11.7: Mechanisms for Resistance (2023)

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    Learning Objectives

    • Explain the concept of drug resistance
    • Describe how microorganisms develop or acquire drug resistance
    • Describe the different mechanisms of antimicrobial drug resistance

    Antimicrobial resistance is not a new phenomenon. In nature, microbes are constantly evolving in order to overcome the antimicrobial compounds produced by other microorganisms. Human development of antimicrobial drugs and their widespread clinical use has simply provided another selective pressure that promotes further evolution. Several important factors can accelerate the evolution of drug resistance. These include the overuse and misuse of antimicrobials, inappropriate use of antimicrobials, subtherapeutic dosing, and patient noncompliance with the recommended course of treatment.

    Exposure of a pathogen to an antimicrobial compound can select for chromosomal mutations conferring resistance, which can be transferred vertically to subsequent microbial generations and eventually become predominant in a microbial population that is repeatedly exposed to the antimicrobial. Alternatively, many genes responsible for drug resistance are found on plasmids or in transposons that can be transferred easily between microbes through horizontal gene transfer. Transposons also have the ability to move resistance genes between plasmids and chromosomes to further promote the spread of resistance.

    Mechanisms for Drug Resistance

    There are several common mechanisms for drug resistance, which are summarized in Figure \(\PageIndex{1}\). These mechanisms include enzymatic modification of the drug, modification of the antimicrobial target, and prevention of drug penetration or accumulation.

    11.7: Mechanisms for Resistance (2)

    Drug Modification or Inactivation

    Resistance genes may code for enzymes that chemically modify an antimicrobial, thereby inactivating it, or destroy an antimicrobial through hydrolysis. Resistance to many types of antimicrobials occurs through this mechanism. For example, aminoglycoside resistance can occur through enzymatic transfer of chemical groups to the drug molecule, impairing the binding of the drug to its bacterial target. For β-lactams, bacterial resistance can involve the enzymatic hydrolysis of the β-lactam bond within the β-lactam ring of the drug molecule. Once the β-lactam bond is broken, the drug loses its antibacterial activity. This mechanism of resistance is mediated by β-lactamases, which are the most common mechanism of β-lactam resistance. Inactivation of rifampin commonly occurs through glycosylation, phosphorylation, or adenosine diphosphate (ADP) ribosylation, and resistance to macrolides and lincosamides can also occur due to enzymatic inactivation of the drug or modification.

    Prevention of Cellular Uptake or Efflux

    Microbes may develop resistance mechanisms that involve inhibiting the accumulation of an antimicrobial drug, which then prevents the drug from reaching its cellular target. This strategy is common among gram-negative pathogens and can involve changes in outer membrane lipid composition, porin channel selectivity, and/or porin channel concentrations. For example, a common mechanism of carbapenem resistance among Pseudomonas aeruginosa is to decrease the amount of its OprD porin, which is the primary portal of entry for carbapenems through the outer membrane of this pathogen. Additionally, many gram-positive and gram-negative pathogenic bacteria produce efflux pumps that actively transport an antimicrobial drug out of the cell and prevent the accumulation of drug to a level that would be antibacterial. For example, resistance to β-lactams, tetracyclines, and fluoroquinolones commonly occurs through active efflux out of the cell, and it is rather common for a single efflux pump to have the ability to translocate multiple types of antimicrobials.

    (Video) Antibiotics vs. Bacteria: Fighting the Resistance

    Target Modification

    Because antimicrobial drugs have very specific targets, structural changes to those targets can prevent drug binding, rendering the drug ineffective. Through spontaneous mutations in the genes encoding antibacterial drug targets, bacteria have an evolutionary advantage that allows them to develop resistance to drugs. This mechanism of resistance development is quite common. Genetic changes impacting the active site of penicillin-binding proteins (PBPs) can inhibit the binding of β-lactam drugs and provide resistance to multiple drugs within this class. This mechanism is very common among strains of Streptococcus pneumoniae, which alter their own PBPs through genetic mechanisms. In contrast, strains of Staphylococcus aureus develop resistance to methicillin (MRSA) through the acquisition of a new low-affinity PBP, rather than structurally alter their existing PBPs. Not only does this new low-affinity PBP provide resistance to methicillin but it provides resistance to virtually all β-lactam drugs, with the exception of the newer fifth-generation cephalosporins designed specifically to kill MRSA. Other examples of this resistance strategy include alterations in

