Bacterial pathogenicity Flashcards

1
Q

What are the stages of an infection?

A

Transmission, colonisation, proliferation and further transmission.
All whilst evading immune system destruction.

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2
Q

What is pathogenicity?
What is virulence?

A

Pathogenicity is the ability of an organism to cause disease whereas virulence is the degree of harm caused by the microorganism.

Pathogenicity is just yes or no! whereas virulence has degrees of harm.

Virulence depends on the microbe’s infectivity, invasiveness and degree of damage.

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3
Q

What are virulence factors?

A

Components that contribute to a microorganism’s pathogenicity and virulence:
Involved with adhesion, invasion, evasion, nutrient obtention and toxicity.

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4
Q

How is virulence measured?

A

ID50 = infectious dose, dose needed to infect 50% of hosts.
LD50 = lethal dose, dose needed to kill 50% of hosts.
Whether an infection leads to disease depends on the virulence, no. of bacteria + host resistance…

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5
Q

Salmonella enterica
Bacillus anthracis

A

Leads to food poisoning.
Produces anthrax = very potent toxin.

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6
Q

Direct vs indirect transmission?

A

Direct transmission occurs between host-to-host.
Whereas indirect transmission occurs using a vehicle/vector

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7
Q

What are portals of entry in humans?

What are the direct transmission routes through these portals?

A

Skin = uncommon, unless damaged.
Mucosal surfaces = more favourable = warm, moist, nutrient rich.

Respiratory = in the case of mycobacterium tuberculosis = which causes TB.
Body contact = STDs like gonorrhea, skin infections like warts, or damaged skin = staphylococcus aureus which causes infected wounds!

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8
Q

What are other direct transmission routes?

A

Faecal-oral route = contact, or indirectly via food, and GI tract pathogens like salmonella enterica.

Body fluid = Hepatitis, HIV.

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9
Q

What is vertical transmission?

A

From mother to child or inherited
Prenatal/postnatal etc, or germline through viral DNA for certain leukemias.

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10
Q

What are examples of indirect transmission routes?

A

Via Vehicles = inanimate objects.
Soil, contaminated water = Vibrio cholerae.
Contaminated food = Lysteria monocytogenes = in fridge = invade intracellularly!
Fomites = bedding, toys = Clostridioides difficle = spores can cause infection after competitors eliminated.

Via vectors
Anopheles spp. (mosquitos) can be used as a vector for Plasmodium spp. (malaria)
Warm blooded animals for rabies virus.
and Rat fleas for Yersinia pestis = black death.

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11
Q

Why is adhesion important for infection?
Why is a healthy gut microbiota needed?

A

In order to colonise, bacteria must first adhere to cells/tissues. Adherence to surfaces depends on adhesins.

Pathogenic bacteria need to survive in host environment and compete with normal microbiota - typical gut microbiome provides colonisation resistance.

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12
Q

What are bacterial adhesins?

A

Required for bacterial adhesion to cells/tissue.
Proteins: Fimbrial/Pili.
Tips of Pili interact with surface molecules like collagen binding protein.

Polysaccharides: Capsules, Teichoic/Lipoteichoic acid.
Polysaccharide adhesions tend to be aspecific.
Capsules = slime coats.
Teichoic acids are found on cell wall of Gram +ve bacteria.

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13
Q

How does E.Coli adhere to cells?

A

Escherichia coli causes UTIs.
Type 1 pili bind to sugar moieties on glycolipids of epithelial cells in the urinary tract.
fimH mutants had tips of Type 1 pili missing and didn’t cause UTI.

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14
Q

How do bacteria invade?

A

Intracellularly = penetrate cells + survive intracellularly + avoid antibodies.
OR extracellularly = invasion into tissue by breaking tight junctions/tissue barriers.

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15
Q

How is extracellular invasion carried out?

A

Enzymes attack ECM = degrade collagen with collagenases.
Degrade carbohydrate-protein complexes between cells.
Disrupt cell surface.

= Allows bacteria to access niches within the tissue, nutrient-rich, aid proliferation + spreading.

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16
Q

What are some common methods of extracellular invasion?

A

Streptococci and streptococci secrete Hyaluronidase to degrade Hyaluronan in ECM, streptokinase to digest fibrin clots and Haemolysin to lyrse RBCs.

Proteases/Glycanases.

Clostridium perfringes = Gangrene = secrete collagenases.

17
Q

What are obligate intracellular invaders?

A

Rickettsia spp and Mycobacterium leprae.
Typically microbes with small genomes that cannot survive independently, so require host machinery for survival intracellularly.

18
Q

How do no-obligate intracellular invaders work?

A

Intracellular invasion is a means of proliferation or spreading.

Phagocytic cells invade via phagocytosis, whereas non-phagocytic cells invade with systems inducing phagocytosis-like process.

19
Q

What is the process of bacterial invasion using phagocytosis?

A

Bacterium adhesion to the cell surface of phagocytic cell.
Phagocytic cell spreads the membrane around the bacterium, creating the phagosome.
The phagosome engulfs the bacteria and moves into the cytoplasm.
Phagosome fuses with lysosomes with digestive enzymes to form phagolysosome.

Phagocytic bacterium can survive within the phagolysosome or can escape phagosome before lysosome fusion.
However, most often, the phagocytic cell prevents lysosome fusion with phagosome.

20
Q

How do some species survive phagocytosis?

A

Coxiella burnetti can reside in the phagolysosome.
Salmonella and Mycobacterium spp can reside in unfused phagosome, preventing the fusion of lysosomes.
Lysteria monocytogenes or Rickettsia rickettsii can destroy/escape phagosome to reside in cytosol.

21
Q

What is the process of invasion for non-phagocytic cells?

A

Bacterium recruits host proteins to induce phagocytosis.
Salmonella + Pseudonomas use T3SS = Type 3 secretion system.
T3SS used to inject invasion proteins into host cell = activating the recruitment of actin + actin polymerisation to wrap around the bacterium.

22
Q
A