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Antibiotic

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Antibiotic
Drug class
Staphylococcus aureus (AB Test).jpg
Testing the susceptibility of Staphylococcus aureus to antibiotics by the Kirby-Bauer disk diffusion method – antibiotics diffuse from antibiotic-containing disks and inhibit growth of S. aureus, resulting in a zone of inhibition.

These are substances produced by microorganisms, which selectively suppress the growth of or kill other microorganisms at very low concentrations. This definition excludes other natural substances which also inhibit microorganisms but are produced by higher forms (e.g. antibodies) or even those produced by microbes but are needed in high concentrations (ethanol, lactic acid, H2O2).

Initially the term ‘chemotherapeutic agent’ was restricted to synthetic compounds, but now since many antibiotics and their analogues have been synthesized, this criterion has become irrelevant; both synthetic and microbiologically produced drugs need to be included together. It would be more meaningful to use the term Antimicrobial agent (AMA) to designate synthetic as well as naturally obtained drugs that attenuate microorganisms.

History

The history of chemotherapy may be divided into 3 phases.

(a) The period of empirical use: of ‘mouldy curd’ by Chinese on boils, chaulmoogra oil by the Hindus in leprosy, chenopodium by Aztecs for intestinal worms, mercury by Paracelsus (16th century) for syphilis, cinchona bark (17th century) for fevers.

(b) Ehrlich’s phase of dyes and organometallic compounds (1890–1935): With the discovery of microbes in the later half of 19th century and that they are the cause of many diseases; Ehrlich toyed with the idea that if certain dyes could selectively stain microbes, they could also be selectively toxic to these organisms. He tried methylene blue, trypan red, etc. He developed the arsenicals—atoxyl for sleeping sickness, arsphenamine in 1906 and neoarsphenamine in 1909 for syphilis. He coined the term ‘chemotherapy’ because he used drugs of known chemical structure (that of most other drugs in use at that time was not known) and showed that selective attenuation of infecting parasite was a practical proposition.

Staphylococcus aureus susceptibility
Staphylococcus aureus susceptibility

(c) The modern era of chemotherapy was ushered by Domagk in 1935 by demonstrating the therapeutic effect of Prontosil, a sulfonamide dye, in pyogenic infection. It was soon realized that the active moiety was paraamino benzene sulfonamide, and the dye part was not essential. Sulfapyridine (M & B 693) was the first sulfonamide to be marketed in 1938.

Pasteur

The phenomenon of antibiosis was demonstrated by Pasteur in 1877: growth of anthrax bacilli in urine was inhibited by air-borne bacteria. Fleming (1929) found that a diffusible substance was elaborated by Penicillium mould which could destroy Staphylococcus on the culture plate. He named this substance penicillin but could not purify it. Chain and Florey followed up this observation in 1939 which culminated in the clinical use of penicillin in 1941. Because of the great potential of this discovery in treating war wounds, commercial manufacture of penicillin soon started.

Waksman

In the 1940s, Waksman and his colleagues undertook a systematic search of Actinomycetes as source of antibiotics and discovered streptomycin in 1944. This group of soil microbes proved to be a treasure-house of antibiotics and soon tetracyclines, chloramphenicol, erythromycin and many others followed. All three groups of scientists, Domagk, Fleming-Chain-Florey and Waksman received the Nobel Prize for their discoveries.

Semisynthetic antibiotics

In the past 40 years emphasis has shifted from searching new antibiotic producing organisms to developing semisynthetic derivatives of older antibiotics with more desirable properties or differing spectrum of activity. Few novel synthetic AMAs, e.g. fluoroquinolones, oxazolidinones have also been produced.

CLASSIFICATION

Antimicrobial drugs can be classified in many ways:

