Oral infections: viral and fungal Flashcards
Viral infections of oral importance (4)
Herpes viruses – Simplex 1 and 2 – Varicella zoster – Cytomegalovirus – Epstein Barr Coxsackie viruses (Measles) Human papilloma virus
What is herpes simplex? (5)
• Enveloped, DNA virus, highly cytolytic, infects via heparan sulphate • Type 1 associated with skin and oral mucous membranes • Type 2 associated with genital mucosa • Transmitted by droplet spread or intimate contact • 90-100% individuals have antibodies to herpes simplex
Herpes simplex type 1 - virus (4)
• Virus enters trigeminal sensory neurones
• Migrates to the ganglion by retrograde axonal flow
• Latency
- 50% of cases lies dormant
Herpes simplex type 1 - reactivation (4)
In 30% of cases virus is reactivated Migrates to peripheral nerve endings Virus is shed Reactivation can be caused by •UV •Stress • Illness •Immunosuppression
Herpes simplex - primary gingivostomatitis - natural history (4)
– Children, young adults – Incubation period 5 days – Heal within 10-14 days – Many cases are subclinical and so asymptomatic
Herpes simplex - primary gingivostomatitis - signs and symptoms (5)
– Malaise and fever – Vesicles which ulcerate – Secondary infection – Erythematous gingivitis – Extra-oral lesions
Diagnosis of herpes simplex - primary gingivostomatitis (2)
- Made on clinical features
* Patients have a rising antibody titre to herpes simplex.
Pathogenesis of herpes simplex - primary gingivostomatitis (3)
– Herpes virus replicates in epithelial cells
– causes epithelial cell destruction and
“ballooning” degeneration of cells
– Results in intra-epithelial vesicles
Clinical features of herpes labialis (5)
– "Cold sore" – Prodromal tingling – Vesicles at the muco-cutaneous junction – Ulcerate and crust over – Lasts 7-10 days
How common is herpes labialis (1)
Occurs in 30% of patients
Main difficulty in diagnosing herpes labialis (1)
Differentiating erythema multiforme
Treatment for herpes labialis (3)
Effective in prodromal stage
Aciclovir cream (Zovirax)
Penciclovir
What is herpes (varicella) zoster virus (4)
Type 3 herpes virus
Primary infection - chicken pox
Secondary lesion - shingles
Most commonly affects one of the divisions of the trigeminal nucleus
3 phases of herpes zoster (3)
Pre-herpetic neuralgia
-pain in the affected division; may mimic dental pain
Rash
-unilateral vesicles; ophthalmic, maxillary, mandibular
-ulcers (mucosa); crusting lesions (skin)
-lasts 2-3 weeks
Post-herpetic neuralgia
-burning pain, affects 10-20%
-more common in the elderly
Management of herpes zoster (4)
Aciclovir 800mg 5x daily, 7 days – Valaciclovir 1g 3x daily, 7 days – Famciclovir 250mg 3x daily, 7 days Analgesics and other supportive measures Referral to Ophthalmology if eye involved Post-herpetic neuralgia – Treat pain with neuropathic pain drugs – Gabapentin, antidepressants
What is Epstein-Barr virus? (5)
HV4 Infectious mononucleosis -tonsils -petechiae on soft palate -cervical lymphadenopathy Burkitt's lymphoma Nasopharyngeal carcinoma Hairy leukoplakia
Oral hairy leukoplakia (4)
Corrugated white patches
Bilateral on lateral borders of tongue
Seen in 25% of HIV infected patients
Can occur in non-HIV patients
Diagnosis of oral hairy leukoplakia (1)
Demonstration of EBV in tissues
Pathogenesis of cytomegalovirus (HV5) (2)
Inclusion bodies
Dormant in lymphocytes - interferences with MHC1 presentation
Rare appearances of HV5 (2)
Glandular fever-like illness (no lymphadenopathy)
Salivary gland swelling
HV5 in immunocompromised (3)
Large ragged oral mucosal ulcers
Salivary gland swelling
Retinitis
HV5 in new born (1)
Life threatening
Cocksackie A viruses - which cause the most problems? (4)
Types 4, 5, 10, 16
Cocksackie A viruses - herpangina (6)
– CVA4 (occ. Others) – Usually trivial; mild febrile illness – Young children and young adults – Vesicles and ulcers on soft palate – Lasts a few days – Usually no treatment • analgesic mouthwash • e.g Difflam
Cocksackie A viruses - hand, foot and mouth disease (4)
– CV A16 – Similar to herpangina; mild systemic upset – Rash/vesicles on palms of hands and soles of feet – Intra-oral vesicles and ulcers
Measles - what is it and features (5)
Paramyxovirus infection Systemically unwell Koplik’s spots – White papules on buccal and palatal mucosa during prodromal phase Skin rash Long term effects
