Antibiotic
Antibiotic | |
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Kirby-Bauer disk diffusion method – antibiotics diffuse from antibiotic-containing disks and inhibit growth of S. aureus, resulting in a zone of inhibition. | |
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In Wikidata |
An antibiotic is a type of
Sometimes, the term antibiotic—literally "opposing life", from the
Antibiotics have been used since ancient times. Many civilizations used topical application of moldy bread, with many references to its beneficial effects arising from ancient Egypt,
Etymology
The term 'antibiosis', meaning "against life", was introduced by the French bacteriologist Jean Paul Vuillemin as a descriptive name of the phenomenon exhibited by these early antibacterial drugs.[8][18][19] Antibiosis was first described in 1877 in bacteria when Louis Pasteur and Robert Koch observed that an airborne bacillus could inhibit the growth of Bacillus anthracis.[18][20] These drugs were later renamed antibiotics by Selman Waksman, an American microbiologist, in 1947.[21]
The term antibiotic was first used in 1942 by
The term "antibiotic" derives from anti + βιωτικός (biōtikos), "fit for life, lively",[25] which comes from βίωσις (biōsis), "way of life",[26] and that from βίος (bios), "life".[27][28] The term "antibacterial" derives from Greek ἀντί (anti), "against"[29] + βακτήριον (baktērion), diminutive of βακτηρία (baktēria), "staff, cane",[30] because the first bacteria to be discovered were rod-shaped.[31]
Usage
Medical uses
Antibiotics are used to treat or prevent bacterial infections,[32] and sometimes protozoan infections. (Metronidazole is effective against a number of parasitic diseases). When an infection is suspected of being responsible for an illness but the responsible pathogen has not been identified, an empiric therapy is adopted.[33] This involves the administration of a broad-spectrum antibiotic based on the signs and symptoms presented and is initiated pending laboratory results that can take several days.[32][33]
When the responsible pathogenic microorganism is already known or has been identified, definitive therapy can be started. This will usually involve the use of a narrow-spectrum antibiotic. The choice of antibiotic given will also be based on its cost. Identification is critically important as it can reduce the cost and toxicity of the antibiotic therapy and also reduce the possibility of the emergence of antimicrobial resistance.[33] To avoid surgery, antibiotics may be given for non-complicated acute appendicitis.[34]
Antibiotics may be given as a
The use of antibiotics for secondary prevention of coronary heart disease is not supported by current scientific evidence, and may actually increase cardiovascular mortality, all-cause mortality and the occurrence of stroke.[37]
Routes of administration
There are many different
Global consumption
Antibiotic consumption varies widely between countries. The
Side effects
Antibiotics are screened for any negative effects before their approval for clinical use, and are usually considered safe and well tolerated. However, some antibiotics have been associated with a wide extent of adverse side effects ranging from mild to very severe depending on the type of antibiotic used, the microbes targeted, and the individual patient.[43][44] Side effects may reflect the pharmacological or toxicological properties of the antibiotic or may involve hypersensitivity or allergic reactions.[4] Adverse effects range from fever and nausea to major allergic reactions, including photodermatitis and anaphylaxis.[45]
Common side effects of oral antibiotics include
Some antibiotics may also damage the
Interactions
Birth control pills
There are few well-controlled studies on whether antibiotic use increases the risk of
In cases where antibiotics have been suggested to affect the efficiency of birth control pills, such as for the broad-spectrum antibiotic
Alcohol
Interactions between alcohol and certain antibiotics may occur and may cause side effects and decreased effectiveness of antibiotic therapy.[57][58] While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side effects.[59] Therefore, potential risks of side effects and effectiveness depend on the type of antibiotic administered.[60]
Antibiotics such as
Pharmacodynamics
The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial.[62] The bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells.[63] These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection.[62][64] Since the activity of antibacterials depends frequently on its concentration,[65] in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial.[62][66] To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.[67]
Combination therapy
In important infectious diseases, including tuberculosis,
In addition to combining one antibiotic with another, antibiotics are sometimes co-administered with resistance-modifying agents. For example,
Classes
-
Molecular targets of antibiotics on the bacteria cell
-
Protein synthesis inhibitors (antibiotics)
Antibiotics are commonly classified based on their
Production
With advances in
Since the first pioneering efforts of
Resistance
The emergence of
Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug.[80] For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment.[81] Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.[82]
Resistance may take the form of biodegradation of pharmaceuticals, such as sulfamethazine-degrading soil bacteria introduced to sulfamethazine through medicated pig feces.[83] The survival of bacteria often results from an inheritable resistance,[84] but the growth of resistance to antibacterials also occurs through horizontal gene transfer. Horizontal transfer is more likely to happen in locations of frequent antibiotic use.[85]
Antibacterial resistance may impose a biological cost, thereby reducing
Paleontological data show that both antibiotics and antibiotic resistance are ancient compounds and mechanisms.[87] Useful antibiotic targets are those for which mutations negatively impact bacterial reproduction or viability.[88]
Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains.
