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pm 226 > infectious diseases > Flashcards

infectious diseases Flashcards

1
Q

virulence factors of staphylococcus and their function

A
  • Cell wall anchored (CWA) proteins: Adhere to host matrix proteins (ECM) bound to host tissues/cells
  • Capsule: Inhibits chemotaxis and phagocytosis; inhibits proliferation of mononuclear cells
  • Slime layer: Facilitates adherence to foreign bodies
  • Peptidoglycan: Provides osmotic stability; stimulates production of endotoxin- like activity; inhibits phagocytosis
  • Teichoic acid: Binds to fibronectin
  • Protein A: Inhibits antibody-mediated clearance by binding IgG Fc receptors; leukocyte chemoattractant; anticomplementary
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2
Q

biological effects of secreted factors in staphylococcus aureus

A

enzymes:
- coagulase: Converts fibrinogen to fibrin
- hyaluronidase: Hydrolyzes hyaluronic acids in connective tissue
- nuclease: Hydrolyze DNA
- lipase: Hydrolyze lipids

toxins:
- cytotoxins: Toxic to erythrocytes, fibroblasts, leukocytes, macrophages and platelets
- exfoliative toxins: Serine proteases, disrupt skin epidermis layer

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3
Q

classify streptococci

A
  • alpha-haemolytic: partial haemolysis
  • beta-haemolytic: complete haemolysis
  • gamma-haemolytic: no hemolysis
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4
Q

virulence factors of streptococci pyogenes

A

Adhesins: Proteins expressed on surface
• Lipoteichoic acids
· Facilitate binding to host cells, colonisation
• F-protein
· binds to host fibronectin in epithelial cells -> internalisation of bacteria into host cells
• M-protein
· fibrils on cell surface
· bind plasma proteins and fibronectin
· anti-phagocytic and anti-complement
· invasion into epithelial cells
• M-like proteins

Toxins and Enzymes
• C5a peptidase (SapA)
· immune-modulating serine endopeptidase
· inactivates human C5a -> hinders complement & neutrophil response
· mediates resistance to phagocytosis
• Streptolysin S
· responsible for β-hemolysis
· lyses erythrocytes, lymphocytes, neutrophils, platelets
· affect phagocytes and help to introduce bacteria across skin barrier

Hyaluronidase:
• their producer attaches to ephitelia
• allow pathogen to invade deeper tissues

Streptokinase:
• disolves clot
• release pathogen to bloodstream and deeper tissues

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5
Q

which type of bacterial infections can streptococci pyogenes cause

A

skin infections:
- impetigo
- erypelas
- cellulitis
super respiratory track infections

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6
Q

what is diphtheria toxin and which bacteria causes it

A

definition: cell damage or death
caused by corynebacterium diphtheriae

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7
Q

what does corynebacterium diptheria affects

A
  • tonsils
  • throat
  • nose
  • skin
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8
Q

what bacteria causes bronchitis and pneumonia

A

haemophilus influenzae and streptococcus pneumoniae

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9
Q

clasification of pneumonia

A
  • community-acquired pneumonia (CAP)
  • hospital-acquired pneumonia (HAC)
  • walking/atypical pneumonia
  • ventilator-associated pneumonia (VAC): early and later infections
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10
Q

immunity of fungi and bacteria

A

intracellular phase:
· cytotoxic T cells: kill host infected cells and activate macrophages
· helper T cells: activate macrophages (IFN) to kill bacteria by MHC recognition

extracellular phase:
· Phagocytes
· Antibody
· Complement

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11
Q

immunity of viruses:

A

intracellular phase:
· interferon
· NK cells
· cytotoxic T cells

extracellular phase:
· antibodies

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12
Q

viruses characteristics

A
  1. NOT CLASSIFIED AS CELLS
  2. Nucleic acid wrapped in a protein coat
  3. Require a host cell for replication and ‘energy production’
  4. Extracellular form -> virion
  5. Receptors (e.g. CCR5 for HIV)
  6. Classification is based on:
    · Envelope
    · Nucleic Acid
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13
Q

bacteria characteristics

A
  1. Unicellular organisms
  2. Fully independent existence
  3. Genome and machinery necessary for survival
  4. Prokaryotes
  5. Extracellular or intracellular
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14
Q

how can the cell wall of bacterias be

A

gram-positive (e.g. staphylococcus): thicker peptidoglycan layer and no outer lipid membrane
acid-fast (e.g. micobacterium tuberculosis)
gram-negative (e.g. E.coli): thinner layer

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15
Q

which diseases can bacteria cause

A

gut diseases / skin diseases / respiratory diseases

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16
Q

differences between a vegetative form and a resting form

A

vegetative form (trophozoite):
resting form (cyst)

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17
Q

steps of lung injury caused by Strep. pneumoniae

A

LytA causes bacterial autolysis
2. Release of pneumolysin -> pore formation in neutrophil membrane
3. induction of neutrophil cell death
4. neutrophil elastase released by dead neutrophils
5. impairs phagocytic activity of macrophages impaired
6. neutrophil elastase may induce IL-8 production from alveolar epithelial cells
7. neutrophil elastase triggers epithelial cell death

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18
Q

Pathogenicity island types and definitions

A

PI-I encodes a salmonella-secreted invasion proteins
Type III secretion system: unique virulence mechanism enabling them to inject bacterial effector proteins directly into the host cell cytoplasm
PI-II: Intracellular replication / immune system evasion

