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Microbiology > final > Flashcards

final Flashcards

1
Q

who was the first to discover vaccines?

A

Edward jenner, with cow pox

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2
Q

variolation

A

inoculation of cowpox into the skin

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3
Q

herd immunity

A

vaccination leads to it, vaccinated people act as barriers to protect unvaccinated people, lead to dramatic declines of certain disease

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4
Q

why was eradication of small pox possible?

A

no subclinical infections (easily identified)

no carries

humans are the only ones that can be infected

the vaccines was effective

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5
Q

measles worldwide before vaccination

A

2.6 million death/year , highly contagious ,

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6
Q

vaccination to measles decreased deaths by…

A

74%

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7
Q

why are cases of measles increasing now??

A

adults not getting their boosters, young babies can’t get their first vaccines for measles til month 12

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8
Q

hot spots for measles

A

Europe, Africa, Asia

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9
Q

SB277 law

A

children have to get vaccinated to go to school

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10
Q

how do vaccines work??

A

suspension of organism, fractions of organism or its products induce immunity.

  • antibodies and memory cells are produced
  • produce rapid and intense 2nd response
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11
Q

types of vaccines

A

attenuated, inactivated/ killed vaccines, toxoids, subunit, conjugated, nucleic acid

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12
Q

attenuated vaccines

advantage and disadvantage

A

-live, weakened microbes
-mimics the actual infection
-adv: highly effective, strong immunity
-disad: live, can become virulent
FLU shot, Swine flu

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13
Q

inactivated/ killed vaccines

A

dead microbes

  • safer, but may require boosters
  • rabies, flue , swine flu
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14
Q

toxoids

A
  • inactivated toxins
  • series of injection, require boosters
  • tetanus
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15
Q

subunit

A

(antigenic components of microbes)

  • safer, fewer adverse effects
  • havested hep B
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16
Q

conjugated vaccine

A

antigen and protein to boost immune response

-to prevent meningitis in young children

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17
Q

nucleic acid vaccines

A

DNA vaccines

-

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18
Q

what should an ideal vaccine be?

A
  • effective, safe, few side effects
  • give long lasting protections
  • ideally low in cost, stable, easy to administer
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19
Q

immunodeficiencies

A

inability of body to make and sustain adequate immune response

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20
Q

congenital

A

due to defective or missing genes

-DiGeorge Syndrome: no thymus gland

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21
Q

acquired

A

results of infection to other stressor
due to drugs, cancers, or infection
-develops during an individuals life time

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22
Q

AIDS

A

acquired immunodeficiency syndrome

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23
Q

what cells does HIV virus infect

A

CD4+

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24
Q

how was HIV discovered?

A

cluster of pheomocystis pneumonia, Kaposi’s Sarcoma , and loss of CD4+ cells

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25
Q

origin of HIV

A

SIV endemic to monkeys and Chimps in africa

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26
Q

why did HIV cross humans

A

in 1908 crossed to humans when animals skinned and used as food

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27
Q

how did HIV spread??

A

in Africa in results to urbanization and sexual promiscuity

-throughout the world via modern transportation and unsafe sexual activity

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28
Q

when did it enter the US?

A

1970s

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29
Q

Stages of HIV

A

HIV infection, HIV disease, AIDS

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30
Q

HIV infection

A

virus enters body and is replicating

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31
Q

HIV disease

A

infection causes signs and symptoms

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32
Q

AIDS

A

finals stages of HIV infection CD4+ cell count drop by a lot

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33
Q

Characteristics of HIV virus:

A

retrovirus, enveloped with spikes, has protein capsid, and 3 enzymes: reverse transcriptase, protease, and integrate
genetic material: two copies of ssRNA

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34
Q

How does the HIV infect the CD4 cell?

A

attachment with cd4 receptors recognized by spike of virus
fusion of HIV with cell
HIV entry and uncoats and relates its RNA

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35
Q

what happens when the virus is inside the cell?

A

viral RNA transcribes to cDNA by reverse transcriptase
viral cDNA is then integrated by integrase
translation of viral DNA, so made and then parts are integrated

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36
Q

diseases that follow after HIV has weakened the immune system?

A
  • fungal infections (pheumocystis jirovecii, histoplasma capsulatun, Candida albicans)
  • taxoplasma Gondi, mycobacterium tuberculosis, cytomegalovirus , herpes simplex,
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37
Q

How is HIV transmitted?

A

by direct contact with infected body fluids

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38
Q

in what fluid can you find the HIV virus? artificial insemmation

A

sweat, urine, saliva, tears, blood

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39
Q

how can you get infected with HIV

A

sexual contact, blood contaminated needles, blood transfusion or organs, artificial insemmation, vertical transmission (placenta

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40
Q

treatment for HIV

A

no cure, but there is treatment to help you live longer

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41
Q

HIV medications….

