If bacterial resistance randomly occur, then why limit broad-spectrum antibiotic use?

If bacterial resistance randomly occur, then why limit broad-spectrum antibiotic use?

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If there is importance to study some discipline, then one of the main matters is its applications, so besides the primary goal of knowing the truth of the matter regarding what that discipline is investigating, applicability or usefulness of that study in other fields or in the field itself is a very important matter. I'll direct my attention here to Evolution, and its mechanisms. So accordingly if something that I personally want to come up with is application of that knowledge to the field of my work.

In reality we don't study evolution extensively at college level in medicine, since it doesn't have a direct clinical impact on the diagnosis and treatment of patients in most of the cases. However, one possible area of interaction is "bacterial resistance to antibiotics", since this is related to "mutations", and generally viewed as a mechanism whereby the bacterium adapts to its environment.

Now all of my life in medicine from college through specialty and academic teaching, we've never ceased being reminded about not dispensing antibiotics liberally, and the main concern outlined is "emergence of resistant strains of bacteria" due to this liberal use of antibiotics itself. There are other reasons of course, like side effects and cost, but they are not the main concern most of the times.

During my recent review of Evolution, looking at the introductory courses that were cited to me by many participants here, in particular this page of Evo101 titled "Mutations are Random" I was really shocked to know that even the mutations that resulted in bacterial resistance were not "directed mutations", i.e. it is not the case that the exposure to the antibiotic caused the bacteria to have that mutation in the first place, actually the page mentions Esther and Joshua Lederberg experiments showing that those resistant bacteria were already there before the population was exposed to the antibiotics?

So why have we been always reminded by bacteriologists of limiting our antibiotic usage if emergence of drug resistance is not due to exposure to it?

Actually, its not only that, many lectures we attend, which are pretty much delivered by official bodies, does mention of emergence of antibiotic resistance as a DIRECTED mutation response to exposure to the particular antibiotic, that almost most of us we clinicians became to think that this is a fact. For example hospital bacteria are of the most resistant ones, especially those in intensive care facilities. The association between exposure to antibiotics and emergence of drug resistant bacteria to them is almost hammered in our brains, that to discover that the mutation was already there before exposure to the antibiotic seems quite shocking, at least to me in person.

My question here is the following:

Is it a scientific fact that emergence of bacterial resistance through mutations is always random, i.e. in the sense that it is not a directed response to exposure of the population to that antibiotic?

For instance this seems to be a counter-example.

If that is the case then why bother about liberal use of broad-spectrum antibiotics? I mean as far as emergence of bacterial resistance is concerned!

I mean its not the case that I'm going to eradicate the "useful bacterial" that could rival the pathogenic resistant bacteria, by that liberal use of broad-spectrum antibiotics. If that happens temporarily we can in principle replace them back, like with the use of probiotics.

During my surfing of the web I found that page addressing the same point, but the responses are not that explicit, and far from being convincing?

You're correct, this is extremely relevant, and it's unfortunate that your medical education didn't include good instruction about evolution.

You point to some very useful and interesting studies. I'm particularly fond of the studies that demonstrate the early existence of antibacterial resistance genes, e.g., in ancient permafrost.

Now to your question

Is it a scientific fact that emergence of bacterial resistance through mutations is always random, i.e. in the sense that it is not a directed response to exposure of the population to that antibiotic?

I think the issue here is a conflation of two separate concepts. Mutation is one mechanism for producing variation. Mutation can be understood as a stochastic process, causing changes in the genome of an individual by chance.

Evolution occurs because of existing variation. Evolution is not a stochastic process. It is a biased process, a change in the distribution of existing variation.

The emergence of antibacterial resistance is evolution that results from selection acting on existing variation. Emergence here refers to emergence of a resistant variant within a population. Selective pressure (application of antibiotics) causes a predictable change in the frequency of genes that would allow reproduction in that environment, the frequency of existing resistance genes increases in the bacterial population.