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19
Q

phenotypes of Escherichia coli and diseases they cause

A

· Intestinal / Diarrhoeagenic E. coli (DEC)
Gastroenteritis

·Extra-intestinal E. coli (ExPEC)
UTIs
Meningitis
Sepsis

20
Q

antimicrobial definition and types

A

A natural or synthetic chemical that kills/inhibits microbial growth.
- Antibiotics
* Produced by variety of bacteria and fungi
* Sole function of inhibiting or killing other microorganisms
- Antiseptics and Germicides
* Chemical compounds that kill/inhibit microbial growth * Nontoxic – can be applied to living tissues
* Often added to soaps, mouthwash, detergents

21
Q

define susceptible and resistant in antimicrobials

A

· Susceptibility - level of vulnerability of a microorganism to an antimicrobial
· Resistance - ability of microorganism to avoid the harmful effects of an antimicrobial

22
Q

Antimicrobial drug resistance is based on

A

· mutation of existing genes (SNPs) e.g. PBPs
· acquisition of foreign resistance determinants due to horizontal gene transfer (Plasmids, Transposons, Resistance islands)

23
Q

definition drug resistance

A

Acquired ability of microorganism to resist effects of an antimicrobial compound to which is it normally susceptible

24
Q

peptidoglycan cell wall

A

10-65 glycan chains connected by short peptides

25
Q

are gram-negative bacterias more resistant to antibiotics than gram-positves?

A

NO. The outer membrane is doesn’t make them more resistant at all. they are both the same.

26
Q

definition of human microbiome

A

full array of microorganisms (the microbiota) that live on and in humans.

27
Q

colonizing microorganism definition

A

Bacteria growing on exposed body sites, without necessarily causing any infection

is a complication in chronic wounds/ulcers

28
Q

biofilm definition

A

Complex consortia of adherent microorganisms
encased in a polymeric matrix

29
Q

what receptors are essential for TLR signalling

A

Toll/Interleukin-1 receptor (TIR)

30
Q

name 3 Bacterial TIR proteins

A

Escherichia coli
Salmonalla enterica
Yersinia pestis

31
Q

mechanisms of host evasion (6)

A

Inhibition of phagocytosis
Inactivation of complement
Inactivation of antibody
Intracellular growth
Manipulating antibiotic penetration
Changing antigenic appearance

32
Q

what does sterol aport to the fungi cell membrane

A

stability and permeability of lipid membrane

33
Q

types of candidiasis and explanation

A

Thrush –thick white adherent growth on mucous membranes, mouth and throat
Vulvovaginal infection –painful inflammatory –ulceration and discharge
Cutaneous candidiasis – moist areas of skin and burn patients

34
Q

definition of Polymorphism / dimorphism

A

Can grow as yeas

35
Q

virulence in candidiasis

A

Adhesion - Range of adhesins produced including agglutinin like sequence (ALS) proteins such as Als3 and glycophosphatidyl (GPI)-linked cell surface glycoproteins.
Biofilm Formation - Growth of pseudohyphae and hyphae concomitant with production of extracellular matrix . Efflux pumps CDR1 and CDR2 = antifungal resistance
Invasion - kills immune cells and enables invasion of tissues and dissemination through blood.

36
Q

name an important chemokine in c.albicans

A

CCL28 - mucosal associated / recruits neutrophils and is an antifungal peptide

37
Q

what is imoortant granuloma for

A

primary fungal pathogens

38
Q

Antifungal Vaccine

A

Currently there are no preventative antifungal vaccines for humans!
ALS3 (Candida albicans) and BAD-1 (Blastomyces) adhesins currently being investigated

39
Q

Antifungal Drugs

A
  • Exploit differences between fungal and mammalian cells
  • Need to inhibit the fungal enzyme but not the human enzyme

· Griseofulvin
- Dermatophytes
- Taken orally - binds to keratin
- Taken-up by fungi , binds to fungal microtubules
- Mitosis arrests at metaphase

40
Q

Sterol functions fungal cell membrane

A
  • Stabilise the cell membrane
  • Essential component of cell in many organisms
  • Required for stability and permeability of lipid membrane
41
Q

Antimicrobial Resistance (AMR) definition

A

The ability of microbes to grow in the presence of a chemical that would normally kill them or limit their growth

42
Q

symbiosis defintion Symbiosis

A

The ability of microbes to grow in the presence of a chemical that would normally kill them or limit their growth

43
Q

parasitism definition

A

“An organism living in or on another living organism, obtaining from it part, or all, of its organic nutriment, usually to the detriment of its host.”

44
Q

exo-erthrocytic stage

A
45
Q

erythrocytic stage in plasmodium cycle

A
  • invade red blood cells (erythrocytes) by endocytosis
  • it feeds on haemoglobin (produces 12-16 new merozoites)
  • the duration of this erythrocytic stage depends on the parasite species
  • Not all of the merozoites make more merozoites;
    some differentiate into gametocytes,
    and if a mosquito bites someone with gametocytes in their blood, it’s the gametocytes that will complete the parasite life cycle in the mosquito stomach.
46
Q

exo-erthrocytic stage in plasmodium cycle

A
  • happens away from red blood cells
  • the parasites invade liver cells (hepatocytes) and form a developmental stage called a schizont, inside which tens of thousands of merozoites develop.
  • the infected liver cells burst, releasing all those merozoites into the bloodstream,

pm 226 (2 decks)

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