module 3: microbial disease & control, antibiotics, immune systems, and vaccines Flashcards

1
Q

what does it mean to be “sterilizing”

A

sterile. 100% microbe free. absolutely no microbes

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2
Q

what does it mean to be “sanitizing”

A

acceptable.

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3
Q

what does it mean to be “antiseptic”

A

mouth wash or concerning the skin

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4
Q

what does it mean to be “disinfectant”

A

fomites. non-living things. wipes

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5
Q

what does it mean to be “microbicidal”

A

“to kill”; bactericidal, fungicidal, viricidal

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6
Q

what does it mean to be “bacteriostatic”

A

to slow the growth

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7
Q

what is a nosocomial infection, or HAI

A

Hospital Acquired Infection

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8
Q

list some chemical controls used to sanitize:

A
  • antiseptic (alcohol hand sanitizer)
  • disinfectants (chlorine)
  • heavy metals
  • detergents
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9
Q

what is the test used for antibiotic resistance?

A

Kirby Bauer test

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10
Q

list the main types of transmission:

A
  • skin to skin
  • respiratory
  • indirect (shared through object)
  • food
  • insect
  • rabid animal
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11
Q

MRSA - hospital acquired infection is referring to ____________________

A

antibiotic resistant Staphylococcus aureus

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12
Q

before the invention of antibiotics, what were the top 1 and 2 causes of death?

A

Pneumonia and Tb

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13
Q

after antibiotics, what are the top 1 and 2 causes of death?

A

heart disease & cancer

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14
Q

list the microorganisms that cause communicable/
infections disease

A
  • bacteria: Tb
  • fungi: yeast – mycosis
  • parasites: malaria
  • viruses: SARS-CoV 2
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15
Q

define “symptom”

A

some sort of physical condition that represents disease (ex. swelling)

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16
Q

what is an “opportunistic pathogen?”

A

an infection you get from a microbe that lives in/on you all the time, but all of a sudden causes disease
** example: yeast infection! Candida albicans **

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17
Q

what are “primary infections”

A

having a cold, the flu, or covid

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18
Q

what are “secondary infections”

A

12 days after the primary infection, getting a headache/mucus/sinus pressure
bacteria overtake from the damage the initial virus has caused, upsets the balance

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19
Q

what are “localized infections”

A

infection in a surgical wound, like a knee replacement

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20
Q

what are “systemic infections”

A

localized infection goes deeper and roots into the tissue, even into blood

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21
Q

what is “bacteremia”

A

bacteria in the blood. VERY bad

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22
Q

what is “septicemia”

A

bacteria progresses and infects organs. creates a massive immune system explosion which can lead to sepsis, and death

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23
Q

what are the 3 modes of transmission?

A

contact (direct, droplet, indirect)
vehicle (water, air, food)
vector (animal, insect, mite, tick)

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24
Q

what does it mean to be “antimicrobial”?

A

an umbrella term. any therapeutic chemical drug or treatment used to stop microbes (fungi, viruses, bacteria, etc)

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25
Q

what does it mean to be “antibacterial”?

A

a drug treating bacteria / bacterial infection. they are anti-living, and fight another living thing

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26
Q

how do antibacterial drugs work?

A

block vital processes in bacteria
kill the bacteria
stop them from multiplying.
all this relies on the patient having a working immune system

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27
Q

describe selective toxicity

A

antibiotics are toxic to bacteria, NOT human eukaryotic cells

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28
Q

where do antibiotics come from?

A

come from other microbes, but can now be synthesized in labs. in the past we’ve used soil bacteria

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29
Q

what decade was the start of antibiotics?

A

1940s

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30
Q

describe the chemotherapeutic index

A

ratio of the maximum tolerated dose of a chemical agent used in chemotherapy to its minimum dose. having a high therapeutic index is good!

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31
Q

what does it mean to have a high therapeutic index?

A

not toxic to us, but very toxic to bacteria

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32
Q

what is the broad vs narrow spectrum?

