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MICROBIO BIOL-160 LEC > Antimicrobial Drugs > Flashcards

Antimicrobial Drugs Flashcards

1
Q

how were INFECTIONS treated before ANTIMICROBIALS were developed?

A
  • thought of HUMORS (ex. BLOOD, PHLEGM, BLACK/YELLOW BILE) have to be in BALANCE to PRESERVE HEALTH
  • thought INFECTIONS = EXCESS OF BLOOD (use of TECHNIQUE of BLOODLETTING)
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2
Q

what were some other medieval medical practices ?

A
  • use of HERBRAL REMEDIES
    use of DRIED CINCHONA BARK (grounded into POWDER) + MIXED WITH WATER
  • used to treat FEVER; BARK CONTAINED QUININE
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3
Q

how FATAL were diseases before ANTIBIOTICS?

A
  • EXTREMELY FATAL!!
  • Streptococcus pyogenes; the CAUSE OF HALF of POST-BIRTH DEATHS + DEATH FROM BURNS
    -    PNEUMONIA CASES – fatality rate 30 - 40%
  • **Staphylococcus aureous – fatal in 80% INFECTED WOUNDS + TB `
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4
Q

describe Paul Ehrlich–the Magic Bullet

A
  • developed and SPECULATED there are certain CHEMICALS that can DESTROY THE BACTERIA without harm to host
  • development of the idea CHEMOTHERAPY; therapy for diseases using CHEMICALS
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5
Q

describe Alexander Fleming

A
  • the first to discover the FIRST ANTIBIOTIC
  • discovered PENICILLIUM FUNGUS–create of antibiotic PENICILLIN; kills S. aureus
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6
Q

definition of ANTIBIOTIC

A

substance naturally produced by a MICROORGANISM that INHIBITS or KILLS another microorganism

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7
Q

definition of SYNTHETIC DRUGS

A
  • other group of antimicrobial
  • 1st; was the SULFA DRUGS–found by german scientists while screening SULFONAMIDE DYES
  • used in WWIi
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8
Q

describe ANTIBIOTICS

A
  • very easy to find in the ENVIRONMENT
  • USEFUL;
  • can find the SAME ONES OVER AND OVER
  • TOXICITY for the HOST
  • LOW EFFECTIVENESS in the HOST
  • around half of all ANTIBIOTICS made from Streptomyces spp. (type of FILAMENTOUS BACTERIA found in the SOIL)
  • MOLDS
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9
Q

describe antibiotics in the MODERN AGE

A
  • heavy use of HIGH-THROUGHPUT SCREENING METHODS
  • allows for greater screening of compounds and look for TREATMENT OPTIONS
  • only a COUPLE OF NEW ANTIBIOTICS FOUND
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10
Q

what is the MAIN GOAL of ANTIBIOTICS

A

target the pathogen while MINIMIZING HOST DAMAGE

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11
Q

what are the specific pathways to TARGET THE PATHOGEN (6)

A
  • target CELL WALL
  • target PROTEIN SYNTHESIS/RIBOSOMES
  • target CELL MEMBRANE
  • target METABOLISM
  • target NUCLEIC ACID SYNTHESIS
  • target specific ATTACHMENT and RECOGNITION
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12
Q

definition of BACTERICIDAL vs. BACTERIOSTATIC

A

BACTERICIDAL:

  • KILLS PATHOGEN

BACTERIOSTATIC:

  • only STOPS GROWTH of pathogen
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13
Q

describe MICROBIAL CHARACTERISTICS–who are they more effective against?

A
  • many antibiotics MORE EFFECTIVE towards GRAM POSITIVE BACTERIA–due to LIPOPOLYSACC in GRAM NEGATIVE OUTER MEMBRANE
  • Pseudomonas & Burkholderia are typically RESISTANT (due to PORINS–has selective ability for what goes in and out)
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14
Q

describe MYCOBACTERIUM

A
  • resistant to LOTS OF CHEMICALS
  • has WAXY LIPID RICH LAYER in CELL WALL; makes them ACID FAST + greater PROTECTION
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15
Q

describe RANGE OF ORGANISMS

A

BROAD SPECTRUM

  • affects a WIDE RANGE OF ORGANISMS (BOTH GRAM + and -)

NARROW SPECTRUM

  • affects only a FEW/SPECIFIC ORGANISMS targeted (ex. affects only GRAM + or MYCOBACTERIUM)
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16
Q

what happens when the PATHOGEN is EUKARYOTIC?

