actinomyces and candida Flashcards
actinomyces properties and habitat
gram + filamentous uneven staining sometimes shows branching form colonies facultatively anaerobic habitat commensal of mouth gut vagina
diagnosis of actiomycosis
- microbiological culture
- immunoassay
- MRI
what does actinomycosis affect and clinical presentation
- affected people often have just had dental treatment, poor OH, periodontal disease
Clinical presentation
- Large abscesses
- can penetrate bone and muscle to the skin
- can break open leaking pus
histology of actinomycosis
chronic inflammation fibrosis eosinophilic terminal clubs asteroid bodies (light blue area) pus - often termed sulphur granules
what are splendour-hoeppli reactions in histology
asteroid bodies
- between cationic proteans and lipids
involved in AgAb complexes tissue debris and fibrin
known as amorphous protein pS matrix
what is the purpose of splendour-hoeppli reactions (asteroid bodies)
wall off infection rom the body
stops immune cells entering the area
- thought to be a localised immunological response to an AbAg precipitate related to fungi ect
virulence of acitnomyces
- induction of chronic inflammation
- walling off from defences
- slow growth as large aggregates in matrix
no toxins or aggressive enzymes
treatment of actinomyces
- attempt at thorough surgical drainage Antibiotics 6-8 weeks - amoxicillin - penicillin - tetracycline
what is candida and its types
Dimorphic fungus (Trimorphic) – a polymorphic organism
- blastopore (yeast)
- psudohyphae
- hyphae (chlamydospores)
yeast
- smaller cells are daughter cells
- can have budding scars, thickening of the wall as the daughter cell buds off
- under certain environmental factors can form psudohypae
psudohypae
- connected to mother via wall to wall interactions
- loosely connected but two separate organisms
- these can form hyphe
hyphae
- still connected to mother cell
- no wall off
- thinner and longer than psudo
- all interconnected
- can bud (spores)
habitat of candida Albans
- mouth
- gut
- vagina
what can candida be cultured in and its appearance
- What tests can be used to test for candida albicans
Sabourauds dextrose medium
- white creamy colonies
- bread/beer smell (yeast)
1) germ tube test
Hypae start to form from the yeast form (3 hours in serum , 37 degrees or pH above 7)
2) Sugar utilisation tests
- as sole source of carbon
- grow on certain types of sugars
what is chromatic agar
Incorporates two chromogens that indicate the presence of the target enzymes
- some candida species have enzymes and some don’t so will lead to different results
what is X-NAG
detects activity of hexosaminidase
what is BCIP
detect alkaline phosphatase activity
how can candida develop
candida is a commensal - individual has an underlying predisposing factor (e.g. immunosuppressed) affects mucosa /skin oral vaginal
candida infection systemically
endocariditis
septicaemia
examples of candida infections in the mouth
acute psudomembranous (thrush) chronic atrophic chronic hyperplastic acute atrophic erythematous- HIV angular cheilitis
thrush/ acute psudomembranous
- candidia grows on the surface of oral mucosa
- tongue, back of throat
- white patches
- can scrape patches off and will show red patch underneath
chronic atrophic candidacies (candidosis infeciton)
- candida under denture, between palate
- penetrate epithelium and damages
chronic hyperplastic (candidosis infeciton)
- junction of lips
- predisposing factor smoking
- only form of candida which is associated with dysplasia and cancer progression
acute atrophic
- red tongue
- associated with those on corticoid steroids (immunosuppressant) or on long term antibiotics
erythematous
- red dots
- associated with those with HIV
angular cheilitis
- cracked lip at junction
- predisposing factors diet and nutrition, HIV, immunosupressents
predisposing factors to candida infection(exam)
- prostheses on top of epithelium, epithelium cannot shed off excess bacteria (no exfoliation)
- low saliva (no flow, low soluble defences, candida can attach more firmly)
- antibiotics (reduced bacterial competition)
- immunosuppression (no T cell defence, diabetes, immunodeficiency)
forms of candida and pathogenicity
1) yeast forms
- commensal
2) hyphal forms
- pathogenic
factors which affect hypal transition
1) pH
- less than 6 favours yeast, greater than 7 favours hyphae
2) nutrients
- serum favours hyphae
when are candida gees expressed pathogenic
when in hyphen form
pathogenic/virulence factors of candida
agglutinin like sequence (only expressed by hyphae, important in adhesion to cells)
hyphen wall protein (mediates adhesion to oral epithelial cells)
adhesion and invasion to oral epithelium of candida
1) Yeast
- genetically engineered candida that cannot form hyphae
- sit on top of the wall
2) hyphal
- mass penetration and destruction of the epithelium
3) Wild type
- natural form, not GM
- some yeast and some hyphal penetrating the epithelium
how does candida invade tissues
Yeast to hyphal transition and growth is essential for virulence and pathogenesis
Hyphae secrete Candidalysin
- pore forming toxin that kills human cells and also initiates an immune response
- secreted as monomers, come together to form a complex with pore in the middle
- punches holes in epithelium
apart from candida lysin what is also used to invade and move through epithelial cells
1) Sap 1-3
- needed for mucosal infection
2) Sap 1-3
- degrade complement
3) Sap 4-6
- contribute to systemic infection
sap secreted at the tip of hyphae so the hyphae can progress
Lipases/phospholipases
- breakdown epithelial plasma membranes during hyphal penetration
- initial access through the plasma membranes of the cell surfaces
pathogenesis at mucosal surfaces of candida yeast spores
1) Yeast form attaches and starts to form hyphae (via a predisposing factor to for hyphae)
- ALS5 and ALS1 protein on yeast cell surface which binds to the receptor on epithelial cell receptor
- Beta glucan (sugar in the candida cell wall) binds to EphA2 on epithelial cells
2) epithelial invasion
- Hyphae generated, B glucans still involved
- ALS3 drives attachment (only expressed in hyphae not yeast)
- HWP binds to epithelial cells as well
- once hyphae bind, flicks down into cell and saps are generated, lipases secreted punching holes in epithelial cell membrane
3) growth
- secretes candilysisin to punch holes in nearby cells
4) damage
how can systemic pathogenesis occur
need a lesion to get access to blood stream
how is candida treated
1) identify and remove pre disposing factor (eg low saliva, antibiotics)
2) Antifungal drugs
- nystastin
- micronazole
Above are topical
- fluconazole
- amphotericin B (quite toxic)
Above are systemic
how do polyenes work
(Nystatin, AmphotericinB)
- bind to ergosterol
- causing membrane leakage of candida
how do imidazole work
(micronazole, fluconazole)
- inhibit cytochrome P450 demethylase (converts lanosterol to ergosterol so affects membrane synthesis)
