List of antibiotic-resistant bacteria

Last updated

The evolution of bacteria on a "Mega-Plate" petri dish [1]

A list of antibiotic resistant bacteria is provided below. These bacteria have shown antibiotic resistance (or antimicrobial resistance).

Contents

Enzyme NDM-1 (New Delhi Metallo-beta-lactamase-1)

NDM-1 is an enzyme that makes bacteria resistant to a broad range of beta-lactam antibiotics.[ citation needed ]

NDM-1 (New Delhi Metallo-beta-lactamase-1) originated in India. In Indian hospitals, hospital-acquired infections are common, and with the new super-bugs on rise in India, this can make them dangerous. [2] Mapping of sewage and water supply samples that were NDM-1-positive indicates widespread infection in New Delhi already back in 2011. [2]

NDM-1 was first detected in a Klebsiella pneumoniae isolate from a Swedish patient of Indian origin in 2008. It was later detected in bacteria in India, Pakistan, the United Kingdom, the United States, [3] Canada, [4] and Japan. [5]

Gram positive

Clostridium difficile

Clostridium difficile is a nosocomial pathogen that causes diarrheal disease worldwide. [6] [7] Diarrhea caused by C. difficile can be life-threatening. Infections are most frequent in people who have had recent medical and/or antibiotic treatment. C. difficile infections commonly occur during hospitalization. [8]

According to a 2015 CDC report, C. difficile caused almost 500,000 infections in the United States over a year period. Associated with these infections were an estimated 15,000 deaths. The CDC estimates that C. difficile infection costs could amount to $3.8 billion over a 5-year span. [9]

C. difficile colitis is most strongly associated with fluoroquinolones, cephalosporins, carbapenems, and clindamycin. [10] [11] [12]

Some research suggests the overuse of antibiotics in the raising of livestock is contributing to outbreaks of bacterial infections such as C. difficile.[16]

Antibiotics, especially those with a broad activity spectrum (such as clindamycin) disrupt normal intestinal flora. This can lead to an overgrowth of C. difficile, which flourishes under these conditions. Pseudomembranous colitis can follow, creating generalized inflammation of the colon and the development of "pseudomembrane", a viscous collection of inflammatory cells, fibrin, and necrotic cells.[4] Clindamycin-resistant C. difficile was reported as the causative agent of large outbreaks of diarrheal disease in hospitals in New York, Arizona, Florida, and Massachusetts between 1989 and 1992. [13] Geographically dispersed outbreaks of C. difficile strains resistant to fluoroquinolone antibiotics, such as ciprofloxacin and levofloxacin, were also reported in North America in 2005. [14]

Enterococcus

Multidrug-resistant Enterococcus faecalis and Enterococcus faecium are associated with nosocomial infections. [15] These strains include: penicillin-resistant Enterococcus , vancomycin-resistant Enterococcus, and linezolid-resistant Enterococcus . [16]

Mycobacterium tuberculosis

Tuberculosis (TB) resistant to antibiotics is called MDR TB (multidrug-resistant TB). Globally, MDR TB causes 150,000 deaths annually. [17] The rise of the HIV/AIDS epidemic has contributed to this. [18]

Mycobacterium tuberculosis is an obligate pathogen that has evolved to ensure its persistence in human populations. [19] This is evident in that Mycobacterium tuberculosis must cause a pulmonary disease in order to be successfully transmitted from one person to another. Tuberculosis better known as TB has one of the highest mortality rates among pathogens in the world. Mortality rates have not seen a significant decrease due to its growing resistance to certain antibiotics. [17] Although years of research have been devoted to the creation of a vaccine, one still does not exist. TB is extremely transmissible, contributing significantly to its very high level of virulence. TB was considered one of the most prevalent diseases, and did not have a cure until the discovery of streptomycin by Selman Waksman in 1943. [20] However, the bacteria soon developed resistance. Since then, drugs such as isoniazid and rifampin have been used. M. tuberculosis develops resistance to drugs by spontaneous mutations in its genomes. These types of mutations can lead to genotype and phenotype changes that can contribute to reproductive success, leading to the evolution of resistant bacteria. Resistance to one drug is common, and this is why treatment is usually done with more than one drug. Extensively drug-resistant TB (XDR TB) is TB that is also resistant to the second line of drugs. [18] [21]