A
  • has more SPECIFIC TARGETS–shares a lot in COMMON PATHWAYS + ENZYMES with the HOST
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17
Q

what happens with VIRAL INFECTIONS?

A
  • use of HOST MACHINERY
  • targets the VIRAL INFECTION PROCESS;
    ENTRY, FUSION, ASSEMBLY, REPLICATION, and releases MECHANISMS + PROTEINS that are specific to the VIRUS
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18
Q

describe how antibiotics INTERFERE with CELL WALL SYNTHESIS

A
  • interfers with SYNTHESIS of the PEPTIDOGLYCAN CELL WALL of bacteria
  • is more of a NARROW SPECTRUM; against GRAM + ORGANISMS
  • have different MODES OF ACTIONS

ex. VANCOMYCIN interferes with peptidoglycan, but not in the same way that PENICILLIN does

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19
Q

how does PENICILLIN interfere with cell wall synthesis?

A
  • PENICILLIN–belongs to GROUP of 50 related antibiotics (known as Beta-Lactams)
  • works by PREVENTING CROSSLINKING of the PEPTIDOGLYCAN CELL WALL
  • WEAKENS CELL WALL&raquo_space;> leads to CELL LYSIS
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20
Q

describe characteristics of NATURAL PENICILLIN and SEMI-SYNTHETIC PENICILLIN

A

NATURAL PENICILLIN:

  • have PENICILLIN G (injected) + PENICILLIN V (oral)
  • susceptible to Beta-lactamase (begins to INACTIVATE PENICILLIN)

SEMI-SYNTHETIC PENICILLIN:

  • developed by SCIENTIST to overcome the DISADVANTAGES of NATURAL PENICILLIN
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21
Q

describe the SUBGROUPS in SEMI-SYNTHETIC PENICILLIN

A
  • METHICILLIN - beta-lactamase RESISTANT PENICILLIN
  • AMPICILLIN/AMOXICILLIN - has a more EXTENDED SPECTRUM
  • effective against BOTH GRAM +/- ORGANISMS
  • AUGMENTIN - has AMOXICILLIN (penicillin) + B-lactamase inhibitor (CLAVULANIC ACID)
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22
Q

describe Cephalosporins

A
  • NATURALLY OCCURRING – within the FUNGI of the GENUS ACREMONIUM
  • is bactericidal
  • has the SAME MODE OF ACTION as B-lactam antibiotics
  • LESS SUSCEPTIBLE to B-lactamases
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23
Q

describe Polypeptide antibiotics

A
  • BACITRACIN
  • active against GRAM +
  • INHIBITS CELL WALL SYNTHESIS
  • restricted TOP TOPICAL (can cause KIDNEY DAMAGE)
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24
Q

