Biological Sciences

Bacterial Resistance to Antibiotics

Bacterial resistance to antibiotics refers to the ability of bacteria to withstand the effects of antibiotics, making the drugs ineffective in treating infections. This resistance can develop through genetic mutations or the acquisition of resistance genes from other bacteria. Overuse and misuse of antibiotics in both humans and animals contribute to the widespread occurrence of bacterial resistance.

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11 Key excerpts on "Bacterial Resistance to Antibiotics"

  • Book cover image for: Emerging Epidemics
    eBook - ePub

    Emerging Epidemics

    Management and Control

    • Prakash S. Bisen, Ruchika Raghuvanshi(Authors)
    • 2013(Publication Date)
    • Wiley-Blackwell
      (Publisher)

    Chapter 21

    Antimicrobial Resistance

    Introduction

    Antibiotics have revolutionized how patients with bacterial infections are treated; they have further contributed to reducing the mortality and morbidity from bacterial diseases. They are also an essential tool for modern medicine and several surgical procedures, such as transplantation, chemotherapy for cancer, and even the orthopaedic surgery, could not be performed without the administration of potent antibiotics. Antibiotic resistance is currently the greatest challenge to the effective treatment of infectious diseases globally. It is a type of resistance in which a microorganism is able to survive exposure to a specific antibiotic. The drug resistance can be acquired by a spontaneous or induced genetic mutation in bacteria. Genes conferring drug resistance can be transferred between bacteria horizontally by any of the methods of genetic recombination, including conjugation, transduction, or transformation. Thereby, a gene for antibiotic resistance, which had evolved via natural selection, may be shared, and an evolutionary stress, such as exposure to antibiotics, then selects for the antibiotic resistant trait. Most of the antibiotic resistance genes reside on plasmids (an extra chromosomal material), facilitating their easy transfer. In case a bacterium carries several resistance genes against different antibiotics, it is called multidrug resistant (MDR), or informally, a superbug or superbacterium.
    Genes for resistance to antibiotic drugs, like the antibiotics themselves, are ancient (D’Costa et al., 2011). However, the increasing prevalence of drug-resistant bacterial infections commonly observed in clinical practice stems from antibiotic use both within human medicine and veterinary medicine. The use of antibiotics can increase selective pressure in a population of bacteria and allow the resistant bacteria to thrive and the susceptible bacteria to die off. As resistance toward antibiotics becomes more common, there arises a greater need for alternative treatments. However, despite a discovery of new antibiotic therapies, there has been a continued decline in the number of newly approved drugs (Donadio et al., 2010). Antibiotic resistance poses a significant problem, and it is also important to understand international patterns of resistance with globalization booming. The excessive use of antibiotics both inside and outside of medicine is playing a significant role in the emergence of resistant bacteria. Although initially there were few pre-existing antibiotic-resistant bacteria before the widespread use of antibiotics, evolutionary pressure from their use has played a role in the development of multidrug resistance varieties and the spread of resistance against more than one drug between bacterial species.
  • Book cover image for: Antibiotic Resistant Bacteria
    eBook - PDF

    Antibiotic Resistant Bacteria

    A Continuous Challenge in the New Millennium

    • Marina Pana(Author)
    • 2012(Publication Date)
    • IntechOpen
      (Publisher)
    Part 1 Assessment of Antibiotic Resistance in Clinical Relevant Bacteria 1 Antibiotic Resistance: An Emerging Global Headache Maimoona Ahmed King Abdul Aziz University Hospital, Jeddah, Saudi Arabia 1. Introduction The discovery of antibiotics was one of the greatest achievements of the twentieth century. The subsequent introduction of sulphonamides, penicillin and streptomycin, broad spectrum bacteriostatic antibiotics, bactericidal antibiotics, synthetic chemicals and highly specific narrow spectrum antibiotics to clinical medicine transformed the treatment of bacterial diseases (Baldry, 1976). However, due to the excessive and inappropriate use of antibiotics there has been a gradual emergence of populations of antibiotic –resistant bacteria, which pose a global public health problem (Komolafe, 2003). According to the WHO, a resistant microbe is one which is not killed by an antimicrobial agent after a standard course of treatment (WHO, 1998). Antibiotic resistance is acquired by a natural selection process. Antibiotic use to combat infection, forces bacteria to either adapt or die irrespective of the dosage or time span. The surviving bacteria carry the drug resistance gene, which can then be transferred either within the species/genus or to other unrelated species (Wise, 1998). Clinical resistance is a complex phenomenon and its manifestation is dependent on the type of bacterium, the site of infection, distribution of antibiotic in the body, concentration of the antibiotic at the site of infection and the immune status of the patient (Hawkey, 1998). Antibiotic resistance is a global problem. While several pathogenic bacteria are resistant to first line broad spectrum antibiotics, new resistant strains have resulted from the introduction of new drugs (Kunin, 1993, Sack et al , 1997, Rahal et al, 1997, Hoge, 1998).
  • Book cover image for: Revenge of the Microbes
    eBook - PDF

