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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
Pre disposing factors to Aspergillus(2)
[1] pre-existing lung damage - Tb - cystic fibrosis [2] underlying disease - leukaemia - immunosuppression
26
Saprophytic aspergillus
[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
Allergic aspergillosis
Allergic bronchopulmonary aspergillosis (ABPA) - 25% of asthmatics - 10% of CF sufferers Fungus survives in mucus and secreted toxins =>allergic response
28
Invasive aspergillosis
Lungs or other tissues Angiovasive aspergillosis - lesions invade blood vessels - hyphae kill tissue as colony expands Defenceless leukocyte-mediated immune response
29
Virulence determinants of aspergillus (general factors)
Sporulation Omnipresence Spore size Germination of spores (rapid) Growth 37-38C Adhesins Nutritional requirements:low; absorb from air
30
Virulence determinants of aspergillus (offensive factors)
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
Virulence determinants of aspergillus (defensive factors)
Thermo tolerance - up to 42C Cell wall
32
Virulence determinants of aspergillus (defensive factors) **cell wall** (6)
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
Gliotoxin
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
Fumagillin
Produced during hyphal development and growth Retards the ciliary beat of epithelial cells May play role in immunosuppression
35
Fumagillin inhibits [6]
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
Aspergillus therapy
Surgery Chemotherapy - amphotericin B -> cell leakage => death - caspofungin -> disrupt cell wall biosynthesis
37
Aspergillus prevention
Air filtration Isolation Preventative chemotherapy
38
Immune response to fungal pathogens **intact skin**
Prevents entry; continually renewed
39
Immune response to fungal pathogens **pulmonary immunity**
Muco-ciliary elevator - removes dust, spores - defective in asthma Alveolar macrophages - phagocytose spores - prevent germination Neutrophil - attack hyphae - destroy growing fungus
40
Immune response to candida
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
Immunocompetent lung
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
ABPA
Hyphae -> Fumagillin and gliotoxin which inhibits mucocilliary elevator and neutrophils Inflammatory Resp. Esosinophils and neutrophils -> tissue necrosis and severe pulmonary damage
43
Antifungal agents [3]
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
Polyenes
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
AmpB
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
Azoles
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
Azole resistance **Alteration in sterol biosynthesis**
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
Azole resistance **mutation in ERG11 gene**
Encodes drug target enzyme 14-alpha-demethylase and not get binding of Azole to target site
49
Azole resistance **overexpression of ERG11 gene**
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
Azole resistance **overexpression of genes encoding efflux pumps**
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
Caspofungin
Cell wall target As effective as AmpB but less nephrotoxic Pre-exposure to H2O2 increases resistance to caspofungin
52
How does C.Albicans respond to caspofungin? (2 pathways)
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
Polyene resistance
Resistance induced by growth in sterol medium or selection of inherent resistance due to prolonged Polyene gene

Miguel (8 decks)

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