    • ribosome subunits, providing resistance to macrolides, tetracyclines, and aminoglycosides;
    • lipopolysaccharide (LPS) structure, providing resistance to polymyxins;
    • RNA polymerase, providing resistance to rifampin;
    • DNA gyrase, providing resistance to fluoroquinolones;
    • metabolic enzymes, providing resistance to sulfa drugs, sulfones, and trimethoprim; and
    • peptidoglycan subunit peptide chains, providing resistance to glycopeptides.

    Target Overproduction or Enzymatic Bypass

    When an antimicrobial drug functions as an antimetabolite, targeting a specific enzyme to inhibit its activity, there are additional ways that microbial resistance may occur. First, the microbe may overproduce the target enzyme such that there is a sufficient amount of antimicrobial-free enzyme to carry out the proper enzymatic reaction. Second, the bacterial cell may develop a bypass that circumvents the need for the functional target enzyme. Both of these strategies have been found as mechanisms of sulfonamide resistance. Vancomycin resistance among S. aureus has been shown to involve the decreased cross-linkage of peptide chains in the bacterial cell wall, which provides an increase in targets for vancomycin to bind to in the outer cell wall. Increased binding of vancomycin in the outer cell wall provides a blockage that prevents free drug molecules from penetrating to where they can block new cell wall synthesis.

    Target Mimicry

    A recently discovered mechanism of resistance called target mimicry involves the production of proteins that bind and sequester drugs, preventing the drugs from binding to their target. For example, Mycobacterium tuberculosis produces a protein with regular pentapeptide repeats that appears to mimic the structure of DNA. This protein binds fluoroquinolones, sequestering them and keeping them from binding to DNA, providing M. tuberculosis resistance to fluoroquinolones. Proteins that mimic the A-site of the bacterial ribosome have been found to contribute to aminoglycoside resistance as well.1

    Exercise \(\PageIndex{1}\)

    List several mechanisms for drug resistance.

    (Video) What causes antibiotic resistance? - Kevin Wu

    Multidrug-Resistant Microbes and Cross Resistance

    From a clinical perspective, our greatest concerns are multidrug-resistant microbes (MDRs) and cross resistance. MDRs are colloquially known as “superbugs” and carry one or more resistance mechanism(s), making them resistant to multiple antimicrobials. In cross-resistance, a single resistance mechanism confers resistance to multiple antimicrobial drugs. For example, having an efflux pump that can export multiple antimicrobial drugs is a common way for microbes to be resistant to multiple drugs by using a single resistance mechanism. In recent years, several clinically important superbugs have emerged, and the CDC reports that superbugs are responsible for more than 2 million infections in the US annually, resulting in at least 23,000 fatalities.2 Several of the superbugs discussed in the following sections have been dubbed the ESKAPE pathogens. This acronym refers to the names of the pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter spp.) but it is also fitting in that these pathogens are able to “escape” many conventional forms of antimicrobial therapy. As such, infections by ESKAPE pathogens can be difficult to treat and they cause a large number of nosocomial infections.

    Methicillin-Resistant Staphylococcus aureus (MRSA)

    Methicillin, a semisynthetic penicillin, was designed to resist inactivation by β-lactamases. Unfortunately, soon after the introduction of methicillin to clinical practice, methicillin-resistant strains of S. aureus appeared and started to spread. The mechanism of resistance, acquisition of a new low-affinity PBP, provided S. aureus with resistance to all available β-lactams. Strains of methicillin-resistant S. aureus (MRSA) are widespread opportunistic pathogens and a particular concern for skin and other wound infections, but may also cause pneumonia and septicemia. Although originally a problem in health-care settings (hospital-acquired MRSA [HA-MRSA]), MRSA infections are now also acquired through contact with contaminated members of the general public, called community-associated MRSA (CA-MRSA). Approximately one-third of the population carries S. aureus as a member of their normal nasal microbiota without illness, and about 6% of these strains are methicillin resistant.3,4