Resistance of Mycobacterium tuberculosis to isoniazid, rifampin, and other common treatments has become an increasingly relevant clinical challenge. Evidence is lacking for whether these bacteria have plasmids. [22] M. tuberculosis lack the opportunity to interact with other bacteria in order to share plasmids. [22] [23]

Mycoplasma genitalium

Mycoplasma genitalium is a small pathogenic bacterium that lives on the ciliated epithelial cells of the urinary and genital tracts in humans. It is still controversial whether or not this bacterium is to be recognized as a sexually transmitted pathogen. Infection with Mycoplasma genitalium sometimes produces clinical symptoms, or a combination of symptoms, but sometimes can be asymptomatic. It causes inflammation in the urethra (urethritis) both in men and women, which is associated with mucopurulent discharge in the urinary tract, and burning while urinating.[ citation needed ]

Treatment of Mycoplasma genitalium infections is becoming increasingly difficult due to rapidly developing multi-drug resistance, and diagnosis and treatment is further hampered by the fact that M. genitalium infections are not routinely detected. [24] Azithromycin is the most common first-line treatment, but the commonly-used 1 gram single-dose azithromycin treatment can lead to the bacteria commonly developing resistance to azithromycin. [25] An alternative five-day treatment with azithromycin showed no development of antimicrobial resistance. [26] Efficacy of azithromycin against M. genitalium has decreased substantially, which is thought to occur through SNPs in the 23S rRNA gene. The same SNPs are thought to be responsible for resistance against josamycin, which is prescribed in some countries. [27] Moxifloxacin can be used as a second-line treatment in case azithromycin is not able to eradicate the infection. However, resistance against moxifloxacin has been observed since 2007, thought to be due to parC SNPs. [27] [28] Tetracyclines, including doxycycline, have a low clinical eradication rate for M. genitalium infections. [29] A few cases have been described where doxycycline, azithromycin and moxifloxacin had all failed, but pristinamycin was still able to eradicate the infection. [27]

Staphylococcus aureus

Staphylococcus aureus is one of the major resistant pathogens. It caused more than 100,000 deaths attributed to AMR in 2019 and MRSA was present in 748,000 global deaths that year. [30] Found on the mucus membranes and the human skin of around a third of the population, it is extremely adaptable to antibiotic pressure. It was one of the earlier bacteria in which penicillin resistance was found, in 1947, just four years after mass-production began. Methicillin was then the antibiotic of choice, but has since been replaced by oxacillin because of significant kidney toxicity. Methicillin-resistant Staphylococcus aureus (MRSA) was first detected in Britain in 1961, and it is now "quite common" in hospitals[ citation needed ]. MRSA was responsible for 37% of fatal cases of sepsis in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline, and erythromycin.[ citation needed ]

Streptococcus

Streptococcus pyogenes (Group A Streptococcus: GAS) infections can usually be treated with many different antibiotics. Strains of S. pyogenes resistant to macrolide antibiotics have emerged; however, all strains remain uniformly susceptible to penicillin. [31]

Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing worldwide. It was identified as one of six leading pathogens for disease associated with resistance in 2019 and that year there were 596,000 deaths globally of people with drug-resistant infection from the pathogen. [30] The major mechanism of resistance involves the introduction of mutations in genes encoding penicillin-binding proteins. Selective pressure is thought to play an important role, and use of beta-lactam antibiotics has been implicated as a risk factor for infection and colonization. S. pneumoniae is responsible for pneumonia, bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis. [31]

Gram negative

Campylobacter

Campylobacter causes diarrhea (often bloody), fever, and abdominal cramps. Serious complications such as temporary paralysis can also occur. Physicians rely on ciprofloxacin and azithromycin for treating patients with severe disease although Campylobacter is showing resistance to these antibiotics. [8]

Neisseria gonorrhoeae

Neisseria gonorrhoeae is a sexually transmitted pathogen that causes gonorrhea, a sexually transmitted disease that can result in discharge and inflammation at the urethra, cervix, pharynx, or rectum. [8] It can cause pelvic pain, pain on urination, penile and vaginal discharge, as well as systemic symptoms. It can also cause severe reproductive complications. [8]

