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Pathogenic Microbes > Virulence factors > Flashcards

Virulence factors Flashcards

1
Q

Toxigenicity

A

P produce a wide range of biological poisons used to damage tissues, facillitate invasion and damage host’s defence mechanisms

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2
Q

Exotoxins

A

Produced by living P

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3
Q

Endotoxins

A

Lipopolysaccharides, componets of the cell wall of gram negative that are released from dead B or those undergoing division

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4
Q

Exo vs endo

A

insert

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5
Q

Exotoxin catrgories

A
  • A-B toxins: specific cellular targets
  • Cytolytic toxins- membrane disrupting
    -Superantigens: cause immune overactivation
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6
Q

A-B exotoxins

A

-B component, like a viral receptor, is responsible for cellular specificty of toxin and mediates initial attachment to cell surface receptors
-Once A-B toxins binds to host cell, it is brought into cell by endocytosis and entrapped in a vacuole
-A and B subunits separate as vacuole acidifies after fusion with lysosome. The A subunit enters the cell cytoplasm and interferes with specific internal cell function that it targets

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7
Q

diptheria toxin

A

-An ACleavagB toxin produced by cells of Corynebacterium diphtheria which binds to the host cytoplasmic membrane by way of its B subunit
-Cleavage of toxin allows A subunit to calayse ADP-ribosylation of elongation factor (EF2) which prevents it from binding to ribisome
-Prevents prtotein synthesis and results in cell death
-B has to be infected by phage to be harmful

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8
Q

Neurological exotoxins

A

Clostridum tetani
Clostridium botulinum

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9
Q

Botulinum toxin mechanism

A

-Most potent AB toxin
-Botulinum toxin acts at the motor end plate and prevents release of acetylcholine from vesicles
-Results in lack of stimulus to muscle fibers, irreversible relaxation of muscles and flaccid paralysis

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10
Q

Acetylcholine mechanism

A

-Acetylcholine is normally released from vesicles at neuronal side of motor end plate
-it then binds to specific muscle receptors inducing contraction

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11
Q

Glycine mechanism

A

-released from inhibitory interneurons and acts on motor neurons to block excitation and rlease of acetylcholine at motor end plate

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12
Q

Tetanus mechanism

A

Tetanus binds to interneuron to prevent release of glycine from vesicles, resulting in a lack of inhibitory signals to motor neurons
-Results in constant release of acetylcholine to muscle fibers
-Irreversible contraction of muscles and spastic paralysis

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13
Q

Cytolytic exotoxins

A

They degrade the cytoplasmic membrane integrity which causes cells lysis and death
-or it forms pores in cytoplasmic membrane causing an increase in membrane permeability

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14
Q

Hemolysins

A

Lyse red blood cells

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15
Q

E. hemolysins

A

Staohlococcal alpha toxin kills nucleated cells and lyses erythrocytes

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16
Q

E.Cytolysins

A

Cytolysins from Acinetobacter sp. target immune cells like macrophages

17
Q

Staphylococcal alpha toxin mechanism

A

-pore forming cytotoxin produced by Staphylococcus aureus
-Released as seven identical subunits which oligomerize in cytoplasmic membrane of target to form a pore which releases cell content
-In red blood cells, hemolysis occurs which indiactes cell lysis

18
Q

Superantigen toxin

A

-Cause an overstimulation and therefore dysregulation of immune system
-often result of localised infection but with systemic effects

19
Q

Superantigen producers

A

Gram-positive B, such as Staphylococcus aureus and Streptococcus pyogenes
-Superantigen poisoning can be triggered by food poisoning ( S.aureus), by toxic shock syndrome or by pyrogenic fever

20
Q

Superantigen mechanism

A

-They crosslink MHC-II Antigen Presenting Receptor and T cell receptor resulting in T-cell activation
-It bypasses specific affinity and causes the activation of any Th cells and this results in overactivation of immune system

21
Q

Superantigen lethal concentration

A

Concentration of less than 0.1pg/ml will stimulate T lymphocytes in an uncontrolled manner resulting in fever, shcock and death

22
Q

Mitogen

A

Factor that promotes cell proliferation

23
Q

do some gram negative not have endotoxins

A

No. The Lipid A component of the LPS is relatively consevred across different genera of gram negative B and is responsible for toxic properties of molecule
-therefore, toxic properties of Lipid A are similar regardless of gram-negative P

24
Q

Lipid A mechanism

A

Triggers immune system’s inflammatory response which is usually beneficial
-Too much LPS in blood can cause an excessive inflammatory response, leading to severe drop in blood pressure, multi-organ failure and death

25
Q

Detection of endotoxin

A

Presence can be detected by Limulus amoebocyte lysate (LAL) assay
-Overharvesting of horseshoe crabs is a concern as their blood is used in this assay
-These crabs have primitve blood that lyse in presence of LPS

26
Q

Iron significance and need for iron transporters

A

-It is essential in biological processes such as e transfer, TCA cycle, nitrogen metabolism
-Iron is not freely availible in host organism but is complexed to storage proteins or bound to proteins/metal complexes such as heme, transferrin, ferritin

27
Q

Siderophores

A

Virulence factors produced by both gram types
-They are high-affinity iron chelating molecules produced in response to iron deficiency
-P virulence is proportional to siderophore production
-Role is to sequester iron and transfer to B

28
Q

Siderophore uses

A

Biofilm formation
toxicity towards mitochondria
-Used to deliver antibiotics to resistant B via membrane transporters

29
Q

Trojan horse strategy

A

siderophores combined with antibiotic which allows it to be transferred into B

30
Q

Virulence factor genetics

A

They are encoded on integrative genetic elements (MIGEs) within B chromosome and mobile elements such as plasmides and bacteriophages

31
Q

Phage role in Virulence genetics (Prophage)

A

Many VF are encoded by prophages:
-Bacteriophages infect B and integrate into its genome to become prophages
-Prophage carries within its genome the VF genes

32
Q

Prophage diseases

A

-Cholera and diptheria are caused by prophages that express the toxin
-Necotising fasciitis caused by prophage in Streptococcus

33
Q

PAI

A

Pathogenicity islands
-Several virulence genes are clustered together on a chromosome
-seen in salmonella

34
Q

PAI acquisition

A

Horizontal gene transfer via transduction, conjugation (sex pili) and transformation (phage) allow B to adapt very quickly to host mmune system

35
Q

AbaR-type resistance islands

A

AbaR-type resistance islands (antibiotic resistance) are found in drug resistant Acinetobacter baumanii hospital strains
-Have transposon-like motility

Pathogenic Microbes (7 decks)

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