describe VANCOMYCIN

A
  • treatment for LIFE-THREATENING INFECTIONS by GRAM + BACTERIA that are UNRESPONSIVE to other antibiotics
  • targets CELL WALL SYNTHESIS
  • the LAST LINE OF DEFENSE AGAINST MRSA (INTRAVENOUS)
  • has now widespread use; have now VANCOMYCIN RESISTANT ENTEROCOCCI (VRE)
  • has become an OPPORTUNISTIC PATHOGEN in hospital settings
25
describe PROTEIN SYNTHESIS INHIBITORS
- ribosomes in PROKARYOTES are DIFFERENT from EUKARYOTES (70s vs. 80s) - have TWO SUBUNITS; 50s & 30s -- INDEPENDENTLY TARGETED - mitochondria also have 70s ribosomes
26
what are the PROTEIN SYNTHESIS INHIBITORS for the 50s SUBUNIT?
- CHLORAMPHENICOL - CLINDAMYCIN
27
describe CHLORAMPHENICOL
- inhibits the FORMATION OF PEPTIDE BONDS - is SYNTHETIC; isolated from Streptomyces - BACTERIOSTATIC - has a BROAD SPECTRUM
28
describe CLINDAMYCIN
- similar MODE OF ACTION to CHLORAMPHENICOL - has BROAD SPECTRUM - useful in infections caused by MRSA - can RARELY CAUSE LIVER DAMAGE
29
what are the PROTEIN SYNTHESIS INHIBITORS of the 30s SUBUNIT?
- AMINOGLYCOSIDES - TETRACYCLINE
30
describe AMINOGLYCOSIDES (3)
- interferes with the 30S SUBUNIT by changing its SHAPE; leads to ERROR in mRNA reading - is BROAD SPECTRUM - targets AEROBIC GRAM +/- organisms TYPES: - STREPTOMYCIN (gives PERMANENT DAMAGE to auditory nerves/kidneys) - GENTAMYCIN (against PSEUDOMONAS) - NEOMYCIN TOPICAL
31
describe TETRACYCLINE
- interferes with tRNA ATTACHMENT - BROAD SPECTRUM - can enter small amounts in MAMMALIAN CELLS--can be used in intercellular bacteria (Rickettsia + Chlamydia)
32
describe MACROLIDES
- group of antibiotics that have a MACROCYCLIC LACTONE RING - ERYTHROMYCIN; - binds to 50S + BLOCKS mRNA MOVEMENT - is BACTERIOSTATIC - similar spectrum to PENICILLIN G
33
how have new antibiotics developed? (2)
- developed in RESPONE TO VANOMYCIN RESISTANCE - LINEZOLID - mainly used vs. MRSA - RETAPAMULIN - TOPICAL USE against GRAM + ORGANISMS
34
describe the MECHANISM OF ACTION; injuring the CELL MEMBRANE
- both EUKARYOTES + PROKARYOTES have similar cell membranes - needs FATTY ACIDS - can target specific FATTY ACID SYNTHESIS PATHWAYS within PROKARYOTES - however BACTERIA CAN SCROUNGE LIPIDS FROM HOST - have specific antibiotics that ATTACK PLASMA MEMBRANES of BACTERIA
35
describe DAPTOMYCIN and POLYMIXIN B
DAPTOMYCIN - is BACTERICIDAL - against GRAM + BACTERIA POLYMIXIN B - attacks membranes of GRAM - BACTERIAL CELLS (topical only)
36
describe NUCLEIC ACID SYNTHESIS INHIBITORS
- have GYRASE and TOPOISOMERASE IV (EUKARYOTIC CELLS do NOT HAVE THESE) - can INTERFERE WITH ENZYMES --antibiotics can prevent BACTERIAL MULTIPLICATION
37
describe RIFAMPICIN
- inhibits RNA SYNTHESIS in both GRAM +/- BACTERIA - binds to BACTERIAL RNA POLYMERASE and INHIBITS TRANSCRIPTION
38
describe HOW ANTIBIOTICS INTERFERE WITH METABOLISM
- DOES NOT ATTACK COMMON PATHWAYS like glycolysis or Krebs - attacks PATHWAYS UNIQUE to PROGANISM ex. FOLIC ACID SYNTHESIS
39
describe ANTIFUNGAL DRUGS
- affects the STEROLS IN PLASMA MEMBRANE of FUNGI - has the PRINCIPAL TARGET of ERGOSTEREOL; important in FUNGAL CELL MEMBRANES--determines FLUDITY, PERMEABILITY, AND ACITIVITY of its MEM-ASSO. PROTEINS - begins to AFFECT FUNGAL CELL WALL - affects NUCLEIC ACID SYNTHESIS
40
describe POLYENES (affects STEROLS)
- AMPHOTERICIN B - can be TOXIC, only have LIMITED USE
41
describe AZOLES (affects STEROLES) - 2
- the MOST WIDELY USED - have IMIDAZOLE (topical use) - have KETOCONAZOLE (less toxic - can be taken ORALLY)
