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Micro Biology > Chapter 16 > Flashcards

Chapter 16 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

A) What does symbiosis mean?

A

live together

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2
Q

B) What is mutualism? Give an example.

A

both benefit from relationship. some produse vit k and b which the host needs. host provides safe environment for bacteria to grow

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3
Q

C) What is commensalism? Give and example.

.

A

one is benefited but the other is unharmed: microbes on skin do not hurt it, but the skin provides food

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4
Q

D) What is parasitism? Give an example

A

one damaged the other to benefit itself: all pathogens, protozoa, and hemilinths

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5
Q

A) What are the normal microbiota in the body? [Figure 16.1]

A

ones normally found in the healthy body.

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6
Q

1) What is the normal microbiota most significant contribution?

A

protection against pathogens.

  • taking up nutrients
  • covering binding sites
  • producing toxins
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7
Q

2) How does the normal microbiota stimulate adaptive immunity?

A

they can influence development of mucousa- lymphiod tissues. The andtibodies that are produced against normal flora can bind to pathogens. T cells can also recognize harmless microbiota and therefore keep system from overreacting.

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8
Q

3) What is the hygiene hypothesis?

A

insuficient exposure to microbes can lead to allergies.

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9
Q

A) What does the word colonization mean?

A

microbe establishing and then growing on a surface.

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10
Q

B) When can you call a relationship an infection?

A

it is parasitic

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11
Q

C) What is subclinical infection?

A

mild to no symptoms that are not noticed, but there is and infection

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12
Q

D) What is an infectious disease?

A

results in disease

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13
Q

E) What are symptoms as opposed to signs?

A

are subjective effects of disease by the patient.

signs= objective evidence ie rash etc.

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14
Q

F) What is the difference between primary and secondary infection?

A

initial infection

secondary: a infection that arrises due to the primary

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15
Q

H) What is a primary pathogen?

A

mircobe that causes disease in healthy individuals

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16
Q

I) What is an opportunistic pathogen?

A

takes advantage of a immunocompromised individual.

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17
Q

J) What does the work virulence mean?

A

degree of how pathogenic/ stronf an organism is.

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18
Q

K) What are virulence factors?

A

traits of microo’s that specifically allow it to cause disease.

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19
Q

L) What makes a disease communicable?

A

spread form one host ot another

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20
Q

M) What is the infectious dose and how is it expressed?

A

the number of microbes neccessary to establish an infection

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21
Q

N) What is the course of an infectious disease? [Figure 16.2]

A

includes several stages:

incubation period, illness conalescence, latency, reoccurence

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22
Q

1) What are the different phases?

A

Incubation: time between ehn host was exposed and onset of illness

illness: person will expirience symptoms
- promodal phase of infection: first vague symptoms
convalesence: recovery from disease.

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23
Q

O) What are the differences between a localized infection and a systemic infection?

A

limited to a small area

systemic: spreads through the whole body

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24
Q

P) What does bacteremia mean?

A

bacteria is circulating in the blood stream

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25
Q

Q)What does toxemia mean?

A

toxins are circulating in blood stream

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26
Q

R) What does viremia mean?

A

viral particles are circulating in blood stream

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27
Q

A) What are Koch’s postulates? [Figure 16.3]

A

criteria koch used to determine that Bacillus anthraxis causes anthrax. it provides a foundation for establishing a certain microbe causes a specific infectious disease

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28
Q

2) When does Koch’s postulates not work?

A
  • is organisms cannot be grown in a medium in a lab.
  • some cases of polio and cholera do not expieirence symptoms
  • some are poly microbial meaning that different micro’s together cause a disease
  • some diseases do not infect animal, only humans
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29
Q

B) What are Molecular Koch’s postulates?

A

similair to koch’s postulates, but rely on molecular techniques to study a microbes virulance factors

  • virulant gene is found in pathogenic strains of org
  • mutating virulance gene takes away virulance of pathogen
  • reimplementing the virulance causes the disease/ restores virulance
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30
Q

C) What are the four patterns that pathogenic mechanisms follow?