Though there is evidence for important antibacterial resistance mutations pre-dating the use of antibiotics, this does not rule out the occurrence of spontaneous mutations, as demonstrated in the article you linked. The production of genetic variation by random mutation can be followed by a rapid increase in the frequency of a new genetic variation that is selected for in a given environment. This can be particularly likely in organisms with high error rates, short generation times, and large numbers of individuals. The spontaneous mutation isn't directed, as you say. It is random. The selection of that particular random mutation is directed, though. Once the random mutation occured, then we can say the variation exists. Then selective pressure acts on existing variation, allowing evolution, a change in the frequency of the, in this case, gene for resistance.

Goodman & Gilman, one of my go to pharmacology references, actually has an excellent discussion of these concepts as they relate to antibacterial resistance, in Ch. 48, under the subsection EMERGENCE. There is a good discussion of the various mechanisms of emergence, but this general statement is helpful:

Mutations are not caused by drug exposure per se. They are random events that confer a survival advantage when drug is present. Any large population of drug susceptible bacteria is likely to contain rare mutants that are only slightly less susceptible than the parent. However, suboptimal dosing strategies lead to selective kill of the more susceptible population, which leaves the resistant isolates to flourish.

The mutations are random, the survival and spread of bacteria with said mutations is NOT random.

Evolution and selection are situational.

The careless use of antibiotics causes those mutations and bacteria to spread because they out compete others without resistance. However, often these will not outcompete without antibiotics being present. Often mutations that produce resistance are detrimental when antibiotics are not present, or more precisely the downsides of the mutation are more than offset by the benefits of resistance when antibiotics are present. Meaning even when they occur mutations the produce resistance die out quickly without antibiotics.

Even when they offer no advantage of disadvantage without the presence of antibiotics normal genetic drift can eliminate them, but when antibiotics are present and a mutation occurs the mutation then offers an advantage and spreads. That means a person is more likely to catch a strain that is resistant than if their was no antibiotics present in the bacteria's environment.

Note the "environment" can be anything from the greater ecosphere down to an individual patient. and population can be the population inside an individual or the population of bacteria across the globe.

lets try a pair of scenarios

In each the mutation for resistance occured in 1% of the population of bacteria.

Scenario 1 no antibiotics. You have a 1% chance of catching a resistant strain.

Scenario 2 Antibiotics present. Now selective pressures quickly change the population so that resistant strains now make up the majority (we'll say 75%). Now you have a 75% chance of catching a resistant strain, and worse those resistant strains now have a high chance of meeting other strains with other resistances or of having another resistant mutation occur (now 1% of 75% instead of 1% of 1%) this means the population becomes even more resistant and it does so rather quickly until no antibiotics work.

So emergence, AKA exposure of humans to resistant strains, IS due to use of antibiotics.

Careless use of antibiotics include.

  1. Use of antibiotics on people/animals/things who do not need it.

  2. Disposal of antibiotics in the environment.

  3. Incomplete courses of antibiotics.

But there is a hidden forth and fifth concern, that is the one your paper is concerned with. Patients and doctors are humans and each of these things will inevitably happen, patients fail to take drugs, or impure drugs are improperly disposed of or a hundred other errors expose bacteria population to antibiotics. So a further concern about having useful antibiotics, by limiting which antibiotics we use, that is by only using common ones unless absolutely necessary, we are minimizing the chances of resistance to those less used antibiotics so we have something that works when we run across a resistant strain.

Lastly people already have bacteria present in their system so these microbes can be exposed to antibiotics targeted at other unrelated infections, thus encouraging resistance. Some are even protected by natural barriers that reduce exposure to antibiotics used to treat other things, like bacteria on the outside of the skin for internal antibiotics. Worse, bacteria can transfer resistance horizontally so these microbes can then share resistance with later infections. So even using antibiotic A correctly on a patient to kill microbe X can lead to microbe Z developing resistance just because the treatment for X is not enough to kill all Z. Staph is particularly prone to this since it is everywhere. So even if you use antibiotics correctly you can still produce resistant strains of other bacteria.

