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2nd year - Microbiology > Mycology (Fungus) - Lecture 4 > Flashcards

Mycology (Fungus) - Lecture 4 Flashcards

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Biology 101 flashcards
1
Q 
Describe a fungal infection
Eukaryotic or prokaryotic
unicellular or multicellular
Cell wall contents
Reproducion
A

Eukaryotic, unicellular or multicellular
Multimorphic sturctures and stages
Cell wall contains chitin, ergosterol
Complex life cycles, sexual and asexual reproduction

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2
Q

What are four morphological stages of fungal infections?

A

1) Yeast or yeast-like stages
2) Pseudohyphae stages
3) Hyphae stages
4) Spores and spore-like stages

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3
Q

Describe the yeast or yeast-like stages

A 
Sexual stages (conjugation) and asexual (budding) stages of reproduction
Unicellulare, compromise mold
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4
Q

Describe pseudohyphae stages

A

Multicellular structures produced by incomplete budding

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5
Q

Describe hyphae stages

A

Multicellular structures, intricate connections and communication between cells
Long, filamentous, comprises mycelium

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6
Q

Describe spores and spore-like stages

A

Metabolically dormant, survive harsh environmental conditions, can travel through air
Unicellular structures

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7
Q

What are the four types of mycoses?

give examples of each

A

1) Superficial/cutaneous - Tinea
2) Subcutaneous - Sporothrichosis
3) Systemic - Blastomycosis, Histomycosis
4) Opportunistic - Candidiasis, Cryptococcosis, Pneumocystosis

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8
Q

Describe superficial/cutaneous mycoses

A

Fungal infection of the outermost layers of skin, hair and nails

Superficial - occur OUTSIDE the body
Cutaneous - occur IN the outer layers of the skin

Tinea = ringworm - infection due to fungus (NOT parasite)

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9
Q

Describe tinea capitis

What causes it?

A

Scalp ringworm
Fungal infection of the head and scalp - patches of hair loss, inflammation, itching, scaling, dandruf

Trichophyton and Microsporum cause it most commonly

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10
Q

Describe subcutatneous mycoses

A

Chronic, localized infection of the skin and tissue
may affect lymphatic system
May invade extradermal tissues

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11
Q

Describe sporotrichosis (Sporothrix schenkii)

A

Aka: Rose gardener’s disease
Affects the skin and lymph nodes
Causes nodular leasions at the point of entry and along lymphatic vessels
Can spread to joints, lung, bone

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12
Q

Describe systemic mycoses

A

Pass through the bloodstream

Primary systemic mycoses generally originate in the lung, and undergo hematogenous spread to other organs

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13
Q

What are systemic mycoses casused by?

A

Caused by dimorphic fungal pathogens - assume different morphologies at different body temperatures

  • Mycelial at room temperature
  • Yeast-like (spore) at body temperature
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14
Q

Give four examples of systemic fungal human pathogens

A

Blastomyces dermatiditis
Coccidioides immitis
Histoplasma capsulatum
Paracoccidioides brasiliensis

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15
Q

Who is more likely to get opportunistic mycoses?

A

Associated with immunosuppressed patients

  • HIV-positive patients (AIDS-defining illness)
  • Transplant recipients
  • Elderly
  • Premature babies
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16
Q

Give three examples of opportunistic mycoses

A

Candida albicans
Pneumocystis jiroveci
Cryptococcus neoformans

17
Q

What is candida albicans? (candidiasis)

A

Thrush, ‘yeast infection’

Commensal organism of the skin

18
Q

Describe oral candidiasis

A

Thrush
Associated with transplant patients, HIV-positive patients, cancer patients
White patches/plaques on the tongue, difficulty swallowing

19
Q

Describe vulvo-vaginal candidiasis

A

‘yeast infection’

Pruritis, thick discharge, dysuria

20
Q

What are some other forms of candidiasis?

A

Esophageal, Urinary tract, Penile (Candida balantidis), GI, Renal. Systemic, Disseminated

21
Q

What is pneumocystis jiroveci? (pneumocystosis)

A

Commensal organism of the lung

22
Q

Describe pneumocystosis (symptoms)

A

Fever, chills, non-productive cough, difficulty breathing, tachypnea, tachycardia
Extra-pulmonary complications: CNS, bone marrow, eyes, GI tract (rare)

23
Q

What are prions?

A

Infectious proteins

24
Q

Describe a prion infection

A

Transmitted by transferring a misfolded protein state
Presence of a misfolded protein stimulates the misfolding of normal proteins, disrupting their function
Prion disease cause transmissible spongiform encephalopathy

25
Q

Who is Tikvah Alper/what importance with regards to prions?

A

In the 1960s he discovered infectious cause of scrapie, a disease in sheep, was resistant to ionizing radiation

26
Q

Who is John Stanley Griffith/what importance with regards to prions?

A

In the 1960s he showed mathematical modelling suggests that scrapie is caused by a misfolded protein, which propagates by self-association

27
Q

Who is Stanley Prusiner/what importance with regards to prions?

A

In 1980s he demonstrated that agents that cause transmissible spongiform encephalopathy are resistant to all methods used to destroy nuceic acid, but are sensitive to all methods used to destroy protein
Coined the term prion (proteinaceous infectious particle)
NOBEL PRIZE 1997

28
Q

Describe:
PrP
PrPc
PrPsc

A

PrP - normal cellular protein localized on the surface of healthy nerve cells

PrPc - (cellular) normal form found in animals, and is subject to degredation by cellular proteases

PrPsc - (scrapie) mifolded form (prion form), and is resistant to degradation by proteases

29
Q

What does PrPsc lead to?

A

Leads to accumulation of protein in the brain, followed by lesions (spongioform)

30
Q

Name the prion disease in:

1) Sheep and farm animals
2) Cattle
3) Humans

A

1) Scrapie
2) Mad cow disease, bovine spongioform encephalopathy (BSE) variant CJD
3) Creuztfel-Jakob Disease (CJD), vCJD, Kuru

31
Q

In humans describe the transmission of different CJD

A

Congenital - 5-10% of cases
Spontaneous - >85% of cases
Aquired - infection during medical procedures <1% of cases

32
Q

What is vCJD and how is it transmitted?

A

It is an acquired disease, transmitted by consumption of contaminated products

33
Q

Who is affected by Kuru?

A

Endemic to the Fore tribe of Papua New Guinea

Incidences of Kuru more common in women than men

34
Q

What are clinical features of prion disease in humans?

A

Protein aggregation, amyloid plaque formation
Spongioform change, necrosis and leasions
Neuronal loss, astrocytosis
Poor muscle coordination, memory loss, dementia, coma

35
Q

What are developing treatment strategies for prion disease in humans?

A

Decrease the presence of normal cellular protein (RNAi)

Passive/Active immunization strategies

2nd year - Microbiology (21 decks)

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