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Microbiology Unit 2 > Antimicrobial Drugs (BE # 4) > Flashcards

Antimicrobial Drugs (BE # 4) Flashcards

1
Q

Father of chemotherapy

A

Paul Erlich

guiding principle is selective toxicity - harm the pathogen, not the host

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2
Q

How is an antibiotic different from any other antimicrobial drug?

A

it is naturally produced by a bacterium or fungus

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3
Q

synthetic antibiotics

A

fully synthesized in laboratory

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4
Q

semisynthetic antibiotics

A

chemical modified after being isolated from natural sources, like bacteria & fungi

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5
Q

narrow spectrum antibiotics

A

target G(+) OR G(-) bacteria

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6
Q

broad spectrum antibiotics

A

target G(+) AND G(-) bacteria

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7
Q

What is a major disadvantage to using a broad-spectrum antibiotic?

A

wipes out normal flora bacteria as well, leaving patient more susceptible to super infection

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8
Q

Where do natural antibiotics come from?

A

fungi (Penicillium & Cephalosporium

bacteria (Bacillus & Actinomycetes)

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9
Q

3 major groups of beta lactam antibiotics

A
  1. Penicillin
  2. Cephalosporins
  3. Carbapanems
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10
Q

What is the MOA of beta lactam antibiotics?

A

they target the enzymes that create protein cross linkages between NAGA-NAMA sugar chains in the peptidoglycan cell wall. This creates weak points in the cell wall making the cell osmotically fragile. The cell wall can no longer withstand turgor pressure and lyses.

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11
Q

How are penicillins selectively toxic?

A

They affect the protein cross linkages in the peptidoglycan cell wall. Humans don’t have cell walls, so are not harmed.

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12
Q

Why are some penicillins not as effective against G(-) bacteria?

A

They are too large to fit through the porins (channel proteins) in the outer membrane.

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13
Q

Cephalosporins

A
  • start with “ceph” or “def”

* derived from fungi

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14
Q

What group of beta lactam antibiotics has been altered so it stays in the blood longer?

A

Carbapenems (beta lactam antibiotic + cilastatin sodium)

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15
Q

beta lactamase

A

an enzyme produced by resistant bacteria to break down beta lactam rings

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16
Q

Penicillianase

A

first beta lactamase discovered

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17
Q

MRSA

A

methicillin resistant Staphylococcus aureus

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18
Q

ESBL

A

Extended - Spectrum beta lactamases

Hydrolyzes (breaks down) penicillin & cephalosporin

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19
Q

CRE

A

Carbapenem-resistant Enterobacteriaceae

A family of bacteria resistant to nearly all antibiotics

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20
Q

KPC

A

An enzyme produced by CRE
Klebsiella pneumoniae carbapenemase
G(-)
Confers resistance to all beta lactam antibiotics (penicillins, cephalosporins, carbapenems); hydrolyzes all

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21
Q

NDM-1

A

An enzyme produced by CRE
New Delhi metallo-beta-lactamase
originally found in New Delhi
gene found in E. coli & Klebsiella pneumoniae

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22
Q

Penicillins

A 
Fungus - Penicillium notatum
Beta lactam antibiotics
narrow spectrum against G(+)
Methicillin
Ampicillin
Amoxicillin
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23
Q

Cephalosporins

A 
Fungus - Cephalosporium
Beta lactam antibiotic
broad spectrum
Cephalexin (Keflex)
Ceftriaxone (Rocephin)
Cefuroxime (Ceftin)
Cephadroxil (Duricef)
Cefaclor (Ceclor)
Cefixime (Suprax)
Cefprozil (Cefzil)
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24
Q

Carpapenems

A

Bacteria - Actinomycetes (Streptomycetes)
broader spectrum than cephalosporins

Imipenem (Primaxin) - beta lactam antibiotic + cilastatin sodium = stays in blood longer