A

prolong life, designed to block replication of HIV, generally cocktails of different drugs

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42
Q

what HIV drugs are currently approved for the treatment of HIV

A

They all prevent entry or replication of the virus

  1. fusion/entry inhibitors
  2. reverse transcriptase inhibitor
  3. integrase inhibitors
  4. protease inhibitors
  5. tetherinns
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43
Q

fusion/entry inhibitors

A

prevent HIV entry by stopping fusion of HIV with CD4+ cells

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44
Q

reverse transcriptase inhibitors

A

prevent reverse transcriptase from happening

  • nucleoside reverse transcriptase inhibitors (NRTIs)
  • non-nucleoside reverse transcriptase inhibitors (NNRTIs)
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45
Q

integrase inhibitors

A

viral DNA will not be integrated in host DNA

-inhibits integration of cDNA into hosts

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46
Q

protase inhibitors

A

inhibit cleaving of viral DNA precursor proteins into structural and functional proteins

47
Q

tetherins

A

tether viruses to cells, prevent their release and spread

48
Q

what is Highly Active Antiretroviral Therapy (HAART)

A

a combination of at least 3 drugs to of the drugs above incase one misses, the other one won’t

49
Q

how can you prevent aids??

A

abstinence, public education, interrupt mother to child transmission , health case workers (use glove, gowns, masks, goggles, not recap needles )

50
Q

how can a mother transmit HIV to its child??

A

breast feeding, or at birth (through blood exchange)

51
Q

antimicrobial drugs

A

chemicals that interfere with growth of microbes within host

52
Q

antibiotic

A

substance produced by a microbe to inhibit another microbe

53
Q

chemotherapy

A

the use of drugs to treat diseases

54
Q

discovery of penicillin

A

discovered by Fleming
- penicillin In 1928
-

55
Q

who were the guys who actually did clinical trials on penicillin

A

Howard Florey and Ernest Chain

-mass production during WW2

56
Q

characteristics of antibiotics

A

bactericidal : kill bacteria

bacteriostatic : inhibit growth of bacteria

57
Q

why are antibiotics said to have selective toxicity?

A
  • inhibit or kill microbial pathogen w/o damaging the host

- target components different from or absent in human cells

58
Q

advantage and disadvantage of broad spectrum of antibiotic

A

advantage: kill wide range of bacteria
disadvantage: harms normal microbiota

59
Q

narrow spectrum of antibiotics

A

effective against few bacteria

60
Q

synergistic effects of antibiotics (better outcome)

A

you get a better outcome when you combine drugs

61
Q

antagonistic effects of antibiotics

A

decreases function of one drug or both

62
Q

good antibiotics must:

A

reach area of infection

63
Q

some antibiotics can not reach the area of infection

A
  • are not absorbed from the GI tract
  • do not cross blood-brain barrier
  • cannot enter abscesses or phagocytic cells
64
Q

antibiotics that inhibit cell wall synthesis

A

penicillin, oxacillin, ampicillin, Bacitracin, vancomycin, isoniazid, ethambutol

65
Q

why id inhibiting the cell wall important in an antibiotic??

A

because eukaryotic cells do not have cell walls

66
Q

how does penicillin work? (bactericidal )

A

prevent cross linking of peptidoglycan

-only affects growing cells
-most effect towards gram (+) cocci (narrow range )
-

67
Q

important structure in penicillin

A

beta lactam ring, natural penicillin is highly susceptible to penicillin—-> breaks the ring

68
Q

what breaks the beta lactam ring in penicillin ?

A

penicillinase

69
Q

semisynthetic penicillin ???

A

produced by mold and modified chemically by the addition of side chain

70
Q

what are the polypeptide antibiotics???

A

bacitracin and vancomycin

71
Q

bacitracin

A

for topical use only, effective against gram (+) bacteria especially staph and strep.

  • produced by bacillus
  • interferes with synthesis of linear strand of PTG
72
Q

vancomycin

A

glyco-peptide that prevent cross inking of peptides in PTG

  • does not affect gram (-) bacteria
  • last line against antibiotic resistant S. aureus
73
Q

antibiotics against mycobacterium

A
  • streptomycin and Rifampicin

- isoniazid and ethambutol

74
Q

streptomycin and rifampicin

A

traditional antibiotics again mycobacterium

75
Q

isoniazid antibiotic

A

effective against mycobacterium tuberculosis

-inhibits mycolic acid synthesis

76
Q

ethambutol

A

weaker antibiotic for mycobacterium to prevent resistance

-inhibits mycelia acids

77
Q

how do antibiotics that inhibit protein synthesis work?

A

they trigger the 70s ribosome

78
Q

antibiotics that inhibit protein synthesis?