Antibacterial-resistant strains and species, sometimes referred to as "superbugs", now contribute to the emergence of diseases that were, for a while, well controlled. For example, emergent bacterial strains causing tuberculosis that are resistant to previously effective antibacterial treatments pose many therapeutic challenges. Every year, nearly half a million new cases of
Misuse
Per The ICU Book "The first rule of antibiotics is to try not to use them, and the second rule is try not to use too many of them."
Common forms of antibiotic misuse include excessive use of
Several organizations concerned with antimicrobial resistance are lobbying to eliminate the unnecessary use of antibiotics.[102] The issues of misuse and overuse of antibiotics have been addressed by the formation of the US Interagency Task Force on Antimicrobial Resistance. This task force aims to actively address antimicrobial resistance, and is coordinated by the US Centers for Disease Control and Prevention, the Food and Drug Administration (FDA), and the National Institutes of Health, as well as other US agencies.[108] A non-governmental organization campaign group is Keep Antibiotics Working.[109] In France, an "Antibiotics are not automatic" government campaign started in 2002 and led to a marked reduction of unnecessary antibiotic prescriptions, especially in children.[110]
The emergence of antibiotic resistance has prompted restrictions on their use in the UK in 1970 (Swann report 1969), and the European Union has banned the use of antibiotics as growth-promotional agents since 2003.
Despite pledges by food companies and restaurants to reduce or eliminate meat that comes from animals treated with antibiotics, the purchase of antibiotics for use on farm animals has been increasing every year.[117]
There has been extensive use of antibiotics in animal husbandry. In the United States, the question of emergence of antibiotic-resistant bacterial strains due to use of antibiotics in livestock was raised by the US Food and Drug Administration (FDA) in 1977. In March 2012, the United States District Court for the Southern District of New York, ruling in an action brought by the Natural Resources Defense Council and others, ordered the FDA to revoke approvals for the use of antibiotics in livestock, which violated FDA regulations.[118]
Studies have shown that
Other forms of antibiotic associated harm include
History
Before the early 20th century, treatments for infections were based primarily on
The use of antibiotics in modern medicine began with the discovery of synthetic antibiotics derived from dyes.[8][128][11][129][9]Various Essential oils have been shown to have anti-microbial properties.[130] Along with this, the plants from which these oils have been derived from can be used as niche anti-microbial agents.[131]
Synthetic antibiotics derived from dyes
Synthetic antibiotic chemotherapy as a science and development of antibacterials began in Germany with
now called arsphenamine.This heralded the era of antibacterial treatment that was begun with the discovery of a series of arsenic-derived synthetic antibiotics by both Alfred Bertheim and Ehrlich in 1907.[129][9] Ehrlich and Bertheim had experimented with various chemicals derived from dyes to treat trypanosomiasis in mice and spirochaeta infection in rabbits. While their early compounds were too toxic, Ehrlich and Sahachiro Hata, a Japanese bacteriologist working with Ehrlich in the quest for a drug to treat syphilis, achieved success with the 606th compound in their series of experiments. In 1910, Ehrlich and Hata announced their discovery, which they called drug "606", at the Congress for Internal Medicine at Wiesbaden.[132] The Hoechst company began to market the compound toward the end of 1910 under the name Salvarsan, now known as arsphenamine.[132] The drug was used to treat syphilis in the first half of the 20th century. In 1908, Ehrlich received the Nobel Prize in Physiology or Medicine for his contributions to immunology.[133] Hata was nominated for the Nobel Prize in Chemistry in 1911 and for the Nobel Prize in Physiology or Medicine in 1912 and 1913.[134]
The first
