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Microbiology > Lesson 2.7 & 2.8 - Antimicrobial Resistance > Flashcards

Lesson 2.7 & 2.8 - Antimicrobial Resistance Flashcards

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1
Q

Define antimicrobials

A

Medications that kill microorganisms or inhibit their growth; grouped according to what they act against

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2
Q

Define antibiotics

A
  • Treat bacterial infections
  • Bactericidal (kill) vs. bacteriostatic (stop growth)
  • ‘against life’
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3
Q

Define antifungal / antimycotic

A
  • Kill fungi, prevent fungal infection (mycosis)
  • i.e. athlete’s foot, ringworm, candidiasis, cryptococcal meningitis
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4
Q

Define antiviral

A
  • Treat viral infections, don’t directly attack/kill viruses
  • Target aspect of viral life cycle
    • Attachment, penetration, uncoating, syntehsis, assembly, release
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5
Q

Plant products [before antibiotics existed]

A
  • Opium, morphine
  • Quinine, caffeine, cocaine
  • Salicin, digitoxin
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6
Q

Amputation [before antbiotics existed]

A

Ulcerous wound, gangrene

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7
Q

Diptheria toxin serum ca. 1891 [before antibiotics existed]

A

Horse antibodies neutralize toxin (if allergic, then patient gets anaphylactic shock)

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8
Q

Salvarsan for syphilis ca. 1911 [before antibiotics existed]

A

Arsenic compound; high toxicity (risk for poisoning if too strong)

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9
Q

Prontonsil ca. 1932 [before antibiotics existed]

A

Red dye w/ antitmicrobial activity & low toxicitiy

1st sulfonamide; technically a antimicrobial

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10
Q

Paul Ehrlich

A

Coined term “magic bullets;” aka selective toxicity (killing microbes without harming human cells)

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11
Q

Spanish flu (1918-19)

A
  • 675k U.S. deaths, 50 million worldwide
  • Infecctious disease was main cause of death before antibiotics existed
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12
Q

Death rates 1901 vs. 1996

A

Deaths per 100,000

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13
Q

Alexander Fleming (1928)

A

Discovered Penicillium spp. (fungus) inhibited bacteria on Petri disk; named compound pencillin & was not widely available until after WWII

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14
Q

Nobel Prize in Physiology or Medicine (1945)

A
  • Sir Alexander Fleming
    • Physician; antimicrobial compounds, original observation
  • Ernst Borin Chain
    • Chemist; purification
  • Sir Howard Walter Florey
    • Pathologist; production & clinical trials
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15
Q

Nobel Prize in Chemistry (1964)

A
  • Dorothy Crowfoot Hodgkin
  • Structure of penicillin using x-ray crystallography
    • +vit. B12 structure, insulin, etc.
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16
Q

Golden Age of Antibiotic Discovery

A

1940 - 1970

No need to memorize specific events

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17
Q

Sources of antibiotics

A
  • Fungi & bacteria (natural product)
    • Combinatorial chemistry = synthetic product made
  • Small # by de novo
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18
Q

Phylum Actinobacteria

A
  • Source of most antibiotics
  • Ubiquitous soil microorganisms also in fresh/marine ecosystems
  • Grow via hyphae
  • e.g. Streptomyces (80% of antibiotics from this phylum)
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19
Q

Products of Phylum Actinobacteria

A
  • Streptomycin, cephalosporin, tetracycline, vancomycin, chloramphenicol
  • Antiviral, antifungals, antiparasitic, insecticidal compounds
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20
Q

Original Hypothesis of how Fungi / Bacteria produce antibioitcs

A
  • Micoorganisms have geast or famine lifestyle
    • r-selected (good = up & bad = down)
      • Not k-selected (stable populations, i.e. elephants)
  • Survival of the fittest paradigms
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21
Q

Contemporary Hypothesis of how Fungi / Bacteria produce antibiotics

A
  • Antibiotics = signaling / communication molecules (like quorum sensing)
  • Sub-lethal concentrations change transcriptional pattern of target organism
  • Hormesis: positive response at low concentration; negative response at high concentrations (e.g. caffeine)
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22
Q

Targets of antibiotics (6)

A
  • Cell wall synthesis
  • Cell membrane
  • DNA replication
  • Transcription
  • Translation
  • Metabolic pathway
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23
Q

(6) Self-resistance mechanisms for producers

Study These Flashcards
A
  • Hidden by proteins
  • Efflux pumps it out
  • Target molecule protected
  • Enzymes inactivate it within cytoplasm
  • Binds to decoy molecules; it bypasses
  • Modified during biosynthesis to be inactive to producer

BE METH!

