exotoxins are soluble proteins that are secreted by bacteria that can have pathogenic effects on the host, whereas endotoxins are bound to the bacteria cell wall. a common structural arrangement for toxins is a division between A and B subunits, where the A subunit contains the pathogenic element and the B subunit facilitates binding to the host cell. toxins have a host of potentially negative effects on host cells, such as affecting enzyme activity (inactivating ADP, ribosylating proteins involved in enzyme synthesis), damaging cellular structures (s. aureus can form holes in RBC membranes), and altering cell physiology (preventing neurotransmitter release, for example). toxins are a category within "virulence factors", which also includes enzymes that bacteria can release that can alter host cell physiology (see chart for more detail).several ideas/theories about disease and infections: Dr. Kate presented us with three models of how disease occurs-- first is invasion and inflammation, where the presence of the bacteria is the main pathogenic factor. second is infection with toxin production, where the bacteria plus the toxin both produce pathogenic effects. third is intoxication, where the toxin itself is the main pathogenic factor (as in food poisoning). in addition, there are three different types of infections based on the virulence of the pathogen: frank pathogens can cause disease in healthy individuals, such as v. cholera or b. pertussis. opportunistic pathogens such as p. auruginosas can only infect immunocompromised individuals. finally, superinfections are when bacterial infections grow to the point of overtaking other bacteria in the host, as in yeast infections.
there are 5 "stages" of disease. during the incubation period the bacteria multiply in the host without causing any noticable signs or symptoms. in the prodromal phase, signs and symptoms begin to manifest, but on a systemic, ambiguous level-- such as malaise or fatigue. in the illness phase, bacterial populations are at their max, signs and symptoms are severe and characteristic of a particular disease. the decline phase sees bacterial population and signs/symptoms disappearing because of treatment or immunity. finally, tissue repair and recovery occurs in the convalescence stage.
questions
basic ideas in pathogenesis...
1. what is meant by a "reservoir" in reference to a pathogen?
2. what is meant by "transmission"?
3. "entry"?
4. "fomites"?
5. what are three ways in which bacteria can cause disease?
6. what is invasion / inflammation characterized by?
7. describe the infection with toxin production method of causing disease.
8. describe "intoxication".
toxins...
9. what are exotoxins?
10. what are endotoxins?
11. what are the effects of endotoxin release on hosts?
12. what is the relationship between toxin production and Fe?
13. what are the transferrin and siderphore serum proteins?
14. what is a common structural arrangement for toxins?
15. what are some specific examples of the effects that toxins can have on cells?
16. how do toxins affect enzymatic activity?
17. what is an example of cellular structural alteration by toxin?
18. what are some examples of how toxins alter cell physiology?
19. give an example of a pathogen that produces a heat stable exotoxin.
20. what are the effects of the toxin from question 19 on the host? what foods have high potential for containing this pathogen?
different virulence factors...
21. what are virulence factors?
22. what does collagenase do and which bacteria produce it?
23. what does lecithinase do and which bacteria produce it?
24. what does coagulase do and which bacteria produce it?
25. what does leucocidin do and which bacteria produce it?
26. what does streptokinase do and which bacteria produce it?
27. what does staphylokinase do?
28. what does hyaluronidase do and which bacteria produce it?
29. and what about hemolysins?
types of infections...
30. what is a "frank pathogen"? what are some examples?
31. what is an "opportunistic pathogen"? what are some examples?
32. what is a "superinfection"? what are some examples?
what are some of the bacteria that are normally present in these body areas...
33. large intestine...
34. mouth...
35. skin...
36. vagina...
37. eyes...
38. nose...
39. throat...
40. what are transient microbiota?
41. what is sepsis?
42. septicemia?
43. bacteremia?
44. septic shock?
stages of infectious disease...
45. what are the stages of infection?
46. what is incubation period characterized by?
47. what is the prodromal phase characterized by?
48. what is the illness phase characterized by?
49. what is the decline phase characterized by?
50. what is the convalescence period characterized by?
definitions...
51. etiology / etiologic agent
52. iatrogenic
53. nosocomial
54. epidemiology
55. pyogenic
56. pyrogenic
57. what are koch's postulates?
answers
1. the normal place where a given pathogen can grow and persist.
2. the method by which pathogen gets from host to host.
3. the means by which the pathogen enters the host.
4. inanimate objects which can temporarily house pathogens, allowing them to be transmitted from host to host.
5. invasion / inflammation, infection with toxin production, intoxication.
