lessions in each stage of syphilis are quite different from
each other. In primary, it consists initially of a firm nodule about a centimetre across. In
secondary, it typically causes mild fever with malaise, headache etc.
In tertiary, the onset is insidious and during the latent period, patient may appear well.
CONT…
 Oral findings
Primary chancre in primary syphilis. In seconsary, there are oral lessions rarely
appearing without the rash and mainly affecting the tonsils.
 Diagnosis
Depends on serological tests for syphilis, VDRL, RPR, FTA,ABS
 Investigations
TPHA,FTA-Abs, ELISA
 Management
Antibiotics.
Secondary syphils
GONORRHEOA
 SDL
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Ulcerative and infective vesiculobullous lesions

  • 1. ULCERATIVE AND INFECTIVE VESICULOBULLOUS LESIONS PRESENTERS: SSEMAGANDA ADDINAN RAJAB CHAKA TUI NAMUWAYA SUMAYA
  • 3. CLASSIFICATION OF INFECTIVE VESICULLOBULLOUS LESIONS  Based on etiology – viral, fungal and bacterial Viral – Herpes simplex 1,cytomegalo virus, varicella zoster, coxsackie virus, hand-foot-and-mouth disease, herpangina and NUG & NUP. Also (acute and multiple) Bacterial- syphilis, tuberclosis Fungal- histoplasmosis, blastomycoses, mucomycoses (Also they are single single ulcers)  Based on the length of time - Acute or Chronic  Based on number of lesions – Single or Multiple  Recurent – herpes labialis infection
  • 4. VIRAL INFECTIOUS LESION  Herpes simplex virus (HSV) infection  Etiology - HSV 1 (lesions above the waist) and 2 (below the waist).  Transmission - contact of the virus through secretions from mucosa, skin and eyes.  Age – common children 6mon-5years.  Pathogenesis - travels through sensory nerve and axons up to sensory ganglion where it establishes chronic latent infection. In case of recrudescent HSV on the lips is called recurrent herpes labialis.  Clinical manifestation – normally it is self limiting, resolves in 10-14 days.
  • 5. CONT … Early symptoms of fever, headache, myalgia and loss of appetite.  Oral findings Primary gingivostomatitis Pharyngotonsolitis Erythema and clusters of vesicles Later ulcers appear on keratinized mucosa(hard palate, gingiva and dorsum of the tongue) non keratinized mucosa (buccal, labial and ventral of the tongue)  Differentials- cosaxkie virus and necrotizing ulcerative gingivitis.  Lab test- HSV culture, PCR, direct fluorescent antigen  Management- control pain, supportive care and antivirals (acyclovir)
  • 6. Fungal Infectious Lesions  HISTOPLASMOSIS.  Etiology and Pathogenesis - Fungus Histoplasma capsulatum, a dimorphic fungus that grows in yeast form in infected tissue. The infection results from inhaling dust contaminated with infected bats or birds.  Clinical manifestation – it’s a self limiting pulmonary disease primarily In progressive disease, it results in cavitation and dissemination Mostly common in HIV/AIDs patients
  • 7. CONT …  Oral Findings.  Begin as an area of erythema that forms a papule and eventually form a painful granulomatous lesion.  Cervical lymphnodes are alyways enlarged and firm  Differential Diagnosis  TB lesions  Squamous cell carcinoma  Lymphoma
  • 8. CONT …  Smear  Culture  PCR and DNA Probes  Management  Supportive, definitive treatment
  • 9. Blastomycosis  Etiology and Pathogenesis Caused by Blastomyces dermatitidis. Found in soil mostly affects agricultural and construction workers. It begins by inhalation of fungus then later primary pulmonary infection that’s self limiting  Clinical manifestations The primary infection is always asymptomatic, always follows a chronic course with mild symptoms like malaise, low grade fever and mild cough If untreated, it can worsen to shortness of breath, blood sputum and weight loss. Can metastatise through the lymphatic system.  Oral findings Non specific painless verricous ulcers with indulated boarders Hard nodules and radioluscent jaw lesions
  • 10. CONT …  Investigations Culture, serology basing on enzyme immune assay  Management Drugs like ketoconazole, fluconazole or itraconazole for mild disease and amphotericin B in severe cases
  • 11. Mucormycosis Etiology and pathogenesis  An infection of a saprophytic fungus that occurs in soil or as a mold on decaying food  Its an opportunistic infection and rarely a pathogen  Clinical manifestations  It occurs in patients with decreased host resistance  In rhinomaxillary form of the fungus is inhaled and invades the arteries and cause damage due to thrombosis.  Oral findings  Ulceration of d palate, gingiva, lip alveolar ridge  The lesion is large and deep causing denudation of the underlying bone.  Necrosis and occlusion of vessels.