    Clavulanic Acid: Penicillin's Little Helper

    With the introduction of penicillin in the early 1940s, and its subsequent mass production, society began to think of antibiotics as miracle cures for a wide range of infectious diseases. Unfortunately, as early as 1945, penicillin resistance was first documented and started to spread. Greater than 90% of current S. aureus clinical isolates are resistant to penicillin.5

    Although developing new antimicrobial drugs is one solution to this problem, scientists have explored new approaches, including the development of compounds that inactivate resistance mechanisms. The development of clavulanic acid represents an early example of this strategy. Clavulanic acid is a molecule produced by the bacterium Streptococcus clavuligerus. It contains a β-lactam ring, making it structurally similar to penicillin and other β-lactams, but shows no clinical effectiveness when administered on its own. Instead, clavulanic acid binds irreversibly within the active site of β-lactamases and prevents them from inactivating a coadministered penicillin.

    Clavulanic acid was first developed in the 1970s and was mass marketed in combination with amoxicillin beginning in the 1980s under the brand name Augmentin. As is typically the case, resistance to the amoxicillin-clavulanic acid combination soon appeared. Resistance most commonly results from bacteria increasing production of their β-lactamase and overwhelming the inhibitory effects of clavulanic acid, mutating their β-lactamase so it is no longer inhibited by clavulanic acid, or from acquiring a new β-lactamase that is not inhibited by clavulanic acid. Despite increasing resistance concerns, clavulanic acid and related β-lactamase inhibitors (sulbactam and tazobactam) represent an important new strategy: the development of compounds that directly inhibit antimicrobial resistance-conferring enzymes.

    Vancomycin-Resistant Enterococci and Staphylococcus aureus

    Vancomycin is only effective against gram-positive organisms, and it is used to treat wound infections, septic infections, endocarditis, and meningitis that are caused by pathogens resistant to other antibiotics. It is considered one of the last lines of defense against such resistant infections, including MRSA. With the rise of antibiotic resistance in the 1970s and 1980s, vancomycin use increased, and it is not surprising that we saw the emergence and spread of vancomycin-resistant enterococci (VRE), vancomycin-resistant S. aureus (VRSA), and vancomycin-intermediate S. aureus (VISA). The mechanism of vancomycin resistance among enterococci is target modification involving a structural change to the peptide component of the peptidoglycan subunits, preventing vancomycin from binding. These strains are typically spread among patients in clinical settings by contact with health-care workers and contaminated surfaces and medical equipment.

    VISA and VRSA strains differ from each other in the mechanism of resistance and the degree of resistance each mechanism confers. VISA strains exhibit intermediate resistance, with a minimum inhibitory concentration (MIC) of 4–8 μg/mL, and the mechanism involves an increase in vancomycin targets. VISA strains decrease the crosslinking of peptide chains in the cell wall, providing an increase in vancomycin targets that trap vancomycin in the outer cell wall. In contrast, VRSA strains acquire vancomycin resistance through horizontal transfer of resistance genes from VRE, an opportunity provided in individuals coinfected with both VRE and MRSA. VRSA exhibit a higher level of resistance, with MICs of 16 μg/mL or higher.6 In the case of all three types of vancomycin-resistant bacteria, rapid clinical identification is necessary so proper procedures to limit spread can be implemented. The oxazolidinones like linezolid are useful for the treatment of these vancomycin-resistant, opportunistic pathogens, as well as MRSA.

    (Video) Macrolides: Mechanisms of Action and Resistance

    Extended-Spectrum β-Lactamase–Producing Gram-Negative Pathogens

    Gram-negative pathogens that produce extended-spectrum β-lactamases (ESBLs) show resistance well beyond just penicillins. The spectrum of β-lactams inactivated by ESBLs provides for resistance to all penicillins, cephalosporins, monobactams, and the β-lactamase-inhibitor combinations, but not the carbapenems. An even greater concern is that the genes encoding for ESBLs are usually found on mobile plasmids that also contain genes for resistance to other drug classes (e.g., fluoroquinolones, aminoglycosides, tetracyclines), and may be readily spread to other bacteria by horizontal gene transfer. These multidrug-resistant bacteria are members of the intestinal microbiota of some individuals, but they are also important causes of opportunistic infections in hospitalized patients, from whom they can be spread to other people.

