Antibiotics

From Wikipedia, the free encyclopedia

Testing the susceptibility ofStaphylococcus 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.
An antibiotic is an agent that either kills or inhibits the growth of a microorganism.[1][2]
The term antibiotic was first used in 1942 by Selman Waksman and his collaborators in journal articles to describe any substance produced by a microorganism that
isantagonistic to the growth of other microorganisms in high dilution.[3] This definition excluded substances that kill bacteria but that are not produced by microorganisms
(such as gastric juices and hydrogen peroxide). It also excluded synthetic antibacterial compounds such as the sulfonamides. Many antibacterial compounds are
relatively small molecules with a molecular weight of less than 2000 atomic mass units.
With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds.[4] These include, for example, the betalactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated
from living organisms are the aminoglycosides, whereas other antibacterialsfor example, the sulfonamides, the quinolones, and the oxazolidinonesare produced solely
by chemical synthesis. In accordance with this, many antibacterial compounds are classified on the basis of chemical/biosynthetic origin into natural, semisynthetic, and
synthetic. Another classification system is based on biological activity; in this classification, antibacterials are divided into two broad groups according to their biological effect
on microorganisms: Bactericidal agents kill bacteria, and bacteriostatic agents slow down or stall bacterial growth.
Contents
[hide]
1 History
1.1 Etymology

2 Medical uses
3 Pharmacodynamics
4 Classes
5 Production
6 Administration
7 Side-effects
8 Drug-drug interactions
o

8.1 Birth control pills

8.2 Alcohol
9 Resistance

9.1 Misuse
10 Alternatives

10.1 Resistance-modifying agents

10.2 Vaccines
11 Status of new antibiotics development

12 See also
13 References
14 External links
History[edit]
See also: Timeline of antibiotics

Penicillin, the first natural antibiotic discovered byAlexander Fleming in 1928

Before the early 20th century, treatments for infections were based primarily on medicinal folklore. Mixtures with antimicrobial properties that were used in treatments of
infections were described over 2000 years ago.[5] Many ancient cultures, including the ancient Egyptians and ancient Greeks, used specially selected mold and plant
materials and extracts to treat infections.[6][7] More recent observations made in the laboratory of antibiosis between micro-organisms led to the discovery of natural
antibacterials produced by microorganisms. Louis Pasteur observed, "if we could intervene in the antagonism observed between some bacteria, it would offer perhaps the
greatest hopes for therapeutics".[8]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.[9][10] 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.[11] These drugs were later renamed antibiotics by Selman Waksman, an American microbiologist, in 1942.[3]
[9]
Synthetic antibiotic chemotherapy as a science and development of antibacterials began in Germany with Paul Ehrlich in the late 1880s.[9] Ehrlich noted that certain dyes
would color human, animal, or bacterial cells, whereas others did not. He then proposed the idea that it might be possible to create chemicals that would act as a selective
drug that would bind to and kill bacteria without harming the human host. After screening hundreds of dyes against various organisms, he discovered a medicinally useful
drug, the synthetic antibacterial Salvarsan[9][12][13] now called arsphenamine.
The effects of some types of mold on infection had been noticed many times over the course of history (see: History of penicillin). In 1928 Alexander Fleming noticed the
same effect in a petri dish where a number of disease-causing bacteria were killed by a fungus of the genus Penicillium. Fleming postulated that the effect is mediated by an
antibacterial compound he named penicillin, and that its antibacterial properties could be exploited for chemotherapy. He initially characterized 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. [14][15]

Alexander Fleming
The first sulfonamide and first commercially available antibacterial, Prontosil, was developed by a research team led by Gerhard Domagk in 1932 at the Bayer Laboratories
of the IG Farben conglomerate in Germany.[13] Domagk received the 1939 Nobel Prize for Medicine for his efforts. Prontosil had a relatively broad effect against Grampositivecocci, but not against enterobacteria. Research was stimulated apace by its success. The discovery and development of this sulfonamide drug opened the era of
antibacterials.
In 1939, coinciding with the start of World War II, Rene Dubos reported the discovery of the first naturally derived antibiotic, tyrothricin, a compound of 20% gramicidin and
80% tyrocidine, from B. brevis. It was one of the first commercially manufactured antibiotics universally and was very effective in treating wounds and ulcers during World
War II.[16] Gramicidin, however, could not be used systemically because of toxicity. Tyrocidine also proved too toxic for systemic usage. Research results obtained during that
period were not shared between the Axis and the Allied powers during the war.
Florey and Chain succeeded in purifying the first penicillin, penicillin G, in 1942, but it did not become widely available outside the Allied military before 1945. The chemical
structure of penicillin was determined by Dorothy Crowfoot Hodgkin in 1945. Purified penicillin displayed potent antibacterial activity against a wide range of bacteria and had
low toxicity in humans. Furthermore, its activity was not inhibited by biological constituents such as pus, unlike the synthetic sulfonamides. The discovery of such a powerful
antibiotic was unprecedented, and the development of penicillin led to renewed interest in the search for antibiotic compounds with similar efficacy and safety.[17] For their
successful development of penicillin, which Fleming had accidentally discovered but could not develop himself, as a therapeutic drug, Ernst Chain and Howard Florey shared
the 1945 Nobel Prize in Medicine with Fleming. Florey credited Dubos with pioneering the approach of deliberately and systematically searching for antibacterial compounds,
which had led to the discovery of gramicidin and had revived Florey's research in penicillin. [16]
Etymology[edit]
The term "antibiotic" derives from anti + (bitikos), "fit for life, lively",[18] which comes from (bisis), "way of life",[19] and that from (bios), "life".[20] [21]
The term "antibacterial" derives from Greek (anti), "against"[22] + (baktrion), diminutive of (baktria), "staff, cane",[23] because the first ones to be
discovered were rod-shaped.[24]
Medical uses[edit]