Gamma proteobacteria

Enterobacteriaceae

As of 2013 hard-to-treat or untreatable infections of carbapenem-resistant Enterobacteriaceae (CRE), also known as carbapenemase-producing Enterobacteriaceae (CPE), were increasing among patients in medical facilities. CRE are resistant to nearly all available antibiotics. Almost half of hospital patients who get bloodstream CRE infections die from the infection. [8]

Klebsiella pneumoniae

Klebsiella pneumoniae carbapenemase (KPC)-producing bacteria are a group of emerging highly drug-resistant Gram-negative bacilli causing infections associated with significant morbidity and mortality whose incidence is rapidly increasing in a variety of clinical settings around the world. Klebsiella pneumoniae was identified as one of six leading pathogens for disease associated with resistance in 2019 and that year there were 642,000 deaths globally of people with drug-resistant infection from the pathogen. [30] Klebsiella pneumoniae includes numerous mechanisms for antibiotic resistance, many of which are located on highly mobile genetic elements. [32] Carbapenem antibiotics (heretofore often the treatment of last resort for resistant infections) are generally not effective against KPC-producing organisms. [33]

Salmonella and E. coli

Infection with Escherichia coli and Salmonella can result from the consumption of contaminated food and polluted water. Both of these bacteria are well known for causing nosocomial (hospital-linked) infections, and often, these strains found in hospitals are antibiotic resistant because of adaptations to wide spread antibiotic use. [34] When both bacteria are spread, serious health conditions arise. Many people are hospitalized each year after becoming infected, with some dying as a result. Since 1993, some strains of E. coli have become resistant to multiple types of fluoroquinolone antibiotics.[ citation needed ]E. coli was identified as one of the six leading pathogens for deaths associated with resistance in 2019 and that year there were 829,000 deaths globally of people with drug-resistant infection from the pathogen. [30]

Although mutation alone plays a huge role in the development of antibiotic resistance, a 2008 study found that high survival rates after exposure to antibiotics could not be accounted for by mutation alone. [35] This study focused on the development of resistance in E. coli to three antibiotic drugs: ampicillin, tetracycline, and nalidixic acid. The researchers found that some antibiotic resistance in E. coli developed because of epigenetic inheritance rather than by direct inheritance of a mutated gene. This was further supported by data showing that reversion to antibiotic sensitivity was relatively common as well. This could only be explained by epigenetics. [35] Epigenetics is a type of inheritance in which gene expression is altered rather than the genetic code itself. There are many modes by which this alteration of gene expression can occur, including methylation of DNA and histone modification; however, the important point is that both inheritance of random mutations and epigenetic markers can result in the expression of antibiotic resistance genes. [35] Resistance to polymyxins first appear in 2011. [36] An easier way for this resistance to spread, a plasmid known as MCR-1 was discovered in 2015. [36]

Pseudomonadales

Acinetobacter

Acinetobacter is a gram-negative bacteria that causes pneumonia or bloodstream infections in critically ill patients. Multidrug-resistant Acinetobacter have become very resistant to antibiotics. [8] Acinetobacter baumannii was identified as one of the six leading pathogens for deaths associated with resistance in 2019 and that year there were 423,000 deaths globally of people with drug-resistant infection from the pathogen. [30]

On November 5, 2004, the Centers for Disease Control and Prevention (CDC) reported an increasing number of Acinetobacter baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom were treated. Most of these showed multidrug resistance (MRAB), with a few isolates resistant to all drugs tested. [37] [38]

Pseudomonas aeruginosa

Pseudomonas aeruginosa is a highly prevalent opportunistic pathogen. It was identified as one of the six leading pathogens for deaths associated with resistance in 2019 and that year there were 334,000 deaths globally of people with drug-resistant infection from the pathogen. [30] One of the most worrisome characteristics of P. aeruginosa is its low antibiotic susceptibility, which is attributable to a concerted action of multidrug efflux pumps with chromosomally encoded antibiotic resistance genes (e.g., mexAB-oprM, mexXY) and the low permeability of the bacterial cellular envelopes. [39] P. aeruginosa has the ability to produce 4-hydroxy-2-alkylquinolines (HAQs), and it has been found that HAQs have prooxidant effects and overexpressing modestly increased susceptibility to antibiotics. The study experimented with the P. aeruginosa biofilms and found that a disruption of relA and spoT genes produced an inactivation of the Stringent response (SR) in cells with nutrient limitation, which provides cells be more susceptible to antibiotics. [40]

