actinomyces and candida Flashcards

(39 cards)

1
Q

actinomyces properties and habitat

A
gram +
filamentous
uneven staining
sometimes shows branching
form colonies
facultatively anaerobic
habitat
commensal of mouth gut vagina
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2
Q

diagnosis of actiomycosis

A
  • microbiological culture
  • immunoassay
  • MRI
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3
Q

what does actinomycosis affect and clinical presentation

A
  • 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
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4
Q

histology of actinomycosis

A
chronic inflammation
fibrosis
eosinophilic terminal clubs
asteroid bodies (light blue area)
pus - often termed sulphur granules
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5
Q

what are splendour-hoeppli reactions in histology

A

asteroid bodies
- between cationic proteans and lipids
involved in AgAb complexes tissue debris and fibrin

known as amorphous protein pS matrix

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6
Q

what is the purpose of splendour-hoeppli reactions (asteroid bodies)

A

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

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7
Q

virulence of acitnomyces

A
  • induction of chronic inflammation
  • walling off from defences
  • slow growth as large aggregates in matrix

no toxins or aggressive enzymes

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8
Q

treatment of actinomyces

A
-	attempt at thorough surgical drainage
Antibiotics 6-8 weeks
-	amoxicillin
-	penicillin
-	tetracycline
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9
Q

what is candida and its types

A

Dimorphic fungus (Trimorphic) – a polymorphic organism

  • blastopore (yeast)
  • psudohyphae
  • hyphae (chlamydospores)
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10
Q

yeast

A
  • 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
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11
Q

psudohypae

A
  • connected to mother via wall to wall interactions
  • loosely connected but two separate organisms
  • these can form hyphe
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12
Q

hyphae

A
  • still connected to mother cell
  • no wall off
  • thinner and longer than psudo
  • all interconnected
  • can bud (spores)
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13
Q

habitat of candida Albans

A
  • mouth
  • gut
  • vagina
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14
Q

what can candida be cultured in and its appearance

  • What tests can be used to test for candida albicans
A

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

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15
Q

what is chromatic agar

A

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

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16
Q

what is X-NAG

A

detects activity of hexosaminidase

17
Q

what is BCIP

A

detect alkaline phosphatase activity

18
Q

how can candida develop

A
candida is a commensal
- individual has an underlying predisposing factor (e.g. immunosuppressed)
affects mucosa /skin
oral
vaginal
19
Q

candida infection systemically

A

endocariditis

septicaemia

20
Q

examples of candida infections in the mouth

A
acute psudomembranous (thrush)
chronic atrophic
chronic hyperplastic
acute atrophic
erythematous- HIV
angular cheilitis
21
Q

thrush/ acute psudomembranous

A
  • candidia grows on the surface of oral mucosa
  • tongue, back of throat
  • white patches
  • can scrape patches off and will show red patch underneath
22
Q

chronic atrophic candidacies (candidosis infeciton)

A
  • candida under denture, between palate

- penetrate epithelium and damages

23
Q

chronic hyperplastic (candidosis infeciton)

A
  • junction of lips
  • predisposing factor smoking
  • only form of candida which is associated with dysplasia and cancer progression
24
Q

acute atrophic

A
  • red tongue

- associated with those on corticoid steroids (immunosuppressant) or on long term antibiotics

25
erythematous
- red dots | - associated with those with HIV
26
angular cheilitis
- cracked lip at junction | - predisposing factors diet and nutrition, HIV, immunosupressents
27
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)
28
forms of candida and pathogenicity
1) yeast forms - commensal 2) hyphal forms - pathogenic
29
factors which affect hypal transition
1) pH - less than 6 favours yeast, greater than 7 favours hyphae 2) nutrients - serum favours hyphae
30
when are candida gees expressed pathogenic
when in hyphen form
31
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)
32
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
33
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
34
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
35
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
36
how can systemic pathogenesis occur
need a lesion to get access to blood stream
37
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
38
how do polyenes work
(Nystatin, AmphotericinB) - bind to ergosterol - causing membrane leakage of candida
39
how do imidazole work
(micronazole, fluconazole) | - inhibit cytochrome P450 demethylase (converts lanosterol to ergosterol so affects membrane synthesis)