Exam3Lec8MedicalMycology Flashcards

Question

What is the Morphological form in diseased tissue of Cryptococcus neoformans | what is its virulence factor?

Answer 1

The **polysaccharide capsule** is the most prominent virulence factor Induces alternate complement pathway Capsule is immunogenic BUT makes **fungus difficult to phagocytose** NOTE: Acapsular strains are avirulent ## Footnote you are going to build an immune response but the capsule makes it hard to phag, so IS cant fight off easily

Answer 2

Commensal found on mucosal surfaces of oral, gastrointestinal, and urogenital tract. ## Footnote naturally it is found here

Answer 3

it is the most common causative agent of fungal-associated diseases such as: **Oral thrush** **Fungal myocarditis** **Fatal disseminated candidiasis** **Biofilm formation (e.g. catheters)** Important** opportunistic pathogen** of hospitalized patients, immunocompromised individuals and burn victims

Answer 4

**Yeast to hypahe** transformation is critical for Candida pathogenicity prior to tissue invasion

Answer 5

Adherence – Main adhesin = mannoproteins (outersurface) Hyphal formation – Yeast-to-hyphae transformation Protease secretion – Secrete aspartyl proteases and cytolysins Thigmotropism – Enhances hyphal penetration by contact sensing ## Footnote Aspartyl Proteases: Enzymes which enhance destruction of host tissue and fungal penetration Cytolysins: After phagocytosis of fungus, this enzyme ensures release from phagolysosome to evade destruction. Contact Sensing: Hyphae find intracellular junctions or microscopic breaks on mucosal surfaces

Answer 6

inhalation of conidia (asexual spores) which can result in a variety of diseases ## Footnote condida are little spores that sits on the flower and is responsible for reproduction and spread. Think of it as pollen o on a flower Conidia are inhaled into lung alveoli, attach to endothelial cells, and then hyphae penetrate microvasculature.

Answer 7

1. Healthy → no sequel 2. Cavitary lung disease → Aspergilloma 3. Chronic lung disease → Chronic necrotizing aspergillosis 4. Mildly immunocompromised → Chronic necrotizing aspergillosis 5. Severely immunocompromised host → (Angio)invasive pulmonary aspergillosis (IPA) 6. Asthma→ Allergic bronchopulmonary aspergillosis (ABPA) ## Footnote Infects immunocompromised patients, especially neutropenic patients (!!!) Laz said we will most likely be tested on either 5 or 6

Answer 8

**Mold only phase – no dimorphism (no change in morphology)** Adherence – Cell wall components Cell wall pigments (**melanin**) – **interferes with phagocytosis** Toxin & enzyme secretion – lead to hemorrhage and tissue necrosis Angioinvasive properties – **invasion of tissue and vasculature** ## Footnote Toxins include: Haemolysin – leads to hemmorrhage and tissue necrosis Gliotixin – slows ciliary beat frequency of human respiratory ciliated epithelium

Answer 9

Aspergillus growing in heart muscle, note the characteristic Y-shaped filaments

Answer 10

Primarily **subcutaneous infection** known as rose gardener’s disease Virulence Factors: Dimorph Thermotolerance Extracellular enzymes

Answer 11

Histoplasmosis: pulmonary infection caused by inhalation of microconidia Also known as “cave disease” because it associated with decaying bat guano or bird droppings

Answer 12

>95%, 5% Immuno-competent → Lung lesions calcify Immuno-compromised → Severe pneumonia leading to disseminating disease

Answer 13

Dimorph – inhalation of **fungal microconidia** leads to transformation to **yeast **at 37 C Survives/Multiplies within phagolysosome of non-activated macrophages Escapes phagocytosis ## Footnote starts at mold phase and when it enters host it enters the yeast phase where it sits inside macrophages and kupffer cells

Answer 14

Coccidiodomycosis: **pulmonary infection** caused by inhalation of **fungal arthrospores** (mold phase)

Answer 15

60% of these infections are asymptomatic 40% have mild to severe symptoms: 5% ->Erythema nodosum (painful inflammation of fat cells undern skin) 5%--> Disseminated disease (i.e. “valley fever”) ## Footnote Erythema nodosum are painful subcutaneous nodules but a good sign of disease prognosis and outcome because the host’s immune system is responding to the infection.

Answer 16

1. Mold Phase: Produce fungal **arthrospores** which are inhaled by host and cause disease. How? Arthrospores have anti-phagocytic activity Arthrospores swell to begin yeast phase 2. Yeast Phase: **Spherules** are filled with **endospores** which are released Spherules are too large for phagocytosis ## Footnote mold phase with arthrospores yeast phase with endospores The two phases of the Coccidioides immitis life cycle make a dimorph

Answer 17

1. Phagocytose fungi at the site of infection 2. Transport to the lymph nodes for antigen 3. presentation to lymphocytes 4. Production of antibodies 5. Activation of TH1/TH2 cells

Answer 18

T-cell + Antibody Inter dependency An intact T-cell function is required for Ab-mediated protection. (without funcational T-cells we WILL NOT have proper IR against fungi, leading to disease) Abs might have an influence over the Th1/Th2-type cytokine balance and the induction of regulatory T cells. ## Footnote T-cells required as well. Thus activation of Th and T(reg) cells is crucial for proper immune response. Remember: 1. TH1 Cells release IFN-gamma and TNF (Cytokines) which lead to macrophage activation 2. TH2 Cells release IL-3, IL-10, IL-13 (cytokines) which lead to inactivation of macrophages

Answer 19

Cell membrane - inhibition of ergosterol synthesis

Answer 20

Direct cell membrane damage (binds to ergosterol)

Answer 21

Inhibition of nucleic acid synthesis

Answer 22

Cell wall - inhibition of glycan synthesis

Answer 23

Nikkomycin Cell wall - inhibition of chitin synthesis Griseofulvin Inhibition of mitosis (disruption of microtubules) Sordarins Inhibition of protein synthesis