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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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Biology 101 flashcards
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

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

A
  • Lag phase
  • Exponential phase
  • Stationary phase
  • Death phase
25
Q

Lag phase

A
  • Brief or extended, depending on start culture
  • Cells adjust to medium; gene expression occurs
26
Q

Exponential / logarithmic phase

A
  • Cell population doubles every generation
    • Time varies
      • Shorter generation time = faster growth
      • Vice versa
27
Q

Stationary phase

A
  • 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
Q

Death phase

A
  • 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
Q

Primary (1°) metabolite

A
  • Produced during tropophase
  • Thigns req. for growth, development, reproduction
  • Nucleotides, AAs, FAs, monosaccharides, fermentation products
30
Q

Secondary (2°) metabolite

A
  • 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
Q

Bacteriostatic antibiotics

A
  • Inhibit bacterial growth
    • Requires higher concentration to kill bacteria
  • Host immune system eliminates infection
  • MBC/MIC ratio > 4
32
Q

Bactericidal antibiotics

A
  • Kill bacteria
  • Inhibit /disrupt a vital cell function
  • MBC/MIC ratio ≤ 4
33
Q

Minimum inhibitory concentration (MIC)

A
  • Lowest concentration that inhibits visible bacterial growth at 24 hrs.
  • Specific medium, °C, & [CO2]
34
Q

Minimum bactericidal concentration (MBC)

A
  • Lowest concentration for a 1000-fold reduction (death) in bacterial density @ 24 hrs
  • Specific medium, °C, & [CO2]
35
Q

Which is better, bacteriostatic or bactericidal?

A

Bacteriostatic = superior & cost-effective; choice depends on what organism it is

36
Q

Broad-spectrum antibiotics

A
  • Effective against wide range (e.g. 30S subunits)
  • Used when causative organism unknown
  • Kills normal microbiome
  • Higher risk of resistance
37
Q

Narrow-spectrum antibiotics

A
  • Effective against fewer range
  • Used only if causative organism is identified
  • Does not kill as many normal microbiomes
  • Lesser chance of resistance
38
Q

Antibiotic resistance sprectrum continuum (chart)

A
39
Q

Tetracycline

A

Binds reversibly to 30S, inhibit aminoacyl-tRNA entry

Effective against Gram (-) & Gram (+)

40
Q

Sulfa drugs

A

Effective against Gram (+) & Gram (-)

41
Q

Streptomycin

A

Effective against Gram (-) & acid-fast bacteria

42
Q

Erythromycin

A

Effective against Gram (+) & bacteria w/o cell walls (mycoplasma)

43
Q

Penicillins

A

Original penicillin G mainly against Gram (+); newer have broader range, including Gram (-)

44
Q

Isoniazid

A
  • Effective against acid-fast bacteria only;
  • Inhibit cell wall mycolic acid formation in Mycobacterium spp.
  • Tuberculosis, leprosy, & atypical pneumonia
45
Q

Antibiotic Reistance Crisis

A
  • 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
Q

MDRO Infections (statistics)

A
  • 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
Q

ICD-10-CM

A

International Classification of Diseases, Clinical Modification

Codes relative to COVID-19 effective Jan 1, 2021. No codes in 2020.

48
Q

Klebsiella pneumoniae (Reno in 2016)

A
  • Resistant to 26 antibiotics
  • Right femur fracture & osteomyelitis of femur & hip
  • Travel to India
  • New Delhi metallo-beta-lactamase (NDM)
49
Q

Antibiotic Paradox

A

More antibiotics = misuse, overuse = more resistance and less effectiveness

50
Q

Antibiogram

A
  • 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
Q

MSSA stands for

A

Methicillin sensitive S. aureus

High resistance to ciprofloxacin

52
Q

MRSA stands for

A

Methicillin Resistant Staphylococcus aureus

53
Q

CoNS

A
  • Coagulase-negative staphylococci
  • Nonpathogens that incite nosocomial infections
    • Associated with intravascular catheter & immune compromised patients
54
Q

Multiple Drug Resistance (MDR)

A
  • Resistant to more than one antibiotic
    • Nonsusceptibility to at least one agent in 3+ categories
  • i.e. most MRSA are MDR
55
Q

Extensively drug-resistant (XDR)

A
  • Nonsusceptibility to at least one agent
    • Susceptible to only 1-2 categories
  • i.e. Mycobacterium tuberculosis
56
Q

Mycobacterium tuberculosis

A
  • Commonly resistant to isoniazid & rifampicin
  • A fluoroquinolone
  • 1/3 second-line parenteral drugs (non-oral method)
    • i.e. amikacin, kanamycin, or capreomycin
57
Q

Pan-drug resistant (PDR)

A
  • Resistant to all antibiotics
  • Nonsusceptibility to errrrrrythang

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