As a side note some confusion is caused by is a quirk of language and terminology in the study of evolution. If X produces an environment in which a mutation that produces trait Z is favored causing that mutation and thus Z to spread in a population often scientists will just say X caused Z, just to save time. humans are lazy and typing out "X produces an environment in which a mutation that produces trait Z is favored causing said mutation to spread in the population and thus Z to spread in a population." takes much longer and uses more space than "X causes Z to spread" or just X causes Z. Other evolutionary scientists know what they mean but it can be confusing for everyone else. It is not a great practice but jargon creeps into all science.

As a personal note it has always been a concern for me that medical schools don't require an understanding of evolution at least for research fields; infection, cancer, and a million other weird quirks of anatomy and physiology are caused by evolution or evolutionary baggage. Heck infection and cancer ARE evolutionary competitions, and some of the most predictable ones.

Evolutionary causes and consequences of bacterial antibiotic persistence

Antibiotic treatment failure is of growing concern. Genetically encoded resistance is key in driving this process. However, there is increasing evidence that bacterial antibiotic persistence, a non-genetically encoded and reversible loss of antibiotic susceptibility, contributes to treatment failure and emergence of resistant strains as well. In this Review, we discuss the evolutionary forces that may drive the selection for antibiotic persistence. We review how some aspects of antibiotic persistence have been directly selected for whereas others result from indirect selection in disparate ecological contexts. We then discuss the consequences of antibiotic persistence on pathogen evolution. Persisters can facilitate the evolution of antibiotic resistance and virulence. Finally, we propose practical means to prevent persister formation and how this may help to slow down the evolution of virulence and resistance in pathogens.


The ribosome is one of the main antibiotic targets in the bacterial cell. Crystal structures of naturally produced antibiotics and their semi-synthetic derivatives bound to ribosomal particles have provided unparalleled insight into their mechanisms of action, and they are also facilitating the design of more effective antibiotics for targeting multidrug-resistant bacteria. In this Review, I discuss the recent structural insights into the mechanism of action of ribosome-targeting antibiotics and the molecular mechanisms of bacterial resistance, in addition to the approaches that are being pursued for the production of improved drugs that inhibit bacterial protein synthesis.

About Antibiotic Resistance

Antibiotic resistance happens when germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them. That means the germs are not killed and continue to grow.

Infections caused by antibiotic-resistant germs are difficult, and sometimes impossible, to treat. In most cases, antibiotic-resistant infections require extended hospital stays, additional follow-up doctor visits, and costly and toxic alternatives.

Antibiotic resistance does not mean the body is becoming resistant to antibiotics it is that bacteria have become resistant to the antibiotics designed to kill them.

Antibiotic Resistance Threatens Everyone

On CDC&rsquos website, antibiotic resistance is also referred to as antimicrobial resistance or drug resistance.

Antibiotic resistance has the potential to affect people at any stage of life, as well as the healthcare, veterinary, and agriculture industries, making it one of the world&rsquos most urgent public health problems.

Each year in the U.S., at least 2.8 million people are infected with antibiotic-resistant bacteria or fungi, and more than 35,000 people die as a result.

No one can completely avoid the risk of resistant infections, but some people are at greater risk than others (for example, people with chronic illnesses). If antibiotics lose their effectiveness, then we lose the ability to treat infections and control public health threats.

Many medical advances are dependent on the ability to fight infections using antibiotics, including joint replacements, organ transplants, cancer therapy, and treatment of chronic diseases like diabetes, asthma, and rheumatoid arthritis.

Brief History of Resistance and Antibiotics

Learn how CDC is leading efforts to combat antibiotic resistance through the Antibiotic Resistance Solutions Initiative.

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

Penicillin-resistant Staphylococcus aureus

Penicillin-resistant Streptococcus pneumoniae

Penicillinase-producing Neisseria gonorrhoeae

Vancomycin-resistant Staphylococcus aureus

Find more information on the development of antibiotic resistance in the latest AR Threats Report.