Treatment

Bacterial infection

Protozoan infection, e.g., metronidazole is effective against several parasitics

Immunomodulation, e.g., tetracycline, which is effective in periodontal inflammation, and dapsone, which is effective in autoimmune diseases such
as oral mucous membrane pemphigoid[25]
Prevention of infection

Surgical wound

Dental antibiotic prophylaxis[26][27]

Conditions of neutropenia, e.g. cancer-related

Pharmacodynamics[edit]
Main article: Antimicrobial 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.[28] A bactericidal activity of antibacterials may depend on the bacterial growth phase,
and it often requires ongoing metabolic activity and division of bacterial cells.[29] These findings are based on laboratory studies, and in clinical settings have also been shown
to eliminate bacterial infection.[28][30] Since the activity of antibacterials depends frequently on its concentration, [31] in vitro characterization of antibacterial activity commonly
includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial.[28][32] 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.[33]
[34]

Classes[edit]
Main article: List of antibiotics

Molecular targets of antibiotics on the bacteria cell

Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth
processes.[9] Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes
(rifamycins,lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are
usually bacteriostatic (with the exception of bactericidal aminoglycosides).[35] Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial
antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following
a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use:
cyclic lipopeptides (such as daptomycin), glycylcyclines (such astigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).[36][37]
Production[edit]
Main article: Production of antibiotics
Since the first pioneering efforts of Florey and Chain in 1939, the importance of antibiotics, including antibacterials, to medicine has led to intense research into producing
antibacterials at large scales. Following screening of antibacterials against a wide range of bacteria, production of the active compounds is carried out using fermentation,
usually in strongly aerobic conditions.[38]
Administration[edit]
Oral antibiotics are taken by mouth, whereas intravenous administration may be used in more serious cases,[citation needed] such as deep-seated systemic infections. Antibiotics
may also sometimes be administered topically, as with eye drops or ointments.
Side-effects[edit]

Health advocacy messages such as this one encourage patients to talk with their doctor about safety in using antibiotics
Antibiotics are screened for any negative effects on humans or other mammals before approval for clinical use, and are usually considered safe and most are well-tolerated.
However, some antibiotics have been associated with a range of adverse side effects.[39] Side-effects range from mild to very serious depending on the antibiotics used, the
microbial organisms targeted, and the individual patient.[citation needed] Safety profiles of newer drugs are often not as well-established as for those that have a long history of
use.[39] Adverse effects range from fever and nausea to major allergic reactions, including photodermatitis and anaphylaxis.[citation needed] Common side-effects includediarrhea,
resulting from disruption of the species composition in the intestinal flora, resulting, for example, in overgrowth of pathogenic bacteria, such as Clostridium difficile.
[40]
Antibacterials can also affect the vaginal flora, and may lead to overgrowth of yeast species of the genus Candida in the vulvo-vaginal area.[41] Additional side-effects can
result from interaction with other drugs, such as elevated risk of tendon damage from administration of a quinolone antibiotic with a systemic corticosteroid. Some scientists
have hypothesized that the indiscriminate use of antibiotics alter the host microbiota and this has been associated with chronic disease.[42][43]
Drug-drug interactions[edit]
Birth control pills[edit]
The majority of studies indicate antibiotics do not interfere with contraceptive pills,[44] such as clinical studies that suggest the failure rate of contraceptive pills caused by
antibiotics is very low (about 1%).[45] In cases where antibacterials have been suggested to affect the efficiency of birth control pills, such as for the broad-spectrum
antibacterial rifampicin, these cases may be due to an increase in the activities of hepatic liver enzymes' causing increased breakdown of the pill's active ingredients.
[44]
Effects on the intestinal flora, which might result in reduced absorption of estrogens in the colon, have also been suggested, but such suggestions have been inconclusive
and controversial.[46][47] Clinicians have recommended that extra contraceptive measures be applied during therapies using antibacterials that are suspected to interact with
oral contraceptives.[44]
Alcohol[edit]
Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy.[48][49]
"It is sensible to avoid drinking alcohol when taking medication. However, it is unlikely that drinking alcohol in moderation will cause problems if you are taking
most common antibiotics. However, there are specific types of antibiotics with which alcohol should be avoided completely, because of serious side-effects." [50]
Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief
that alcohol and antibiotics should never be mixed is widespread.
Antibiotics such as metronidazole, tinidazole, cephamandole, latamoxef, cefoperazone, cefmenoxime, and furazolidone, cause a disulfiram-like chemical reaction with
alcohol by inhibiting its breakdown byacetaldehyde dehydrogenase, which may result in vomiting, nausea, and shortness of breath.[50]
Other effects of alcohol on antibiotic activity include altered activity of the liver enzymes that break down the antibiotic compound. [21] In addition, serum levels of
doxycycline and erythromycinsuccinate[clarification needed] two bacteriostatic antibiotics (see above) may be reduced by alcohol consumption, resulting in reduced efficacy and
diminished pharmacotherapeutic effect.[51]
Resistance[edit]
Main article: Antibiotic resistance