Penicillin and other natural antibiotics
Observations about the growth of some microorganisms inhibiting the growth of other microorganisms have been reported since the late 19th century. These observations of antibiosis between microorganisms led to the discovery of natural antibacterials. Louis Pasteur observed, "if we could intervene in the antagonism observed between some bacteria, it would offer perhaps the greatest hopes for therapeutics".[138]
In 1874, physician Sir William Roberts noted that cultures of the mould Penicillium glaucum that is used in the making of some types of blue cheese did not display bacterial contamination.[139]
In 1895 Vincenzo Tiberio, Italian physician, published a paper on the antibacterial power of some extracts of mold.[140]
In 1897, doctoral student
In 1928, Sir Alexander Fleming postulated the existence of penicillin, a molecule produced by certain moulds that kills or stops the growth of certain kinds of bacteria. Fleming was working on a culture of disease-causing bacteria when he noticed the spores of a green mold, Penicillium rubens,[143] in one of his culture plates. He observed that the presence of the mould killed or prevented the growth of the bacteria.[144] Fleming postulated that the mould must secrete an antibacterial substance, which he named penicillin in 1928. Fleming believed that its antibacterial properties could be exploited for chemotherapy. He initially characterised some of its biological properties, and attempted to use a crude preparation to treat some infections, but he was unable to pursue its further development without the aid of trained chemists.[145][146]
Florey credited
Late 20th century
During the mid-20th century, the number of new antibiotic substances introduced for medical use increased significantly. From 1935 to 1968, 12 new classes were launched. However, after this, the number of new classes dropped markedly, with only two new classes introduced between 1969 and 2003.[152]
Antibiotic pipeline
Both the WHO and the
A few antibiotics have received marketing authorization in the last seven years. The cephalosporin ceftaroline and the lipoglycopeptides oritavancin and telavancin have been approved for the treatment of acute bacterial skin and skin structure infection and community-acquired bacterial pneumonia.[158] The lipoglycopeptide dalbavancin and the oxazolidinone tedizolid has also been approved for use for the treatment of acute bacterial skin and skin structure infection. The first in a new class of narrow spectrum macrocyclic antibiotics, fidaxomicin, has been approved for the treatment of C. difficile colitis.[158] New cephalosporin-lactamase inhibitor combinations also approved include ceftazidime-avibactam and ceftolozane-avibactam for complicated urinary tract infection and intra-abdominal infection.[158]
- β-lactamaseinhibitor combination (cell wall synthesis inhibitor). FDA approved on 19 December 2014.
- Ceftazidime/avibactam (ceftazidime/NXL104): antipseudomonal cephalosporin/β-lactamase inhibitor combination (cell wall synthesis inhibitor).[159] FDA approved on 25 February 2015.
- MRSAcephalosporin/ β-lactamase inhibitor combination (cell wall synthesis inhibitor).
- Cefiderocol: cephalosporin siderophore.[159] FDA approved on 14 November 2019.
- Imipenem/relebactam: carbapenem/ β-lactamase inhibitor combination (cell wall synthesis inhibitor).[159] FDA approved on 16 July 2019.
- Meropenem/vaborbactam: carbapenem/ β-lactamase inhibitor combination (cell wall synthesis inhibitor).[159] FDA approved on 29 August 2017.
- Delafloxacin: quinolone (inhibitor of DNA synthesis).[159] FDA approved on 19 June 2017.
- Plazomicin (ACHN-490): semi-synthetic aminoglycoside derivative (protein synthesis inhibitor).[159] FDA approved 25 June 2018.
- Eravacycline (TP-434): synthetic tetracycline derivative (protein synthesis inhibitor targeting bacterial ribosomes).[159] FDA approved on 27 August 2018.
- Omadacycline: semi-synthetic tetracycline derivative (protein synthesis inhibitor targeting bacterial ribosomes).[159] FDA approved on 2 October 2018.
- Lefamulin: pleuromutilin antibiotic.[159] FDA approved on 19 August 2019.