    Revenge of the Microbes

    How Bacterial Resistance is Undermining the Antibiotic Miracle

    • Brenda A. Wilson, Brian T. Ho(Authors)
    • 2023(Publication Date)
    • ASM Press
      (Publisher)
    71 Revenge of the Microbes: How Bacterial Resistance Is Undermining the Antibiotic Miracle, Second Edition. Brenda A. Wilson and Brian T. Ho. © 2023 American Society for Microbiology. Antibiotic use has become so pervasive in modern times and so varied in its application that it is sometimes difficult even for scientists and physicians to keep up with the most recent incarnation of the antibiotic resistance problem. However, the rapidity with which some bacteria have developed antibiotic resistance mecha- nisms should not have come as a surprise, especially for researchers with any background in the basic biology of bacteria. In this chapter, we will consider some of the ways bacteria counter or subvert the action of antibiotics. HOW DO BACTERIA BECOME RESISTANT TO ANTIBIOTICS? In general, bacterial populations become resistant to antibiotics in a two-step process. The first step involves random mutations in individual bacterial cells, either through spontaneous errors during DNA replication or through acquisition of foreign genetic material (DNA). Occasionally, such mutations can cause these individual cells to become more resistant to a particular antibiotic. These muta- tions can be very subtle, only conferring a slight tolerance for a particular antibiotic compared to the original wild-type bacteria, but they can also be very drastic, espe- cially when acquiring foreign DNA, potentially conferring complete immunity to some antibiotics. In either case, so long as the mutation is not too inherently detri- mental to cellular growth, these now-resistant, mutant bacteria will be able to propagate as a subset of the larger bacterial population. Bacteria Reveal Their Adaptability and Gain Resistance 6 72 • Revenge of the Microbes The second step required for the establishment of antibiotic resistance is for the bacterial population to experience a selective antibiotic pressure—that is, they need to actually be exposed to the antibiotic.
  • Book cover image for: Emerging Infections
    • John I. Gallin, Anthony S. Fauci(Authors)
    • 1998(Publication Date)
    • Academic Press
      (Publisher)
    8 ANTIBIOTIC RESISTANCE IN BACTERIA JULIAN DAVIES and VERA WEBB Department of Microbiology and Immunology University of British Columbia Vancouver, British Columbia, Canada We must swim with the microbes and study their sur- vival and adaptation to new habitats. Richard M. Krause (1994) I. INTRODUCTION The development of antibiotic resistance can be viewed as a global problem in microbial genetic ecology. It is a very complex problem to contemplate, let alone solve, due to the geographic scale, the variety of environmental factors, and the enormous number and diversity of microbial participants. In addition, the situ- ation can only be viewed retrospectively, and what has been done was uncon- trolled and largely unrecorded. Simply put, since the introduction of antibiotics for the treatment of infectious diseases in the late 1940s, human and animal microbial ecology has been drastically disturbed. The response of microbes to the threat of extinction has been to find genetic and biochemical evolutionary routes that led to the development of resistance to every antimicrobial agent used. The result is a large pool of resistance determinants in the environment. The origins, evolution, and dissemination of these resistance genes is the subject of this review. II. MECHANISMS OF RESISTANCE: BIOCHEMISTRY AND GENETICS The use of antibiotics should have created a catastrophic situation for microbial populations; however, their genetic flexibility allowed bacteria to survive (and even thrive) in hostile environments. The alternatives for survival for threatened microbial populations were either mutation of target sites or acquisition of Emerging Infections Copyright © 1998 by Academic Press. All rights of reproduction in any form reserved. 239
  • Book cover image for: Genetics and Evolution of Infectious Diseases
    • Michel Tibayrenc(Author)
    • 2010(Publication Date)
    • Elsevier
      (Publisher)