    Carbapenem-Resistant Gram-Negative Bacteria

    The occurrence of carbapenem-resistant Enterobacteriaceae (CRE) and carbapenem resistance among other gram-negative bacteria (e.g., P. aeruginosa, Acinetobacter baumannii, Stenotrophomonas maltophila) is a growing health-care concern. These pathogens develop resistance to carbapenems through a variety of mechanisms, including production of carbapenemases (broad-spectrum β-lactamases that inactivate all β-lactams, including carbapenems), active efflux of carbapenems out of the cell, and/or prevention of carbapenem entry through porin channels. Similar to concerns with ESBLs, carbapenem-resistant, gram-negative pathogens are usually resistant to multiple classes of antibacterials, and some have even developed pan-resistance (resistance to all available antibacterials). Infections with carbapenem-resistant, gram-negative pathogens commonly occur in health-care settings through interaction with contaminated individuals or medical devices, or as a result of surgery.

    Multidrug-Resistant Mycobacterium tuberculosis

    The emergence of multidrug-resistant Mycobacterium tuberculosis (MDR-TB) and extensively drug-resistant Mycobacterium tuberculosis (XDR-TB) is also of significant global concern. MDR-TB strains are resistant to both rifampin and isoniazid, the drug combination typically prescribed for treatment of tuberculosis. XDR-TB strains are additionally resistant to any fluoroquinolone and at least one of three other drugs (amikacin, kanamycin, or capreomycin) used as a second line of treatment, leaving these patients very few treatment options. Both types of pathogens are particularly problematic in immunocompromised persons, including those suffering from HIV infection. The development of resistance in these strains often results from the incorrect use of antimicrobials for tuberculosistreatment, selecting for resistance.

    Exercise \(\PageIndex{2}\)

    (Video) ß-Lactams: Mechanisms of Action and Resistance

    How does drug resistance lead to superbugs?

    To learn more about the top 18 drug-resistant threats to the US, visit the CDC’s website.

    Factory Farming and Drug Resistance

    Although animal husbandry has long been a major part of agriculture in America, the rise of concentrated animal feeding operations (CAFOs) since the 1950s has brought about some new environmental issues, including the contamination of water and air with biological waste, and ethical issues regarding animal rights also are associated with growing animals in this way. Additionally, the increase in CAFOs involves the extensive use of antimicrobial drugs in raising livestock. Antimicrobials are used to prevent the development of infectious disease in the close quarters of CAFOs; however, the majority of antimicrobials used in factory farming are for the promotion of growth—in other words, to grow larger animals.

    The mechanism underlying this enhanced growth remains unclear. These antibiotics may not necessarily be the same as those used clinically for humans, but they are structurally related to drugs used for humans. As a result, use of antimicrobial drugs in animals can select for antimicrobial resistance, with these resistant bacteria becoming cross-resistant to drugs typically used in humans. For example, tylosin use in animals appears to select for bacteria also cross-resistant to other macrolides, including erythromycin, commonly used in humans.

    Concentrations of the drug-resistant bacterial strains generated by CAFOs become increased in water and soil surrounding these farms. If not directly pathogenic in humans, these resistant bacteria may serve as a reservoir of mobile genetic elements that can then pass resistance genes to human pathogens. Fortunately, the cooking process typically inactivates any antimicrobials remaining in meat, so humans typically are not directly ingesting these drugs. Nevertheless, many people are calling for more judicious use of these drugs, perhaps charging farmers user fees to reduce indiscriminate use. In fact, in 2012, the FDA published guidelines for farmers who voluntarily phase out the use of antimicrobial drugs except under veterinary supervision and when necessary to ensure animal health. Although following the guidelines is voluntary at this time, the FDA does recommend what it calls “judicious” use of antimicrobial drugs in food-producing animals in an effort to decrease antimicrobial resistance.