  • Chemical structure
  1. Sulfonamides and related drugs: Sulfadiazine and others, Sulfones—Dapsone (DDS), Para aminosalicylic acid (PAS).
  2. Diaminopyrimidines: Trimethoprim, Pyrimethamine.
  3. Quinolones: Nalidixic acid, Norfloxacin, Ciprofloxacin, Gatifloxacin, etc.
  4. β-Lactam antibiotics: Penicillins, Cephalosporins, Monobactams, Carbapenems.
  5. Tetracyclines: Oxytetracycline, Doxycycline, etc.
  6. Nitrobenzene derivative: Chloramphenicol.
  7. Aminoglycosides: Streptomycin, Gentamicin, Amikacin, Neomycin, etc.
  8. Macrolide antibiotics: Erythromycin, Clarithromycin, Azithromycin, etc.
  9. Lincosamide antibiotics: Lincomycin, Clindamycin.
  10. Glycopeptide antibiotics: Vancomycin, Teicoplanin.
  11. Oxazolidinone: Linezolid.
  12. Polypeptide antibiotics: Polymyxin-B, Colistin, Bacitracin, Tyrothricin.
  13. Nitrofuran derivatives: Nitrofurantoin, Furazolidone.
  14. Nitroimidazoles: Metronidazole, Tinidazole, etc.
  15. Nicotinic acid derivatives: Isoniazid, Pyrazinamide, Ethionamide.
  16. Polyene antibiotics: Nystatin, Amphotericin-B, Hamycin.
  17. Azole derivatives: Miconazole, Clotrimazole, Ketoconazole, Fluconazole.
  18. Others: Rifampin, Spectinomycin, Sod. fusidate, Cycloserine, Viomycin, Ethambutol, Thiacetazone, Clofazimine, Griseofulvin.
  1. Inhibit cell wall synthesis: Penicillins, Cephalosporins, Cycloserine, Vancomycin, Bacitracin.
  2. Cause leakage from cell membranes: Polypeptides—Polymyxins, Colistin, Bacitracin. Polyenes—Amphotericin B]], Nystatin, Hamycin.
  3. Inhibit protein synthesis: Tetracyclines, Chloramphenicol, Erythromycin, Clindamycin, Linezolid.
  4. Cause misreading of m-RNA code and affect permeability: Aminoglycosides—Streptomycin, Gentamicin, etc.
  5. Inhibit DNA gyrase: Fluoroquinolones— Ciprofloxacin and others.
  6. Interfere with DNA function: Rifampin, Metronidazole.
  7. Interfere with DNA synthesis: Acyclovir, Zidovudine.
  8. Interfere with intermediary metabolism: Sulfonamides, Sulfones, PAS, Trimethoprim, Pyrimethamine, Ethambutol.
  • Type of organisms against which primarily active
  1. Antibacterial: Penicillins, Aminoglycosides, Erythromycin, etc.
  2. Antifungal: Griseofulvin, Amphotericin B, Ketoconazole, etc.
  3. Antiviral: Acyclovir, Amantadine, Zidovudine, etc.
  4. Antiprotozoal: Chloroquine, Pyrimethamine, Metronidazole, Diloxanide, etc.
  5. Anthelmintic: Mebendazole, Pyrantel, Niclosamide, Diethyl carbamazine, etc.
  • Spectrum of activity
  1. Narrow-spectrum: Penicillin G, Streptomycin, Erythromycin.
  2. Broad-spectrum: Tetracyclines, Chloramphenicol.
  • Type of action
  1. Primarily bacteriostatic: Sulfonamides, Erythromycin, Tetracyclines, Ethambutol, Chloramphenicol, Clindamycin, Linezolid.
  2. Primarily bactericidal: Penicillins, Cephalosporins, Aminoglycosides, Vancomycin, Polypeptides, Nalidixic acid, Rifampin, Ciprofloxacin, Isoniazid, Metronidazole, Pyrazinamide, Cotrimoxazole.
  • Antibiotics are obtained from
  1. Fungi: Penicillin, Griseofulvin, Cephalosporin.
  2. Bacteria: Polymyxin B, Tyrothricin, Colistin, Aztreonam, Bacitracin.
  3. Actinomycetes: Aminoglycosides, Macrolides, Tetracyclines, Polyenes, Chloramphenicol.

Overuse of antibiotics

Antibiotics save lives, but any time antibiotics are used, they can cause side effects and lead to antibiotic resistance. In U.S. doctors’ offices and emergency departments, at least 47 million antibiotic prescriptions each year are unnecessary, which makes improving antibiotic prescribing and use a national priority, according to the CDC.

Antibiotic sensitivity and resistance.jpg

Antibiotic resistance

Antibiotic resistance is one of the biggest public health challenges of our time. Each year in the U.S., at least 2.8 million people get an antibiotic-resistant infection, and more than 35,000 people die, according to the CDC.

History of antibiotic resistance

Penicillin, the first commercialized antibiotic, was discovered in 1928 by Alexander Fleming. Ever since, there has been discovery and acknowledgement of resistance alongside the discovery of new antibiotics. In fact, germs will always look for ways to survive and resist new drugs. More and more, germs are sharing their resistance with one another, making it harder for us to keep up.

Select Germs Showing Resistance Over Time

Select Germs Showing Resistance Over Time
Antibiotic Approved or Released Year Released Resistant Germ Identified Year Identified
Penicillin 1941

Penicillin-resistant Staphylococcus aureus

Penicillin-resistant Streptococcus pneumoniae

Penicillinase-producing Neisseria gonorrhoeae

1942

1967

1976

Vancomycin 1958

Plasmid-mediated vancomycin-resistant Enterococcus faecium

Vancomycin-resistant Staphylococcus aureus

1988

2002

Amphotericin B 1959 Amphotericin B-resistant Candida auris 2016
Methicillin 1960 Methicillin-resistant Staphylococcus aureus 1960
Extended-spectrum cephalosporins 1980 (Cefotaxime) Extended-spectrum beta-lactamase- producing Escherichia coli 1983
Azithromycin 1980 Azithromycin-resistant Neisseria gonorrhoeae 2011
Imipenem 1985 Klebsiella pneumoniae carbapenemase (KPC)-producing Klebsiella pneumoniae 1996
Ciprofloxacin 1987 Ciprofloxacin-resistant Neisseria gonorrhoeae 2007
Fluconazole 1990 (FDA approved) Fluconazole-resistant Candida 1988
Caspofungin 2001 Caspofungin-resistant Candida 2004
Daptomycin 2003 Daptomycin-resistant methicillin-resistant Staphylococcus aureus 2004
Ceftazidime-avibactam 2015 Ceftazidime-avibactam-resistant KPC-producing Klebsiella pneumoniae 2015

Antibiotic stewardship

Antibiotic stewardship is the effort to measure antibiotic prescribing; to improve antibiotic prescribing by clinicians and use by patients so that antibiotics are only prescribed and used when needed; to minimize misdiagnoses or delayed diagnoses leading to underuse of antibiotics; and to ensure that the right drug, dose, and duration are selected when an antibiotic is needed.

Benefits of antibiotic stewardship

Antibiotic stewardship can be used in all health care settings in which antibiotics are prescribed and remains a cornerstone of efforts aimed at improving antibiotic-related patient safety and slowing the spread of antibiotic resistance.

Goal of antibiotic stewardship

The goal of antibiotic stewardship is to maximize the benefit of antibiotic treatment while minimizing harm both to individual persons and to communities.

External links

Some templates adapted from Wikipedia (CC BY-SA 3.0)

Latest research - Antibiotic

PubMed
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