    Mechanisms acting on gene variability, including mutation and recombination, facilitated in their turn by processes as tandem amplification, might trigger the evolution of pre-resistance genes into resistance genes, or from these to variants with higher resistance efficiency. Exposure to various antibiotics might contribute to the diversification of resistance genes, as with CTX-M enzymes. The density of resistant variants depends on environmental processes as selection (reducing variability) and genetic drift (affecting equally to all variants), in combination with the effective population size, which differs in opportunistic and pathogenic (as Mycobacterium tuberculosis) bacteria. The success in the dispersion of particular clones and mobile genetic elements by reasons other than antibiotic selection greatly influences the epidemiology of antibiotic resistance. Antibiotic resistance is becoming an ecological problem, and its control should be based on predictive studies and epidemiological and ecological interventions. 12.1. Introduction What is antibiotic resistance? This expression was obviously coined first in relation to medical microbiology and the therapy of infections. Antibiotic resistance refers to the property of bacteria which prevents the inhibition of their growth by antimicrobial agents used in the clinical setting. During the past decade many research, editorial, and review articles have focused on antibiotic resistance (Levy and Marshall, 2004 Pitout and Laupland, 2008 and Livermore, 2009). The problem is dramatic in some countries (Vatopoulos, 2008) and especially worrying in highly pathogenic species such as Mycobacterium tuberculosis (Wright et al., 2009), methicillin-resistant Staphylococcus aureus (MRSA) (De Lencastre and Tomasz, 2008), Acinetobacter baumanii (Karageorgopoulos and Falagas, 2008), enterococci (Arias and Murray, 2008), or Klebsiella pneumoniae (Souli et al., 2008)
  • Book cover image for: Veterinary Public Health: New Trends
    • Rahman, H(Authors)
    • 2021(Publication Date)
    • Biotech
      (Publisher)
    Nonetheless, the ability of bacteria to acquire resistance genes from other organisms, including those that constitute the normal bacterial flora of humans, under the selective pressure of use of antibiotics should not be underestimated (Davies, 1994). SELECTIVE PRESSURE Selective pressure refers to the environmental conditions that enhance the ability of bacteria to develop resistance to antibiotics and to proliferate. This ability to survive may be the result of acquisition of new DNA (as is often the case with vancomycin resistant enterococci – VRE) or it may be due to spontaneous mutation, as is often the case for rifampin-resistant organisms. This ebook is exclusively for this university only. Cannot be resold/distributed. Expanded use of antibiotics in hospitals and in sites outside the hospital ( e.g. , long-term care facilities, day care centers, animal feedlots, and other agricultural sites) increases the selective pressure for resistant organisms to emerge in these settings. The intensity of use of antibiotics appears to be proportional to the resistance levels in organisms in hospital settings (Nicolle et al ., 1996, Dupont and Steele, 1987). MOLECULAR APPROACHES FOR STUDYING ANTIBIOTIC RESISTANCE The determination of antimicrobial susceptibility of a clinical isolate is often crucial for the optimal antimicrobial therapy of infected patients. This need is only increasing with increasing resistance and the emergence of multidrug-resistant microorganisms. Testing is required not only for therapy but also to monitor the spread of resistant organisms or resistance genes throughout the hospital and community (Fluit et al. , 2000a, Fluit et al ., 2000b, Fluit et al ., 2001). Nucleic acid-based detection systems offer rapid and sensitive methods to detect the presence of resistance genes and play a critical role in the elucidation of resistance mechanisms.
  • Book cover image for: Antibiotic Development and Resistance
    • Diarmaid Hughes, Dan I Andersson, Diarmaid Hughes, Dan I Andersson(Authors)
    • 2001(Publication Date)
    • CRC Press
      (Publisher)

    10. Fitness and Virulence of Antibiotic Resistant Bacteria

    Dan I.Andersson§ , Johanna Björkman§ # and Diarmaid Hughes#

    § Swedish Institute for Infectious Disease Control, Department of Bacteriology, S-171 82 Solna, Sweden
    # Uppsala University, Department of Cell and Molecular Biology, BMC, Box 596, S-751 24 Uppsala, Sweden