SEM depicting methicillin-resistant Staphylococcus aureusbacteria

The emergence of resistance of bacteria to antibiotics is a common phenomenon. 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. [52] For example,
antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the LuriaDelbrck experiment.[53] 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.[54]
Resistance may take the form of biodegredation of pharmaceuticals, such as sulfamethazine-degrading soil bacteria introduced to sulfamethazine through medicated
pig feces.[55] The survival of bacteria often results from an inheritable resistance,[56] 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.[57]
Antibacterial resistance may impose a biological cost, thereby reducing fitness of resistant strains, which can limit the spread of antibacterial-resistant bacteria, for
example, in the absence of antibacterial compounds. Additional mutations, however, may compensate for this fitness cost and can aid the survival of these bacteria. [58]
Paleontological data show that both antibiotics and antibiotic resistance are ancient compounds and mechanisms. [59] Useful antibiotic targets are those for which
mutations negatively impact bacterial reproduction or viability.[60]
Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. [61] For example,
an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extrachromosomal DNA.[61] Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to,
antibacterial-resistant strains.[62][63] The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic
recombination of DNA by horizontal genetic exchange.[56] For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species
viaplasmids that carry these resistance genes.[56][64] Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. [64] Crossresistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial
compound.[64]
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 (TB) that are resistant to previously effective antibacterial treatments pose many therapeutic challenges.
Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide.[65] For example, NDM-1 is a newly identified
enzyme conveying bacterial resistance to a broad range of beta-lactam antibacterials.[66] The United Kingdom's Health Protection Agency has stated that "most isolates
with NDM-1 enzyme are resistant to all standard intravenous antibiotics for treatment of severe infections."[67]
Misuse[edit]

This poster from the U.S. Centers for Disease Control and Prevention "Get Smart" campaign, intended for use in doctors' offices and other healthcare facilities,
warns that antibiotics do not work for viral illnesses such as the common cold.
Main article: Antibiotic misuse
Per the The ICU Book "The first rule of antibiotics is try not to use them, and the second rule is try not to use too many of them." [68]
Inappropriate antibiotic treatment and overuse of antibiotics have contributed to the emergence of antibiotic-resistant bacteria. Self prescription of antibiotics is an
example of misuse.[69] Many antibiotics are frequently prescribed to treat symptoms or diseases that do not respond to antibiotics or that are likely to resolve without
treatment. Also incorrect or suboptimal antibiotics are prescribed for certain bacterial infections. [39][69] The overuse of antibiotics, like penicillin and erythromycin, have
been associated with emerging antibiotic resistance since the 1950s.[54][70] Widespread usage of antibiotics in hospitals has also been associated with increases in
bacterial strains and species that no longer respond to treatment with the most common antibiotics. [70]
Common forms of antibiotic misuse include excessive use of prophylactic antibiotics in travelers and failure of medical professionals to prescribe the correct dosage of
antibiotics on the basis of the patient's weight and history of prior use. Other forms of misuse include failure to take the entire prescribed course of the antibiotic,
incorrect dosage and administration, or failure to rest for sufficient recovery. Inappropriate antibiotic treatment, for example, is their prescription to treat viral infections
such as thecommon cold. One study on respiratory tract infections found "physicians were more likely to prescribe antibiotics to patients who appeared to expect
them".[71]Multifactorial interventions aimed at both physicians and patients can reduce inappropriate prescription of antibiotics. [72]
Several organizations concerned with antimicrobial resistance are lobbying to eliminate the unnecessary use of antibiotics. [69] The issues of misuse and overuse of
antibiotics have been addressed by the formation of the U.S. 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 (NIH), as well as other US agencies.[73] An NGO campaign group is Keep Antibiotics Working.[74] 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. [75]
The emergence of antibiotic resistance has prompted restrictions on their use in the UK in 1970 (Swann report 1969), and the EU has banned the use of antibiotics as
growth-promotional agents since 2003.[76] Moreover, several organizations (e.g., The American Society for Microbiology (ASM), American Public Health Association
(APHA) and the American Medical Association (AMA)) have called for restrictions on antibiotic use in food animal production and an end to all nontherapeutic uses.
[citation needed]
However, commonly there are delays in regulatory and legislative actions to limit the use of antibiotics, attributable partly to resistance against such
regulation by industries using or selling antibiotics, and to the time required for research to test causal links between their use and resistance to them. Two federal bills
(S.742[77] and H.R. 2562[78]) aimed at phasing out nontherapeutic use of antibiotics in US food animals were proposed, but have not passed.[77][78]These bills were
endorsed by public health and medical organizations, including the American Holistic Nurses' Association, the American Medical Association, and the American Public
Health Association (APHA).[79]

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 U.S.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.[80]
Alternatives[edit]
The increase in bacterial strains that are resistant to conventional antibacterial therapies has prompted the development of bacterial disease treatment strategies that
are alternatives to conventional antibacterials.
Resistance-modifying agents[edit]
One strategy to address bacterial drug resistance is the discovery and application of compounds that modify resistance to common antibacterials. For example, some
resistance-modifying agents may inhibit multidrug resistance mechanisms, such as drug efflux from the cell, thus increasing the susceptibility of bacteria to an
antibacterial. Targets include:

The efflux inhibitor Phe-Arg--naphthylamide.[81]

Beta-lactamase inhibitors, such as clavulanic acid and sulbactam.