Biology and Diseases of Ferrets

Joerg Mayer Dr., MSc, Dipl. ACZM, Dipl. ECZM (small mammal), Dipl. ABVP (ECM) , . James G. Fox DVM, MS, DACLAM , in Laboratory Animal Medicine (Third Edition) , 2015


Broad-spectrum antibiotic therapy may be instituted pending culture and sensitivity results of the milk. Enrofloxacin (10 mg/kg BID PO) is often effective. Jills may require aggressive care, because acute mastitis may progress rapidly and animals may become septicemic and moribund ( Liberson et al., 1983 ). Oral antibiotic administration to kits nursing on affected jills is recommended ( Bell, 1997a ). Supplementation of kits with milk replacer may also be necessary, because jills with acute mastitis are reluctant to nurse, and jills with the chronic form have diminished lactation as milk-producing tissue is replaced by scar tissue ( Bell, 1997a ). Surgical resection and debridement of affected glands and supportive care may be necessary for jills with acute mastitis. In the laboratory setting, in which foster mothers are often available, it is far more common to remove and foster the kits, after which jills are treated medically. When cross-fostering kits is required, kits may spread infection to healthy jills. Maintaining thorough personal hygiene practices when handling affected jills is important in minimizing spread to other lactating jills. Jills with the chronic form of mastitis should be culled ( Bell, 1997a ).

Bacterial Antibiotic Resistance: on the Cusp of a Post-antibiotic World

The specific aim of this article is to provide evidence that antibiotic resistance (AR) has become a human disease unto itself and to describe the current means of preventing, treating, and reversing AR in individuals and in affected populations.

Recent findings

An ever-increasing number of infections are being classified as multidrug resistant (MDR). Low and middle-income countries are most likely to increase the spread of AR due to limited healthcare infrastructure coupled with policies that promote unregulated access to antibiotics. The genetic basis for AR has become more thoroughly understood as efforts move toward a global big data approach to surveille and implement effective public health measures.


Antibiotic Stewardship (AS) programs are critical to prevent the spread of AR. As resistant pathogens reside in patients for many years after they are initially integrated into the microbiome, the potential for future infection increases substantially. This property contributes to the conclusion that AR is in and of itself a human disease that must be treated appropriately. While all bacteria are at risk to become AR, Staphylococcus, Klebsiella, Mycobacterium, Acinetobacter, and Pseudomonas represent the greatest challenges in infectious disease treatment as rapid AR acquisition leads to MDR infections.


The emergence and spread of bacterial resistance to clinical antibiotics is a growing public health concern worldwide [1]. Moreover, it is increasingly appreciated that antibiotic tolerance can also contribute to the failure of treatments for infections [2] and that tolerance can lead to the evolution of resistance [3,4]. Yet bacterial resilience to antibiotics is anything but new: Microbes in environments like soil have been producing natural antibiotics and evolving mechanisms of tolerance and resistance for millions of years [5,6]. Here, we define tolerance as the ability to survive a transient exposure to an otherwise lethal antibiotic concentration and resistance as the ability to grow in the presence of an antibiotic, similar to recent recommendations [2,7,8].

Considering that most of the antibiotics used today are derived from microbially produced molecules, we hypothesized that molecular defenses that originally evolved to protect cells from a natural antibiotic in the environment might also promote tolerance and/or resistance to structurally or mechanistically similar clinical drugs. Indeed, several clinical antibiotic resistance genes are thought to have originated in nonpathogenic soil bacteria, but it has often been assumed that intermediate steps of horizontal gene transfer are necessary in order for such genes to be acquired by human pathogens [6]. In this study, we asked whether there could be a direct link between production of natural antibiotics by an opportunistic human pathogen and its recalcitrance to clinical antibiotic treatment due to shared protective mechanisms. In addition, we sought to determine whether in the presence of such a natural antibiotic producer, recalcitrance to clinical antibiotics could also be observed in other opportunistic pathogens found together with it in polymicrobial infections. Given that many opportunistic pathogens share their natural environment (e.g., soil), we posited that the evolutionary legacy of natural antibiotic–mediated ecological interactions between these microbial species could have important implications for antibiotic tolerance and resistance in the clinical context.