    INTRODUCTION

    The use, overuse and misuse of antibiotics, since their introduction about 50 years ago, has resulted in the evolution and spread of antibiotic resistance with a concomitant increase in the frequency of resistant bacteria (Cohen, 1992, Davies, 1994; Levy, 1992; McCormick, 1998). A consequence of this is that infections previously treatable with antibiotics might require treatment with more expensive or less efficient drugs. Clearly, antibiotic resistance represents a growing threat to public health and is a cause of major medical and economic concern. Whether this unwanted trend can be slowed down or reversed is unclear. That depends on some factors which we can in principle control, such as the volume of antibiotic use, but also on factors outside our control, such as the fitness costs resistance places on bacteria and the rate and extent to which natural selection reduces or eliminates these costs.
    A problem in the above context is that, at present, we lack the experimental knowledge required to propose and implement rational strategies on how to reduce the frequency of resistance or to evalute the success of any such strategy. This is mainly due to a lack of data on the factors affecting the rate and stability of antibiotic resistance combined with a lack of knowledge on how to incorporate these data into quantitative models which describe and predict resistance development. Thus, there is a need for experimental, epidemiological and theoretical studies where we obtain: (i) the experimental and conceptual background knowledge required to rationally predict and assess the risks of antibiotic resistance development in society, (ii) the data required to allow us to develop policies for the use of antibiotics in clinical settings so as to minimize resistance development without compromising treatment efficacy, and (iii) the data required to provide criteria for pharmaceutical companies, drug-licensing agencies and physicians on how to evaluate the risks of resistance development towards both new compounds and already marketed antibiotics.
  • Book cover image for: New Strategies Combating Bacterial Infection
    • Iqbal Ahmad, Farrukh Aqil(Authors)
    • 2008(Publication Date)
    • Wiley-Blackwell
      (Publisher)
    This chapter will discuss recent strategies to obtain novel antibacterials from microbial products to combat drug-resistant bacteria. Further, roles of alternative therapy (phage therapy) and antibiotic use policy are discussed as possible ways to minimize the problem of drug resistant bacteria. 2.1 Introduction One of the greatest accomplishments of modern medicine had been the development of antimicrobial drugs for the treatment of infectious diseases. Alexander Fleming discovered the first antibiotic, penicillin, in 1928 and over half century of extensive research most acute bacterial infections had been treated effectively with antibacterial drugs. The remarkable success of antibacterial drugs had given an impression in the late 1960s and early 1970s that infectious diseases had been congruent. However, New Strategies Combating Bacterial Infection. Edited by Iqbal Ahmad and Farrukh Aqil Copyright Ó 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim ISBN: 978-3-527-32206-0 j47 40 years later, infectious diseases still remain the third leading cause of death in the United States [1] and the second leading cause of death worldwide [2]. This is mainly due to the development of drug resistance, emergence of new infectious agents and nonavailability of suitable drugs for many infectious diseases. Indiscriminate and excessive use of antibiotics in medical as well as nonmedical settings has resulted in the selection and development of antibiotic resistance among clinical isolates. Bacterial pathogens have developed several mechanisms to overcome antibiotic pressure and now thrive even in the presence of multidrugs. Bacteria may develop resistance by mutation and by acquisition of new genes through bacterial genetic exchange mechanisms (conjugation, transformation and transduction).
  • Book cover image for: Antibiotic Resistance
    eBook - PDF

    Antibiotic Resistance

    Origins, Evolution, Selection and Spread

    • Derek J. Chadwick, Jamie A. Goode, Derek J. Chadwick, Jamie A. Goode(Authors)
    • 2008(Publication Date)
    • Wiley
      (Publisher)
    In addition to morbidity and mortality caused by failure to cure those individuals who are infected by resistant pathogens, society as a whole must pay for the research and development of new antibiotics to keep pace with continually evolving pathogens. It is clear, therefore, that there are major costs associated with antibiotic resistance from the perspective of human society. But is there any cost associated with antibiotic resistance from the perspective of a bacterium? In an environment that contains antibiotic, possession of a corresponding resistance gene is clearly beneficial to a bacterium. However, in the absence of antibiotic, resistant genotypes may have growth rates that are lower than their sensitive counterparts. Mutations that confer resistance do so by disrupting some normal physiological process in the cell, thereby causing detrimental side-effects. In the case of plasmid- encoded resistance functions, bacteria must synthesize additional nucleic acids and 131 132 LENSKI proteins; this synthesis imposes an energetic burden (DaSilva & Bailey 1986) and the products that are synthesized may also interfere with the cell's physiology (Lenski & Nguyen 1988). Resistant bacteria may therefore be inferior competitors to sensitive genotypes in the absence of antibiotics. If so, then a possible strategy for containing the spread of antibiotic resistance would be to suspend the use of a particular antibiotic until the corresponding resistant genotypes had declined to low frequency. Figure 1 shows that the efficacy of this strategy depends on the cost of resistance from the perspective of the bacterium. Assuming that some sensitive genotypes have survived antibiotic treatment (or that they colonized after the treatment ended), the amount of time that would be required to reduce the abundance of resistant bacteria to a specified low level is inversely proportional to the cost of resistance.
  • Book cover image for: Bovine Science
    eBook - PDF