Metabolic stimuli such as sugar can help eradicate a certain type of antibiotic-tolerant bacteria by keeping their metabolism active. [82]
Vaccines[edit]
Vaccines rely on immune modulation or augmentation. Vaccination either excites or reinforces the immune competency of a host to ward off infection, leading to the
activation of macrophages, the production ofantibodies, inflammation, and other classic immune reactions. Antibacterial vaccines have been responsible for a drastic
reduction in global bacterial diseases.[citation needed] Vaccines made from attenuated whole cells or lysates have been replaced largely by less reactogenic, cell-free
vaccines consisting of purified components, including capsular polysaccharides and their conjugates, to protein carriers, as well as inactivated toxins (toxoids) and
proteins.[83]
Status of new antibiotics development[edit]
In a policy report released by the Infectious Disease Society of America (IDSA) on April 2013, IDSA expressed grave concern over the weak pipeline of antibiotics to
combat the growing ability of bacteria, especially the Gram-negative bacilli (GNB), to develop resistance to antibiotics. Since 2009, only 2 new antibiotics were
approved in United States, and the number of new antibiotics annually approved for marketing continues to decline. The report could identify only seven antibiotics
currently in phase 2 or phase 3 clinical trials to treat the GNB, which includes E. coli, Salmonella, Shigella, and theEnterobacteriaceae bacteria, and these drugs do not
address the entire spectrum of the resistance developed by those bacteria.[84][85] Some of these seven new antibiotics are combination of existent antibiotics, including:

Ceftolozane/tazobactam (CXA-201; CXA-101/tazobactam): Antipseudomonal cephalosporin/-lactamase inhibitor combination (cell wall synthesis inhibitor). In
phase 3.

Ceftazidime/avibactam (ceftazidime/NXL104): Antipseudomonal cephalosporin/-lactamase inhibitor combination (cell wall synthesis inhibitor). In phase 3.

Ceftaroline/avibactam (CPT-avibactam; ceftaroline/NXL104): Anti-MRSA cephalosporin/ -lactamase inhibitor combination (cell wall synthesis inhibitor)

Imipenem/MK-7655: Carbapenem/ -lactamase inhibitor combination (cell wall synthesis inhibitor). In phase 2.

Plazomicin (ACHN-490): Aminoglycoside (protein synthesis inhibitor). In phase 2.

Eravacycline (TP-434): A synthetic tetracycline derivative / protein synthesis inhibitor targeting the ribosome being developed by Tetraphase. Phase 2 trials
complete.[86]

Brilacidin (PMX-30063): Peptide defense protein mimetic (cell membrane disruption). In phase 2.

The IDSAs prognosis for sustainable R&D infrastructure for antibiotics development will depend upon clarification of FDA regulatory clinical trial guidance that would
facilitate the speedy approval of new drugs, and the appropriate economic incentives for the pharmaceuticals companies to invest in this endeavor.[85] On 12 December
2013, the Antibiotic Development to Advance Patient Treatment (ADAPT) Act of 2013 was introduced in the U.S. Congress. The ADAPT Act aims to fast track the drug
development in order to combat the growing public health threat of 'superbugs'. Under this Act, FDA can approve antibiotics and antifungals needed for life-threatening
infections based on data from smaller clinical trials. The CDC will reinforce the monitoring of the use of antibiotics that treat serious and life-threatening infections and
the emerging resistance, and make the data publicly available. The FDA antibiotics labeling process, 'Susceptibility Test Interpretive Criteria for Microbial Organisms' or
'breakpoints' is also streamlined to allow the most up-to-date and cutting-edge data available to healthcare professionals under the new Act. [87][88]
List of antibiotics
From Wikipedia, the free encyclopedia
The following is a list of antibiotics, sorted by class. The highest division is between bactericidal antibiotics and bacteriostatic antibiotics. Bactericidals kill bacteria directly,
whereas bacteriostatics prevent them from dividing. However, these classifications are based on laboratory behavior. In practice, both can prevent a bacterial infection. [1]
See also pathogenic bacteria for a list of antibiotics sorted by target bacteria.

Antibiotics by class

Generic name

Brand names

Common uses[2]

Aminoglycosides

Possible side effects[2]

Mechanism of action

Amikacin

Amikin

Gentamicin

Garamycin

Kanamycin

Kantrex

Neomycin

Neo-Fradin[3]

Netilmicin

Netromycin

Tobramycin

Nebcin

Paromomycin

Humatin

Streptomycin
Spectinomycin

Infections caused by Gram-negative bacteria,

such as Escherichia
coli and Klebsiella particularlyPseudomonas
aeruginosa. Effective against Aerobic bacteria
(not obligate/facultative anaerobes)
andtularemia.

Binding to the
bacterial 30S ribosomal subunit (some
work by binding to the 50Ssubunit),
inhibiting the translocation of the
peptidyl-tRNA from the A-site to the PVertigo
site and also causing misreading of
mRNA, leaving the bacterium unable to
Kidney damage synthesize proteins vital to its growth.
Hearing loss

Tuberculosis
Trobicin

Gonorrhea
Ansamycins

Geldanamycin

Experimental, as antitumor antibiotics

Herbimycin
Rifaximin

Xifaxan

Traveler's diarrhea caused by E. coli

Carbacephem

Loracarbef

Lorabid

Ertapenem

Invanz

Doripenem

Doribax

Imipenem/Cilastatin

Primaxin

prevents bacterial cell division by

inhibiting cell wall synthesis.

Discontinued
Carbapenems

Meropenem

Merrem

Bactericidal for both Gram-positive and Gramnegative organisms and therefore useful for
empiric broad-spectrum antibacterial coverage.
(Note MRSA resistance to this class.)