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25
Q

Bacitracin

A

Bacteria - Bacillus subtilis

MOA - inhibits synthesis of glycan strands in peptidoglycan molecule, so wall structure is compromised & can no longer withstand turgor pressure. They lyse

Only used topically; part of triple antibiotic ointment

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26
Q

Glycopeptides (ex. Vancomycin)

A

Bacteria - Actinomycetes

MOA - binds to glycan strands to prevent protein cross-linking (doesn’t bind to enzyme like beta lactam antibiotics). Cell wall is compromised, can’t withstand turgor pressure, it lyses

Used against G(+) bacteria

Traditionally, “drug of last resort” against MRSA & entercocci

27
Q

Polymycin B

A

Bacteria - Bacillus poymyxa

MOA - disrupts cell membrane; act as detergents; attach to LPS’s and phospholiipids in outer membrane & plasma membrane; membranes are disrupted & get leaky.

Not very selectively toxic since eukaryotes have plasma membrane, too.

Only used topically; usually in triple antibiotic ointment

Effective agains G(-) because of outer membrane

28
Q

Quinolones

A

Nalidixi acid - uti’s traveler’s diarrhea (E. coli)
Ciprofloxacin Hydrochloride (Cipro) - anthrax
Levofloxacin (Levaquin) - bronchitis, pneumonia, chlamydia, gonorrhea, skin infections, uti

MOA - inhibition of DNA replication; targets enzyme that unwinds DNA prior to replication

29
Q

Metronidazole (Flagyl)

A

Flagyl

MOA - inhibition of DNA replication; taken up into DNA, forming unstable molecules. Only occurs when drug is reduced in anaerobic bacteria

Sleelctive toxicity: only affects anaerobic bacteria, not human cells, which are aerobic, or aerobic bacteria

effective against Clostridium difficile, protistan infections

30
Q

Rifamycins (Rifmapin)

A

Rifampin
Bacteria - Actinomycete

MOA - inhibits transcription; targets the enzyme, RNA polymerase, involve in transcription

Selective toxicity: prokaryotic RNA polymerase is different than eukaryotic RNA polymerase, so won’t affect humans

31
Q

Aminoglycosides

  • Streptomycin
  • Tobramycin
  • Neomycin
  • Gentamycin Sulfate
A

Bacteria - Actinomycetes

MOA - target the large or small subunit of the prokaryotic ribosome, interfering with some step in translation.

Selective toxicity - there’s a difference between prokaryotic & eukaryotic ribosomes. The ration of RNA proteins is different in prokaryotes & eukaryotes.

32
Q

Tetracyclines (Sumycin, Doxycycline)

A

Bacteria - Actinomycetes

  • Widest spectrum of activity of any antibiotic
  • Most common antibiotic added to animal feed
  • Can cause mild to severe toxic effects

MOA - target the large or small subunit of the prokaryotic ribosome, interfering with some step in translation.

Selective toxicity - there’s a difference between prokaryotic & eukaryotic ribosomes. The ration of RNA proteins is different in prokaryotes & eukaryotes.

Used to treat Lyme disease, can, uti’s

33
Q

Chloramphenicol

A

origninally obtained from Streptmyces bacteria, but now fully synthesized in lab

  • cheap & easy to manufacture - easy to get in Mexico
  • toxic to bone marrow
  • last drug of choice in US
  • used to treat bacterial meningitis
  • can cross blood brain barrier, so used to treat brain abscesses

MOA - target the large or small subunit of the prokaryotic ribosome, interfering with some step in translation.

Selective toxicity - there’s a difference between prokaryotic & eukaryotic ribosomes. The ration of RNA proteins is different in prokaryotes & eukaryotes.

34
Q

Macrolides

  • Erythromycin
  • Clarithromycin (Clarem)
  • Azithromycin (Zithromax = Zpac)
A

bacteria - Actinomycetes

  • Bacteristatic against most G(+)
  • valuable in treating infections caused by penicillin resistant orgs or those allergic

Erythromycin is considered one of the least toxic of commonly used antibiotics
MOA - target the large or small subunit of the prokaryotic ribosome, interfering with some step in translation.

