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Chapter 10 Flashcards

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Biology 101 flashcards
1
Q

Ancient history of antibiotics

A
  • ancient Egyptians, Chinese, and Indians of Central America used molds to treat infected wounds
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2
Q

Ancient history of antibiotics
- tetracycline
- red soils found in Jordan
- traditional Chinese Medicine (TCM)

A

Tetracycline found in bones 350-550 CE Late Roman period
• Only comes from ingesting the compound
• Incorporate into mineral portion of bone, enamel
Red soils in Jordan
• Antibiotic producing bacteria
• Actinomycin peptides (bind to forms of replicating DNA)
Traditional Chinese Medicine (TCM)
• Qinhaosu (artemisinin) extracted from plants
• Anti-malarial drug

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3
Q

History of antibiotics - anti and bios

A
  • an antibiotic is a chemical substance produces by one organism that is destructive to another.
    • anti: against
    • bios: life
  • antibiotic came from the word antibiotics, which means a process by which life could be used to destroy life
  • not just ‘the golden era’ of microbiology
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4
Q

The history of antibiotic agents
- Paul Ehrlich

A
  • “magic bullets”
    • arsenic compounds that killed microbes
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5
Q

The history of antibiotic agents
- Alexander Fleming

A
  • penicillin released from penicillium
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6
Q

The history of antibiotic agents
- Gerhard Domagk

A
  • he discovered sulfanilamide
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7
Q

The history of antibiotic agents
- Selman Waksman

A
  • antibiotics
    - antimicrobial agents were produced naturally by organisms
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8
Q

The foundation of the antibiotic era

A

Paul Ehrlich- Had an idea of magic bullet that would selective target only disease- causing microbes
• Synthetic dyes could stain specific microbes, but not others
1904-large –scale screening program to find drug against syphilis
• STD-caused by spirochete Treponema pallidum
• Mercury salts
1909: drug 606, cured syphilis-infected rabbits
• Hoechst manufactured and named Salvarsan, Neosalvarsan
Screening programs still remain
Sulfa drugs: sulfaanilamide

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9
Q

Antimicrobial chemotherapy

A

Goal of antimicrobial chemotherapy:
• Administer a drug to an infected person that destroys the infective agent without harming the host’s cells
A drug must be able to:
• Be easy to administer and able to reach the infectious agent anywhere in the body
• Be absolutely toxic to the infectious agent and absolutely nontoxic to the host
• Remain active in the body as long as needed and be safely and easily broken down and excreted

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10
Q

Characteristics of the ideal antimicrobial drug

A

• Toxic to the microbe but nontoxic to host cells
• Microbicidal rather than microbistatic
• Relatively soluble; functions even when highly diluted in body fluids
• Remains potent long enough to act and is not broken down or excreted prematurely
• Does not lead to the development of antimicrobial resistance
• Complements or assists the activities of the host’s defenses
• Remains active in tissues and body fluids
• Readily delivered to the site of infection
• Does not disrupt the host’s health by causing allergies or predisposing the host to other infection

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11
Q

Prophylaxis

A

Use of a drug to prevent infection of a person at risk
action taken to prevent disease, especially by specified means or against a specified disease.
- something like taking an antibiotic to prevent illness before having dental work done if you have metal in your body

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12
Q

Antimicrobial chemotherapy
Antimicrobials

A

Antimicrobial chemotherapy - the use of drugs to control infection (not just cancer treatment, but the use of drugs to eliminate infection)

Antimicrobials - all-inclusive term for any antimicrobial drug, regardless of its origin

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13
Q

Antibiotics

A

Substances produced by the natural metabolic processes of some microorganisms that can inhibit or destroy other microorganisms; generally, the term is used for drugs targeting bacteria and not other types of microbes

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14
Q

Semisynthetic drugs
Synthetic drugs

A

Semisynthetic - drugs that are chemically modified in the laboratory after being isolated from natural sources (modified after they come from a natural source like a lab)

Synthetic - drugs produced entirely by chemical reactions (produced entirely in the lab)