Gastrointestinal
upset and diarrhea
Nausea
Seizures

Inhibition of cell wall synthesis

Headache

Rash and
allergic reactions

Gastrointestinal
upset and diarrhea

Nausea (if
alcohol taken
concurrently)

Allergic
reactions

Gastrointestinal
upset and diarrhea

Nausea (if
alcohol taken
concurrently)

Allergic
reactions

Cephalosporins (First generation)

Cefadroxil

Duricef

Cefazolin

Ancef

Cefalotin or Cefalothin

Keflin(discontinued)
Good coverage against Gram-positive
infections.

Cefalexin

Keflex

Same mode of action as other betalactam antibiotics: disrupt the

synthesis of thepeptidoglycan layer of
bacterial cell walls.

Cephalosporins (Second generation)

Cefaclor

Distaclor

Cefamandole

Mandol(discontinued)

Cefoxitin

Mefoxin(discontinued)

Cefprozil

Cefzil

Cefuroxime

Ceftin, Zinnat(UK)

Less Gram-positive cover, improved Gramnegative cover.

Same mode of action as other betalactam antibiotics: disrupt the

synthesis of thepeptidoglycan layer of
bacterial cell walls.

Cephalosporins (Third generation)

Cefixime

Suprax

Cefdinir

Omnicef, Cefdiel

Cefditoren

Spectracef, Meiact

Cefoperazone

Cefobid(discontinued)

Cefotaxime

Claforan

Cefpodoxime

Vantin

Ceftazidime [Unlike most third-

Fortaz

Improved coverage of Gram-negative

organisms, except Pseudomonas. Reduced
Gram-positive cover.

Same mode of action as other betalactam antibiotics: disrupt the

Gastrointestinal synthesis of thepeptidoglycan layer of
upset and diarrhea
bacterial cell walls.
Nausea (if
alcohol taken
concurrently)

generation agents, ceftazidime is

active against Pseudomonas
aeruginosa]
Ceftibuten

Cedax

Ceftizoxime

Cefizox (discontinued)

Ceftriaxone

Rocephin

Allergic
reactions

Gastrointestinal
upset and diarrhea

Nausea (if
alcohol taken
concurrently)

Allergic
reactions

Gastrointestinal Same mode of action as other betaupset and diarrhea

lactam antibiotics: disrupt the
synthesis of thepeptidoglycan layer of
bacterial cell walls.
Allergic
reaction

Cephalosporins (Fourth generation)

Cefepime

Maxipime

Covers pseudomonal infections.

Same mode of action as other betalactam antibiotics: disrupt the

synthesis of thepeptidoglycan layer of
bacterial cell walls.

Cephalosporins (Fifth generation)

Ceftaroline fosamil

Teflaro

Used to treat MRSA

Ceftobiprole

Zeftera

Used to treat MRSA

Gastrointestinal
upset and diarrhea

Nausea (if
alcohol taken
concurrently)

Allergic
reactions

Same mode of action as other betalactam antibiotics: disrupt the

synthesis of thepeptidoglycan layer of
bacterial cell walls.

Glycopeptides
Teicoplanin

Targocid (UK)

Vancomycin

Vancocin

Telavancin

Vibativ

Clindamycin

Cleocin

Lincomycin

Lincocin

Active against aerobic and anaerobic Grampositive bacteria including MRSA;

Vancomycin is used orally for the treatment
of C. difficile

inhibiting peptidoglycan synthesis

Lincosamides
Serious staph-, pneumo-, and streptococcal
infections in penicillin-allergic patients, also
anaerobic infections; clindamycin topically
for acne

Possible C. difficileBind to 50S subunit of bacterial

relatedpseudomembranous ribosomal RNA thereby inhibiting
enterocolitis
protein synthesis

Lipopeptide

Daptomycin

Cubicin

Bind to the membrane and cause rapid

depolarization, resulting in a loss of
membrane potential leading to
inhibition of protein, DNA and RNA
synthesis

Gram-positive organisms

Macrolides
Azithromycin

Dirithromycin

Zithromax,Sumamed,Xithrone Streptococcal infections, syphilis, upper

respiratory tract infections, lower respiratory
Biaxin
tract infections,mycoplasmal infections, Lyme
disease
Dynabac(discontinued)

Erythromycin

Erythocin,Erythroped

Clarithromycin

Roxithromycin
Troleandomycin

Tao (discontinued)

Nausea,
vomiting, and
diarrhea (especially
at higher doses)

Prolonged
cardiacQT
interval(especially
erythromycin)

Hearing loss
(especially at higher
doses)

Jaundice

inhibition of bacterial protein

biosynthesis by binding reversibly to
the subunit 50S of the
bacterial ribosome, thereby inhibiting
translocation of peptidyl tRNA.

Visual Disturbance, Liver

Toxicity.[4]

Telithromycin

Ketek

Pneumonia

Spiramycin

Rovamycine

Mouth infections
Monobactams

Aztreonam

Azactam

Gram-negative bacteria

Furazolidone

Furoxone

Bacterial or protozoal diarrhea or enteritis

Nitrofurantoin

Macrodantin,Macrobid

Urinary tract infections

Same mode of action as other betalactam antibiotics: disrupt the

synthesis of thepeptidoglycan layer of
bacterial cell walls.