Selective toxicity - there’s a difference between prokaryotic & eukaryotic ribosomes. The ration of RNA proteins is different in prokaryotes & eukaryotes.

35
Q

Lincosamide (Clindamycin)

A

semisynthetic

  • common side effect is Clostridium difficile - associate diarrhea (CLASSICALLY LINKED TO CLINDAMYCIN USE)

MOA - inhibition of translation; target the large or small subunit of the prokaryotic ribosome, interfering with some step in translation.

Selective toxicity - there’s a difference between prokaryotic & eukaryotic ribosomes. The ration of RNA proteins is different in prokaryotes & eukaryotes.

36
Q

Sulfonamides or Sulfa drugs

* Sulfamethoxazole (Bactrim or Septra)

A

Molecular mimicry - drug mimics the normal molecule, which inhibits a reaction in some way

First & only effective antibacterial available before penicillin

MOA - sulfa drug is very similar in structure to the compound PABA, so binds to the enzyme so that PABA can’t. Many bacteria require PABA to make folic acid (Vit B) which they use to synthesize nucleic acids & other compounds. When sulfa drug binds to the enzyme, bacterium can’t make folic acid.

Selective toxicity: animals obtain folic acid from diets, so don’t have the enzymes to make it themselves so are unaffected by the drug.

37
Q

Why is Augmentin, which contains a penicillin, effective against bacteria that produces beta lactamases?

A

Another antibiotic, clavulanic acid, is added to amoxicillin. Clavulanic acid binds to beta lactamases & prevents them from inactivating the amoxicillin.

broad-spectrum

38
Q

What is molecular mimicry?

A

a drug mimics the normal molecule, inhibiting a chemical reaction in some way.

39
Q

Explain how super infections occur.

A

They are caused by antibiotic use. Antibiotics kill off normal flora bacteria, changing the environment & making the patient more susceptible to other infections.

40
Q

Example of superinfection

A 
yeast infection (Candida albicans)
Clostridium difficile (diarrhea)
41
Q

What are 2 ways to deal with super infection caused by Candida albicans and Clostridium difficult?

A

take probiotics to restore natural flora

fecal bacteriotherapy (fecal transplant)

42
Q

instrinsic antibiotic resistance

A

innate / natural ability of a bacterial species to resist the activity of an antibiotic through its inherent structure or function. Ex. some beta lactam antibiotics have no effect on G(-) bacterial cell walls because they are too large to fit through porins in the outer membrane

43
Q

Acquire antibiotic resistance

A

mutations - during reproduction

genetic transfer (gene swapping) - resistant genes found on R plasmids can be transferred to another through conjugation through pili, transduction (viral vector) or transformation.

44
Q

How does natural selection allow resistant strains become dominant?

A

if a mutant is resistant to a drug, it will survive, but the nonresistant ones will die. After a few generations, most of the survivors will be resistant to the drug.

45
Q

cross resistance

A

resistance to 2 or more antibiotics via a common mechanism. Ex. penicillin contains beta lactam rings. Bacteria with the enzyme beta lactamase will break the rings. These bacteria are also resistant to some cephalosporins (they have beta lactam rings, too).

46
Q

Kirby Bauer method

A

Determines microbial sensitivities to antibiotics.

  • Bacteria is spread evenly on agar plate.
  • Filter paper disks are saturated with drug & placed on plate
  1. zones of inhibition - clear areas around bacteria
  2. bacteria are sensitive to drug - if there’s a clear area around disk (use it!)
  3. bacteria are intermediate - small zone w/ or w/o mutants (don’t use!)
  4. resistant - no zone (don’t use!)
47
Q

Why is it more difficult to treat fungal disease than bacterial disease?