24
Q

Phases of Microbial Growth Cycle

Study These Flashcards
A
  • Lag phase
  • Exponential phase
  • Stationary phase
  • Death phase
25
Lag phase
* Brief or extended, depending on start culture * Cells adjust to medium; gene expression occurs
26
Exponential / logarithmic phase
* Cell population doubles every generation * Time varies * Shorter generation time = faster growth * Vice versa
27
Stationary phase
* Cell growth limited * Nutrient limitation (all C consumed) / buildup of waste * Cryptic growth, but balanced by cell death * Metabolism & biosynthetic functions continue * Physiologically different from exponential phase ANTIBIOTICS PRODUCED DURING THIS PHASE!
28
Death phase
* Viability decreases - lysis may or may not occur * Rate of death slower than growth * Metabolic & biosynthetic functions usually continue * Cells physiologically different from exponential
29
Primary (1°) metabolite
* Produced during **tropophase** * Thigns req. for growth, development, reproduction * Nucleotides, AAs, FAs, monosaccharides, fermentation products
30
Secondary (2°) metabolite
* Producing during **idiophase** * Not directly in growth, development, repro. * Important in ecological / environmental situations * Antibiotics, growth factors, toxins, pheromones, aromatic compounds, heat shock proteins
31
Bacteriostatic antibiotics
* Inhibit bacterial growth * Requires higher concentration to kill bacteria * Host immune system eliminates infection * MBC/MIC ratio \> 4
32
Bactericidal antibiotics
* Kill bacteria * Inhibit /disrupt a vital cell function * MBC/MIC ratio ≤ 4
33
Minimum inhibitory concentration (MIC)
* Lowest concentration that inhibits visible bacterial growth at 24 hrs. * Specific medium, °C, & [CO2]
34
Minimum bactericidal concentration (MBC)
* Lowest concentration for a 1000-fold reduction (death) in bacterial density @ 24 hrs * Specific medium, °C, & [CO2]
35
Which is better, bacteriostatic or bactericidal?
Bacteriostatic = superior & cost-effective; choice depends on what organism it is
36
Broad-spectrum antibiotics
* Effective against wide range (e.g. 30S subunits) * Used when causative organism unknown * Kills normal microbiome * Higher risk of resistance
37
Narrow-spectrum antibiotics
* Effective against fewer range * Used only if causative organism is identified * Does not kill as many normal microbiomes * Lesser chance of resistance
38
Antibiotic resistance sprectrum continuum (chart)
39
Tetracycline
Binds reversibly to 30S, inhibit aminoacyl-tRNA entry Effective against Gram (-) & Gram (+)
40
Sulfa drugs
Effective against Gram (+) & Gram (-)
41
Streptomycin
Effective against Gram (-) & acid-fast bacteria
42
Erythromycin
Effective against Gram (+) & bacteria w/o cell walls (mycoplasma)
43
Penicillins
Original penicillin G mainly against Gram (+); newer have broader range, including Gram (-)
44
Isoniazid
* Effective against acid-fast bacteria only; * Inhibit cell wall mycolic acid formation in *Mycobacterium* spp. * Tuberculosis, leprosy, & atypical pneumonia
45
Antibiotic Reistance Crisis
* Nonsuscpetible * ~2.8 million Americans acquire a resistant infection * ~35,000 Americans die (CDC) * $8 billion/year in healthcare costs * Antibiotic resistance adds $1,383 in treatment costs
46
MDRO Infections (statistics)
* Multiple drug resistant organisms * Estimated $2.9 billion to treat infection alone * MDRO sepsis could cause 70,837 inpatient deaths/year * 715k inpatient deaths * 34.4% due to sepsis * 28.8% due to MDR pathogens * Would make MDR bacteria 3rd highest cause of death in US
47
ICD-10-CM
International Classification of Diseases, Clinical Modification Codes relative to COVID-19 effective Jan 1, 2021. No codes in 2020.
48
*Klebsiella pneumoniae* (Reno in 2016)
* Resistant to 26 antibiotics * Right femur fracture & osteomyelitis of femur & hip * Travel to India * New Delhi metallo-beta-lactamase (NDM)
49
Antibiotic Paradox
More antibiotics = misuse, overuse = more resistance and less effectiveness
50
Antibiogram
* Antimicrobial suspectibility profile; screening for resistance * Advantages: * Helps identify best antibiotic treatment plan * Monitor trends (zone of inhibition) * Limitations: * Doesn't take into account patient history * May or may not apply to other patients * Doesn't demonstrate cross resistance
51
MSSA stands for
Methicillin sensitive *S. aureus* High resistance to ciprofloxacin
52
MRSA stands for
Methicillin Resistant *Staphylococcus aureus*
53
CoNS
* Coagulase-negative staphylococci * Nonpathogens that incite nosocomial infections * Associated with intravascular catheter & immune compromised patients
54
Multiple Drug Resistance (MDR)
* Resistant to more than one antibiotic * Nonsusceptibility to at least one agent in 3+ categories * i.e. most MRSA are MDR
55
Extensively drug-resistant (XDR)
* Nonsusceptibility to at least one agent * Susceptible to only 1-2 categories * i.e. *Mycobacterium tuberculosis*
56
*Mycobacterium tuberculosis*
* Commonly resistant to isoniazid & rifampicin * A fluoroquinolone * 1/3 second-line parenteral drugs (non-oral method) * i.e. amikacin, kanamycin, or capreomycin
57
Pan-drug resistant (PDR)
* Resistant to all antibiotics * Nonsusceptibility to errrrrrythang

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