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Micro > lecture 5/6 - antibiotics > Flashcards

lecture 5/6 - antibiotics Flashcards

1
Q

antiviral

A

treat viral infections

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2
Q

antifungal

A

treat fungal infections

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3
Q

antibiotics treat …

A

treat bacterial infection

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4
Q

antimicrobials

A

treat any microbial infection (virus, bacteria, protists, fungal)

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5
Q

what are the two forms of antimicrobial resistance?

A
  1. natural resistance
    - natural feature of any microbe; encoded in microbe’s chromosome
    - Existed before antibiotic use
  2. Acquired resistance
    - arises in some strains of species; mutations occur on chromosome, plasmid, or transposon.
    - increased with antibiotic use
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6
Q

where do antibiotics come from?

A

metabolic products from aerobic bacteria and fungi.

-new drugs arise from altering the natural structure

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7
Q

what is minimum inhibitory concentration (MIC)

A

LOWEST concentration of antibiotic in which a species CANT GROW

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8
Q

what are the consequences of treating microbes with lower doses than MIC

A

-adds pressure but allows for microbial survival and potential for evolution of resistance.

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9
Q

In vitro kinetics

A

Done in broth or plate cultures to find the concentration of the antibiotic that inhibits growth.

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10
Q

In vivo kinetics

A

Diffusion in tissues, host protein interaction, drug interactions, immune system, multiple simultaneous infections, virulence of organism, site and severity of infection, dosage maintenance*

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11
Q

what are the goals of antimicrobials

A

Disrupt the cell processes or structures of bacteria, fungi, and protozoa
-inhibit viral replication

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12
Q

how do antimicrobial drugs work?

A
  • interfere with the function of enzymes required to synthesize and assemble macromolecules
  • or, destroy structures already formed in the cell
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13
Q

selectively toxic

A

drugs kill or inhibit microbial cells without damaging host tissues

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14
Q

name the 5 targets of antimicrobials

A
  1. protein synthesis inhibitors acting on ribosomes
  2. folic acid synthesis in the cytoplasm
  3. cell wall inhibitors
  4. cell membrane
  5. DNA/RNA
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15
Q

why isn’t the cell membrane the best target?

A

-poor selective toxicity d/t all organisms having cell membranes

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16
Q

what do organisms use to supercoil DNA?

A

gyrase —- critical for growth

** in all organisms

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17
Q

what type of antimicrobials inhibit DNA gyrase?

A

broad spectrum

Quinolone

ex) Nalidixic acid
ex) Ciprofloxacin

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18
Q

antimicrobials that act on RNA synthesis inhibit which replication action?

A

Transcription - copying of DNA into RNA

**works well because it is essential for all bacteria

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19
Q

what type of agents inhibit RNA synthesis?

A

Rifampin

  • binds to RNA polymerase (enzyme) tp prevent elongation of transcription
  • only bacteria
  • usful for TB

Pyronins

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20
Q

antimicrobials that act on Protein synthesis inhibit which replication action?

A

Translation - coding of RNA into proteins

**works well as it is a part of all bacterial replication

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21
Q

how do agents that block enzyme functioning work?

A

“competitive inhibition”

-antibiotic mimics normal substrate to block enzyme binding

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22
Q

what is a sulpha drug?

A

sulfanilamide inhibits folic acid synthesis in bacteria and protozoans by blocking enzyme receptors.

-folic acid is an essential nutrient made by PABA (we get from diet)

23
Q

Even pathogens with few virulence factors can infect through this portal of entry:

A

Intravenous
- HIV is able to get through the skin barrier via a needle and can infect us due to the lack of body defenses once in the blood stream

24
Q

Why are culture independent techniques important in the lab for identifying pathogens?

A

Many pathogens and most microorganisms don’t grow in the lab. Need alternate techniques that don’t need us to culture them- ex: virus so need culture independent to study and identify them. DNA sequencing, antibody-based techniques, PCR- aren’t strictly culture independent (refers to pathogen itself)

25
Q

Briefly describe the difference between an infection and a disease.

A

Infection: body colonized by infection can spread, may not be sick (many people can be carriers, but they don’t recognize they are sick ex: HIV (infectious agent), AIDS (disease)
Disease is when you’re actually showing symptoms

26
Q

what makes antibiotics effective?

A

harm the microbe and not the host

27
Q

what action is taken when a micro becomes resistant to antibiotics? what is the consequence of this?

A

Pathogens become resistance to first line so we move to second and third line defences
-increases the risk of them harming us while they are hurting the disease (less selective toxicity)

28
Q

what are the two main issues related to antibiotic use?

A
  1. Antibiotic-resistant bacteria

2. Complications from the use of antibiotics, such as Clostridium difficile colitis.

29
Q

CRE

A

carbapenem-resistent enterobacteriaceae

  • *resistant to nearly all antibiotics
  • only old drugs c/ significant toxicities and side effects work
  • kills 1/2 people who go septic c/ CRE
30
Q

MRSA

A

methicillin resistant Staphylococcus aureus

  • popular . 80000/year –> >11000 deaths
  • sask accounts for 8% of cases
  • **nosocomial infection
  • normal flora of skin, rose, respiratory tract, GI tract.

** commonly causes skin/ bone tissue infections, pneumonia, sepsis

31
Q

what does MRSA resistance mean?

A

first line treatments will FAIL.
second line drugs are LESS EFFECTIVE and have more SIDE EFFECTS
infections that might be treated with pills, now need IV medication

32
Q

VRE

A

vancomycin-resistant Enterococcus

  • few to no treatment options d/t natural resistance
  • emerged in 1988
  • 20000 cases per year, 1300 deaths
  • normal flora of bowels
33
Q

how is VRE transferred and why is VRE a fear?