    Bovine Science

    A Key to Sustainable Development

    • Sadashiv S. O., Sharangouda J. Patil, Sadashiv S. O., Sharangouda J. Patil(Authors)
    • 2019(Publication Date)
    • IntechOpen
      (Publisher)
    The other mechanism is known as co-selection. This is a phenomenon in which the genes for resistance against a myriad of antibiotics are located in the single plasmid or the mobile genetic element. In this case this mobile genomic element or the plasmid confers the resistance against all the antibiotics. In contrary to this, the other mechanism is that when one bacterium becomes resistant against one microbe, then it exhibits an increased susceptibility against the other antibiotic [28]. 4.6.1. Mechanisms of the antibacterial drug resistance Table 2 illustrates the mechanisms of the bacterial resistance against different drugs. It also depicts various genes involved in the emergence of resistance against that drug. 4.7. Mechanisms of antibacterial resistance transfer in bacteria One of the major problems is that bacteria not only become resistant to many antibacterial drugs by a variety of phenomena, but they are also capable of transferring this resistance to other bacteria of same as well as with other genera. The main reason for transfer of genetic resistance is because the genes for antibacterial resistance are mainly present on the moveable genomic elements (MGE), e.g., integrons, plasmids, and transposons. But the changes at gene level may also occur in chromosomes although they are extremely rare (except in Mycobacte-rium ). This often occurs because there is a change in the drug target and, thus, the antibacterial drug cannot bind to the appropriate binding site, leading to the loss of efficacy of that partic-ular antibiotic. If the use of antibiotics is inappropriate, e.g., not following the well-established dosage regimen for a particular drug against a particular disease, it can dramatically increase the chances of the development of the resistance against that drug because of the selective advantage of changing their genomic elements. One of the main important locations of antibacterial resistance is the bacterial plasmids.
  • Book cover image for: Antibiotics and Antibiotic Resistance in the Environment
    • Carlos F. Amabile-Cuevas(Author)
    • 2015(Publication Date)
    • CRC Press
      (Publisher)
    1.2.1.2 Co-selection: the plot thickens Antibiotic usage leds to antibiotic resistance; this we know for sure. But it is not quite as simple: there are non-antibiotic agents that can select for antibiotic resistance; and antibiotics can select traits different from antibiotic resistance. Furthermore, some antibiotics can select for resistance to other, unrelated antibiotics. Most of these inter-actions are based on co-selection, and have been reviewed before (Amábile-Cuevas, 2013); cross-resistance ( i . e . , a single resistance mechanism providing protection against several drugs on the same family, or even against chemically unrelated compounds, such as the MLS B phenotype) that can also account for some of these phenom-ena, is rather obvious. Important to keep in mind while discussing resistance in the environment are the following: – Genetic linkage of antibiotic resistance determinants and some other traits, can explain why non-antibiotic agents, or unrelated antibiotics, select for antibiotic resistance genes. For this to happen, resistance genes must reside on the same genetic element: many antibiotic resistance genes have been found along with heavy-metal ( e . g . , mercury, cadmium) and/or disinfectant ( e . g . , quaternary ammo-nium compounds) resistance genes in the same plasmids or other mobile elements. Hence, the presence of such compounds select for the entire genetic element that carries antibiotic resistance determinants, in the absence of antibiotics. It is per-haps relevant to state that the same, or even worst confusion over the definition of “resistance’’ prevails when referring to disinfectants (Gilbert and McBain, 2003). However, while the role of genes that confer only protection against slightly higher disinfectant concentrations could be negligible in houses or hospitals, it may be Definitions and basic concepts 19 particularly relevant in environmental settings where such biocides are diluted.
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