6. a disease in which the bacteria itself is an integral part of the disease. often pyogenic.
7. an infection where the toxins are the main pathogenic factor, as in cholera.
8. an infection where the toxin is the main pathogenic factor and the bacterial organism is not necessarily present (such as food poisoning)
9. generally secreted proteins that produce pathogenic effects on a host. can be coded for on chromosome, plasmid, bacteriophage.
10. the lipid A portion of LPS on all gram negative bacteria.
11. diarrhea, nausea, fever, cramping, septic shock.
12. Fe plays a regulatory role in toxin production: as Fe concentration goes down, toxin production is induced.
13. transferrin is a carrier of Fe in the serum of humans. siderphore is a protein that bacteria uses to gather iron from transferrin for use in the bacteria.
14. two units, A and B. A is the functional, pathogenic unit, B is the binding unit.
15. affecting specific enzymatic activity, altering cellular structures, and inhibiting cell physiology.
16. by covalent inactivation of ADP, ribosylation of proteins involved in protein/enzyme synthesis.
17. s. aureus alpha toxin causes holes to form in RBC's.
18. tetanus blocking release of glycine by neurons, botulinum toxin blocking acetylcholine release.
19. staphylococcus aureus, which produces an enterotoxin.
20. symptoms include nausea, vomiting, diarrhea. no fever and rapid recovery. ham, custards, mayonnaise, high salt all risky foods.
21. enzymes or toxins that pathogens can make that can produce pathogenic effects in host.
22. breaks down collagen. produced by s. aureus, clostridium perfringens.
23. lyses cell membranes, especially with RBC's. staphylococcus, streptococcus.
24. coagulates fibrin in blood to protect bacteria against phagocytosis. s. aureus. s. epidermidis is coagulase-.
25. kills leukocytes by degrading lysosomes. s. aureus and streptococcus pyogenes.
26. breaks down fibrin in blood clots in order to facilitate spreading of pathogen. streptococcus pyogenes.
27. same action as streptokinase. staphylococcus aureus.
28. breaks down extracellular matrix and causes tissue damage. clostridium perfringes, streptococcus pyogenes, pseudomonas aeruginosa.
29. involved in hemolytic reactions via two mechanisms: punching holes in RBC membranes, and enzymatically degrading phospholipids in membrane. C. perfringens, streptococus pyogenes, staphylococcus spp.
30. a pathogen that can cause infection in a healthy individual, such as vibrio cholerae, bordetella pertussis, clostridium tetani.
31. a pathogen that can cause infection only in debilitated or immunocompromised individuals, such as psudomonas aeruginosa, burn patients, cystic fibrosis patients.
32. infection in which the bacteria overgrows other bacteria; commonly due to antibiotic treatment. examples: candida albicans, clostridium difficle.
33. gram negative facultative organisms, anaerobic rods, enterococcus
34. mostly aerobes, anaerobes at the teeth. viridans strep, staph, neisseriae, branhamella...
35. aerobic, anaerobic diphtheroid bacilli, corynebacteria and propionibacterium, s. epidermidis, fungi, yeast.
36. lactobacilli during first few weeks and after puberty (thrives in more acid environment). cocci and bacilli during neutral pH (before puberty)
37. corynebacteria and diptheroids.
38. s. pneumonia and s. aereus.
39. s. pneumonia, hemophilus, staph, strep, neisseria, diphteroids, mycoplasma.
40. organisms only present for a limited period of time, such as those that infect newborns.
41. the presence of unwanted bacteria.
42. infection with bacteria multiplying in blood.
43. bacteria present in blood.
44. caused primarily by LPS.
45. incubation, prodromal, illness, decline, convalescence.
46. multiplying of bacteria without any signs or symptoms.
47. manifestation of vague, systemic symptoms such as fatigue or malaise.
48. bacterial numbers are at their highest, signs and symptoms are severe, might lead to severe weakness or death.
49. treatment or immunity leads to lowering bacterial numbers and amelioration of signs / symptoms.
50. tissue repair and recovery.
51. the organism that causes disease.
52. infection resulting from treatment.
53. infection resulting from a hospital stay.
54. how and why diseases occur in a population.
55. pus forming.
56. fever forming.
57. a set of postulates that must be fulfilled for a pathogen to be the considered the etiologic agent for a particular disease: identify the pathogen that causes the disease. isolate outside of infected host and grow in vitro. reintroduce into healthy host and cause disease. re-isolate the same pathogen from newly infected host.
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