A

not every antibiotic is going to have the same effect on every pathogen

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33
Q

broad spectrum =

A

kill any

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34
Q

narrow spectrum =

A

very targeted

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35
Q

list some qualities of an ideal antibacterial drug:

A
  • selective target
  • bactericidal
  • narrow spectrum
  • high therapeutic index
  • few adverse reactions
  • various routes of administration
  • good distribution to site of infection
  • emergence of resistance is slow
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36
Q

MOA: Beta-Lactams

A

inhibit cell walls.
stops the building of peptidoglycan.
the drug targets transpeptidase, the peptidoglycan builder

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37
Q

MOA: Vancomycin

A

different structure from B-Lactams, but still attacks peptidoglycan in cell walls

38
Q

MOA: Aminoglycosides, Tetracycline, and Macrolides

A

inhibits protein synthesis.
some stop transcription from happening at the mRNA step,
others stop translation with the ribosome.
has to find targets that are specific to prokaryotes

39
Q

MOA: Polymixin

A

inhibits plasma membrane.
external only
contains 3 antibiotics (bacitracin, neomycin, polymixin) so the pathogens cannot mutate and take over all 3

40
Q

MOA: Quinolones

A

external & extremely broad spectrum
Cipro targets DNA gyrase
and Rifampin targets RNA polymerase

41
Q

MOA: Sulfonamides

A

inhibits a metabolic pathway through competitive inhibition
sulfonamide/trimethoprim act as imposters of the actual enzyme & block the building of folic acidsw

42
Q

what do antivirals do?

A

have varying MOA but prevent viral uncoating, replication, or release

43
Q

what do antifungals do?

A

inhibit the plasma membrane, specifically ergesterol

44
Q

what do antiparasitics do?

A

MOA is very specific and tricky, since parasites are eukaryotic just like human cells

45
Q

describe the issue of drug resistance:

A

antimicrobial resistance is on the rise as a result of…
- selection of drug-resistant strains in clinical environments
- the overuse and misuse of antibacterials
- the issue of not completing a prescribed dose
- poor patient compliance with antibacterial drug therapies

46
Q

what does broad spectrum antibiotic use increase?

A

increases the risk of resistance

47
Q

describe “antibiotic resistant mechanism”

A

a whole gene going from one pathogen, getting shared with another via horizontal gene transfer. happens in a population as an accidental mutation

48
Q

what is Augmentin?

A

contains penicillin & β-lactamase inhibitor

49
Q

what are biofilm infections?

A

1,000x more resistant to drugs than other infections. inner ear, surgical sites, joint replacements

50
Q

image with “blocked penetration, target modification, inactivation of enzymes, efflux pump”… what is this saying?

A

the image is saying all the ways bacteria can fight infections

51
Q

define “innate defenses”

A

non-specific, no memory

52
Q

what are the 3 kinds of innate defenses?

A

physical, chemical, cellular

53
Q

physical defense: skin

A

protects us from the outside world
epidermis, dermis, microbiota

54
Q

physical defense: lymphatic system

A

glands, lymph nodes, spleen
(lymph nodes = where white blood cells mature)

55
Q

physical defense: respiratory system

A

coughing, sneezing… expelling microbes from the body
(misc: eyelids tearing, urinating. also examples of physical)

56
Q

chemical defense:

A

natural compounds that inhibit bacteria growth.
chemicals produced by humans

57
Q

list some examples of chemical defense mechanisms:

A

salt in sweat, tears, breast milk (lysozyme)
stomach acid, sebum, urine, earwax
antimicrobial peptides/proteins
complement proteins (attack proteins in plasma)
cytokines

58
Q

describe/define cytokines

A

chemical communicators (like the commander).
signals that are communicated between cells.
produced by Leukocytes

59
Q

what are the different kinds of cytokines?

A
  • interferon: interferes with viral infection
  • complement cascade: important 4 blood, attack proteins in plasma
  • defensins: protein fighting microbe
  • histamines: swells
  • prostaglandins: temperature control
60
Q

what are Interkeukins?