42
describe ECHINOCANDINS (fungal cell wall)
- UNIQUE--gives good target - inhibits the SYNTHESIS OF GLUCANS for the cell wall
43
describe FLUCYTOSINE (nucleic acid synthesis - fungal)
- seen in FUNGI ONLY - converted into 5-FLUOROURACIL = interferes with RNA SYNTHESIS
44
describe ANTIPROTOZOAN DRUGS
- QUININE used to CONTROL PROTOZOAN DISEASE - use of CHOLROQUINE - used to TREAT MALARIA (now have a lot of RESISTANT STRAINS - use of ARTEMISININ - kills the ASEXUAL STAGES of PLASMODIUM
45
describe ANTIHEMINTHIC + THREE TYPES
- greater increase of TAPEWORM due to consumption of SUSHI TYPES: - NICLOSAMIDE (is not absorbed in intest.) - PRAZIQUANTEL (affects PERMEABILITY OF WORM PLASMA MEMBRANE - IVERMECTIN (WIDE RANGE OF TARGETS)
46
how do we test SUSCEPTIBILITY
- use of DIFFUSION SUSCEPTIBILITY TEST; KIRBY0BAUER TEST-- shows ZONES OF INHIBITION - yields SUSCEPTIBILITY; look to see who is SUSCEPTIBLE or RESISTANT
47
describe COMPONENTS OF DIFFUSION SUSCEPTIBILITY TEST
- has MINIMUM INHIBITORY CONCENTRATION (MIC) - HAS MINIMUM BACTERICIDAL CONCENTRATION (MBC) - see and look for SERIAL DILUTIONS OF TREATMENT agent against growth
48
how do we ADMINISTER ANTIBIOTICS
- depends on ROUTES - DELIVERY focuses on the PROPER QUANTITIY TREATMENT + CORRECT DESTINATION + FASTEST DELIVERY - think of SAFETY - think of the LEAST DISRUPTION TO THE HOST
49
what are the DELIVERY METHODS (3)?
ORAL + LOCAL - SIMPLE BUT SLOW - can be SELF-ADMIN - have BLOOD EFFICACY (low and variable) IM - NEEDLES - BLOOD EFFICACY (intermediate) IV - have HYPODERMIC NEEDLE SYSTEm - BLOOD EFFICACY (high + cont.)
50
describe DRUG RESISTANCE
- bacteria are HIGHLY RESOURCEFUL - not all bacteria are EQUALLY SENSITIVE--have changes in GENOMIC MUTATIONS + HORIZONTAL TRANSFER (transformation + conjugation + transduction) - SURVIVE BETTER = ADVANTAGE (natural selection/evolution)
51
describe the MECHANISMS of DRUG RESISTANCE (5)
- INACTIVATES OR DESTROYS DRUGS - PREVENTION OF DRUG ENTRY - METABOLIC ADAPTATION - RESISTANCE PUMPS - TARGET MODIFICATION
52
describe how organism INACTIVATES/DESTROYS DRUG
- have creation of MUTANT B-LACTAMASES - start to DIGEST METHICILLLIN - MRSA resistant - more resistance to VANOMYCIN
53
describe how organism PREVENTS DRUG ENTRY
- modification of MEMBRANE PROTEINS - has RESISTANCE PUMPS--has a RAPID EFFLUX OF DRUGS
54
describe how organism has METABOLIC ADAPTION
- increase concentration of TARGET PROTEIN TO OVERCOME DRUG EFFECT
55
describe TARGET MODIFICATION
- changes its TARGET to be NO LONGER SUSCEPTIBLE
56
why do we have drug resistance; MISUSE
- have an OVERUSE OF ANTIBITOICS - a lot of diseases are VIRAl; continue to PRESCRIBE ANTIBIOTICS - feeding animals ANTIBIOTICS FOR GROWTH
57
why do we have drug resistance; THIRD-WORLD NATIONS
- have vary low rates of PRESCRIBED ANTIBIOTICS - leads to OVERUSE and IMPROPER USE
58
how to AVOID MAKING MORE DRUG RESISTANCE
- greater maintenance of HIGH CONCENTRATION - have PROPER TIME FRAME - LIMITATION OF DISTRIBUTION - use of MULTIPLE ANTIMICROBIAL to inhibit growth without exception
59
describe MULTIPLE DRUG RESISTANCE
- where DRUG IS RESISTANT TO MORE THAN ONE DRUG - typically acquired by PLASMIDS - often created in HOSPITALS - due to HIGH ANTIMICROBIAL TREATMENT LEVELS - ELIMINATION OF SENSITIVE CELLS + selective GROWTH OF RESISTANT CELLS

MICROBIO BIOL-160 LEC (21 decks)

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