See also

Related Research Articles

<span class="mw-page-title-main">Antibiotic</span> Antimicrobial substance active against bacteria

An antibiotic is a type of antimicrobial substance active against bacteria. It is the most important type of antibacterial agent for fighting bacterial infections, and antibiotic medications are widely used in the treatment and prevention of such infections. They may either kill or inhibit the growth of bacteria. A limited number of antibiotics also possess antiprotozoal activity. Antibiotics are not effective against viruses such as the ones which cause the common cold or influenza; drugs which inhibit growth of viruses are termed antiviral drugs or antivirals rather than antibiotics. They are also not effective against fungi; drugs which inhibit growth of fungi are called antifungal drugs.

<span class="mw-page-title-main">Antimicrobial resistance</span> Resistance of microbes to drugs directed against them

Antimicrobial resistance (AMR) occurs when microbes evolve mechanisms that protect them from the effects of antimicrobials. All classes of microbes can evolve resistance where the drugs are no longer effective. Fungi evolve antifungal resistance, viruses evolve antiviral resistance, protozoa evolve antiprotozoal resistance, and bacteria evolve antibiotic resistance. Together all of these come under the umbrella of antimicrobial resistance. Microbes resistant to multiple antimicrobials are called multidrug resistant (MDR) and are sometimes referred to as superbugs. Although antimicrobial resistance is a naturally occurring process, it is often the result of improper usage of the drugs and management of the infections.

<span class="mw-page-title-main">Mycoplasma genitalium</span> Species of bacterium

Mycoplasma genitalium is a sexually transmitted, small and pathogenic bacterium that lives on the mucous epithelial cells of the urinary and genital tracts in humans. Medical reports published in 2007 and 2015 state that Mgen is becoming increasingly common. Resistance to multiple antibiotics, including the macrolide azithromycin, which until recently was the most reliable treatment, is becoming prevalent. The bacteria was first isolated from the urogenital tract of humans in 1981, and was eventually identified as a new species of Mycoplasma in 1983. It can cause negative health effects in men and women. It also increases the risk factor for HIV spread with higher occurrences in those previously treated with the azithromycin antibiotics.

<i>Klebsiella pneumoniae</i> Species of bacterium

Klebsiella pneumoniae is a Gram-negative, non-motile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium. It appears as a mucoid lactose fermenter on MacConkey agar.

<span class="mw-page-title-main">Azithromycin</span> Antibiotic

Azithromycin, sold under the brand names Zithromax and Azasite, is an antibiotic medication used for the treatment of a number of bacterial infections. This includes middle ear infections, strep throat, pneumonia, traveler's diarrhea, and certain other intestinal infections. Along with other medications, it may also be used for malaria. It can be taken by mouth or intravenously.

<span class="mw-page-title-main">Hospital-acquired infection</span> Infection that is acquired in a hospital or other health care facility

A hospital-acquired infection, also known as a nosocomial infection, is an infection that is acquired in a hospital or other healthcare facility. To emphasize both hospital and nonhospital settings, it is sometimes instead called a healthcare-associated infection. Such an infection can be acquired in hospital, nursing home, rehabilitation facility, outpatient clinic, diagnostic laboratory or other clinical settings. A number of dynamic processes can bring contamination into operating rooms and other areas within nosocomial settings. Infection is spread to the susceptible patient in the clinical setting by various means. Healthcare staff also spread infection, in addition to contaminated equipment, bed linens, or air droplets. The infection can originate from the outside environment, another infected patient, staff that may be infected, or in some cases, the source of the infection cannot be determined. In some cases the microorganism originates from the patient's own skin microbiota, becoming opportunistic after surgery or other procedures that compromise the protective skin barrier. Though the patient may have contracted the infection from their own skin, the infection is still considered nosocomial since it develops in the health care setting. Nosocomial infection tends to lack evidence that it was present when the patient entered the healthcare setting, thus meaning it was acquired post-admission.