A
  • micro o must be present in every case of disease
  • org must be grown in pure culture from diseased host
  • same disease must be produced when pure cultures is introduced to suseptible host
  • organinsm must be recovered from infected host.
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31
Q

D) What is balanced pathogenicity?

A

pathogens and host evolve. the pathogen becomes less virulent while the host becomes less suceptible.

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32
Q

A) Where are adhesins located and how are they used? [Figure 16.4]

A

bacteria use them. usually located on tips of pili.

can also be on curface structures

33
Q

1) Where do the adhesins attach?

A

the receptor.

34
Q

2) How specific is adhesin-receptor binding?

A

highly specific

35
Q

B) How do microorganisms colonize a mucosal surface?

A

they must produce their own iron binding molecules so they can survive on it ( cause lactoferrin and transferrin use up all fe )

36
Q

1) What are siderophores used for?

A

produce, or bind to hosts fe molecules

37
Q

2) How do these microorganisms avoid secretory IgA?

A

they have rapid turn over pilli and IgA prtoease which cleases IgA antibodies

38
Q

C) How does the type III secretion system work and what does it do? [Figure 16.5]

A

these are when pathogens “gives a shot” of protiens into eukaryotic cells to induce changes in it. some cause it to engulf the bacteria

39
Q

A) Which bacteria rely on skin damaging injuries to penetrate.

A

staphylococcus aureus, and yersina pestis

40
Q

B) How do pathogens enter the mucous membrane?

A

2 ways

  • direct uptake by cells
  • exploiting antigen sampling processes
41
Q

1) What is membrane ruffling and when does it occur? [Figure 16.6]

A

this is when gram neg bacteria inject effector protiens into host. These protiens changes the cytosplams and causes the membrane to ruffle. These ruffles enclose bacteria and bring then into the cell.

42
Q

2) How can a pathogen exploit the antigen-sampling process? [Figure 16.7]

A

this is when bacteria take advantage of the MALT system which brings in the bacteria to the macrophages, but some can kill the macrophages before they destroy them

43
Q

A) How do pathogens hide in host cells? [Figure 16.8]

A

they stay within the cell and cause ti to make an actin tail which propels it around and rams into other cells to transfer bacteria

44
Q

B) What are serum resistant bacteria? How do they avoid be killed?

A

these are bacteria that avoid being killed by compliment systems. They hijack hosts cells mechanisms that they use to trigger compliment system.

45
Q

C) How do pathogens prevent encounters with phagocytes?

A

They so this by avoiding macrophages and neutrophils altogether.

46
Q

1) What is C5a peptidase?

A

This degrades compliment systen C5 ( a chemoatractant)

47
Q

2) How do membrane-damaging toxins do what they do?

A

kill phagocytes by forming pores in phagocytes membranes

48
Q

D) How do pathogens avoid being recognized by phagocytes?

A

they prevent osponins, or other antibodies from coating it and therefore avoiding recognition by phagocytes.

49
Q

1) What benefit are capsules to pathogens?

A

They bind the hosts regulatory protiens of C3b mechanism

50
Q

2) How does the m protein benefit Streptococcus pyogenes?

A

binds to C3b regulatory protiens in hosts cell

51
Q

3) What do Fc receptors do? [Figure 16.10]

A

bind in the Fc regions of antibodies interfering with their function as osponins (Fc= red flag of antibody)

52
Q

E) How do some pathogens survive within phagocytes?

A
  • they escape from the phagosome before it joins with the lysosomes and then they multiply in the hosts cells cytoplasm
  • Prevent fusion of phagosome to lysosome: so this by prod. protien that blocks the fusion
  • Survive in the pagolysosome- able to withstand the conditions
53
Q

F) What mechanisms do pathogens have for avoiding antibodies?

A
  • IgA protease- tgus cleaves to IgA ( antibody found in mucous)
  • Antigenic Variation: routinely alter the structure of surface antigens
  • mimicking host molecules: pathogens cover themselves in molecules normally found in host.
54
Q

A) What are exotoxins? What are some examples? [Table 16.1]

A

protiens produced which have very specific damaging effects. botulism( can cause paralysis), diptheria( destrys cells, pus and blood all form a membrabe that disloges in back of airway and blocks it),

55
Q

2) What does the immune system do when exotoxins are present?