    Key Concepts and Summary

    • Antimicrobial resistance is on the rise and is the result of selection of drug-resistant strains in clinical environments, the overuse and misuse of antibacterials, the use of subtherapeutic doses of antibacterial drugs, and poor patient compliance with antibacterial drug therapies.
    • Drug resistance genes are often carried on plasmids or in transposons that can undergo vertical transfer easily and between microbes through horizontal gene transfer.
    • Common modes of antimicrobial drug resistance include drug modification or inactivation, prevention of cellular uptake or efflux, target modification, target overproduction or enzymatic bypass, and target mimicry.
    • Problematic microbial strains showing extensive antimicrobial resistance are emerging; many of these strains can reside as members of the normal microbiota in individuals but also can cause opportunistic infection. The transmission of many of these highly resistant microbial strains often occurs in clinical settings, but can also be community-acquired.

    Footnotes

    1. D.H. Fong, A.M. Berghuis. “Substrate Promiscuity of an Aminoglycoside Antibiotic Resistance Enzyme Via Target Mimicry.” EMBO Journal 21 no. 10 (2002):2323–2331.
    2. Centers for Disease Control and Prevention. “Antibiotic/Antimicrobial Resistance.” http://www.cdc.gov/drugresistance/index.html. Accessed June 2, 2016.
    3. A.S. Kalokhe et al. “Multidrug-Resistant Tuberculosis Drug Susceptibility and Molecular Diagnostic Testing: A Review of the Literature. American Journal of the Medical Sciences 345 no. 2 (2013):143–148.
    4. Centers for Disease Control and Prevention. “Methicillin-Resistant Staphylococcus aureus (MRSA): General Information About MRSA in the Community.” http://www.cdc.gov/mrsa/community/index.html. Accessed June 2, 2016
    5. F.D. Lowy. “Antimicrobial Resistance: The Example of Staphylococcus aureus.” Journal of Clinical Investigation 111 no. 9 (2003):1265–1273.
    6. Centers for Disease Control and Prevention. “Healthcare-Associated Infections (HIA): General Information about VISA/VRSA.” www.cdc.gov/HAI/organisms/vis...visa_vrsa.html. Accessed June 2, 2016.

    Contributor

    • Nina Parker, (Shenandoah University),Mark Schneegurt (Wichita State University),Anh-Hue Thi Tu (Georgia Southwestern State University), Philip Lister (Central New Mexico Community College), and Brian M. Forster (Saint Joseph’s University) with many contributing authors. Original content via Openstax(CC BY 4.0; Access for free athttps://openstax.org/books/microbiology/pages/1-introduction)

    (Video) Foundations of Blockchains (Lecture 11.7: Pros and Cons of Burning Fees)

    FAQs

    What are the mechanisms of resistance? ›

    The main mechanisms of resistance are: limiting uptake of a drug, modification of a drug target, inactivation of a drug, and active efflux of a drug.

    How long does it take to become resistant to antibiotics? ›

    Different types and strains of bacteria behave differently. And the exact antibiotic affects how long antibiotic resistance takes. But some studies have shown that bacteria can begin to develop antibiotic resistance as early as 11 days.

    What are the three mechanisms for antibiotic resistance explain each mechanism? ›

    The three fundamental mechanisms of antimicrobial resistance are (1) enzymatic degradation of antibacterial drugs, (2) alteration of bacterial proteins that are antimicrobial targets, and (3) changes in membrane permeability to antibiotics.

    What does it mean to be resistant to a drug? ›

    Drug resistance is simply defined as the ability of disease-causing germs (e.g., bacteria or viruses) to continue multiplying despite the presence of drugs that usually kill them.

    What are the different mechanisms of metal resistance? ›

    There are five main mechanisms of heavy metal resistance in bacteria extracellular barrier, active transport of metal ions (efflux), extracellular sequestration, intracellular sequestration, reduction of metal ions.

    What are the five mechanisms of antimicrobial resistance? ›

    Acquired antimicrobial resistance generally can be ascribed to one of five mechanisms. These are production of drug-inactivating enzymes, modification of an existing target, acquisition of a target by-pass system, reduced cell permeability and drug removal from the cell.

    What to do if you have antibiotic resistance? ›

    How are antibiotic-resistant bacterial infections treated? If an infection shows signs of antibiotic resistance, your healthcare provider may try a different drug. The new drug may have more severe side effects, and trying a different antibiotic also raises the risk of developing resistance to that drug.

    How bad is antibiotic resistance? ›

    Resistance to even one antibiotic can mean serious problems. For example: Antimicrobial-resistant infections that require the use of second- and third-line treatments can harm patients by causing serious side effects, such as organ failure, and prolong care and recovery, sometimes for months.