  • 12. CONT…  Investigations Culture Biopsy  Management Debridement of the infected area and systemic administration of amphotericin b for 3 months Proper management of the underlying disorder.
  • 14. Oral candidiasis  Etiology and pathogenesis  3 pieces c albicans ctropicalis c glabrata  Most common cause is Candida albicans  Microorganism must adhere to the epithelial surfaces then penetrate by their produced lipases  Local Predisposing conditions  Denture wearing  Smoking  Inhalation steroid  Topical steroids  quality and quantity of saliva
  • 15. General predisposing factors  Immunosuppressive disease  Impaired health status  Chemotherapy  Endocrine disorders  Classification of oral candidiasis  Erythematous candidiasis  It applies to patchy red mucosal macules due to c albicans infection in HIV  Mostly affects the hard palate, dorsum of the tongue and soft palate  Pseudomembranous candidiasis  Common in infants and HIV infected
  • 16. Thrush  Thrush forms soft friable and creamy coloured plaques of mucosa.  They can easily be wipped off and at times cause bleeding  Mostly common in HIV pts and those on steroid inhalers  Management  Control the local cause  Nystatin lozenges  Fluconazole to the immune suppressed
  • 17. Denture induced stomatitis  Denture induced stomatitis  Candidal infection caused by well fitting denture  Enclosed mucosa is cut off of salivary protection mucosal erythema is restricted to areas covered by the denture.  Angular stomatitis frequently associated  Show gram positive hyphae  They resolve after elimination of c albicans with antigungal treatment
  • 18. CONT …  Angular stomatitis  Oral candidiasis associated with HIV  Most common type is pseudomembranous candidiasis,erythematous candidiasis angular chelitis and chronic hyperplastic candidiasis  Clinical manifestations  Secondary oral candidiasis accompanied by systemic mucocutanous candida and other immune deficiencies  Management  Identify the predisposing factor and treat  Use antifungal drugs.
  • 19. VARICELLA ZOSTER VIRUS (vzv) INFECTION  Etiology and pathogenesis Caused by varicella virus Primary infection is chicken pox (varicella) and latency reactivation produces HZI (shingles). Transmission is through oral route and establishes in the dorsal root ganglia of cranial nerves (mainly the trigeminal nerve).  Age – children in varicella adults and elderly in herpes zoster For HZI mainly affects the elderly and immunosuppressed.
  • 20.
  • 21. CONT…  Clinical features- low grade fever, malaise, intense pruritic maculopapular rash, early onset of vesicles which rapidly rapture and leave erosions. Vesicular eruption follows the distribution of sensory nerves, segmental and unilateral. Resolution in 2-4 weeks If its disseminate- cerebellar ataxia, encephalitis, myocarditis. In HZI – facial palsy, acute retinal necrosis and postherpetic neuralgia. Oral findings-  Differentials- HSV, Pemphigus or Pemphigoid and NUP.  Investigations- culture, PCR, direct fluorescent antibody  Management – pain control(ibuprofen), acyclovir and valacyclovir.
  • 22. CYTOMEGALOVIRUS INFECTION  Etiology and pathogenesis.  Transmission- from person to person through intimacy, blood products and organ transplant. Establishes latency in connective tissue cells.  Clinical features  fever, malaise, myalgia  Thrombocytopenia, lymphocytosis, meningoencephalitis  Can be life threatening in children and it’s more common in AIDS people.
  • 23. CONT…  Oral findings In immunocompromised people – painful single necrotic large ulcer at any site present for weeks or months. Mandibular osteomyelitis and exfoliation of teeth.  Differentials- HSV, VZV, Squamous cell carcinoma  Investigations- biopsy, PCR, blood culture (systemic infection).  Management The infection resolves spontaneously in immunocopetent people. In immunocompromised-Ganciclovir, valganciclovir Topical anesthetic for ulcerative lesion pain
  • 24.