Nitrofurans

Oxazolidonones

Linezolid

Zyvox

Posizolid

Phase II clinical trials

Radezolid

Phase II clinical trials

Torezolid

Phase II clinical trials

Amoxicillin

Novamox,Amoxil

Ampicillin

Principen (discontinued)

Thrombocytope
nia

VRSA

Peripheral
neuropathy

Gastrointestinal
upset and diarrhea

Allergy with
seriousanaphylactic
reactions

Brain and
kidney damage (rare)

Protein synthesis inhibitor; prevents

the initiation step

Penicillins

Azlocillin
Carbenicillin

Geocillin (discontinued)

Cloxacillin

Tegopen (discontinued)

Dicloxacillin

Dynapen (discontinued)

Flucloxacillin

Floxapen(Sold to European
generics Actavis Group)

Mezlocillin

Mezlin (discontinued)

Methicillin

Staphcillin (discontinued)

Nafcillin

Unipen (discontinued)

Oxacillin

Prostaphlin (discontinued)

Penicillin G

Pentids (discontinued)

Penicillin V

Veetids (Pen-Vee-K)
(discontinued)

Piperacillin

Pipracil (discontinued)

Penicillin G

Pfizerpen

Temocillin

Negaban (UK) (discontinued)

Ticarcillin

Ticar (discontinued)

Wide range of infections; penicillin used

forstreptococcal infections, syphilis, and Lyme
disease

Same mode of action as other betalactam antibiotics: disrupt the

synthesis of thepeptidoglycan layer of
bacterial cell walls.

Penicillin combinations
Amoxicillin/clavulanate

Augmentin

Ampicillin/sulbactam

Unasyn

Piperacillin/tazobactam

Zosyn

Ticarcillin/clavulanate

Timentin

The second component prevents

bacterial resistance to the first
component
Polypeptides

Bacitracin

Colistin

Polymyxin B

Coly-Mycin-S

Eye, ear or bladder infections; usually applied

directly to the eye or inhaled into the lungs;
rarely given by injection, although the use of
Kidney and nerve damage
intravenous colistin is experiencing a
(when given by injection)
resurgence due to the emergence of multi drug
resistant organisms.

Inhibits isoprenyl pyrophosphate, a

molecule that carries the building
blocks of
thepeptidoglycan bacterial cell
wall outside of the inner membrane[5]
Interact with the Gramnegative bacterial outer
membrane and cytoplasmic
membrane, displacing bacterial
counterions, which destabilizes the
outer membrane. Act like a detergent
against the cytoplasmic membrane,
which alters its permeability.
Polymyxin B and E are bactericidal
even in an isosmotic solution.

Quinolones/Fluoroquinolone
Ciprofloxacin

Cipro,Ciproxin, Ciprobay

Enoxacin

Penetrex

Gatifloxacin

Tequin

Gemifloxacin

Factive[6]

Levofloxacin

Levaquin

Lomefloxacin

Maxaquin

Moxifloxacin

Avelox

Nalidixic acid

NegGram

Norfloxacin

Noroxin

Ofloxacin

Floxin, Ocuflox

Trovafloxacin

Trovan

Withdrawn

Grepafloxacin

Raxar

Withdrawn

Sparfloxacin

Zagam

Withdrawn

Temafloxacin

Omniflox

Withdrawn

Urinary tract infections, bacterial prostatitis,

community-acquired pneumonia, bacterial
diarrhea,mycoplasmal infections, gonorrhea

Nausea (rare), irreversible

damage tocentral nervous
system (uncommon),
tendinosis (rare)

inhibit the bacterial DNA gyrase or

the topoisomerase IV enzyme, thereby
inhibitingDNA replication and
transcription.

Sulfonamides
Mafenide

Sulfamylon

Sulfacetamide

Sulamyd, Bleph-10

Sulfadiazine

Micro-Sulfon

Silver sulfadiazine

Silvadene

Sulfadimethoxine

Di-Methox, Albon

Sulfamethizole

Thiosulfil Forte

Sulfamethoxazole

Gantanol

Sulfanilimide (archaic)
Sulfasalazine

Azulfidine

Sulfisoxazole

Gantrisin

Urinary tract infections (except sulfacetamide,

used for eye infections, and mafenide and
silver sulfadiazine, used topically for burns)

Nausea,
vomiting, and
diarrhea

Allergy (includi Folate synthesis inhibition. They

are competitive inhibitors of the
ng skin rashes)
enzymedihydropteroate synthetase,
DHPS. DHPS catalyses the conversion
Crystals in
of PABA (para-aminobenzoate)
urine
to dihydropteroate, a key step
in folate synthesis. Folate is necessary
for the cell to synthesize nucleic
Kidney failure
acids (nucleic acids are essential
building blocks of DNA and RNA),
and in its absence cells cannot divide.
Decrease
in white blood
cell count

TrimethoprimSulfamethoxazole(Co-trimoxazole) Bactrim, Septra

(TMP-SMX)

Sulfonamidochrysoidine(archaic)

Sensitivity to
sunlight

Gastrointestinal
upset

Sensitivity to
sunlight

Potential
toxicity to mother
and fetus during
pregnancy

Enamel
hypoplasia (staining
of teeth; potentially
permanent)

transient
depression of bone
growth

Prontosil
Tetracyclines

Demeclocycline

Declomycin

Doxycycline

Vibramycin

Minocycline

Minocin

Oxytetracycline

Terramycin

Tetracycline

Sumycin,Achromycin
V, Steclin

Syphilis, chlamydial infections, Lyme

disease,mycoplasmal infections,
acne rickettsial infections, *malaria *Note:
Malaria is caused by a protist and not a
bacterium.

