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last lecture Flashcards

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Biology 101 flashcards
1
Q

commensals

A

coexist (neutral relationship) however, the commensals are kind of beneficial when kept in check as they gobble up resources that would otherwise be used by more harmful bacteria

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2
Q

opportunists pathogens

A

pathogens that take advantage of breaks/disruption in the host defense system

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3
Q

primary pathogens

A

cause disease on their own

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4
Q

what environments are dental plaque found

A

fissures, approximal surfaces, gingival crevices

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5
Q

what are the nutrient sources for dental plaque found in fissures, ph, and redox potential

A

saliva and diet, neutral-acidic, positive

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6
Q

what are the nutrient sources for dental plaque found in approximate surface

A

saliva, diet GCF, neutral to acidic, slightly negative

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7
Q

what are the nutrient sources for dental plaque found in gingival crevice

A

GCF, neutral-alkaline, negative

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8
Q

biofilm

A

a community of bacteria attached to a surface that is encased in an extracellular polymer substances of “EPS”.

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9
Q

biofilm formation aids the participating bacteria by

A

1) providing protection against host defenses
2) limit the diffusion of nutrients
3) protection against antimicrobial substance
4) providing energy storage
5) quorum sensing

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10
Q

quorum sensing

A

a form of bacterial communication that allows a community of bacteria to coordinate gene expression in response to the size of the population or environmental cues

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11
Q

autoinducers

A

molecules released during quorum sensing. released by all members of a particular species. once enough of these molecules bind to transcriptional regulators on the cell surface, target gene expression is induced

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12
Q

threshold value

A

how many molecules needed for a specific particular transcriptional regulator in quorum sensing

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13
Q

what are the 4 virulence factors of s. mutant that contribute to dental caries

A
  1. acidogenic
  2. acid tolerant
  3. glycolsyltranferase (GTF)
  4. gluten binding proteins
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14
Q

acidogenic

A

ability to metabolize carbohydrates and produce acid

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15
Q

acid tolerant

A

ATR more tolerant to acid environment than commensal bacteria

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16
Q

glycosyltransferase

A

extracellular enzyme that forms polymers of glucose from sucrose, liberating fructose. BIOFILM formation

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17
Q

gluten binding proteins

A

surface proteins that bind to glucan

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18
Q

what are the three commensal bacteria that prevent dental caries

A
  1. S.oligofermentans
  2. S. australis
  3. S. Gordonil
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19
Q

how do S. oligofermentans help prevent dental caries

A

production of H2O2 from lactic acid which inhibit S. mutans

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20
Q

how do S. australis prevent dental caries

A

production of NH3 from arginine which will raise plaque pH

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21
Q

how do S. gordonii help prevent dental caries

A

production of a protease that degrades CSP and antagonizes S. Mutans

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22
Q

periodontitis

A

chronic inflammatory disease which affects the tooth- supporting tissue and increases risk for other disease like atherosclerosis, diabetes, and rheumatoid arthritis

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23
Q

virulence factors of Pg that contribute to periodontitis

A
  1. capsule- antiphagocyctic, down regulates cytokine production, encapsulated strains more virulent
  2. gingipains- degrades extracellular matrix components, cytokines, immunoglobulin and complaint factors. decreases fibrinogen which increases bleeding
  3. fimbriae- required for binding to host cells
  4. LPS- lipid A modification evade TLR4 interactions
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24
Q

sterilization

A

kills all forms of microbial life
1 Chemical: gas, formaldehyde vapor
2. physical: autoclave, hot air oven, incineration

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25
Q

disinfection

A

doesn’t kill all microorganisms (spores)
1. chemical: alcohol, h2o2, chlorine, chlorhexidine, formaldehyde
2 physical: boiling, filtration, pasteurization

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26
Q

antiseptics

A

can be used with living tissues h202

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27
Q

antimicrobials

A

used for treatment of infectious disease. derived from FUNGI or BACTERIA (penicillin, tetracyclines, sulfonamides)

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28
Q

Nosocomial infections

A

acquired in a hospital, symptoms may show during or after say

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29
Q

sources of nosocomial infections

A
  1. endogenous-patients own microbiota

2. exogenous- transmission from external environment

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30
Q

known nosocomial pathogens

A

MRSA and VRSA often caused by staphylococcus aureus that is commonly on the external skin layers but not within the body

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31
Q

drugs b-Lactams and non b_lactams target

A

cell wall. interfere with cross linking by lysing cell wall (penicillin, vancomycin)

