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54 Cards in this Set

  • Front
  • Back
Pathogenesis
how infections develop
Exposure to pathogens
coughing, sneezing, vectors (insects), fomites (pathogens on inanimate surfaces), injury
Adherence of pathogen to tissue
slime layer, pili, adhesion molecules
Colonization
Factors that allow pathogen to evade immune system, grows within host
Escape
exit strategies.
Virulence
the relative ability of a pathogen to cause disease
Virulence depends on presence of....
cell structures and/or production of toxins or other extra-cellular proteins called virulence factors.
Virulence factor genes are found on....
plasmids, lysogenic phage, and seperately on chromosomes (meaning they can be transferred horizontally).
Virulence factors related to cell structures include...
flagellae, pili, cell membrane (LPS), capsule, OMVs (outer membrane vesivles).
Biofilms are formed by a combination of....
slime and other adhesive molecules.
Some strains of E. coli have specialized fimbriae called ___.
colonization factor antigens (CFAs)
What do colonization factor antigens (CFAs) do?
allow them to adhere to intestinal cells, colonize, and produce disease
What is special about the pili in Neisseria gonorrhoeae and Neisseria menigitides?
They have many pilin genes for different pili that change to evade immune response. They use pili to adhere to urogenital (gonorrhoeae) and upper respiratory epithelial cells (minigitides).
What is key in Vibrio cholerae?
the fimbriae are key to colonization/infection.
Candida Albicans also produces...
fimbriae for adhesion to epithelial cells.
Capsules are usually composes of ____ and help microbes ___.
high molecular weight polysaccharide or amino acids (B. anthracis); evade immune cells (especially phagotcytes).
Some slime layers...
allow adhesion to tissue.
How does a biofilm occur in catheters?
We you puncture the skin it can get in the catheter and cause it to make a biofilm in it. They can also produce toxins.
Capsules of Streptococcus pneumoniae determine....
patient prognosis. The capsules evade the immune system and can kill you before your immune system even knows there is something wrong.
What is the complement way to evade the immune system?
N. Gonorrhoeae has special lipooligosaccharides that prevent MAC formation. There are also species that have complement-specific proteases (Like C5a).
The Ig way to evade the immune system.
N. Gonorrhoeae & others use antigenic variation. Slamonella sp. has many genes for flagella that are expressed; Borrelia burgdorferi constantly changes surface proteins, leading to relapses in Lyme disease.
N. Gonorrhoeae secretes....
an IgA protease.
S. aureus makes....
protein A that binds to IgG in the Fc region that inhibits opsinization.
What is coagulase/streptokinase?
It is a way to evade phagocytosis by allowing microbes to produce, hide in and grow in clots, then are released. Coagulase forms the clot and sterptokinase breaks it down.
What are leukocidans?
They are produced by microbes to evade phagotcytosis by killing phagocytic cells.
_____ all use actin based motility after they escape the phagosome.
L. monocytogenes, Shigella, & Rickettsia
How does Chlamydia evade phagocytosis?
It prevents the fusion of the phago- and lysosome.
What is another way to evade phagocytosis?
Pathogens make factors that inactivate or compensate for lysosomal action (ex. making high levels of super oxide dismutase.)
Explain the new concepts from Outer Membrane Vesicles.
- The bacteria pinch off a part of themselves from the OM and fill it with toxins.
- only Gram negative (ex. P. aeruginosa & E. coli)
- the vesicles fuse with the target cells, delivering cytotoxic molebules & adhesins into the cytoplasm.
- they act as decoys so the cell phagocytoses them and not the pathogen.
Exotoxins are typically....
proteins that are made and released by Gram +/- microbes (many are made from lysogenic phage or plasmid genes).
Neurotoxins
exotoxins that act on nerves to cause/block muscle contraction (C. botulinum, C. tetani)
What are enterotoxins? Two types of enterotoxins and examples.
they act on the GI tract to cause diarrhea.
1. Infectious diarrhea caused by growth of microbe in intestine (V. cholera, E. coli, Shigella sp.)
2. Food poisoning caused by growth of microbe in food, making toxins that are consumed (B. cereus, S. aureus).
What are pyrogenic exotoxins?
Cause the release of cytokines - rash, fever, (S. aureus, S. pyogenes)
What are tissue invasive toxins?
They destroy DNA, NAD, lyse RBCs and WBCs. (S. pyogenes)
What do superantigens do?
They cause pan-activation of the immune system.
Botulism toxins
ingested in food (from canning); spores; not heated enough to kill; binds to motor neurons and blocks release of acetylcholine, resulting in flaccid paralysis (muscles can't contract)
Tetanus toxins
released by C. tetani; work at spinal cord neurons; inhibits the release of other neruotransmitters that normally block the contraction of opposing muscles;
What are AB toxins?
2-component extotoxin produced by many pathogens; B subunit delivers A; ADP ribosyl transferases used NAD to produce ADP Ribose, which leads to cell death; "A" targets vary from elongation factors, things that increase cAMP; but all target proteins are inactivated when ADP Ribose it attached.
Types of Membrane Disrupting Exotoxins
2 types, both end up lysing cell;
1. Pore-forming - leukocidans produced by pneumo-, sterpto-, & staphylococci-; hemolysins also target erythrocytes, releasing iron.
2. Phospholipases - destabilize membranes of attacking immune system cells.
What are superantigens, and what are some examples?
they bind to MCH (I or II) and T cell receptor outside and independent of antigen-binding, causing pan-activation of T-cells and shock.
Toxic shock by S. aureus and scarlet fever by S. pyogenes.
Pathogenicity Islands occur when...
How are they transferred?
many virulence factor genes are clustered together with Insertion Sequences at the end; horizontally on plasmids and/or phage as a group;
What are Type III secretion systems?
Often found in the clusters of Pathogenicity Islands; they allow the direct transfer of toxins into cytoplasm of a host cell; it delays antitoxin response by host.
Chemical composition of exotoxins and endotoxins:
EX: Protein, often with A & B
EN: LPS complex on outer membrane; Lipid A portion is toxic
Disease examples of exotoxins and endotoxins:
EX: Botulism, tetanus, diphtheria
EN: Gram (-) infections, meningococcemia
Effect on host of exotoxins and endotoxins:
EX: Highly variable between each
EN: Similar for all endotoxins
Fever from exotoxins and endotoxins:
EX: No fever
EN: Fever from interleukin-1 and TNF
Genetics of exotoxins and endotoxins:
EX: Carried by plasmids
EN: Synthesized directly from chromosomal genes
Heat stability of exotoxins and endotoxins:
EX: Heat sensitive, inactivated 60-80 degrees C
EN: Heat stable to 250 degrees C
Immune response of exotoxins and endotoxins:
EX: Antitoxins provide host immunity; highly antigenic
EN: Weakly immunogenic; immunogenicity ass. with polysaccharide
Location of exotoxins and endotoxins:
EX: Excreted outside of living cell
EN: Part of outer membrane of gram (-) bacteria
Production of exotoxins and endotoxins:
EX: produced by gram +/- bacteria
EN: Gram (-)
Toxicity of exotoxins and endotoxins:
EX: highly toxic in small quantities
EN: Less potent and less specifif; causes septic shock
Toxoid production of exotoxins and endotoxins:
EX: converted to antigenic, non-toxoids used to immunize
EN: toxoids can't be made
Different ways of dissemination:
1. Within organism: attaching to macrophages; blood
2. From host-to-host: Vectors (arthropod)
3. Exotoxins ofter help spread (coughing, diarrhea, sneezing)
4. Anthrax produces endospores once host dies.