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Miguel > Medical Mycology > Flashcards

Medical Mycology Flashcards

1
Q

Candida and candidosis

A

Opportunistic fungal pathogen
Candida albicans => dimorphic asexual yeast

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2
Q

Candida and candidosis superficial disease

A

Common
Treatable
Curable -> mouth

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3
Q

Candida and candidosis systemic disease

A

Rare
Difficult to treat
Fatal -> multiple organs

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4
Q

Orophangeal candidosis

A

Superficial
Easy to diagnose and treat with antifungal agents
Premature infants, geriatrics, diabetics and HIV+
White plaques on tongue, roof of mouth
Maternal infection; low/underdeveloped immunity; nosocomial infection

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5
Q

Candidosis of skin/nails

A

Cutaneous 10% of patients
Candida onychia and paronychia
- nails and nail folds
- moist conditions
- destroys nails

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6
Q

Vulvovaginal candidosis

A

Frequent; cystitis; can infect neonate during birth
Itching and discharge
Yeast persists regulated by pH an lactobacillus
25% asymptomatic; occurs in healthy women
Pregnancy; diabetes; antibiotic therapy; oral contraceptives

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7
Q

How does pregnancy lead to susceptibility in Vulvovaginal candidosis?

A

Higher levels due to reduced acidity and increased glycogen

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8
Q

Systemic candidosis GIT (3)

A

Oesaphagus
- plaques line tract - painful to swallow
- infection of GI tract
- diabetes, cancer or AIDs

Gastric
- invasion of ulcers
- 73% ulcers => candida

Intestinal
- small intestine and colon
- diarrhea

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9
Q

Systemic candidosis respiratory tract

A

Laryngeal
- hoarseness and fever
- underlying cause
- silicone voice prostheses

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10
Q

Systemic infection urinary tract

A

10^5ml^-1 =>disease
Renal candidosis, underlying disease or cystitis

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11
Q

Predisposing factors to candida infection[3]

A

[1] Compromised host
- HIV+
- immunosuppressive therapy/antibiotic therapy
- drug addiction

[2] Diabetes
- genital candidosis
- 5-15% systemic conditions
- oral candidosis

[3] Malignant disease
- 10% leukaemias develop systemic candidosis

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12
Q

Dimorphism

A

Yeast-hyphal transmission
Hyphal form invades tissues and are more adherent
Both found in specimens

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13
Q

Thigmotropism

A

Ability of germ tubes to ‘explore’ the environment in search of nutrients
Germ tubes respond to charge
Hyphae grow between sheets of cells, finding the line of least resistance in tissue

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14
Q

Adherence virulent factor => pathogenicity

A

More adherence = more pathogenesis

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15
Q

Specific adherence mechanisms (mycology)

A

Ligand-receptor interactions associated with outer fibrillar layer
Adhesions present on yeast surface specific for receptors on host cell surface may target ECM proteins - laminate, fibronectins

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16
Q

Non-specific adherence mechanisms (mycology)

A

Electrostatic charges
Cell surface hydrophobicity
Yeast cells have a net negative charge; must overcome this before they can adhere
Cell surface hydrophobicity increased in galactose culture medium
Increased cell surface hydrophobicity = increased adherence

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17
Q

Extracellular enzymes virulence factor (mycoplasma): secreted acid proteinases

A

PH 4.6-5.5 => active
Synthesised during tissue invasion
C.albicans in VVC produce SAP which cleaves IgA
-> may induce phagocytosis of cells by polymorphs

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18
Q

Extracellular enzymes virulence factor (mycoplasma): phospholipase

A

pHA and lysophosphilase lyse biological membranes located at growing tip of hyphal form of C.albicans
Most adherent yeasts = most phLip
Ruptures membranes
Alter cell surface -> increase adherence

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19
Q

Extracellular enzymes virulence factor (mycoplasma): haemolysin

A

Rupture RBC -> releases iron
Produced by C.albicans

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20
Q

Extracellular enzymes virulence factor (mycoplasma): Canidalysin

A

Role in pathogenesis
Epithelial damage
Immune activation
Phagocyte attraction

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21
Q

Phenotypic switching

A

[1] cell types
- altered shape, size, antigenicity, surface
[2] colony types
- smooth, wrinkled, pitted, rough