    Why won't my UTI clear up with antibiotics? ›

    UTI comes back right after antibiotics because of antibiotic resistance that bacteria develop. Antibiotic resistance indicates that the bacteria causing a UTI do not respond to antibiotic treatment. This occurs because repeated use of antibiotics causes bacteria to evolve.

    Why is there so much concern for antibiotic resistant bacteria? ›

    When bacteria become resistant, the original antibiotic can no longer kill them. These germs can grow and spread. They can cause infections that are hard to treat. Sometimes they can even spread the resistance to other bacteria that they meet.

    How do bacteria gain resistance to antibiotics? ›

    Through mutation and selection, bacteria can develop defense mechanisms against antibiotics. For example, some bacteria have developed biochemical “pumps” that can remove an antibiotic before it reaches its target, while others have evolved to produce enzymes to inactivate the antibiotic.

    What are 2 major mechanisms of antibiotics? ›

    Alteration of Cell Membranes. Inhibition of Nucleic Acid Synthesis.

    How do you get rid of drug resistance? ›

    Here are more tips to promote proper use of antibiotics.
    1. Take the antibiotics as prescribed. ...
    2. Do not skip doses. ...
    3. Do not save antibiotics. ...
    4. Do not take antibiotics prescribed for someone else. ...
    5. Talk with your health care professional. ...
    6. All drugs have side effects.
    Oct 29, 2019

    Can antibiotic resistance be reversed? ›

    “Our findings show that by targeting disulfide bond formation and protein folding, it is possible to reverse antibiotic resistance across several major pathogens and resistance mechanisms.

    What is the strongest antibiotic for bacterial infection? ›

    Vancomycin 3.0 is one of the most potent antibiotics ever created. It is used to treat conditions like methicillin-resistant Staphylococcus aureus-induced meningitis, endocarditis, joint infections, and bloodstream and skin infections.

    What are two metals with high resistance? ›

    Two highly resistant metals are Aluminium and Tungsten.

    What are heavy metal resistant bacteria? ›

    Among these metal-resistant organisms, the species belonging to Bacillus, Erwinia, Myco- bacterium, Pseudomonas and coryneforms were.

    What are the examples of heavy metal resistant bacteria? ›

    Several species of Bacillus, especially from cereus and subtilis groups, are known for their metal ions resistance.

    What are the 7 main mechanisms of action of antimicrobials? ›

    Basis of Antimicrobial Action

    Various antimicrobial agents act by interfering with (1) cell wall synthesis, (2) plasma membrane integrity, (3) nucleic acid synthesis, (4) ribosomal function, and (5) folate synthesis.

    How does drug resistance occur? ›

    How Antimicrobial Resistance Happens. Antimicrobial resistance happens when germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them. Resistant infections can be difficult, and sometimes impossible, to treat. Antimicrobial resistance is a naturally occurring process.

    What are 4 causes of antimicrobial resistance? ›

    The main drivers of antimicrobial resistance include the misuse and overuse of antimicrobials; lack of access to clean water, sanitation and hygiene (WASH) for both humans and animals; poor infection and disease prevention and control in health-care facilities and farms; poor access to quality, affordable medicines, ...

    What are the 7 types of antibiotics? ›

    In this portal, antibiotics are classified into one of the following classes: penicillins, fluoroquinolones, cephalosporins, macrolides, beta-lactams with increased activity (e.g. amoxicillin-clavulanate), tetracyclines, trimethoprim-sulfamethoxazole, lincosamides (e.g. clindamycin), urinary anti-infectives, and other ...

    Who is at high risk for antibiotic resistance? ›

    Who is at risk of antibiotic-resistant infections? Everyone is at risk of antibiotic-resistant infections, but those at the greatest risk for antibiotic-resistant infections are young children, cancer patients, and people over the age of 60.

    Who is most at risk for antibiotic resistance? ›

    Antibiotic resistance can affect anyone, of any age, in any country. Antibiotic resistance occurs naturally, but misuse of antibiotics in humans and animals is accelerating the process.