<span class="mw-page-title-main">Colistin</span> Antibiotic

Colistin, also known as polymyxin E, is an antibiotic medication used as a last-resort treatment for multidrug-resistant Gram-negative infections including pneumonia. These may involve bacteria such as Pseudomonas aeruginosa, Klebsiella pneumoniae, or Acinetobacter. It comes in two forms: colistimethate sodium can be injected into a vein, injected into a muscle, or inhaled, and colistin sulfate is mainly applied to the skin or taken by mouth. Colistimethate sodium is a prodrug; it is produced by the reaction of colistin with formaldehyde and sodium bisulfite, which leads to the addition of a sulfomethyl group to the primary amines of colistin. Colistimethate sodium is less toxic than colistin when administered parenterally. In aqueous solutions it undergoes hydrolysis to form a complex mixture of partially sulfomethylated derivatives, as well as colistin. Resistance to colistin began to appear as of 2015.

Multiple drug resistance (MDR), multidrug resistance or multiresistance is antimicrobial resistance shown by a species of microorganism to at least one antimicrobial drug in three or more antimicrobial categories. Antimicrobial categories are classifications of antimicrobial agents based on their mode of action and specific to target organisms. The MDR types most threatening to public health are MDR bacteria that resist multiple antibiotics; other types include MDR viruses, parasites.

<span class="mw-page-title-main">Carbapenem</span> Class of highly effective antibiotic agents

Carbapenems are a class of very effective antibiotic agents most commonly used for treatment of severe bacterial infections. This class of antibiotics is usually reserved for known or suspected multidrug-resistant (MDR) bacterial infections. Similar to penicillins and cephalosporins, carbapenems are members of the beta-lactam antibiotics drug class, which kill bacteria by binding to penicillin-binding proteins, thus inhibiting bacterial cell wall synthesis. However, these agents individually exhibit a broader spectrum of activity compared to most cephalosporins and penicillins. Furthermore, carbapenems are typically unaffected by emerging antibiotic resistance, even to other beta-lactams.

<i>Acinetobacter baumannii</i> Species of bacterium

Acinetobacter baumannii is a typically short, almost round, rod-shaped (coccobacillus) Gram-negative bacterium. It is named after the bacteriologist Paul Baumann. It can be an opportunistic pathogen in humans, affecting people with compromised immune systems, and is becoming increasingly important as a hospital-derived (nosocomial) infection. While other species of the genus Acinetobacter are often found in soil samples, it is almost exclusively isolated from hospital environments. Although occasionally it has been found in environmental soil and water samples, its natural habitat is still not known.

<span class="mw-page-title-main">New Delhi metallo-beta-lactamase 1</span> Enzyme

NDM-1 is an enzyme that makes bacteria resistant to a broad range of beta-lactam antibiotics. These include the antibiotics of the carbapenem family, which are a mainstay for the treatment of antibiotic-resistant bacterial infections. The gene for NDM-1 is one member of a large gene family that encodes beta-lactamase enzymes called carbapenemases. Bacteria that produce carbapenemases are often referred to in the news media as "superbugs" because infections caused by them are difficult to treat. Such bacteria are usually sensitive only to polymyxins and tigecycline.

Multidrug resistant Gram-negative bacteria are a type of Gram-negative bacteria with resistance to multiple antibiotics. They can cause bacteria infections that pose a serious and rapidly emerging threat for hospitalized patients and especially patients in intensive care units. Infections caused by MDR strains are correlated with increased morbidity, mortality, and prolonged hospitalization. Thus, not only do these bacteria pose a threat to global public health, but also create a significant burden to healthcare systems.

<span class="mw-page-title-main">Rifalazil</span> Antibiotic

Rifalazil is an antibiotic substance that kills bacterial cells by blocking off the β-subunit in RNA polymerase. Rifalazil is used as a treatment for many different diseases. The most common are Chlamydia infection, Clostridium difficile associated diarrhea (CDAD), and tuberculosis (TB). Using rifalazil and the effects that coincide with taking rifalazil for treating a bacterial disease vary from person to person, as does any drug put into the human body. Food interactions and genetic variation are a few causes for the variation in side effects from the use of rifalazil. Its development was terminated in 2013 due to severe side effects.

Carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae (CPE) are Gram-negative bacteria that are resistant to the carbapenem class of antibiotics, considered the drugs of last resort for such infections. They are resistant because they produce an enzyme called a carbapenemase that disables the drug molecule. The resistance can vary from moderate to severe. Enterobacteriaceae are common commensals and infectious agents. Experts fear CRE as the new "superbug". The bacteria can kill up to half of patients who get bloodstream infections. Tom Frieden, former head of the Centers for Disease Control and Prevention has referred to CRE as "nightmare bacteria". Examples of enzymes found in certain types of CRE are KPC and NDM. KPC and NDM are enzymes that break down carbapenems and make them ineffective. Both of these enzymes, as well as the enzyme VIM have also been reported in Pseudomonas.

<i>Clostridioides difficile</i> Species of bacteria

Clostridioides difficile is a bacterium that is well known for causing serious diarrheal infections, and may also cause colon cancer. It is known also as C. difficile, or C. diff, and is a Gram-positive species of spore-forming bacteria. Clostridioides spp. are anaerobic, motile bacteria, ubiquitous in nature and especially prevalent in soil. Its vegetative cells are rod-shaped, pleomorphic, and occur in pairs or short chains. Under the microscope, they appear as long, irregular cells with a bulge at their terminal ends. Under Gram staining, C. difficile cells are Gram-positive and show optimum growth on blood agar at human body temperatures in the absence of oxygen. C. difficile is catalase- and superoxide dismutase-negative, and produces up to three types of toxins: enterotoxin A, cytotoxin B and Clostridioides difficile transferase. Under stress conditions, the bacteria produce spores that are able to tolerate extreme conditions that the active bacteria cannot tolerate.

<span class="mw-page-title-main">Ceftazidime/avibactam</span> Combination antibiotic medication

Ceftazidime/avibactam, sold under the brand name Avycaz among others, is a fixed-dose combination medication composed of ceftazidime, a cephalosporin antibiotic, and avibactam, a β-lactamase inhibitor. It is used to treat complicated intra-abdominal infections, urinary tract infections, and pneumonia. It is only recommended when other options are not appropriate. It is given by injection into a vein.

ESKAPE is an acronym comprising the scientific names of six highly virulent and antibiotic resistant bacterial pathogens including: Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter spp. The acronym is sometimes extended to ESKAPEE to include Escherichia coli. This group of Gram-positive and Gram-negative bacteria can evade or 'escape' commonly used antibiotics due to their increasing multi-drug resistance (MDR). As a result, throughout the world, they are the major cause of life-threatening nosocomial or hospital-acquired infections in immunocompromised and critically ill patients who are most at risk. P. aeruginosa and S. aureus are some of the most ubiquitous pathogens in biofilms found in healthcare. P. aeruginosa is a Gram-negative, rod-shaped bacterium, commonly found in the gut flora, soil, and water that can be spread directly or indirectly to patients in healthcare settings. The pathogen can also be spread in other locations through contamination, including surfaces, equipment, and hands. The opportunistic pathogen can cause hospitalized patients to have infections in the lungs, blood, urinary tract, and in other body regions after surgery. S. aureus is a Gram-positive, cocci-shaped bacterium, residing in the environment and on the skin and nose of many healthy individuals. The bacterium can cause skin and bone infections, pneumonia, and other types of potentially serious infections if it enters the body. S. aureus has also gained resistance to many antibiotic treatments, making healing difficult. Because of natural and unnatural selective pressures and factors, antibiotic resistance in bacteria usually emerges through genetic mutation or acquires antibiotic-resistant genes (ARGs) through horizontal gene transfer - a genetic exchange process by which antibiotic resistance can spread.

Cefiderocol, sold under the brand name Fetroja among others, is an antibiotic used to treat complicated urinary tract infections when no other options are available. It is indicated for the treatment of multi-drug-resistant Gram-negative bacteria including Pseudomonas aeruginosa. It is given by injection into a vein.

<span class="mw-page-title-main">Antimicrobial spectrum</span> Method of assessing antibiotics

The antimicrobial spectrum of an antibiotic means the range of microorganisms it can kill or inhibit. Antibiotics can be divided into broad-spectrum antibiotics, extended-spectrum antibiotics and narrow-spectrum antibiotics based on their spectrum of activity. Detailedly, broad-spectrum antibiotics can kill or inhibit a wide range of microorganisms; extended-spectrum antibiotic can kill or inhibit Gram positive bacteria and some Gram negative bacteria; narrow-spectrum antibiotic can only kill or inhibit limited species of bacteria.