  • 25. COXSACKIEVIRUS(CV) INFECTIONS.An RNA virus in the family of picornaviridae. Coxsackie virus A & B Transmission – fecal-oral. Virus replicate in the mouth then extend to lower GI where shedding takes place. In oral cavity CV infections leads to 3 diseases  Hand foot and mouth disease(HFM)  Herpangina  Lymphonodular pharyngitis
  • 26. HAND FOOT AND MOUTH DISEASE(HFM) Common cause CV-A 16 A common children’s virus causing mouth sores and rashes on the hands and feet. Transmission- direct mucous or saliva contact Clinical features Low grade fever, skin rash (red macular then becomes vesicular) on hands, feet and buttocks. Oral manifestation- sore mouth and throat, vesicles leading to ulcers on tongue, hard and soft palate and buccal mucosa.
  • 27. Rashes in Hand foot and Mouth disease
  • 28. HERPANGINA Vesicular eruption and throat inflammation  Etiology-Caused by CV-A(serotypes 1-10,16 & 22), CV-B 1 and echovirus.  Age – below 10 yrs  Clinical features Fever, headache and myalgia which last for 3 days  Oral manifestation Sore throat, pain on swallowing Erythema of oropharynx and soft palate Small vesicles rapidly break down to form 2-4mm ulcers
  • 29. LYMPHONODULAR PHARYNGITIS A variant of herpangina, associated with CV-A 10  Clinical features Sore throat with nodules like vesicles in the oropharynx.  Differentials for HFM Primary herpetic gingivostomatitis Primary HSV Streptococcal infection Infectious mononucleosis
  • 30. CONT…  Investigations EV-B culture from throat or fecal matter Reverse transcriptase PCR Biopsy  Management CV infections are self limiting Control fever, mouth pain with topical anaesthetics Non-asprin antipyretics
  • 31. Bacterial Oral Lesions TUBERCULOSIS  Etiology caused by the acid and acohol bacillus M.Tuberculosis  Pathogenesis Typical tuberculous granulomas are seen in the flow of the ulcers. Mycobacteria are rarely identifiable in the oral lesion  Age Oral TB is ocassionally seen in immunocompetent persons who are usuall elderly men with pulmonary infection and a chronic cough that has progressed unrecorgnised or who have neglected treatment.  Clinical manifestations Painless lessions in the early stages, lymphnodes usually not affected  Oral findings Typical Angular shape or stellate and over hanging edges of the ulcers of the toungue
  • 32. CONT…  Diagnosis Biobsy, chest radiography and specimen of sputum  Investigations PCR and culture  Management Multi drug chemotherapy for pulmonary infection
  • 34. TB Ulcer on the tip of the toungue
  • 35. SYPHILS  Etiology; It is caused by a spirochete bacteria called Treponema pallidum  Pathogenesis; in primary syphilis, an oral chancre appears 3-4 weeks after infection and may form on the lip-tip of the tongue or rarely other oral sites. The secondary stage develops 1-4 months after infection. Late stage syphilis develops in many patients about 3 or more years after infection. Age; all age groups but commonly in young adults who are sexually active  Clinical manifestations; oral lessions in each stage of syphilis are quite different from each other. In primary, it consists initially of a firm nodule about a centimetre across. In secondary, it typically causes mild fever with malaise, headache etc. In tertiary, the onset is insidious and during the latent period, patient may appear well.
  • 36. CONT…  Oral findings Primary chancre in primary syphilis. In seconsary, there are oral lessions rarely appearing without the rash and mainly affecting the tonsils.  Diagnosis Depends on serological tests for syphilis, VDRL, RPR, FTA,ABS  Investigations TPHA,FTA-Abs, ELISA  Management Antibiotics.
  • 39. THANK YOU FOR LISTENING

Editor's Notes

  1. Normochromic normocytic, susceptible to infection and bleeding tendency often associated SCA: Normocytic
  2. Hypochromic, microcytic Chronic inflammatory: normochromic, normocytic
  3. Normocytic Can acute or chronic Gi hermo, or hypersplenism 2o to portal hyper Def. ofblood coagulation factors syn by hepatocytes
  4. Deter- try to prevent Maternal concerns Fetal concerns Radiography Medication
  5. Anatomical – UW increase from 70gms – 1 kg Volume 10ml-5000ml Supine hypotension – inferior vena cava syndrome CVS- co incre by 40 % TBV 40-50 % HR 10 BPM GIS- esophargeal reflux, constipation, decr gastric mobility RS- U tract infections , nocturnal oedema HS- RBC , PLASMA , BV, increases
  6. Organogenesis- between 2nd to 8th weeks
  7. Hyposalivation- as result of disease s such as Sjogren’s syndrome or the use of drugs with diuretics or antimuscarinic activity
  8. RAS – is uncommon in elderly but if seen should be looked underlying cause Mucosa heals very slowly with age