One organism that is well suited to testing these hypotheses is the opportunistic pathogen Pseudomonas aeruginosa, which is notorious for causing chronic lung infections in cystic fibrosis (CF) patients, as well as other types of infections in immunocompromised hosts [9]. P. aeruginosa produces several redox-active, heterocyclic compounds known as phenazines [10]. Phenazines have been shown to provide multiple benefits for their producers, including by (i) serving as an alternative electron acceptor in the absence of oxygen, thereby promoting redox homeostasis and anaerobic survival [11], which is particularly relevant for oxidant-limited biofilms [12] (ii) acting as signaling molecules [13] (iii) promoting iron acquisition [14] and (iv) killing competitor species [15]. In addition, despite possessing broad-spectrum antimicrobial activity [10], including against P. aeruginosa itself [16], phenazines have recently been shown to promote tolerance to clinical antibiotics under some circumstances, via mechanisms that have yet to be characterized [17,18]. Here, we sought to assess potential broader implications of this phenomenon by investigating whether phenazine-mediated tolerance to clinical antibiotics in P. aeruginosa is driven by cellular defenses that evolved to mitigate self-induced toxicity. We also tested whether phenazine production by P. aeruginosa could promote antibiotic tolerance in other clinically relevant opportunistic pathogens from the Burkholderia and Stenotrophomonas genera. Finally, we explored the ramifications of phenazine-induced tolerance for the evolution of heritable antibiotic resistance, both in P. aeruginosa and in a clinical isolate from the Burkholderia cepacia complex.


Antibiotics are chemicals that kill or inhibit the growth of bacteria and are used to treat bacterial infections. They are produced in nature by soil bacteria and fungi. This gives the microbe an advantage when competing for food and water and other limited resources in a particular habitat, as the antibiotic kills off their competition.

© Dr_Microbe / iStock Fungi Penicillium which cause food spoilage and are used for production of the first antibiotic penicillin. 3D illustration showing spores conidia and conidiophore.

How do antibiotics work

Antibiotics take advantage of the difference between the structure of the bacterial cell and the host&rsquos cell.

They can prevent the bacterial cells from multiplying so that the bacterial population remains the same, allowing the host&rsquos defence mechanism to fight the infection or kill the bacteria, for example stopping the mechanism responsible for building their cell walls.

An antibiotic can also be classified according to the range of pathogens against which it is effective. Penicillin G will destroy only a few species of bacteria and is known as a narrow spectrum antibiotic. Tetracycline is effective against a wide range of organisms and is known as a broad spectrum antibiotic.

Antibiotic resistance

Bacteria are termed drug-resistant when they are no longer inhibited by an antibiotic to which they were previously sensitive. The emergence and spread of antibacterial-resistant bacteria has continued to grow due to both the over-use and misuse of antibiotics.

Treating a patient with antibiotics causes the microbes to adapt or die this is known as &lsquoselective pressure&rsquo. If a strain of a bacterial species acquires resistance to an antibiotic, it will survive the treatment. As the bacterial cell with acquired resistance multiplies, this resistance is passed on to its offspring. In ideal conditions some bacterial cells can divide every 20 minutes therefore after only 8 hours in excess of 16 million bacterial cells carrying resistance to that antibiotic could exist.

How is resistance spread?

Antibiotic resistance can either be inherent or acquired. Some bacteria are naturally resistant to some antibiotics due to their physiological characteristics. This is inherent resistance. Acquired resistance occurs when a bacterium that was originally sensitive to an antibiotic develops resistance. For example resistance genes can be transferred from one plasmid to another plasmid or chromosome, or resistance can occur due to a random spontaneous chromosomal mutation.

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Microbes and food

Food for thought – bread, chocolate, yoghurt, blue cheese and tofu are all made using microbes.

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The function of microbes as tiny chemical processors is to keep the life cycles of the planet turning.

What to know about antibiotics

Antibiotics, also known as antibacterials, are medications that destroy or slow down the growth of bacteria.