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15
Q

Narrow-spectrum (limited spectrum)
Broad-spectrum (extended spectrum)

A

Narrow - Antimicrobials effective against a limited array of microbial types - for example, a drug effective mainly against gram-positive bacteria

Broad - Antimicrobials effective against a wide variety of microbial types - for example, a drug effective against both gram-positive and gram-negative bacteria

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16
Q

Before therapy can begin what three factors should be considered

A

• The identity of the microorganism causing the infection
• The degree of the microorganism’s susceptibility (also called sensitivity) to various drugs
• The overall medical condition of the patient

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17
Q

Identifying the agent

A

Identification of infectious agents should begin as soon as possible:
- first need to know if it is Gram-positive or Gram-negative

• Should occur before antimicrobial drugs are given, before their numbers are reduced
• Direct examination of body fluids, sputum, or stool samples is a rapid method for detection
• Doctors often begin therapy on the basis of immediate findings and informed guesses
• Epidemiological statistics may be required

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18
Q

Testing for drug susceptibility
- four organisms it is necessary for

A

Testing is necessary for the following organisms:
• Staphylococcus species
• Neisseria gonorrhoeae
• Enterococcus faecalis
• Aerobic, gram-negative intestinal bacilli

If the treatment is ineffective for fungal or protozoal infections initially, drug testing is essential. In general, these tests involve exposing a pure culture of the microbe to several different drugs and observing the effects of the drugs on growth.

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19
Q

The Kirby-Bauer Technique

A

• Surface of an agar plate is spread with test bacterium (for example)
• Small discs containing a prepared amount of antibiotic are placed on the plate
• Zone of inhibition surrounding the discs is measured and compared with a standard for each drug
- this is qualitative technically, but in this scenario in bio it is quantitative. The zone for the antibiotic is specific to that antibiotic

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20
Q

What is the tube dilution test

A
  • More sensitive and quantitative than the Kirby-Bauer test
  • Antimicrobial is diluted serially in tubes of broth
  • Each tube is inoculated with a small uniform sample of pure culture, incubated, and examined
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21
Q

Minimum inhibitory concentration (MIC)

A
  • the smallest concentration (highest dilution) of drug that visibly inhibits growth
    • useful in determining the smallest effective dosage and providing a comparative index against other Antimicrobials
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22
Q

Response to treatment

A
  • in vitro activity of a drug is not always correlate with the Vivo effect
    Failure or antimicrobial treatment is due to:
    • The inability of the drug to diffuse into that body compartment (brain, joints, skin); this can include the possibility that the microbes are in a biofilm
    • Resistant microbes in the infection that did not make it into the sample collected for testing
    • An infection caused by more than one pathogen (mixed), some of which are resistant to the drug
    • In outpatient situations you have to also consider the possibility that the patient did not take the antimicrobials correctly
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23
Q

The goals of antimicrobial drugs

A

• Disrupt cell processes or structures of bacteria, fungi, or protozoa
• Inhibit virus replication
• Interfere with the function of enzymes required to synthesize or assemble macromolecules
• Destroy structures already formed in the cell
• Selectively toxic: kill or inhibit microbial cells without damaging host tissues

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24
Q

What are interactions between the drug and the microbe

A

Drugs with excellent selective toxicity block the synthesis of the bacterial cell wall (penicillins):
• Human cells lack the chemical peptidoglycan and are unaffected by the drug
Drugs most toxic to humans:
• Drugs that act upon a structure common to both the infective agent and the host cell (cytoplasmic membrane)
• As characteristics of the infectious agent are more and more similar to the host cell, selective toxicity becomes more difficult to achieve

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25
Q

Drugs that target the cell wall
- penicillin

A

Penicillin and its family are known to inhibit bacterial cell wall synthesis
- Penicillins G and V
• Ampicillin, carbenicillin, amoxicillin
• Nafcillin, cloxacillin
• Clavulanic acid