A

chloramphenicol, erythromycin, tetracycline , and streptomycin

79
Q

chloramphenicol

A

bind so 50s portion and block polypeptide formation

80
Q

erythromycin

A

bond to 50s portion and prevents translocation

81
Q

tetracycline

A

the attachment of tRNA to mRNA to ribosome is inhibited

82
Q

streptomycin

A

changes shape of 30s and mRNA is read wrong

83
Q

inhibitors of nucleic acids

A

-rifampin and quinolone and fluoroquinolone

84
Q

rifampin

A

used for intracellular pathogen

  • inhibit rna pol and mana synthesis
  • readily penetrates tissues, csf, abscesses
85
Q

Quinolones and fluoroguinolones

A

used for urinary tract infections

-block dna synthesis by inhibiting DNA gyrase

86
Q

how do antibiotics that injure the plasma membrane work??

A

drugs can bind and cause structural changes in membrane that can lead to loss of metabolites and membrane function

87
Q

chemicals that damage the plasma membrane

A

lipopeptides B and polymyxin

88
Q

lipopeptides

A

loss of membrane potential and causes cell death

  • against gram +
  • from soil bacteria
89
Q

polymyxin B

A

produced by bacillus polymyxins

  • increase permeability of membrane
  • works with gram + and -
  • topical use only
90
Q

inhibitors of metabolic synthesis, why is this antibiotic a good target ?

A

selective toxicity because human don’t have this pathway

91
Q

inhibitors of metabolic antibiotics (what drugs do they include)

A

most are synthetic antibiotics

  • antimetabolites
  • competitive inhibitors
92
Q

antimetabolites

A

act as competitive inhibitors for essential needs of bacterial metabolism

93
Q

competitive inhibitors

A

sulfonamides

-broad spectrum, inhibit folic acid, bacteriostatic

94
Q

what is the disk diffusion test?

disadvantage

A

to determine effectiveness of an antibiotic against a specific bacteria

-cannot tell if it is bactericidal or bacteriostatic

95
Q

what is the purpose of the E test ?

A

estimates minimal inhibitory concentration (MIC)

96
Q

what is the purpose of Broth Dilution Test ??

A

determine the MIC and MBC of the antibacterial drug

97
Q

MBC

A

minimal bactericidal concentration

98
Q

why are microbes becoming resistant to antimicrobial drugs???

A

-widespread use and misuse of antibiotics

99
Q

how does bacteria acquire resistance??

A
  • -Acquisition of resistance genes

- -mutations

100
Q

what are the mechanisms in which microbes become resistant??

A
  1. block entry
  2. inactivate enzymes (enzymatic destruction of drug)
  3. alteration of target molecule (ribosome)
  4. efflux of antibiotic (rapid ejection of drug)
  5. over-synthesize target enzyme
101
Q

what are the 4 ways humans contribute to antibiotic resistance

A
  1. physicians responsibility to prescribe the right antibiotic and to educate their patient to take it the whole prescription
  2. responsibility of patients: they need to follow directions
  3. educate the public: teach them about antibiotics, they have no effect on viruses
  4. global impacts of antimicrobial drugs: overuse of antibiotics WW, they are used in animal feed
    antibiotics available without prescription, resistant to salmonella
102
Q

how is pneumonia caused ??

A

viruses, bacteria, allergies, amoeba

older people that are in bed for more than 3 days may get pneumonia

103
Q

hospital stay pneumonia

A

5 day stay in the hospital, mortality: 53,000

104
Q

what is pneumonia ??

A

fluid in the lungs

105
Q 
Pneumococcal Pneumonia (most common )
what causes it
A

80-90% of cases

  • kills 1/20 people who get it
  • caused by streptococcus pneumoniae (gram +)
106
Q

symptoms of pneumococcal pneumonia ???

consequences

A

Runny nose and upper respiratory congestion followed by cough w/ sputum, high fever, severe chest pain
-can also lead to other serious infections (meningitis, septicemia)

treated with antibiotics

107
Q

how can pneumococcal pneumonia be prevented ???

A 
with vaccine (pneumococcal polysaccharide vaccine) 
young people and older people are at higher risk to getting infection
108
Q

klebsiella Pneumonia

A

fatal

  • caused by Klebsiella pneumonia
  • 50-80 % mortality if untreated
109
Q

mycoplasmal pneumonia

A

walking pneumonia
caused by mycoplasma pneumonia (small, lacks cell wall)
-inflammation causes difficulty breathing

110
Q

influenza types and structure of virus

A

A, B, C

  • gemone is SSRNA
  • N spike: hemagglutinin (attachment )
  • N spike : neuraminidase (viral spread)
111
Q

how common if the flu??

A

infects 20% of human annually

-many deaths due unvaccinated people

112
Q

Flu in 2017-2018

A

number of cases : 49 million

highest since the swine flu in 2009 at 60 mill cases

113
Q

deaths per year due to the flu

A

79,000

114
Q

why do we have to keep getting new flue shots??

A

because antigenic changes&raquo_space;» antigenic drift (more dramatic changes, genetic reassortment, genetic mixing (new viruses , more virulent )

Microbiology (8 decks)

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