Actinomyces and Candida Flashcards
Morphology and pathogenic features of Actinomyces and Candida species Main pathological conditions caused by these organisms Aspects of treatment
Actinomyces
Most frequent and often found with
Habitat
Gram +ve
Sometimes branch
Uneven staining
21 species
A. israelii - aggregatibacter actinomycetemcomitans
A. oris, odontlyticus and gerencaeseriae –> caries
Mouth, gut, vagina
Culture
Fastidious
FACULTATIVE anaerobe
3-7 days to grow
Clinical presentation of actinomycosis
Aetiology
large abscesses can
Rare infection
Painful slow growing abscesses –> chronic infection
Recent tx, poor OH or periodontal disease
penetrate bone and muscle through to skin –> leak pus
Types of actinomycosis and examples
Histology
Mechanism
Cervicofacial - acute painful 55-65% Abdominopelvic - 10-20% - ileocaecal Thoracic - farmer's lung Cerebral - haematogenous spread Entry - mucosal break
Chronic inflammation, fibrosis and eosinophilic terminal clubs
Eosinophils try to destroy pathogen –> degranulation
Histology of actinomyces related disease
Club shaped lipid complexes around amorphous protein polysaccharide
Locules of pus surrounded by fibrous septa
Pathogenic factors
Virulence mechanisms
No toxins or enzymes
- induction of chronic inflammation
- walling off from defences
- slow growth due to large aggregates in a matrix
Treatment
Surgical drainage 6-8 weeks antibiotic course - amoxicillin - tetracycline - penicillin
Candida
Features of organism opportunistic dimorphic fungus - blastospore - yeast - pseudohyphae - hyphae - chlamydospores
Candida species
Most frequent
C. albicans
Mouth, gut, vagina
Culture and ID of candida
3 methods
- Dextrose medium - +ve creamy colonies
- germ-tube test (for albicans)
- sugar utilisation tests
Candidosis/candidiasis
Pre-Deposing factor
Affects
presentations?
systemic effects?
Immunodeficiency
Mucosa and/or skin - red lesions caused by hyphae breaking open cells and disrupting epithelium
- vulvo-vaginal
- oral
- cutaneous and mucocutaenous
- bronchopulmonary
Endocarditis and septicaemia
Oral candidosis
Different types, what does it effect
Hyphae often live
- Acute pseudomembranous candidosis - thrush - immunodeficiency - redness below white lesion
Hyphae difficult to phagocytose and live within macrophages - Chronic atrophic
- associated with denture wear on hard palate and upper jaw - Chronic hyperplastic - buccal mucosa or tongue border - carcinogenesis and pre malignant lesions - colonise dysplastic lesions t accelerate malignancy
- Acute atrophic
- Angular cheilitis - occurs at corners of mouth
Predisposing factors of candidosis
Prostheses - lack of exfoliation –> XS build up of candida
Low saliva - no flow –> soluble defences and candida build up / low pH due to diet
Antibiotics - reduced competition
Immunosuppression - no cellular defence e.g in diabetes
Pathogenic features
- hyphae
- proteases
Which pH for which
- invasive i.e blastospores and hyphae (inflammatory and anti-inflammatory cytokines)
- secreted aspartyl proteases against proteins
- destroy tissues and secreted from front of hyphae
- mucosal infection
- degradation of complement
- systemic infection
- make space for movement - pH <6
- pH >7 forms anchor points to blast cells open
Other pathogenic factors
- C. albicans hyphae
- phospholipase
- Adhesins
- acid by products of metabolism
- IL-10 - immunosuppressant, candidalysin, blastospores have slow TNF-α production
- breakdown of phospholipid layers
- bind to proteins within cell
- cause cell damage