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32
Q

ahminoglycosides, tetracylines, chloramphenicol and macrolides target

A

protein synthesis. prevent tRNA from itialitng or translocating or prevent ribosomes from completing task

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33
Q

quinolone, sulfonamides, metronidazole and rifampin

A

target nucleic acid synthesis . either DNA or RNA will be broken down and folate synthesis will stop

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34
Q

polymyxin b target

A

cell membrane. permeability lost and cellular material leaks out

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35
Q

things present in bacteria that are not present in host cells

A

bacteria cell wall, 70 s bacterial ribosome, folic acid synthesis

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36
Q

drug resistance

A

drug kill most bacteria and the surviving bacteria are resistant to drug. new bacteria can thrive. antibiotics creates selection for resistance

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37
Q

5 mechanisms of bacterial resistance

A
  1. efflux pump
  2. blocked penetration
  3. altered target
  4. enzymatic activation
  5. genetic resistance
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38
Q

efflux pump

A

happens at cell wall and btonrols what passes through

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39
Q

blocked penetration

A

happens at cell walll

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40
Q

altered target

A

some organisms have altered receptors preventing drugs from binding. MRSA modified so penicillin cannot bind

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41
Q

Enzymatic activation

A
  1. b-lactam ihibitors- where penicillin is inhibited because bacteria modify the shape of the b-lactam ring and open it up so its no longer effective
    2 amino glycoside resistance- where a group of phosphates are removed from the drugs structure inactivating it and preventing it from binding
42
Q

3 types of genetic resistance

A
  1. intrinsic
  2. acquired
  3. mutational
43
Q

intrinsic resistance

A

structure provides a tolerance of certain drugs

44
Q

acquired resistance

A

developing resistance over time

45
Q

mutational resistance

A

resistance due to a genetic mutation

46
Q

pathogen

A

a bacterial species that is able to cause disease when presented with favorable circumstances

47
Q

extracellular pathogen

A

not able to invade host cells

48
Q

facultative intracellular bacteria

A

can invade host cells but can survive in extracellular enviornment

49
Q

obligated pathogens

A

requires host cell for survival

50
Q

pathogencitiy

A

ability of any bacteria to cause damage in a susceptible human host

51
Q

virulence

A

resumes pathogenicity, but allow expression of degrees from low to high

52
Q

low virulence strain

A

streptococcus salvarious. universally presented in oropharyngeal flora of humans

53
Q

moderate virulence strain

A

E. coli, universally found in colon but can cause bladder infection

54
Q

high virulence strain

A

Bordetella pertussis (whopping cough) not found in normal flora

55
Q

extremely high virulence

A

yersinia pestis causes plaque and highly infectious can lead to death in few days

56
Q

3 stages of establishing infection

A
  1. adherence
  2. colonization
  3. bacteria are taken up in host vesciles
57
Q

adherence

A

bacteria attach to host cell through specific pili, biofilms, fimbriae, or receptors. can bind to cell specific receptors mannose or fibronectin. first pili attachment brings organism closer to cell so second adhesion can occur (usually sugars teichoic acid) example. neisseria gonorrhoeae

58
Q

colonization or invasion

A

what are the nutrient sources for dental plaque found ingram neg bacteria have special secretion system that injects proteins into host cells. EFFECTOR PROTEINS promote invasion and suppress host defense

59
Q

bacteria taken up in host vesicle

A

take up through endocytosis in endosomes. endosomes fuse with lysosomes creating endolysosomes. invasive pathogens must disrupt normal cell vesicle trafficking or be able to escape the endosome and into the cytoplasm.

60
Q

ways bacteria can avoid being killed after entering cell

A

modify endosome to facility survival, escape endosome and replicate in cytoplasm, block endosome and lysosome fusion

61
Q

ways bacteria is killed once it enters cell

A

endolysosome digests bacteria, acidification

62
Q

transmission

A

long term survival of bacteria is dependent on ability to replicate, survive and be transmitted to another host

63
Q

modes of transmission

A

airborne, food borne, vector borne, water borne, blood borne

64
Q

inducible innate immunity

A

PAMPs, DAMPs AMPs, IgA, complement, phagocytes

65
Q

non inducible innate immunity

A

lysozyme, cilia of trachea, stomach acid, mucus, intact skin, commensal bacteria, flushing action of urinary tract, sequestration of iron

66
Q

many bacteria have ____ attachment mechanisms

A

multiple; pili or fimbriae and biofilm formation

67
Q

_____ is secreted into mucus; it helps prevent pathogens from adhering to mucosal surfaces aiding in bacterial clearance

A

sIgA

68
Q

sIgA protease

A

enzyme that pathogens have that can degrade that immunoglobulin. it cleaves sIgA in the hinge region to release the Fc portion from the Fab portion