- Brilacidin (PMX-30063): peptide defense protein mimetic (cell membrane disruption). In phase 2.
- Zosurabalpin (RG-6006): lipopolysaccharide transport inhibitor. In phase 1.[160][161]
Possible improvements include clarification of clinical trial regulations by FDA. Furthermore, appropriate economic incentives could persuade pharmaceutical companies to invest in this endeavor.
Replenishing the antibiotic pipeline and developing other new therapies
Because antibiotic-resistant bacterial strains continue to emerge and spread, there is a constant need to develop new antibacterial treatments. Current strategies include traditional chemistry-based approaches such as natural product-based drug discovery,[164][165] newer chemistry-based approaches such as drug design,[166][167] traditional biology-based approaches such as immunoglobulin therapy,[168][169] and experimental biology-based approaches such as phage therapy,[170][171] fecal microbiota transplants,[168][172] antisense RNA-based treatments,[168][169] and CRISPR-Cas9-based treatments.[168][169][173]
Natural product-based antibiotic discovery
Most of the antibiotics in current use are
In addition to screening natural products for direct antibacterial activity, they are sometimes screened for the ability to suppress
Natural products may be screened for the ability to suppress bacterial
Immunoglobulin therapy
Antibodies (
Phage therapy
Some disadvantages to the use of bacteriophages also exist, however. Bacteriophages may harbour virulence factors or toxic genes in their genomes and, prior to use, it may be prudent to identify genes with similarity to known virulence factors or toxins by genomic sequencing. In addition, the oral and
There are considerable regulatory hurdles that must be cleared for such therapies.[196] Despite numerous challenges, the use of bacteriophages as a replacement for antimicrobial agents against MDR pathogens that no longer respond to conventional antibiotics, remains an attractive option.[196][198]
Fecal microbiota transplants
Fecal microbiota transplants involve transferring the full
Antisense RNA-based treatments
Antisense RNA-based treatment (also known as gene silencing therapy) involves (a) identifying bacterial
In addition to silencing essential bacterial genes, antisense RNA can be used to silence bacterial genes responsible for antibiotic resistance.
CRISPR-Cas9-based treatments
In the early 2000s, a system was discovered that enables bacteria to defend themselves against invading viruses. The system, known as CRISPR-Cas9, consists of (a) an enzyme that destroys DNA (the nuclease Cas9) and (b) the DNA sequences of previously encountered viral invaders (CRISPR). These viral DNA sequences enable the nuclease to target foreign (viral) rather than self (bacterial) DNA.[200]
Although the function of CRISPR-Cas9 in nature is to protect bacteria, the DNA sequences in the CRISPR component of the system can be modified so that the Cas9 nuclease targets bacterial resistance genes or bacterial virulence genes instead of viral genes. The modified CRISPR-Cas9 system can then be administered to bacterial pathogens using plasmids or bacteriophages.[168][169] This approach has successfully been used to silence antibiotic resistance and reduce the virulence of enterohemorrhagic E. coli in an in vivo model of infection.[169]
Reducing the selection pressure for antibiotic resistance
In addition to developing new antibacterial treatments, it is important to reduce the
Vaccines
See also
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Further reading
- Gould K (March 2016). "Antibiotics: from prehistory to the present day". The Journal of Antimicrobial Chemotherapy. 71 (3): 572–5. PMID 26851273.
- Davies J, Davies D (September 2010). "Origins and evolution of antibiotic resistance". Microbiology and Molecular Biology Reviews. 74 (3): 417–33. PMID 20805405.
- "Antibiotics: MedlinePlus". nih.gov. Archived from the original on 27 July 2016. Retrieved 19 July 2016.
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- Pugh R, Grant C, Cooke RP, Dempsey G (August 2015). "Short-course versus prolonged-course antibiotic therapy for hospital-acquired pneumonia in critically ill adults". The Cochrane Database of Systematic Reviews. 2015 (8): CD007577. PMID 26301604.
- Giedraitienė A, Vitkauskienė A, Naginienė R, Pavilonis A (1 January 2011). "Antibiotic resistance mechanisms of clinically important bacteria". Medicina. 47 (3): 137–46. PMID 21822035.
External links
- Antibiotic at Curlie