Drugs against mycobacteria

Clofazimine

Lamprene

Antileprotic

Dapsone

Avlosulfon

Antileprotic

Capreomycin

Capastat

Antituberculosis

Cycloserine

Seromycin

Antituberculosis, urinary tract infections

Ethambutol

Myambutol

Antituberculosis

inhibiting the binding of aminoacyltRNA to the mRNAribosome complex. They do so mainly

by binding to the 30S ribosomal
subunit in the mRNA
translationcomplex.

Ethionamide

Trecator

Antituberculosis

Isoniazid

I.N.H.

Antituberculosis

Pyrazinamide

Aldinamide

Antituberculosis

Rifampicin (Rifampin in US)

Rifadin, Rimactane

mostly Gram-positive and mycobacteria

Reddish-orange sweat,
tears, and urine

Rifabutin

Mycobutin

Mycobacterium avium complex

Rash, discolored urine, GI

symptoms

Rifapentine

Priftin

Antituberculosis

Streptomycin

Inhibits peptide synthesis

Antituberculosis

Neurotoxicity,ototoxicity

Binds to the subunit of RNA

polymerase to inhibit transcription

As other aminoglycosides

Others
Arsphenamine

Salvarsan

Spirochaetal infections (obsolete)

Chloramphenicol

Chloromycetin

Meningitis, MRSA, topical use, or for low-cost

internal treatment.
Rarely: aplastic anemia.
Historic: typhus, cholera. Gram-negative, Gra
m-positive, anaerobes

Fosfomycin

Monurol, Monuril

Acute cystitis in women

This antibiotic is not

recommended for children
and 75 up of age

Inactivates enolpyruvyl transferase,

thereby blocking cell wall synthesis

Fusidic acid

Fucidin
Discolored
urine,headache, metallic
taste, nausea; alcoholis
contraindicated

Produces toxic free radicals that

disrupt DNA and proteins. This nonspecific mechanism is responsible for
its activity against a variety of
bacteria, amoebae, and protozoa.

Metronidazole

Flagyl

Infections caused by anaerobic bacteria;

alsoamoebiasis, trichomoniasis, giardiasis

Mupirocin

Bactroban

Ointment for impetigo, cream for infected cuts

Inhibits bacterial protein synthesis by

binding to the 50S subunit of the
ribosome

Inhibits isoleucine t-RNA synthetase

(IleRS) causing inhibition of protein
synthesis

Platensimycin
Quinupristin/Dalfopristin

Synercid

Thiamphenicol

Gram-negative, Gram-positive, anaerobes.

Widely used in veterinary medicine.

A chloramphenicol analog. May

Rash. Lacks known anemic inhibit bacterial protein synthesis by
side-effects.
binding to the 50S subunit of the
ribosome

Tigecycline

Tigacyl

Indicated for complicated skin/skin structure

infections and complicated intra-abdominal
infections.

Teeth discoloration

Tinidazole

Tindamax Fasigyn

Protozoal infections

Upset stomach, bitter taste,

and itchiness

Trimethoprim

Proloprim, Trimpex

Urinary tract infections

Generic Name

Brand Names

Common Uses[2]

Possible Side Effects[2]

Mechanism of action

Ampicillin is an antibiotic useful for the treatment of a number of bacterial infections. It is a beta-lactam antibiotic that is part of the aminopenicillin family and is roughly
equivalent to its successor, amoxicillin in terms of spectrum and level of activity.[1]
It can sometimes result in reactions that range in severity from a rash (in the case of patients who may unwittingly have mononucleosis) to potentially lethal allergic
reactions such as anaphylaxis. However, as with other penicillin drugs, it is relatively nontoxic, and adverse effects of a serious nature are encountered only rarely.
It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.[2]
Medical uses[edit]
Ampicillin is closely related to amoxicillin, another type of penicillin, and both are used to treat urinary tract infections, otitis media, H. influenzaeinfection, salmonellosis,
and Listeria meningitis. It is used with flucloxacillin in the combination antibiotic co-fluampicil for empiric treatment ofcellulitis, providing cover against group A streptococcal
infection whilst the flucloxacillin acts against Staphylococcus aureus. Of concern is the number of bacteria that have become resistant to ampicillin, necessitating
combination therapy or use of other antibiotics.

Demeclocycline (marketed as Declomycin, Declostatin, and Ledermycin) is a tetracycline antibiotic derived from a strain of Streptomyces aureofaciens.[1]
Uses[edit]

It is officially indicated for the treatment of various types of bacterial infections.[2] It is used as an antibiotic in the treatment of Lyme disease, acne, andbronchitis.[citation
needed]

Resistance, though, is gradually becoming more common, and demeclocycline is now rarely used for infections.

It is widely used (though off-label in many countries) in the treatment of hyponatremia (low blood sodium concentration) due to the syndrome of inappropriate antidiuretic
hormone (SIADH) when fluid restriction alone has been ineffective.[3] Physiologically, this works by reducing the responsiveness of the collecting tubule cells to ADH.
The use in SIADH actually relies on a side effect; demeclocycline induces nephrogenic diabetes insipidus (dehydration due to the inability to concentrate urine).[3] The use of
demeclocycline in SIADH was first reported in 1975,[4] and, in 1978, a larger study found it to be more effective and better tolerated than lithium carbonate, the only available
treatment at the time.[5] Demeclocycline has since been the drug of choice for treating SIADH, although it may be superseded as vasopressin receptor antagonists, such
as tolvaptan, become available.[5]