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26
Q

Drugs that target the cell wall
- carbapenems

A

Carbapenems target and inhibit bacterial cell-wall biosynthesis inhibitors
- Doripenem, imipenem
• Aztreonam

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27
Q

Drugs that target the cell wall
- cephalosporins

A

Cephalosporins inhibit the synthesis of the bacterial cell wall
- Cefazolin
• Cefaclor
• Cephalexin, cefotaxime
• Ceftriaxone
• Cefepime
• Cegtaroline

28
Q

Drugs that target the cell wall
- Miscellaneous drugs

A

• Bacitracin
• Isoniazid
• Vancomycin
• Fosfomycin tromethamine

29
Q

Drugs that target protein synthesis
- Aminoglycosides

A

insert on sites on the 30S subunit and cause the misreading of the mRNA, leading to abnormal proteins
- they inhibit protein synthesis by binding with a high level of affinity so the A diet on the 16S ribosomal RNA of the 30S ribosome
• Streptomycin

30
Q

Drugs that target protein synthesis
- macrolides

A

inhibit translocation of the subunit during translation (erythromycin)
- they inhibit protein synthesis by targeting the bacterial ribosome of the cell
• Erythromycin,clarithromycin, azithromycin

31
Q

Drugs that target protein synthesis
- tetracyclines

A

block the attachment of tRNA on the A acceptor site and stop further protein synthesis
- they inhibit protein synthesis by preventing the attachment of aminoacyl-tRNA to the ribosomal acceptor (A) site
• Tetracycline

32
Q

Drugs that target folic acid synthesis

A

Sulfonamides: interfere with folate metabolism by blocking enzymes required for the synthesis of tetrahydrofolate, which is needed by the cells for folic acid synthesis and eventual production of DNA, RNA, and amino acids
- drugs can target folic acid synthesis by blocking the purine and pyrimidine biosynthesis which then inhibits bacterial growth
• Sulfamethoxazole
• Silver sulfadiazine
• Trimethoprim

33
Q

Drugs that target DNA or RNA

A

Fluoroquinolones: inhibit DNA unwinding enzymes or
helicases, thereby stopping DNA transcription
• Ciprofloxacin, ofloxacin
• Levofloxacin
• Miscellaneous Drugs That Target DNA or RNA
• Rifampin

34
Q

Drugs that target cytoplasmic or cell membranes

A

Polymyxins (colistins): interact with membrane phospholipids; distort the cell surface and cause leakage of protein and nitrogen bases, particularly in gram-negative bacteria
- they can bind to the LPA and the phospholipids of the outer cellular membrane of gram-neg bacteria
• Polymyxin B
• Daptomycin

35
Q

Bacteria in biofilms

A

Bacteria in biofilms behave differently than when they are free-living:
• Often unaffected by the same antimicrobials that work against them
• Antibiotics often cannot penetrate the sticky extracellular material surrounding biofilms
• Bacteria in biofilms express a different phenotype and have different antibiotic susceptibility profiles than free-living bacteria

36
Q

Antibiotics in biofilms with bacteria

A

Biofilm treatment strategies:
• Interrupting quorum sensing pathways
• Daptomycin: shown success
• Adding DNAse to antibiotics aids penetration through extracellular debris
• Impregnating devices with antibiotics prior to insertion to prevent colonization
Some antibiotics cause biofilms to form at a higher rate than they normally would

37
Q

Agents that work to treat fungal infections

A

Fungal cells are eukaryotic, present special problems in drug treatment:
• Drugs designed to act on bacteria are ineffective against fungi
• Similarities between fungal and human cells mean that drugs toxic to fungi will harm human tissues
• Only a few agents with special antifungal properties have been developed

38
Q

Antimalarial drug
- Quinine

A
  • principal treatment of malaria for hundreds of years
  • has been replaced by less toxic synthesized quinolones, chloroquine and primaquine
  • several species of Plasmodium and many stages in its life cycle mean that no single drug is universally effective
39
Q