+allows rapid adaptation to environment -> induces variation
+evade attentions of the immune system
+alters pathogen characteristics

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22
Q

Biofilm formation initial adherence

A

Initial adherence facilitated by saliva or serum

23
Q

4 stages in candida invasion

A

[1] epithelial adhesions and colonisation
- adhesions
- hydrophobicity
- biofilm

[2] epithelial penetration
- hyphal formation
- lytic enzymes
- thigmotropism

[3] tissue invasion and dissemination
- lytic enzymes
- thigmotropism

[4] endothelial adhesion and penetration of tissue
- adhesins
- hypha formation
- lytic enzymes

24
Q

Aspergillus and aspergillosis

A

Aspergillus fumigatus, aspergillus niger, aspergillus flavus
Pulmonary pathogen
A.fumigatus => ubiquitous, grows on damp surfaces

25
Q

Pre disposing factors to Aspergillus(2)

A

[1] pre-existing lung damage
- Tb
- cystic fibrosis

[2] underlying disease
- leukaemia
- immunosuppression

26
Q

Saprophytic aspergillus

A

[1] airway colonisation
- asthma
- cystic fibrosis

[2] aspergilloma (fungus ball)
- hyphae, mucus, cell debris
- surrounded by inflamed tissue
- 5% die due to blood loss

27
Q

Allergic aspergillosis

A

Allergic bronchopulmonary aspergillosis (ABPA)
- 25% of asthmatics
- 10% of CF sufferers
Fungus survives in mucus and secreted toxins
=>allergic response

28
Q

Invasive aspergillosis

A

Lungs or other tissues
Angiovasive aspergillosis
- lesions invade blood vessels
- hyphae kill tissue as colony expands
Defenceless leukocyte-mediated immune response

29
Q

Virulence determinants of aspergillus (general factors)

A

Sporulation
Omnipresence
Spore size
Germination of spores (rapid)
Growth 37-38C
Adhesins
Nutritional requirements:low; absorb from air

30
Q

Virulence determinants of aspergillus (offensive factors)

A

Digestive enzymes
- proteases
- induce pro-inflammatory cytokine production
- cell peeling and death
- elastin degradation
Phosphlipase
- degrade cell membrane
Toxins
- gliotoxin, fumagilin
Angioinvasive
- growth within capillaries

31
Q

Virulence determinants of aspergillus (defensive factors)

A

Thermo tolerance - up to 42C
Cell wall

32
Q

Virulence determinants of aspergillus (defensive factors) cell wall (6)

A

Pigments
- melanin - scavenge free radicals

Hydrophobins
- allow dispersion

ROS protection
- catalase, SOD, antioxidants

Efflux pumps
- detoxify immune response

Biofilms
- 3D structure in ECM

Pes 1
- affects clonidine surface and hydrophobicity

33
Q

Gliotoxin

A

Inhibits T and B cell production
Inhibits macrophage phagocytosis of material
Suppresses activity of immune system
- apoptosis in thymus, spleen and lymph nodes
Immunosuppressive agent
Blocks translocation of p47 and p67 in neutrophils

34
Q

Fumagillin

A

Produced during hyphal development and growth
Retards the ciliary beat of epithelial cells
May play role in immunosuppression

35
Q

Fumagillin inhibits [6]

A

Ability of neutrophils to kill yeast cells
Ability of neutrophils to consume O2
Neutrophil degranulation
Translocation of p47 from cytosol to membrane
Release of myeloperoxidase
Formation of F-actin

36
Q

Aspergillus therapy

A

Surgery
Chemotherapy
- amphotericin B -> cell leakage => death
- caspofungin -> disrupt cell wall biosynthesis

37
Q

Aspergillus prevention

A

Air filtration
Isolation
Preventative chemotherapy

38
Q

Immune response to fungal pathogens intact skin

A

Prevents entry; continually renewed

39
Q

Immune response to fungal pathogens pulmonary immunity

A

Muco-ciliary elevator
- removes dust, spores
- defective in asthma

Alveolar macrophages
- phagocytose spores
- prevent germination

Neutrophil
- attack hyphae
- destroy growing fungus

40
Q

Immune response to candida

A

Superficial
- oral cavity -> saliva
- vagina -> pH, microflora

Systemic
- serum ->GT formation -> clumping
->lactoferrin, transferrin (iron scavenging)
- PMN and macrophages
- cytokines recruit immune cells
- MP or monocytes phagocytose
- PMN kill using oxidants