    What happens if an infection doesn t go away with antibiotics? ›

    In some cases, the antibiotic-resistant illness can lead to serious disability or even death. Resistance can happen if the bacterial infection is only partially treated. To prevent this, it is important to finish taking the entire prescription of antibiotics as instructed, even if your child is feeling better.

    How do you get rid of a stubborn urinary tract infection? ›

    Home remedies for a UTI include:
    1. taking acetaminophen to relieve pain and reduce fever.
    2. placing a hot water bottle on the lower stomach to ease discomfort.
    3. drinking plenty of water to flush out the bacteria.
    4. getting plenty of rest to help the body fight the infection.
    5. avoiding sex to reduce discomfort.
    Jun 20, 2018

    What antibiotics treat stubborn UTI? ›

    Ciprofloxacin (Cipro) or levofloxacin (Levaquin)

    These types of antibiotics work slightly better than amoxicillin/potassium clavulanate, cefdinir, and cephalexin. But the risk of serious side effects is higher. Healthcare providers usually save these antibiotics for more complicated or severe types of UTIs.

    What is the strongest natural antibiotic for UTI? ›

    Cranberry juice is one of the most well-established natural treatments for UTIs. People also use it to clear other infections and speed wound recovery. 2020 research into the effectiveness of cranberries for UTIs has found it to be effective.

    How can I reverse antibiotic resistance naturally? ›

    Food ingredients and nutrients such as thyme, mushrooms, ginger, garlic, sage, zinc, echinacea, elderberry, andrographis and pelargonium are examples of natural remedies that have been demonstrated to enhance immunity.

    Can overuse of antibiotics cause resistance? ›

    The overuse of antibiotics in recent years means they're becoming less effective and has led to the emergence of "superbugs". These are strains of bacteria that have developed resistance to many different types of antibiotics, including: MRSA (methicillin-resistant Staphylococcus aureus)

    Can overuse of antibiotics make bacteria more resistant? ›

    Taking antibiotics too often or for the wrong reasons can change bacteria so much that antibiotics don't work against them. This is called bacterial resistance or antibiotic resistance. Some bacteria are now resistant to even the most powerful antibiotics available. Antibiotic resistance is a growing problem.

    How long does it take for antibiotics to work for bacterial infection? ›

    Antibiotics begin to work right after you start taking them. However, you might not feel better for 2 to 3 days. How quickly you get better after antibiotic treatment varies. It also depends on the type of infection you're treating.

    What are the three mechanisms of antibiotics against bacteria? ›

    The following biochemical types of resistance mechanisms are used by bacteria: Antibiotic inactivation, target modification, altered permeability, and “bypass” metabolic pathway.

    How do you test for resistance to drugs? ›

    The standard method for identifying drug resistance is to take a sample from a wound, blood or urine and expose resident bacteria to various drugs. If the bacterial colony continues to divide and thrive despite the presence of a normally effective drug, it indicates the microbes are drug-resistant.

    How long does it take bacteria to lose antibiotic resistance? ›

    We have demonstrated that drug-resistance frequently declines within 480 generations during exposure to an antibiotic-free environment. The extent of resistance loss was found to be generally antibiotic-specific, driven by mutations that reduce both resistance level and fitness costs of antibiotic-resistance mutations.

    Why does my body reject antibiotics? ›

    Antibiotic resistance happens when bacteria are repeatedly exposed to the same medicine. This changes the bacteria, making it harder for the medicine to work. It also can happen when bacteria are left in your body. They will multiply and become stronger.

    What are the harshest antibiotics? ›

    According to reports, fluoroquinolones—a broad spectrum antibiotic that includes Cipro, Levaquin, Avelox, and others—have been associated with a host of devastating side effects, including joint and muscle pain, tendon rupture, aortic aneurysm, nerve damage, delirium, and even death.

    What is the most aggressive antibiotic? ›

    Vancomycin, long considered a "drug of last resort," kills by preventing bacteria from building cell walls. It binds to wall-building protein fragments called peptides, in particular those that end with two copies of the amino acid D-alanine (D-ala).