Antimalarial drug
- artemisinin

A
  • has become the staple for malaria treatment
40
Q

Anti-Protozoal drug
- metronidazole

A

Metronidazole: widely used amoebicide:
• Treats intestinal infections and hepatic disease caused by
Entamoeba histolytica
• Also treats Giardia lamblia and Trichomonas vaginalis

41
Q

Other common drugs with antiprotozoal activities

A

• Quinacrine
• Sulfonamides
• Tetracyclines

42
Q

Four challenges of antihelminthic drug therapy

A

• Flukes, tapeworms, and roundworms are larger parasites
• Their physiology is much more similar to humans
• Blocking reproduction does not usually affect adult worms
• Most effective drugs immobilize, disintegrate, or inhibit the metabolism of all stages of the life cycle

43
Q

List some agents discussed to treat helminthic infections

A

Albendazole inhibit microtubules of worms, eggs, and larvae Pyrantel paralyzes the muscles of intestinal roundworms
Praziquantel:
• Tapeworm and fluke infections
Ivermectin:
• Used for strongyloidiasis and oncocerosis in humans

44
Q

What are five of the agents to treat viral infections

A

• Treatment of viral infections presents unique problems
• Infectious agent relies on a host cell for the vast majority of its metabolic functions
• Disrupting viral metabolism requires disruption of cellular metabolism of host
• Measles, mumps, and hepatitis are prevented through the use of vaccines
• AIDS, influenza, and the common cold attest to the need for more effective medications for the treatment of viral pathogens

45
Q

Actions of antiviral drugs
- inhibition of virus entry:

A

Inhibition of virus entry: Receptor/fusion/uncoating inhibitors
• Enfuvirtide (Fuzeon®); amantadine (Symmetrel®)

46
Q

Actions of antiviral drugs
- inhibition of nucleic acid synthesis

A

Inhibition of nucleic acid synthesis
• Acyclovir (Zovirax®), other “cyclovirs,” vidarabine; ribavirin; Remdesivir; zidovudine (AZT), lamivudine (3TC), didanosine (ddI), zalcitabine (ddC), and stavudine (d4T); nevirapine, efavirenz, delavirdine

47
Q

Actions of antiviral drugs
- inhibition of viral assembly/release

A

Inhibition of viral assembly/release
• Indinavir, saquinavir; zanamivir (Relenza®) and oseltamivir (Tamiflu®)

48
Q

How does resistance develop?
- (penicillin and others)

A
  • Resistance to penicillin developed in some bacteria as early as 1940
  • In the 1980s and 1990s scientists and physicians witnessed treatment failures on a large scale
  • Microbes become newly resistant to a drug after one of the following occurs:
    • Spontaneous mutations in critical chromosomal genes
    • Acquisition of entire new genes or sets of genes via horizontal transfer from another species
    • Slowing or stopping of metabolism so that the microbe cannot be harmed by the antibiotic (“Persisters”)
49
Q

Development of drug resistance
- chromosomal drug resistance

A

Chromosomal drug resistance:
• Usually results from spontaneous random mutation
• Slight changes in drug sensitivity can be overcome with larger doses of the drug

50
Q

The three kinds of threats on drug resistance

A

Urgent threats:
• Clostridioides difficile (C. diff)
• Carbapenem-resistant Enterobacteriaceae (CRE)
• Drug-resistant Neisseria gonorrhoeae
Serious threats:
• Multidrug-resistant Acinetobacter
• Drug-resistant Campylobacter
• Fluconazole-resistant Candida (a fungus)
• Many more
Concerning threats:
• Vancomycin-resistant Staphylococcus aureus (VRSA)
• Erythromycin-resistant Group A Streptococcus
• Clindamycin-resistant Group B Streptococcus

51
Q

New approaches to antimicrobial therapy:
- using RNA interference strategies

A

• Small pieces of RNA that regulate the expression of genes
• Used to shut down the metabolism of pathogenic microbes
• Drug trials have begun to evaluate the effectiveness of synthetic RNAs in treating hepatitis C and respiratory syncytial virus.