A

-fecal contamination from not washing hands; occurs easily esp. in immunocompromised

fear that it could be transferred to other microbes such as MRSA

34
Q

Resistant N. gonorrhoeae

A
  • *urgent threat
  • 1/3 cases are resistant
  • almost 250000 cases of resistance – mostly to tetracycline

Resistance:

  • Control efforts begin to fail, leading to increasing rates of spread.
  • Increase in HIV (infection with Gonorrhoea makes spread of HIV easier)
  • increases susceptibility
  • Increase in Pelvic Inflammatory Disease (major cause of female infertility)
  • Increase in Epididymitis (cause of male infertility)
35
Q

clostridium difficile

A
  • 1/4million infections per year c/ 14000 deaths

- infection occurs as a result of antibiotic use - wipes out good bacteria and allows c.diff to overgrow

36
Q

what is the importance of hand washing?

A

80% of common infections are spread through hand contact

-hand washing can prevent this

37
Q

Carbapenems

A
  • beta-lactam antibiotics, broad spectrum
  • LAST RESORT - esp c/ E.coli
  • resistance rising since 2001

**outbreak in is real (2006) killed 50-70%

38
Q

virus

A

DNA inside a protein shell (capsid)

-hijacks host cell machines to reproduce

39
Q

bacteriophage

A

-specifically infects bacterial cells by poking through cell membranes c/ needle like structure. and injecting viral DNA inside to use machines and replicate its material, assemble viral particles and leave cell to infect more

40
Q

Mycobacterium tuberculosis

A

Cause of TB

  • has been around since 4000 BCE
  • in america since 100 CE
41
Q

Yersinia pestis

A

cause of the 14th century black plague

-killed 75-200 million (30-60% Europe population)

42
Q

how did bacteria affect human health prior to antibiotics?

A
  • -90% of children with bacterial meningitis died
  • -Strep throat was potentially fatal
  • -ear infections could spread to the brain, causing severe problems
  • -1 in 200 women died from infections acquired during childbirth
  • -3 in 10 people died from pneumonia
  • -1 in 10 people with a skin infection (from a scrape, cut, or scratching a bite) lost a limb
  • 1910–> 46% of deaths were d/t infectious disease
43
Q

who discovered penicillin?

A

1928 by Alexander Fleming

  • Ring where bacteria were not growing; discovered that the fungus (Penicillin) produces an antibiotic that prevents growth of and kills bacteria
  • first used in 1941 on a police officer ( worked well while supplies lasted
44
Q

how does antibiotic resistance occur?

A

natural selection
-lots of opportunity for gene mutations as bacteria replicate in 20 mins (some)

-caused by over use and improper use of antibiotics

45
Q

why is antibiotic resistance bad for health care workers and the human population?

A

Increased rates of antibiotic resistant organisms and decreased rates of new antibiotic discovery are leading us to a point where we will no longer have antibiotics to treat or prevent infections.

46
Q

what are three examples of situations in which antibiotics would be administered as a protective measure

A
  • Oncology -(cancer treatment) to prevent opportunistic infections that may kill patient
  • Surgery - hip and knee replacements in elderly pop especially
  • Obstetrics - c sections are safer with antibiotics to prevent infections during childbirth
47
Q

antimicrobial stewartship

A

promoting optimal pt outcomes c/ antibiotic use

-IS IT NECESSARY?
(right drug, dose, duration, route)
-collaborative effort c/ all health care workers in ALL facilities/ places

48
Q

S&S of bacterial infections

A
  • Temperature (> 37°C)
  • White Blood Cell Count (WBC > 10)
  • Vital Signs (respiration, heart rate)
  • Radiology Data
  • Laboratory Data
49
Q

Empiric Therapy

A

Initial treatment of an infection based on the best and most recent ‘evidence’:
Guidelines (best treatment/ what works best)
Medical Studies
Local Algorithm (rules to follow c/ different infections )
Local Antibiogram (road map for what bugs in your local region are resistant to what drugs)

50
Q

Targeted therapy

A

Treatment of an infection based on available test results:
Radiology Tests
Microbiology Results

51
Q

How is the right dose of antibiotic determined?

A

1.The type or severity of infection
-more severe > dose
Example: Upper vs. Lower UTI
2. The site of infection
-Hard to hit areas: CNS, bone, and heart valves have higher doses
3. Patient specific factors
-Liver and Kidney function (alters metabolism)

52
Q

how is the right duration of antibiotics determined?

A

Depends on infection:
Uncomplicated UTI = 3 days
Cellulitis = 5-7 days (if diabetic foot infection = 14 days, if there is bone involvement = up to 3 months)
Prosthetic joint infection = up to 6 weeks
Endocarditis = 2-8 weeks (depends on type of bug/valve)

Prolonged antibiotic use = resistance (BALANCING ACT)

53
Q

how is the right rough determined?

A

Parenteral (IV) versus oral (tablet/capsule/liquid)

1) Type of infection
2) Type of drug
3) Patient factors:
- clinically stable?
- other oral medications?
- regular diet?
- functioning GI tract?

Less time with IV = less chance of picking another infection/another infection
May need IV if low bioavailability as oral
Oral antibiotic is generally better if they are eating/drinking/taking other oral meds

54
Q

How is antimicrobial stewartship enforced?

A 
Prospective audit and feedback
-Hospital units or community settings
-Specific antimicrobials
-Specific disease states
Formulary restriction and preauthorization
-Save the ‘big guns’ for when we need them
Educate
-health care workers
-public
Research

Micro (12 decks)

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