69
Q

extracellular tissue fluid contains ____ that breaks down cell wall of gram + bacteria

A

lysozymes

70
Q

the _____ of ____ bacteria prevents penetration of lysozyme

A

outer membrane; gram -

71
Q

siderophores

A

pathogenic bacteria can produce siderophores which compete with human proteins for available iron, allowing for bacterial growth

72
Q

3 strategies for bacteria to avoid detection by immune system

A
  1. invade and survive inside host cell like macrophages
  2. avoid contact wth phagocytes
  3. inhibit phagocytic engulfment
73
Q

major infections caused by facultative intracellular bacteria

A

Mycobacterium tuverulosis (tuberculosis),, mayobacterium leprae (leprosy)

74
Q

major human infections caused by obligate intracellular bacteria

A

rickettsia rickettsia (rocky mountain spotted fever) rickettsia prowazekkii (endemic typhus)

75
Q

_____ bacteria have special secretion systems that inject proteins into host cells

A

gram negative (effector proteins)

76
Q

effector proteins function

A

promote invasion of host cells or suppress host cell defense

77
Q

how can bacteria avoid inducible innate host defenses

A

avoid phagocytosis by macrophages and PMN (polymorphonuclear leukocytes) by using a capsule

78
Q

capsules bind to ____ present in serum

A

factor h. this degrades complement protein C3b preventing its deposition on bacterial cell surface

79
Q

if the bacteria is able to avoid inducing a ______ then the host is unable to focus phagocytotic defense

A

inflammatory response

80
Q

inhibition of phagocyte chemotaxis

A

streptococcal kills phagocytes and suppresses neutrophil chemotaxis

81
Q

some bacteria can avoid engulfment though ____adaptions

A

specialized surface adaptions

82
Q

PAMSP are recognized by?

A

TLRs toll-like receptors

83
Q

Lipid A affects ____ of bacteria preventing antimicrobial peptides from attacking

A

surface charge

84
Q

how do bacteria avoid innate PAMPs antibodies and adaptive immunity

A

antigenic variation; varying surface antigens presents PAMPs from being recognized

85
Q

varying ____ prevents PAMPs form being recognized

A

sufrace antigenen

86
Q

some pathogens can activate _____ in cells and kill them

A

apoptotic pathways; decreases number of defenders and prevents alarm bells form osunding

87
Q

exotoxin a activates ____ to kill cells

A

apoptotic pathway

88
Q

in order for bacteria to survive they must not only survive dost defuse but also _____

A

distrust host function

89
Q

ways bacteria cause injury to host

A 
exotoxins
endotoxins
hydrolytic enzymes
superantigen
inflammation
90
Q

exotoxins

A

bacterial secreted proteins; have host cell specificity and bind to specific receptors. can have local and systemic effects depending on distribution. toxins can be

91
Q

endotoxins

A

lipid A proteins of LPS of Gram - cavteria. stimulates cytokine release (inflammation); induces fever through release of IL-1 and TNF from macrophages

92
Q

hydrolytic enzymes

A

facilitate tissue invasion (collagenase amor hyaluronidase)

93
Q

superantigen exotoxin

A

stimulate massive cytokine secretion

94
Q

inflammation

A

prolonged immune response to bacteria can damage host tissues (periodontal disease)

95
Q

3 things exotoxins can be

A
  1. inhibitory
  2. stimulatory
  3. fatal
96
Q

a-b exotoxins

A

b subunits bind host cell surface receptor glycoproteins or glycolipids. A (active)subunit gets transported by direct fusion or endocytosis into host cell and act son target protein

97
Q

membrane active exotoxins

A

create pores in host cell membranes. E coli or S. aureus. causes loss of cell integrity and leakage through DAMPs

98
Q

Parts of the endotoxin

A
  1. O antigen polysaccharide side chains
  2. core polysaccharide
  3. lipid a (toxin)
99
Q

lipid a toxin

A

phospholipid with glucosamine instead of glycerol located on outer membrane

100
Q

superantigen

A

polyclonal stimulator of t cells. binds to MMCH II and causes t cells to release cytokines

101
Q

staphylococcus aurees and group a strep

A

toxic shock syndrome

102
Q

pulmonary alveoli filled with OMNs and macrophages due to inflammation cant

A

absorb oxygen

Microbiology (7 decks)

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