<span class="mw-page-title-main">Multidrug-resistant bacteria</span>

Multidrug-resistant bacteria are bacteria that are resistant to three or more classes of antimicrobial drugs. MDR bacteria have seen an increase in prevalence in recent years and pose serious risks to public health. MDR bacteria can be broken into 3 main categories: Gram-positive, Gram-negative, and other (acid-stain). These bacteria employ various adaptations to avoid or mitigate the damage done by antimicrobials. With increased access to modern medicine there has been a sharp increase in the amount of antibiotics consumed. Given the abundant use of antibiotics there has been a considerable increase in the evolution of antimicrobial resistance factors, now outpacing the development of new antibiotics.

References

  1. ↑ Baym M, Lieberman TD, Kelsic ED, Chait R, Gross R, Yelin I, Kishony R (2016-09-09). "Spatiotemporal microbial evolution on antibiotic landscapes". Science. 353 (6304): 1147–1151. Bibcode:2016Sci...353.1147B. doi:10.1126/science.aag0822. ISSN   0036-8075. PMC   5534434 . PMID   27609891.
  2. 1 2 Walsh TR, Weeks J, Livermore DM, Toleman MA (2011). "Dissemination of NDM-1 positive bacteria in the New Delhi environment and its implications for human health: an environmental point prevalence study". The Lancet Infectious Diseases. 11 (5): 355–362. doi:10.1016/s1473-3099(11)70059-7. PMID   21478057.
  3. ↑ Marilynn Marchione (13 September 2010). "New drug-resistant superbugs found in 3 states". Boston Globe.
  4. ↑ Madeleine White (21 August 2010). "Superbug detected in GTA". Toronto Star.
  5. ↑ Yuasa S (8 September 2010). "Japan confirms first case of superbug gene". The Boston Globe.
  6. ↑ Gerding DN, Johnson S, Peterson LR, Mulligan ME, Silva J (1995). "Clostridium difficile-associated diarrhea and colitis". Infect. Control Hosp. Epidemiol. 16 (8): 459–477. doi:10.1086/648363. PMID   7594392.
  7. ↑ McDonald LC (2005). "Clostridium difficile: responding to a new threat from an old enemy". Infect. Control Hosp. Epidemiol. 26 (8): 672–5. doi: 10.1086/502600 . PMID   16156321.
  8. 1 2 3 4 5 6 "Biggest Threats – Antibiotic/Antimicrobial Resistance – CDC". www.cdc.gov. Retrieved 2016-05-05.
  9. ↑ "CDC Press Releases". CDC. January 2016. Retrieved 2016-05-05.
  10. ↑ Baxter R, Ray GT, Fireman BH (January 2008). "Case-control study of antibiotic use and subsequent Clostridium difficile-associated diarrhea in hospitalized patients". Infection Control and Hospital Epidemiology. 29 (1): 44–50. doi:10.1086/524320. PMID   18171186. S2CID   39290661.
  11. ↑ Gifford AH, Kirkland KB (December 2006). "Risk factors for Clostridium difficile-associated diarrhea on an adult hematology-oncology ward". European Journal of Clinical Microbiology & Infectious Diseases. 25 (12): 751–5. doi:10.1007/s10096-006-0220-1. PMID   17072575. S2CID   23822514.
  12. ↑ Palmore TN, Sohn S, Malak SF, Eagan J, Sepkowitz KA (August 2005). "Risk factors for acquisition of Clostridium difficile-associated diarrhea among outpatients at a cancer hospital". Infection Control and Hospital Epidemiology. 26 (8): 680–4. doi:10.1086/502602. PMC   5612438 . PMID   16156323.
  13. ↑ Johnson S, Samore MH, Farrow KA, Killgore GE, Tenover FC, Lyras D, Rood JI, DeGirolami P, Baltch AL, Rafferty ME, Pear SM, Gerding DN (1999). "Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals". New England Journal of Medicine. 341 (23): 1645–1651. doi: 10.1056/NEJM199911253412203 . PMID   10572152.