A

they produce nuetralizing antibodies

56
Q

3) What are toxoids and antitoxins?

A

a suspension of neutralizing bodies that help with syptoms of toxin mediated disease
toxoids: inactivated toxins, used in vaccines ie tetanus and diptheria

57
Q

4) What do neurotoxins damage?

A

damage the nervous system

58
Q

5) What symptoms are associated with enterotoxins?

A

intestinal distrubance, vomiting diareah

59
Q

6) What do cytotoxins damage?

A

interfere with cellular mechanism or cause lycing in a variety of cells

60
Q

7) What are A-B toxins and what do they offer for vaccine development? [Figure 16.11 and A B Exotoxins and Diphtheria Exotoxin video]

A

Two parts the A which carries the toxin and the B which binds to specific surface molecules of cells. This is neat because we can just administer the b part and get the body innoculated and build a defense for it.
They also hope to program the B to bind to specific types of cells and administer medications that way.

61
Q

8) What are membrane-damaging toxins and how do they work?

A

cytotoxins: disrupt plasma membranes causing them to burst. they insert themselves into the membrane and create pores that allow fluids to enter the cell

62
Q

9) How do superantigens affect the body and by what mechanism? [Figure 16.12 and Superantigens video]

A

they are able to overide the specificity of t cells response causing toxic effects due to release of cytokines. it does this by binding to MHC region of cell making the cell think that antigen is present when it probably is not there

63
Q

10) What does the toxin exfoliatin do to skin?

A

this causes it to crack because it degrades material that binds together to seperate

64
Q

B) What are endotoxins and how are the different from exotoxins? [Table 16.2]

A

endotoxins is a lipopolysacharide molecule that makes up outer layer of gram neg cell wall. cannot be converted to toxide to make vaccination. it is heat stable

65
Q

1) What is septic shock? What causes it?

A

when infection is systemic causing drop in bp, and fever.

66
Q

C) What type of damage can me caused by the inflammatory response?

A

leakage of permiable vessles results in sweeling, fever,drop in bp etc

67
Q

D) How do immune complexes affect the kidneys and joints?

A

anitbody-antigen complexes settle in the kidneys and joints to activate compliment system and therefore causing inflamation

68
Q

E) How do cross-reactive antibodies promote and autoimmune response? What’s the consequence?

A

when antibodies formed end up binding to self cells

69
Q

A) How are viruses able to attach to target cells?

?

A

they attatch at specific receptors

70
Q

B) How do viruses avoid the effect of interferons?

A

they end up destroying host genes, or preventing the interferons enzymes from activating

71
Q

C) How do viruses stop apoptosis in host cells and how does this relate to tumors?

A

by controling protien p53 when this is inhibited tuomors will develop

72
Q

D) How can viruses avoid being detected by the cellular immune response? [Figure 16.13]

A

interfere with antigen presentation on mhc. Some like herpes prevent any from showing ( but nk cells will kill cells if they don’t have any to recognize) So some will place false molecules out on their surface

73
Q

E) How do viruses, like HIV, avoid antibodies

A

they do this from moving from one cell to it’s neighbors before antibodies can get them. HIV cause cells to fUSE with their neighbors. This forms a syncyum

74
Q

A) What are dermatophytes how do they invade host tissue?

A

group of fungi that infect the hair, skin and nails, but do not go deep.

75
Q

1) Which fungi cause the most sever infections?

A

caused by dimorphic fungi. tjese occur as mold in environment which can then infect them

76
Q

2) What are mycotoxins and who produces them?

A

toxins produced by fungi. Asperfillus flavus is what grows on grains and nuts and can cause damage to the liver

77
Q

B) How do protozoans and helminthes enter the body?

A

they can either through bites, being ingested, and some can enter through skin themselves

78
Q

1) How do they avoid antibodies?

A

coat themselves in host protiens, they can hide within cells, or change their outer cell antigens

79
Q

2) What kind of damage do they cause?

A

some result in malnutrition, block organs, destroy tissues

Micro Biology (25 decks)

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