A

a type of cytokines, between white blood cells… they regulate immune responses

61
Q

what are Leukocytes?

A

a general category of white blood cell

62
Q

list the different roles of Leukocytes in the innate immune system:

A
  • platelets: clot blood at cut sites
  • basophils
  • eosinophils
  • neutrophils – most active in the blood. high %
    (all 3 listed above are very active in innate immune sys)
  • macrophage/dendritic: gateway cells. important connection between innate & adaptive immune system
  • natural killer
63
Q

how are phagocytic cells activated?

A

cells have the ability to send signals to one another when something is foreign

64
Q

describe the roles of TLR and PAMP

A

these match up, indicate “this is not us” then attack

65
Q

what does PAMP stand for and what does it do?

A

Pathogen Associated Molecular Pattern
its a type of antigen… indication of a foreign thing

66
Q

in regards to bacterial pathogens, how does phagocytosis play a role?

A

it can either clear up the bacterial infection by “gobbling it up”
OR
sometimes small particles are used to teach the acquired immune system what to target

67
Q

what is an antigen presenting cell?

A

the gateway to teach the adaptive immune system by using PAMP and antigen

68
Q

what 3 names all refer back to an antigen presenting cell?

A

can be called antigen presenting cell, macrophage, or dendritic cell

69
Q

describe the main role of the antigen presenting cell

A

it presents an antigen to the acquired immune system by presenting the bacterial pathogen (antigen) to the MHC II

70
Q

what is MHC II?

A

what the antigen presenting cells use to show invaders

71
Q

what is MHC I?

A

the flaggers. they indicate “hey its me, I’m human”….
or it can tell your immune system “one of my cells isn’t doing well. I have a parasite. kill me”

72
Q

what are natural killer cells?

A

one type of lymphocyte in the innate immune system. they take out your body cells that aren’t doing well.

73
Q

how do natural killer cells attach to the MHC I complex?

A

they have a receptor called CD8

74
Q

what do the 5 immunoglobulin cases mean?

A

antibody being made

75
Q

define “antibody”

A

what your immune system makes to fight an invader

76
Q

define “antigen”

A

found on the surface of the pathogen

77
Q

live, attenuated vaccines:

A

reduce the virulence.
teaches the body the exact antigens without getting you sick

78
Q

inactivated vaccines:

A

killed virus.
pathogen that’s going to cause disease is shown to your body, but is completely dead

79
Q

subunit vaccines:

A

antigens.
break PAMP off microbe, but not the whole thing. no risk of causing infection/disease

80
Q

conjugate vaccines:

A

antigen & carrier protein.
no whole bacteria. helper protein attaches to sugars outside the cell

81
Q

briefly describe mRNA vaccines:

A

mRNA vaccines are injection to muscle cells. your ribosomes make polypeptides that say “fight this spike.” dendritic cells, deep in tissues, say “that’s not self” then make antibodies to fight it. they connect CD4 and helper T cells, and elicit the immune system.

82
Q

how does mRNA exposure help your immune system?

A

it has your body cells make the mRNA message, then produce polypeptides. your immune system will see that and carry on making antibodies

83
Q

MMR

A

live attenuated virus
measles, mumps, rubella (highly contagious, all viral)

84
Q

HEP-B

A

subunit vaccine (not entire virus, just antigen)
Hepatitis B virus. liver disease.

85
Q

Dtap, Tdap

A

subunit vaccine & toxoids.
upper respiratory infected

86
Q

Hib

A

conjugate vaccine
polysaccharide antigen

87
Q

PCV

A

Pneumococcal conjugate vaccine
fights Streptococcus pneumoniae

88
Q

IPV

A

inactivated viral vaccine
polio

89
Q

influenza

A

killed/inactivated virus - shot
live attenuated virus - spray
recombinant cell vaccine also available

90
Q

varicella

A

live (attenuated) virus
chicken pox & shingles