Actinomyces and Candida Flashcards
Morphology and pathogenic features of Actinomyces and Candida species Main pathological conditions caused by these organisms Aspects of treatment
Actinomyces are
Gram-positive filaments, unevenly staining, sometimes showing branching
Actinomyces species
21 species - 5 cause majority of disease in man
- A. israelii
- A. oris (naeslundii)
- A. odontolyticus
- A. gerencseriae
- A. meyeri
A. israelii
Most frequent in actinomycosis
-sometimes with Ag. actinomycetemcomitans
A. oris (naeslundii)
2nd most frequent
A. odontolyticus
Important in caries
A. gerencseriae
Important in caries
A. meyeri
Brain abscess
Actinomyces habitat
Mouth, gut, vagina
Actinomyces culture
Fastidious - usuallu use brain-heart infusion
Microaerophilic/ facultatively anaerobic
Slow growing - 3-7 days, ‘molar tooth’ colonies
Actinomycosis cervicofacial
55-65%
Acute painful
Chronic indolent with sinus
No lymphadenopathy
Abdominopelvic actinomycosis
10-20% ileocaecal; IUDs
Thoracic actinomycosis
Aspiration; farmer’s lung
Cerebral Actinomycosis
Haematogenous spread
Locations of actinomycosis
Cervicofacial
Abdominopelvic
Thoracic
Cerebral
Actinomycosis entry
Mucosal break
Actinomycosis histology
Chronic inflammation, fibrosis, eosinophilic terminal clubs
Actinomycosis in pus
‘Sulphur granules’
Actinomyces pathogenic factors
No toxins, no aggressive enzymes Virulence associated with -induction of chronic inflammation -walling off from defences -slow growth as large aggregates in a matrix
Actinomyces treatment
Attempt at thorough surgical drainage Antibiotics - 6-8 weeks -amoxicillin -penicillin -tetracycline
Candida
Dimorphic fungus (trimorphic)
- blastospore (yeast)
- hyphae
- chlamydospores
Candida species
C. albicans (most frequent) C. tropicalis C. krusei C. glabrata C. dubliniensis
Candida habitat
Mouth, gut, vagina
Candida culture and identification
Sabouraud's dextrose medium - creamy colonies C. albicans - germ-tube test -3hr in serum, 37 degrees C Sugar utilisation tests -as sole source of carbon
Candidosis
Predisposing factor Affects mucosa and/ or skin -systemic infection uncommon but serious Oral Vulvo-vaginal Cutaneous; mucocutaneous Bronchopulmonary Systemic - endocarditis, speticaemia
Oral candidosis types
Acute pseudomembranous Chronic atrophic Chronic hyperplastic Acute atrophic Erythematous - HIV Angular cheilitis
Predisposing factors for oral candidosis: mainly
Prosthesis - no exfoliation Low saliva - no flow; soluble defences -low pH induced by high sugar diet Antibiotics - reduced bacterial competition Immuno-suppression - no cellular defence -diabetes
Pathogenic factors oral candidosis
Hypha - invasive structure
-blastospores - pro-inflammatory cytokines
-hyphae - anti-inflammatory cytokines
Proteases - secreted aspartyl proteases
-sap 1-3 needed for mucosal infection
-sap 1-3 degrade complement
-sap 4-6 contribute to systemic infection
Phospholipases
Adhesins
-e.g. Ala3 and Ssa1 bind to E-cadherin
Acid by-products of metabolism cause cell damage
pH on pathogenic factors of oral candidosis
pH <6 favours blastospores
pH >7 favours hyphae production
Other pathogenic factors C. albicans
IL-10 (immuno suppressive)
Slow TNF alpha production
no IL-12 or IFN gamma
Treatment of oral candidosis
Identify and remove predisposing factors Antifungal drugs -nystatin -miconazole -fluconazole -amphotericin B
Topical antifungal drugs
Nystatin
Miconazole
Systemic antifungal drugs
Fluconazole
Amphotericin B
Polyenes antifungal drugs
Nystatin and amphotericin B
Bind to ergosterol, membrane leakage
Imidazoles antifungal drugs
Miconazole and fluconazole
Inhibit cytochrome P450 demethylase
-converts lanosterol to ergosterol, so affects membrane synthesis
