Fungal infection Flashcards

Fungal properties: explain the main differences between fungi (eukaryotes) and bacteria (prokaryotes), and the consequences for treatment of fungal infections Fungal pathogens: list the various types of fungal infection, the major fungal pathogens, and explain the mechanisms by which they cause disease Antifungal drugs: compare the major classes of antifungal drugs, and explain their mechanisms of action Mycoses: define the terms superficial mycoses and deep mycoses, giving named examples of

1
Q

What type of cell are fungi?

A

Eukaryotes

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2
Q

What is another name for ‘higher fungi’?

A

Dikarya

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3
Q

What are the two main classes of dikarya?

A

Ascomycota – moulds that grow on foods. Contains 90% of human infections. Basidiomycota – mushrooms.

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4
Q

What are the differences between fungi and bacteria?

A

Fungi are eukaryotes. Bacteria are prokaryotes.

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5
Q

What is meant by fungi are saprophytes? How can this be symbiotic?

A

Pump enzymes into environment. Secrete hydrolytic enzymes (proteases…) which break down environment and absorb those products. Symbiotic relationship – trees house fungi in roots because they break down chemicals which they can then absorb.

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6
Q

How are fungi transmitted? (x2)

A

Fungi produce lots of spores for dispersion over large distances. Found on our skin (commensal organisms (live on organism without harming or helping that organism)) so can spread through direct contact or vectors (on yoga mats, for example).

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7
Q

What is the lung’s defences against fungal pathogens?

A

Macrophages in the lung ingest spores in the air that enter the lungs.

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8
Q

What are the three types of fungal infection? (x3)

A

Allergies Mycotoxicoses Mycoses

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9
Q

What are the types of mycoses? (x4)

A

SUPERFICIAL, CUTANEOUS, SUBCUTANEOUS, DEEP MYCOSES.

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10
Q

What happens in each mycoses-type infection? Nature of systemic symptoms?

A

SUPERFICIAL MYCOSES: Live on external layer of skin – skin or hair shaft. No living tissue is invaded and there is no cellular response from host, it’s just growing on us. CUTANEOUS MYCOSES: Dig into cutaneous layer of skin, with more dramatic clinical effects the deeper fungi go. Produce extracellular enzymes which hydrolyse KERATIN. This causes inflammation to the metabolic by-products produced by the fungi. SUBCUTANEOUS if reaches that layer. Produce chronic, localised skin infections – caused by trauma that embeds fungus deep e.g. cat scratch. DEEP MYCOSES: Within organs. Also known as systemic mycoses. SYSTMEMIC INFECTIONS TEND TO HAVE BROAD SYMPTOMS.

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11
Q

Examples of superficial mycoses and the fungal infection they cause? (x3)

A

Piedraia hortae: Black Piedra. Trichosporon beigelii: White Piedra. Malessezia globosa: Dandruff.

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12
Q

What is the mechanism of Malassezia globosa?

A

Produces oleic acid which causes inflammation of the stratum corneum (outermost layer of epidermis).

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13
Q

What is the class of pathogens that cause cutaneous mycoses called? Examples of cutaneous mycoses and the infection they cause? (x2)

A

Class: Dermatomycoses. Examples: 1. Candida albican causes candidiasis in immunocompromised individuals. 2. Ringworm, caused by fungi with Genus: Tinea. e.g. Tinea capitis. Highly transmissible. Affecting scalp, eyebrows, eyelashes, hair; Tinea pedis. Athlete’s foot. Affects feet; Tinea corporis. The body.

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14
Q

List examples of subcutaneous mycoses and the infection they cause. (x1)

A

Sporotrichosis (caused by Sporothrix schenckii)

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15
Q

What are the two types of deep mycoses? List examples of deep mycoses and the infection they cause. (x0 and x3)

A

PRIMARY mycoses: able to establish infection in a normal healthy host. OPPORTUNISTIC mycoses: require a compromised host in order to establish infection e.g. immuno-compromised. Geni include: Candida: cause candidiasis; Aspergillus: cause Aspergillosis. Some Fusarium: cause human infections in nails, cornea (onychomycosis and keratomycosis respectively).

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16
Q

What are fungal allergies?

A

There are many fungal spores found in the air. Lungs can become sensitive to certain types of fungal spores = hypersensitivity. Leads to allergic reaction.

17
Q

Major fungal allergy pathogen? (x1)

A

Aspergillus fumigatus – typically found in soil and causes allergic broncho-pulmonary aspergillosis (ABPA) in some asthmatics.

18
Q

What causes mycotoxicosis? How do they cause disease in the body?

A

Mycotoxins! Fungi secrete more than just enzymes. Also produce complex secondary metabolites to protect themselves from their environment e.g. beta-lactams to protect against bacteria that prey on fungi. Produce many types of mycotoxins which are very toxic. This produces a toxic reaction in the body when ingested or inhaled.

19
Q

What are the symptoms of mycotoxicosis? (x4)

A

Breathing problems, dizziness, severe diarrhoea and vomiting, and dehydration. But depends on the mycotoxin.

20
Q

What are the major mycotoxins associated with mycotoxicosis? (x2) And what pathogen are they associated with?

A

Aflatoxins (from the Aspergillus species). Citrinin (from Penicillium citrinum).

21
Q

What effect does the Aflatoxin mycotoxin have? Where do they originate in the food chain?

A

Carcinogenic compound that contaminates grain pre- and post-harvest. Causes liver cancer – particularly if you have pre-existing liver damage from hepatitis B virus.

22
Q

Epidemiologically, what individuals are more susceptible to fungal infections?

A

Immunosuppressed individuals – fungal pathogens are opportunistic.

23
Q

What are the targets for antifungal therapy? (x3) Why for each?

A

CELL MEMBRANE: fungi use principally ergosterol instead of cholesterol. DNA SYNTHESIS: some compounds may be selectively activated by fungi, arresting DNA synthesis. CELL WALL: unlike mammalian cells, fungi have a cell wall.

24
Q

Why are there so few realistic targets for anti-fungal therapy?

A

Fungi and animals are actually closely related. So antifungal drugs likely have some cross-reactivity with our metabolism.

25
What are the four anti-fungal drug classes?
Affect membrane function: Polyenes Affect cell wall synthesis: Echinocandins Disrupt nucleic acid synthesis: 5-Flucytosine Membrane ergosterol biosynthesis interference: AZOLES, Terbinafine and Fenpropimorph.
26
What is the problem with anti-fungal drugs?
Evolving resistance to drugs that we use – all of the main four classes have resistance in some form.
27
How does anti-fungal resistance emerge?
Resistance through evolution in MANY ways. 1. FARMERS use anti-fungal drugs as much as we do. Azoles are interesting – because there’s dual use. Same azoles used in farming on plants is the same as we use in medicine. If farmer spraying a pathogenic fungus – may form a resistance in the environment, which may infect a patient, which may mean that there’s resistance in the human population and drug ineffective. 2. Some of these resistances are acquired by the human population through the environment.
28
Do not try and learn this, just read and absorb: May come in handy.
Candida is found healthily in all of us – in GI tract. But can get out of control = infection. Big fungal infection: Candida. Five species are pathogenic. CANDIDA ALBICANS: causes blood stream infection. Colonise GI tract, respiratory tract, vagina, urethra… It’s in the hospital environment too – so key transmissible area. CANDIDA AURIS: huge issue as it is resistant to many disinfectants. Systemic Candida infections not seen in healthy people. Risk factors: chemotherapy, gut-related surgery, catheters.