41
Q

Immunocompetent lung

A

Conida recognised by PTx3 and SP-D which enhance activation of alveolar macrophages
AM uptake is mediated by Dectin1 and TLRs -> Pro-inflamm Resp.
Conida that escape AM -> penetrate alveolar surface
Neutrophil recruitment -> ROS generation and NET formation inactivate germinating candida and hyphae
Dendritic cells -> process antigens -> adaptive response

42
Q

ABPA

A

Hyphae -> Fumagillin and gliotoxin which inhibits mucocilliary elevator and neutrophils
Inflammatory Resp. Esosinophils and neutrophils -> tissue necrosis and severe pulmonary damage

43
Q

Antifungal agents [3]

A

Polyenes - bind ergesterol and induce cell leakage AmpB
Azoles- interfere with lanesterol demethylase and increase in toxic IM
Echinocandins - disrupt glucan biosynthesis and lead to cell lysis

44
Q

Polyenes

A

Damage CM => alter permeability
Bind to steroids -> differential action on yeast/human cells
Stat.cells are more resistant to Polyenes than exp cells
Protoplast lysed by action of Polyenes - > induce osmotic instability
GT formation in C.albicans
Adherence to buccal epithelial cells
May also increase host immune response

45
Q

AmpB

A

Binds ergesterol -> creates opening
=> amino acids and proteins leak

Cell responds by trying to release more gliotoxin
In systemic infection last chance is AmpB
=> they deteriorate and relapse for days because of this sudden release of gliotoxin by de novo synthesis

46
Q

Azoles

A

Most widely used antifungal agents
Alter permeability of CM by blocking synthesis of ergesterol
- accumulate 14-alpha-methyl-sterols in cells instead of ergosterol due to inhibition of demethylation step in sterol synthesis
- inhibit action of cytochrome p450 involved in sterol synthesis

47
Q

Azole resistance Alteration in sterol biosynthesis

A

Decreased ergosterol in cell membrane and 14-alpha-methyl-3,6-diol
- toxic and growth arrest
ERG3 mutations prevent formation of 14-alpha-methyl and increased 14-alphamethylfecosterol (acts as a substitute for ergosterol in cm)
May also be polyene resistant as no ergosterol

48
Q

Azole resistance mutation in ERG11 gene

A

Encodes drug target enzyme 14-alpha-demethylase and not get binding of Azole to target site

49
Q

Azole resistance overexpression of ERG11 gene

A

Addition of fluconazole => increased ERG11 due to ergosterol depletion and leads to increased lanosterol in C.albicans membrane
Zinc cluster transcription factor IPC2
- regulates expression of ERGII in presence of triazole
Resistance by increased gene expression
=> but may be not be significant clinically

50
Q

Azole resistance overexpression of genes encoding efflux pumps

A

Major facility super-family:
- MDR1: o/e encodes fluconazole resistance only C.dubliniensis
- CDR: o/e encodes multi-drug resistance
- FLU1: mediates azole resistance in C.Albicans

ATP-binding cassette superfamily:
- flu-resistance
- interaction of efflux pumps

51
Q

Caspofungin

A

Cell wall target
As effective as AmpB but less nephrotoxic
Pre-exposure to H2O2 increases resistance to caspofungin

52
Q

How does C.Albicans respond to caspofungin? (2 pathways)

A

Osmotic stress (HOG PATHWAY) -> cascade of reactions -> phosphorylation of HOG1
Moves into nucleus to turn on genes that can deal with the osmotic stress

Oxidative stress (CAP1P pathway) -> phosphorylation of cap1p protein -> translocates into nucleus => turns on expression of genes that code for enzymes or proteins that can deal with oxidative stress

53
Q

Polyene resistance

A

Resistance induced by growth in sterol medium or selection of inherent resistance due to prolonged Polyene gene

Miguel (8 decks)

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