They include a range of powerful drugs and are used to treat diseases caused by bacteria.

Antibiotics cannot treat viral infections, such as cold, flu, and most coughs.

This article will explain what antibiotics are, how they work, any potential side effects, and antibiotic resistance.

Antibiotics are a common medication that doctors prescribe to fight bacteria.

Antibiotics are powerful medicines that fight certain infections and can save lives when used properly. They either stop bacteria from reproducing or destroy them.

Before bacteria can multiply and cause symptoms, the immune system can typically kill them. White blood cells (WBCs) attack harmful bacteria and, even if symptoms do occur, the immune system can usually cope and fight off the infection.

Sometimes, however, the number of harmful bacteria is excessive, and the immune system cannot fight them all. Antibiotics are useful in this scenario.

The first antibiotic was penicillin. Penicillin-based antibiotics, such as ampicillin, amoxicillin, and penicillin G, are still available to treat a variety of infections and have been around for a long time.

Several types of modern antibiotics are available, and they are usually only available with a prescription in most countries. Topical antibiotics are available in over-the-counter (OTC) creams and ointments.

Some medical professionals have concerns that people are overusing antibiotics. They also believe that this overuse contributes toward the growing number of bacterial infections that are becoming resistant to antibacterial medications.

According to the Centers for Disease Control (CDC), outpatient antibiotic overuse is a particular problem. Antibiotic use appears to be higher in some regions , such as the Southeast.

Use of carbapenems, a major class of last-line antibiotics, increased significantly from 2007 to 2010.

Alexander Fleming, speaking in his Nobel Prize acceptance speech in 1945, said:

“ Then there is the danger that the ignorant man may easily underdose himself and by exposing his microbes to non-lethal quantities of the drug, make them resistant.”

As the man who discovered the first antibiotic almost 70 years ago predicted, drug resistance is starting to become commonplace.

There are different types of antibiotic, which work in one of two ways:

  • A bactericidal antibiotic, such as penicillin, kills the bacteria. These drugs usually interfere with either the formation of the bacterial cell wall or its cell contents.
  • A bacteriostatic stops bacteria from multiplying.

Antibiotics are ineffective against viruses.

A doctor prescribes antibiotics for the treatment of a bacterial infection. It is not effective against viruses.

Know whether an infection is bacterial or viral helps to effectively treat it.

Viruses cause most upper respiratory tract infections (URTIs), such as the common cold and flu. Antibiotics do not work against these viruses.

If people overuse antibiotics or use them incorrectly, the bacteria might become resistant. This means that the antibiotic becomes less effective against that type of bacterium, as the bacterium has been able to improve its defenses.

A doctor can prescribe a broad-spectrum antibiotic to treat a wide range of infections. A narrow-spectrum antibiotic is only effective against a few types of bacteria.

Some antibiotics attack aerobic bacteria, while others work against anaerobic bacteria. Aerobic bacteria need oxygen and anaerobic bacteria do not.

In some cases, a healthcare professional may provide antibiotics to prevent rather than treat an infection, as might be the case before surgery. This is the ‘prophylactic’ use of antibiotics. People commonly use these antibiotics before bowel and orthopedic surgery.

Antibiotics commonly cause the following side effects:

  • diarrhea
  • nausea
  • vomiting
  • rash
  • upset stomach
  • with certain antibiotics or prolonged use, fungal infections of the mouth, digestive tract, and vagina

Less common side effects of antibiotics include:

  • formation of kidney stones, when taking sulphonamides
  • abnormal blood clotting, when taking some cephalosporins)
  • sensitivity to sunlight, when taking tetracyclines
  • blood disorders, when taking trimethoprim , when taking erythromycin and the aminoglycosides

Some people, especially older adults, may experience bowel inflammation, which can lead to severe, bloody diarrhea.

In less common instances, penicillins, cephalosporins, and erythromycin can also cause inflamed bowels.

Some people may develop an allergic reaction to antibiotics, especially penicillins. Side effects might include a rash, swelling of the tongue and face, and difficulty breathing.