Doxycycline (IPA: /dksisaklin/) is an antibiotic useful for the treatment of a number of infections. It is in the tetracycline antibiotic class.
Under the brand name Vibramycin, Pfizer's doxycycline product received US Food and Drug Administration approval in 1967.[1] Other brand names include Monodox,
Microdox, Periostat, Vibra-Tabs, Oracea, Doryx,[2] Vibrox, Adoxa, Doxyhexal, Doxylin, Doxoral, Doxy-1 and Atridox (topical doxycycline hyclate for periodontitis) It is on
the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.[3]
Medical uses[edit]
Further information: Oxytetracycline
In addition to the general indications for all members of the tetracycline antibiotics group, doxycycline is frequently used to treat Lyme disease,
chronic prostatitis, sinusitis, pelvic inflammatory disease,[4][5] acne, rosacea,[6][7] and rickettsial infections.[8]

Vancomycin INN /vkmasn/ is an antibiotic useful for the treatment of a number of bacterial infections. It is of the glycopeptide antibiotic class and is effective mostly
against Gram-positive bacteria. Vancomycin was first isolated in 1953 at Eli Lilly, from a soil sample collected from the interior jungles of Borneo by a missionary. It is a
naturally occurring antibiotic made by the soil bacterium Actinobacteria species Amycolatopsis orientalis(formerly designated Nocardia orientalis). It is a complex chemical
compound and an example of a comparatively rare haloorganic natural compound, containing two covalently bonded chlorine atoms(see green "balls" in ball-and-stick
model, right).

The compound was industrially produced by fermentation and given the generic name vancomycin, derived from the term "vanquish." The original indication for vancomycin
was for the treatment of penicillin-resistant Staphylococcus aureus, a use kept alive for many years by the fact that compound had to be given intravenously and thus
provided bacteria fewer opportunities to evolve resistance, and the fact that organisms were relatively slow to evolve/adapt to it, even in experiments.
Vancomyin is primarily used for the treatment of serious infections caused by Gram-(+) bacteria that are known or suspected to be resistant to other antibiotics. The
Infectious Disease Society of America recommends vancomycin as a first line treatment for complicated skin infections, bloodstream infections, endocarditis, bond and joint
infections, and meningitis infections caused by methicillin-resistant Staphylococcus aureus.[1] Orally administered vancomycin is recommended as a treatment for intestinal
infection with Clostridium difficile, a common side effect of treatment with broad spectrum antibiotics. [2]
It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.[3]

Medical uses[edit]
Vancomycin is indicated for the treatment of serious, life-threatening infections by Gram-positive bacteria that are unresponsive to other less-toxic
antibiotics. In particular, vancomycin should not be used to treat methicillin-sensitive Staphylococcus aureus because it is inferior to penicillins such as
nafcillin.

Mafenide (INN; usually as mafenide acetate, trade name Sulfamylon) is a sulfonamide-type medication. It was approved by the FDA in 1948.
Uses[edit]
It is used to treat severe burns.[1][2] It is used topically as an adjunctive therapy for second- and third-degree burns. It is bacteriostatic against many gram-positive and gramnegative organisms, including Pseudomonas aeruginosa. Some sources state that mafenide is more appropriate for non-facial burns,
whilechloramphenicol/prednisolone or bacitracin are more appropriate for facial burns.[3]

Teicoplanin is an antibiotic used in the prophylaxis and treatment of serious infections caused by Gram-positive bacteria, including methicillin-resistantStaphylococcus
aureus and Enterococcus faecalis. It is a semisynthetic glycopeptide antibiotic with a spectrum of activity similar to vancomycin. Its mechanism of action is to inhibit bacterial
cell wall synthesis.
Teicoplanin is marketed by Sanofi-Aventis under the trade name Targocid.
Oral teicoplanin has been demonstrated to be effective in the treatment of pseudomembranous colitis and Clostridium difficile-associated diarrhoea, with comparable efficacy
with vancomycin.[1]
Its strength is considered to be due to the length of the hydrocarbon chain.[2]

Medical uses
Oral teicoplanin has been demonstrated to be effective in the treatment of pseudomembranous colitis and Clostridium difficile-associated diarrhoea, with comparable efficacy
with vancomycin.[1]

Ciprofloxacin (INN) is an antibiotic useful for the treatment of a number of bacterial infections. It is a second-generation fluoroquinolone.[2][3] Its spectrum of activity includes
most strains of bacterial pathogens responsible for respiratory, urinary tract, gastrointestinal, and abdominal infections, including Gram-negative (Escherichia
coli, Haemophilus influenzae, Klebsiella pneumoniae, Legionella pneumophila, Moraxella catarrhalis, Proteus mirabilis, and Pseudomonas aeruginosa), and Grampositive (methicillin-sensitive but not methicillin-resistant Staphylococcus aureus, Streptococcus pneumoniae, Staphylococcus epidermidis, Enterococcus faecalis,
andStreptococcus pyogenes) bacterial pathogens. Ciprofloxacin and other fluoroquinolones are valued for this broad spectrum of activity, excellent tissue penetration, and
for their availability in both oral and intravenous formulations
Medical uses[edit]

Ciprofloxacin is used to treat a wide variety of infections, including infections of bones and joints, endocarditis, gastroenteritis, malignant otitis externa, respiratory tract
infections, cellulitis, urinary tract infections, prostatitis, anthrax, and chancroid.[17]
Ciprofloxacin only treats bacterial infections; it does not treat viral infections such as the common cold. Although for certain uses including acute sinusitis, lower respiratory
tract infections and uncomplicated gonorrhea, ciprofloxacin is not considered a first line agent.