HPV - types (4)
> 40 types DNA virus - just 9 genes Only infects keratinocytes -basal cells - integrins "High risk" oncogenic subtypes -HPV 16 & 18 -cervica, oropharynx and anal cancer
HPV - main oral lesions include (4)
Squamous cell papilloma/ verruca vulgaris
Condyloma accuminatum
Focal epithelial hyperplasia
• HPV13
• Common in small native communities and HIV infection
• Treatment – excision, imiquimod 5% cream
Dysplasia/SCC - controversial
Fungal infections (7)
- Aspergillosis
- Blastomycosis
- Candidosis
- Coccidioidomycosis
- Cryptococcosis
- Histoplasmosis
- Rhinosporidiosis
Candida species (5)
- C.albicans - most common
- C.tropicalis
- C.krusei
- C.glabrata
- C.dubliniensis
Predisposing factors to candida (4)
Prostheses - no exfoliation
Low saliva
Antibiotics - reduced bacterial competition
Immuno-suppresion
Predisposing factors to candida - low saliva (3)
No flow; reduces soluble defences
Low pH induced by high sugar diet
Predisposing factors to candida - Immuno-suppresion (6)
– Very young/old – Diabetes – Corticosteroids, including steroid inhalers – Malignancy – HIV – Immunosuppressive therapy
Pathogenic/ virulence factors (3)
Tissue invasion and pathogenesis
Yeast to hyphal transition and growth is essential for virulence and pathogenesis
Hyphae secrete candidalysin - a pore forming toxin that kills human cells and also initiates an immune response
Proteases - Secreted Aspartyl Proteases (SAP) used to invade between/ through epithelial cells
-sap 1-3 - needed for mucosal infection
-sap 1-3 - degrade complement
-sap 4-6 - contribute to systemic infection
Classification of candida infections (4)
Acute forms
Chronic forms
Candida-associated lesions
HIV-related candidosis
Acute forms of candida (2)
– Acute pseudomembranous candidosis (Thrush)
– Acute atrophic candidosis (antibiotic sore mouth)
Chronic forms of candida (3)
– Chronic atrophic candidosis (denture stomatitis)
– Chronic hyperplastic candidosis (candidal leukoplakia)
– Chronic mucocutaneous candidosis (various: inherited syndromes)
Candida-associated lesions (2)
– Median rhomboid glossitis
– Angular cheilitis
Acute pseudomembranous candidosis (2)
Creamy thick white plaques
-thick biofilm of yeast and hyphal forms
Easily rubbed off
Causes of acute atrophic candidosis (2)
– Prolonged corticosteroid or
antibiotic therapy
– Bacterial flora altered, allows candida to flourish
Treatment of acute atrophic candidosis (1)
Reduce antibiotic use if possible
Management of acute atrophic candidosis (3)
Confirm diagnosis – Swab(s) or oral rinse +/- MC+S Investigate and treat underlying cause Treat with anti-fungal agents – Topical • Miconazole oral gel • Nystatin suspension • Amphotericin B (only available in hospital pharmacies) – Systemic • Fluconazole • Itraconazole
Denture related candidosis (3)
Palate protected from saliva Poor denture hygiene Treatment – Improve denture hygiene • Leave out at night • Clean denture and soak in Milton or Corsodyl – Antifungals • Nystatin +/- Miconazole gel to fitting surface tds • 2-3 weeks
Median rhomboid glossitis (5)
• Erythematous area on dorsum tongue • Epithelial proliferation • Candida in epithelium • Not premalignant • Diagnosis usually on clinical grounds
Angular cheilitis (3)
• Reduced vertical dimension – drooling of saliva • Haematological deficiency – Iron, B12, folate deficiency – Crohn’s disease • Some cases associated with Staph. aureus
Treatment of angular cheilitis (2)
– Address underlying cause
– miconazole cream or fusidic acid, depending on cause
Chronic hyperplastic candidosis (5)
• White or red/white patch, nodular • Can’t be rubbed off • Labial commissures or tongue • Premalignant: – “Candida leukoplakia” – up to 25% risk of malignant change. • Diagnosis by biopsy
Aetiology of chronic hyperplastic candidosis (4)
– Usual candida risk factors – Smoking – Not clear if candida cause the lesion or invade a preexisting lesion. – Some lesions regress following antifungal therapy
Management of hyperplastic candidosis (3)
• Diagnosis
– Biopsy will establish diagnosis
– Assess degree of dysplasia and risk of malignant
transformation
• Treatment
– Systemic antifungals
• 7-14 days fluconazole or amphotericin B
– Smoking cessation
• If no improvement and high risk of malignant
transformation then excise