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History and Modern Development of Antibiotics

The Future of Antibiotics

Bacteria

Timeline of antibiotic development

• Bacteria are unicellular prokaryotic microorganisms. Some bacteria are actually helpful to people by assisting in the digestion of food and producing vitamins.

• However, other bacteria are infectious and can produce toxins that damage tissue.

  • The need for a new class of antibiotic as a long-term solution to reducing the overall level of resistance.
  • The ability to test and identify patients who are carrying a milt-resistant strain is vital in achieving the full potential of this new class of antibiotic.
  • Continuing to create a next generation antibiotic rather than a new class can result in developing a high-level resistance in bacteria.
  • With this new class of antibiotics there needs to be prescription regulation in order to have a significant impact on antibiotic resistance.
  • Phage therapy: Bacteriophages or "phages" are viruses that invade bacterial cells and, in the case of lytic phages, disrupt bacterial metabolism and cause the bacterium to lyse. Phage therapy is the therapeutic use of lytic bacteriophage to treat pathogenic bacterial infections.

Penicillin

Streptomycin

  • Selman Waksman introduced the concept of antimicrobial activity, which describes the effect of small molecules made by a microbe, which antagonized the growth of other microbes.
  • The isolation of streptomycin from a culture of Spretomyces griseus was discovered to treat tuberculosis by Albert Schatz.

o Ancient Egyptians, Chinese and central American Indians used molds and plants to treat infections and wounds

• They did not fully understand the connection of the antibacterial properties of mold.

  • Alexander Fleming
  • treated scarlet fever, pneumonia, diphtheria, and meningitis.
  • Accidently discovered Staphylococcus aureus could be destroyed by mold Penicillium notatum.
  • He described the amount of inhibition and the effect of doubling the dilutions of his “inhibitor” yellow fluid, similar to our concept of minimum inhibitory concentration (MIC) and disk diffusion, and still extremely valuable today in the clinical setting.

1940

1948

1909

1943

1928

Early History

Antibiotics Today

Cephalosporins

Arsphenamine

(salvarsan)

  • Howard Florey + Ernst Chain
  • Mass production and distribution of penicillin in 1945
  • During WWII, Florey himself successfully tested the effects of penicillin on wounded soldiers
  • Fleming, Florey, and Chain shared 1945 Nobel Prize for their work on penicillin
  • The next goals were to identify the chemical structure with antibacterial activity. Later the isolation of 6-aminopenicillanic acid in 1959 made it possible to develop semisynthetic penicillins and the introduction of methicillin in 1960 and ampicillin in 1961.

• Paul Ehrlich

  • Arsphenamine: used for the treatment of syphilis. Most used antimicrobial drug until the 1940s
  • Screening- the systematic testing of chemical compounds and their ability to modify their target, as now practiced in the pharmaceutical industry.

• Giuseppe Brotzu isolated a fungus Cephalosporium acremonium from sewer water. This discovery came about from observing that people from Cagliari, Italy had a lower population of people infected with typhoid fever.

  • Edward Abraham and Guy Newton collaborated with Brotzu to later produce different generations of Cephalosporins

What are antibiotics?

  • There was a splurge in the development of new antibiotics from the 1940s-1960s; however, no new class of antibiotics were discovered until the year 2000.
  • Most current antibiotics used today are synthetic derivatives of previous antibiotics introduced forty to fifty years ago.
  • Over time antibiotics have decreased in their effectiveness due to bacterial resistance.

• Anti-against bios-life “against life”

• An antibiotic is a type of medication that actually kills or prevents the growth of bacteria.

• An antibiotic is selective towards bacteria cells so that it doesn’t kill other cells in your body

Folic Acid Synthesis Inhibitors

• DNA synthesis Inhibitors

o Sulfonamides

o Trimethoprim

o Fluoroquinolones

o Metronidazole

Antibiotic Resistance

Mycolic Acid Synthesis Inhibitors

o Isoniazid

Classifications of Antibiotics

  • Antibiotics can be classified by their structure, chemistry, or mechanism of action
  • In this presentation we will see how antibiotics are classified based on their mechanisms

An antibiotic has lost its ability to kill or inhibit the growth of bacteria. Bacteria become resistant and can survive in the presence of antibiotics.

Reduced drug accumulation

Drug inactivation or modification

Caused by reduced drug permeability or the ability of the bacteria to transport drugs out of the cell

Example: Increasing active efflux (pumping out) of the drugs across the cell surface.

• RNA Synthesis Inhibitors

Enzymatic deactivation of the antibiotic.

Example: penicillin reistant bacteria like E.coli can produce beta-lactamases in order to inactivate the antibiotic. Through hydrolysis, the lactamase enzyme breaks open the beta-lactam ring structure, deactivating the antibiotic.

o Rifampin

• Cell wall synthesis inhibitors

o Penicilllins

o Cephalosporins

o Vancomycin

o Beta-lactamase inhibitors

o Carbapanems

o Aztreonam

o Polymycin

o Bacitracin

Alteration of metabolic pathway

Alteration of

target site

Many drugs target certain parts of metabolic pathways by inactivating enzymes or sequestering substrates. Bacteria can use alternative metabolic pathways or find ways to uptake the necessary nutrients from the environment.

Example: Sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.

No binding or inhibition will take place because the bacteria can either change or camouflage the target site through mutations in genes.

Example: Alteration in penicillin-binding protein (PBPs) leading to reduced affinity of beta-lactam antibiotics (Methicillin-Resistant Staphylococcus aureus)

• Protein Synthesis Inhibitors

o Inhibit 30s subunit

• Aminoglycosides

• Tetracyclines

o Inhibit 50s Subunit

• Macrolides

• Chloramphenicol

• Clindamycin

• Linezolid

• Streptogramins

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