Allergic reactions to antibiotics might be immediate or delayed hypersensitivity reactions.

Anyone who has an allergic reaction to an antibiotic must tell their doctor or pharmacist. Reactions to antibiotics can be serious and sometimes fatal. They are called anaphylactic reactions.

People with reduced liver or kidney function should be cautious when using antibiotics. This may affect the types of antibiotics they can use or the dose they receive.

Likewise, women who are pregnant or breast-feeding should speak with a doctor about the best antibiotics to take.

Individuals taking an antibiotic should not take other medicines or herbal remedies without speaking with a doctor first. Certain OTC medicines might also interact with antibiotics.

Some doctors suggest that antibiotics can reduce the effectiveness of oral contraceptives. However, research does not generally support this.

Nonetheless, people who experience diarrhea and vomiting or are not taking their oral contraceptive during illness because of an upset stomach might find that its effectiveness reduces.

In these circumstances, take additional contraceptive precautions.

People must not stop a course of antibiotics halfway through. If in doubt, they can ask their doctor for advice.

People usually take antibiotics by mouth. However, doctors can administer them by injection or apply them directly to the part of the body with infection.

Most antibiotics start combating infection within a few hours. Complete the whole course of medication to prevent the return of the infection.

Stopping the medication before the course has finished increases the risk that the bacteria will become resistant to future treatments. The ones that survive will have had some exposure to the antibiotic and may consequently develop resistance to it.

An individual needs to complete the course of antibiotic treatment even after they see an improvement in symptoms.

Do not take some antibiotics with certain foods and drinks. Take others on an empty stomach, about an hour before meals, or 2 hours after. Follow the instructions correctly for the medication to be effective. People taking metronidazole should not drink alcohol.

Avoid dairy products when taking tetracyclines, as these might disrupt the absorption of the medication.


The global human community has an ongoing and worsening crisis of antibiotic-resistant infections in patients. We cannot count on new antibiotics to save us from this crisis—the pipeline is inadequate. We must do a much better job of preserving the effectiveness of the antibiotics we have now. We must therefore use fewer antibiotics. Because nearly 80 percent of antimicrobial use in the United States is in livestock, we must do a much better job of reducing antibiotic use in livestock as well as in humans.

It is important that we not be bogged down or distracted by quibbles over the minutiae of the molecular mechanisms by which antibiotic resistance spreads from animals to humans or the precise proportion of antibiotic-resistant infections in humans that is caused by antibiotic use in animals. The fundamental point is that antibiotic-resistant microbes can move from livestock fed antibiotics to humans, that patients are harmed as a result of this process, and that, in some countries, national policies eliminating growth promotion and routine prophylactic use have reverted or slowed antibiotic resistance rates.

Thus, from a policy perspective, the real question is, what is the “pro” of antimicrobial use in animals that might cause society to agree to take on the corresponding “con”—the risk of harming humans by this use? The pro is the ability of industrial farms to take shortcuts in animal husbandry to increase the potential for profit. So this issue—like so many others—boils down to societal priorities. This is not a science question, it is a policy question. Do we, as a society, believe that livestock producers should be afforded the right to profligate antimicrobial use by growing animals in unsanitary and crowded conditions despite the clear associated risk of transmission of antibiotic resistant bacteria from animals to humans, resulting in harm to humans? That is the question that confronts us as a society.

Finally, a critical lesson from this dialogue has not been clearly stated. If we reduce the amount of antibiotics fed to animals by 50 percent per animal, but we grow twice as many animals, we still will be exposing the bacteria in the food production environment to the same amount of antibiotics, driving antibiotic resistance. As a society, if we want to reduce the selection of antibiotic-resistant bacteria, and thereby reduce the risk of antibiotic-resistant infections, we should be consuming less meat. This real, transformative opportunity has had insufficient attention at the level of national health and commerce policy.

Note: Affiliations for the authors of this paper are shown for identification purposes only. The opinions stated in the manuscript do not reflect or represent those of the institutions or employers shown.