52
Q

New approaches to antimicrobial therapy:
- mimicking defense peptides

A

• Peptides of 20 to 50 amino acids secreted as part of the mammalian innate immune system called defensin, magainins, and protegrins
• Bacteria also produce defense peptides called bacteriocins and lantibiotics.
• Insert into membranes and target other structures in cells
• May be more effective than narrowly targeted drugs and less likely to foster re

53
Q

New approaches to antimicrobial therapy
CRISPR

A

CRISPR:

• System found in bacteria that can cause very specific cuts in genes
• May treat antibiotic-resistant infections, together with an antibiotic

54
Q

New approaches to antimicrobial therapy
- drugs from noncultivable bacteria

A

Drugs from noncultivable bacteria:
• 99% of all microbes are noncultivable
• Scientists are developing new ways to grow and harvest their antimicrobial substances

55
Q

Bacteriophages history

A

• The former Soviet Union and other regions used mixtures of bacteriophages as medicine
• Biophage-PA used to treat ear infections caused by Pseudomonas aeruginosa biofilms
• Other researchers are incorporating bacteriophages into wound dressings
• Advantage to bacteriophage is their narrow specificity; only infect one species of bacterium

56
Q

How do we want antibiotics to be effective?

A
  • easy to get and administer
  • affordable
  • long lasting (do not have to take every 30 minutes)
  • non-reactive to allergies
  • works (specific to pathogen its targeting, effective efficiently, non-toxic to healthy cells)
  • can remain active in the body while taking the antibiotic
  • does not lead to microbial resistance in the body
57
Q

Why do we have to have specific ways to kill the eukaryotic organisms?

A
  • they have a nucleus
  • humans are eukaryotes, so we need the identities of the microorganisms
58
Q

Chapter 9 versus chapter 10

A

9:
- disk diffusion
- zone -> yes or no
- qualitative

10:
- Kirby-Bauer
- measuring the zone (ruler)
- measurements specific for each antibiotic
- quantitative

59
Q

According to the ted talk what has proven to have become most reliable to work against bacteria

A

Viruses

60
Q

What does folic aid synthesis do

A
  • it is a building block
  • works with metabolism in the body
61
Q

Cell wall inhibitors that block synthesis and repair

A
  • penicillins
  • cephalosporins
  • carbapenems
  • vancomycin
  • bacitracin
  • fosfomycin
  • isoniazid
62
Q

What do cephalosporins target

A
  • the cell wall
63
Q

The mechanisms and steps by which Antimicrobials can target prokaryotic ribosomes to inhibit proteins synthesis

A

1) the mRNA is misread because of the wrong shape of the ribosome
2) the peptide then cannot dock since the tetracycline (4 green dots) block the formation of tetracycline attaching to the mRNA
3) then the chloramphenicol blocks the peptide bond and peptide chain formation. This is through blocking the amino acids from bonding with the peptides to form the peptide bonds (or chains)
4) then the lincosamides or macrolides can bind to the larger 50s unit of the ribosome which blocks the correct way for the mRNA to move throughout the ribosomes which causes a temporary stop to the synthesis
5)

64
Q

With the anti metabolic action of sulfanilamides in inhibiting nucleic acid synthesis, what happens if you do not have one precursor?

A

If one precursor, or enzyme needed to create the next thing is not there then the anti metabolic action can not be completed. Without PABA you can’t have dihydrofolic acid, without dihydrofolic acid you can’t have tetrahydrofolic acid, without tetrahydrofolic acid you can’t have purines and pyramiding nucleotides, without purine and pyrimidine nucleotides you can’t make DNA or RNA
- without all steps there is death and incompletion

65
Q

Amoxicillin
Clavulanic acid
Cephalosporins
Carbapenems -> doripenem, imipenem

A

These all target the cells wall

Amoxicillin -
Clavulanic acid -
Cephalosporins -
Carbapenems - inhibit bacterial cell-wall biosynthesis inhibitors
Carbapenems -> doripenem -
Carbapenems -> imipenem -

Microbiology (23 decks)

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