    What are the top 3 antibiotics? ›

    Top 10 most prescribed antibiotics of 2022
    RankDRUG name% of all prescriptions dispensed in 2022
    1Amoxicillin29.00%
    2Azithromycin15.40%
    3Amoxicillin and Clavulanate Potassium13.10%
    4Cephalexin12.00%
    6 more rows
    Mar 17, 2023

    What are the mechanisms of resistance intrinsic and acquired? ›

    Resistance Mechanisms

    There are two types of bacterial resistance: intrinsic and acquired. In intrinsic resistance, the antibiotic never possessed activity against the pathogen (TABLE 3). Acquired resistance is achieved through the transfer of genetic material that confers resistance.

    What mechanisms result in acquired resistance? ›

    The acquired resistance mechanisms, on the other hand, are generally obtained by horizontal gene transfer (HGT, described later) and include plasmid-encoded specific efflux pumps (such as TetK and TetL of S.

    What is the tolerance mechanism of resistance? ›

    Tolerance is a decrease in response to a drug that is used repeatedly. Resistance is development of the ability to withstand the previously destructive effect of a drug by microorganisms or tumor cells. Examples of drugs that result in tolerance include alcohol and opioids.

    What are the biochemical mechanisms of resistance to antibiotics? ›

    The antimicrobial resistance is recognized as a major problem in the treatment of microbial infections. The biochemical resistance mechanisms used by bacteria include the following: antibiotic inactivation, target modification, altered permeability, and “bypass” of metabolic pathway.

    What are the mechanisms of resistance in AML? ›

    Role of gene mutations in AML chemotherapy resistance. The mechanism of AML cell resistance to chemotherapy can be caused by gene mutations. Among them are the FMS-like tyrosine kinase (FLT3) gene and DNA methyltransferase 3A (DNMT3A) gene mutations.

    What is an example of acquired resistance? ›

    For example, the bacterium Staphylococcus aureus can acquire the resistance gene mecA and produce a new penicillin-binding protein. These proteins are needed for bacterial cell wall synthesis and are the targets of β-lactam antibiotics.

    What are 2 mechanisms by which bacteria can acquire resistance to an antibiotic? ›

    Through mutation and selection, bacteria can develop defense mechanisms against antibiotics. For example, some bacteria have developed biochemical “pumps” that can remove an antibiotic before it reaches its target, while others have evolved to produce enzymes to inactivate the antibiotic.

    What causes acquired resistance? ›

    The second type of resistance to immunotherapy is acquired resistance at the level of the individual tumour cell4. This occurs because tumour cells alter their gene expression in response to interactions with immune cells or their products.

    What is the intrinsic resistance? ›

    Intrinsic resistance is defined as resistance of all or almost all isolates of one species to a certain drug—e.g., the resistance of Candida krusei to fluconazole.

    What does intrinsically resistant mean? ›

    Overview. Intrinsic resistance is when a bacterial species is naturally resistant to a certain antibiotic or family of antibiotics, without the need for mutation or gain of further genes. This means that these antibiotics can never be used to treat infections caused by that species of bacteria.

    What is an example of tolerance mechanism? ›

    Examples of drugs that result in tolerance include alcohol and opioids. One mechanism responsible for tolerance is accelerated metabolism, for example, by induction of hepatic enzymes such as the cytochrome P-450 system enzymes.

    What does tolerance vs resistance mean? ›

    Tolerance is a decrease in response to a drug that is used repeatedly. Resistance is development of the ability to withstand the previously destructive effect of a drug by microorganisms or tumor cells. Examples of drugs that result in tolerance include alcohol and opioids.

    What is the definition and mechanism of tolerance? ›

    Thus, tolerance can be defined as a lack of reactivity to self-antigens or foreign tissue antigens in an organ graft achieved without the need for long-term immunosuppression while retaining immune competence and reactivity to all other foreign antigens.

    Videos

    1. When Antibiotics Don't Work (full documentary) | FRONTLINE
    (FRONTLINE PBS | Official)
    2. How can we solve the antibiotic resistance crisis? - Gerry Wright
    (TED-Ed)
    3. Antibiotic Resistance | Are we creating super bacteria?
    (ABC Science)
    4. Rise of the Superbug - Antibiotic-Resistant Bacteria: Dr. Karl Klose at TEDxSanAntonio
    (TEDx Talks)
    5. Gene Regulation and the Order of the Operon
    (Amoeba Sisters)
    6. Resistant starch — the carb with no calories (kinda)
    (Adam Ragusea)
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