A

They are eukaryotes like us, so there are fewer differences between cells. It’s more difficult to follow the principle of selective toxicity).

48
Q
  1. Why would a bacteriostatic antibiotic not be a good choice for an AIDS patient?
A

Bacteriostatic antibiotics inhibit bacteria so the immune system can get rid of them. AIDS patients are immunocompromised, so would not have the ability to fit them off.

49
Q

What is the MOA of many anti-fungals & how are they selectively toxic?

A

Many anti-fungals target egrosterol in the plasma membrane, which creates pore in it & causes leakage & death. Our plasma membrane cholesterol has a slightly different structure, so is unaffected.

50
Q

Polyenes (Amphotericin B & Nystatin)

A

produced by Streptomyces

  • binds to ergosterols, creating pores in membranes
  • used for treatment of systemic fungal diseases
  • used topically for Candida infections
  • toxic to kidneys
51
Q

Lotrimin (Clotrimazole)

A

an Azole

  • inhibits ergosterol synthesis
  • used for treatment of athlete’s food, jock itch, ringworm, nail infections
  • less toxic
52
Q

Lamisil (Terbinafine)

A
  • inhibits ergosterol synthesis
  • taken systemically for nail fungus
  • hepatoxic (liver) class action lawsuits
53
Q

Griseofulvin

A
  • blocks mirotubule assembly (proteins involved in mitosis)
  • binds to keratin in skin
  • used to treat tine capitis (ringworm) of hair, nails
54
Q

Miconazole (Monistat)

A

an Azole

  • inhibits ergosterol synthesis
  • OTC used for treatment of vaginal yeast infections
  • less toxic
55
Q

Fluconazole (Diflucan)

A

an Azole

  • inhibits ergosterol synthesis
  • often given as a single oral dose for treatment of vaginal Candida infections
56
Q

Name 5 ways drug resistance can be limited.

A
  1. maintain high levels of antibiotics long enough to kill pathogens and mutants
  2. administer 2 antibiotics together (Augmentin)
  3. Restrict antibiotic use to essential use only
  4. Take all of antibiotic
  5. Culture so you know exactly what is causing infection
57
Q

Nucleoside ananlog drugs

A

Antiviral drug

MOA - nucleosides are precursors to nucleotides (nucleoside = nitrogenous base + sugar). The analog drugs are similar in structure to nucleosides. They take the place of natural nucleosides, blocking the completion of a viral DNA chain.

Selective toxicity - Viruses incorporate these “fakes” more rapidly than do cells.

58
Q

Acyclovir (Zovirax)

A

Antiviral - Nucleoside Analog

treat herpes simplex & herpes zoster (chicken pox/shingles)

59
Q

Valtrex (Valocyclovir)

A

Antiviral - Nucleoside Analog

treatment of herpes zoster (chicken pox/shingles) & herpes simplex infections

60
Q

Ribavirin (Virazole)

A

Antiviral - Nucleoside Analog

  • treats respiratory syncytial virus (RSV).
  • In combo with interferons, shows some efficacy against Hep. C
61
Q

Azidothymidine (AZT)

A

MOA - HIV is RNA so must first go thru reverse transcription to make DNA from its RNA. AZT inhibits reverse transcriptase, the enzyme that makes DNA from viral mRNA. Viral replication is then stopped.

Selective toxicity - Humans don’t have this enzyme since our cells make mRNA from DNA in regular transcription (don’t do reverse transcription).

62
Q

Relenza & Tamiflu

A

MOA - work by blocking the function of the viral neuraminidase protein; virus cannot release from cell after budding from host.

treats influenza

63
Q

Flumadine (Rimantadine or Amantadine)

A

MOA - not fully understood; appears to inhibit the uncoating of the virus.

64
Q

Abreva

A

MOA - not fully understood; appears to inhibit fusion of enveloped herpes virus to human cells

OTC treatment of oral Herpes Simplex Virus

Microbiology Unit 2 (6 decks)

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