  14. ↑ Loo VG, Poirier L, Miller MA, Oughton M, Libman MD, Michaud S, Bourgault AM, Nguyen T, Frenette C, Kelly M, Vibien A, Brassard P, Fenn S, Dewar K, Hudson TJ, Horn R, René P, Monczak Y, Dascal A (2005). "A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality". N Engl J Med. 353 (23): 2442–9. doi: 10.1056/NEJMoa051639 . PMID   16322602.
  15. ↑ Hidron AI, Edwards JR, Patel J, Horan TC, Sievert DM, Pollock DA, Fridkin SK (November 2008). National Healthcare Safety Network Team; Participating National Healthcare Safety Network Facilities. "NHSN annual update: antimicrobial-resistant pathogens associated with healthcare-associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006–2007". Infect Control Hosp Epidemiol. 29 (11): 996–1011. doi:10.1086/591861. PMID   18947320. S2CID   205988392.
  16. ↑ Kristich CJ, Rice LB, Arias CA (2014-01-01). Gilmore MS, Clewell DB, Ike Y, Shankar N (eds.). Enterococcal Infection—Treatment and Antibiotic Resistance. Boston: Massachusetts Eye and Ear Infirmary. PMID   24649502.
  17. 1 2 "Antimicrobial Resistance Still Poses a Public Health Threat: A Conversation With Edward J. Septimus, MD, FIDSA, FACP, FSHEA, Clinical Professor of Internal Medicine at Texas A&M Health Science Center". Agency for Healthcare Research and Quality. 2013-04-17. Retrieved 2013-09-26.
  18. 1 2 LoBue P (2009). "Extensively drug-resistant tuberculosis". Current Opinion in Infectious Diseases. 22 (2): 167–73. doi:10.1097/QCO.0b013e3283229fab. PMID   19283912. S2CID   24995375.
  19. ↑ Brites D, Gagneux S (2013-04-17). "Co-evolution of Mycobacterium tuberculosis and Homo sapiens, Brites, D., & Gagneux, S. (2015)". Immunol Rev. 264 (1): 6–24. doi:10.1111/imr.12264. PMC   4339235 . PMID   25703549.
  20. ↑ Herzog H (1998). "History of Tuberculosis". Respiration. 65 (1): 5–15. doi:10.1159/000029220. PMID   9523361. S2CID   202645306.
  21. ↑ Gao Q, Li X (2010). "Transmission of MDR tuberculosis". Drug Discovery Today: Disease Mechanisms. 7: e61–e65. doi:10.1016/j.ddmec.2010.09.006.
  22. 1 2 Zainuddin ZF, Dale JW (1990). "Does Mycobacterium tuberculosis have plasmids?". Tubercle. 71 (1): 43–9. doi:10.1016/0041-3879(90)90060-l. PMID   2115217.
  23. ↑ Louw GE, Warren RM, Gey van Pittius NC, McEvoy CR, Van Helden PD, Victor TC (2009). "A Balancing Act: Efflux/Influx in Mycobacterial Drug Resistance". Antimicrobial Agents and Chemotherapy. 53 (8): 3181–9. doi:10.1128/AAC.01577-08. PMC   2715638 . PMID   19451293.
  24. ↑ Suneta S, Parkhouse A, Gillian D (24 April 2017). "Macrolide and quinolone-resistant Mycoplasma genitalium in a man with persistent urethritis: the tip of the British iceberg?". Sexually Transmitted Infections. 93 (8): 556–557. doi:10.1136/sextrans-2016-053077. PMID   28438948. S2CID   9178150 . Retrieved 6 October 2017.
  25. ↑ Yew HS, Anderson T, Coughlan E, Werno A (2011). "Induced macrolide resistance in Mycoplasma genitalium isolates from patients with recurrent nongonococcal urethritis". Journal of Clinical Microbiology. 49 (4): 1695–1696. doi:10.1128/JCM.02475-10. PMC   3122813 . PMID   21346049.
  26. ↑ Anagrius C, Loré B, Jensen JS, Coenye T (2013). "Treatment of Mycoplasma genitalium. Observations from a Swedish STD Clinic". PLOS ONE. 8 (4): e61481. Bibcode:2013PLoSO...861481A. doi: 10.1371/journal.pone.0061481 . PMC   3620223 . PMID   23593483.
  27. 1 2 3 Unemo M, Jensen JS (10 January 2017). "Antimicrobial-resistant sexually transmitted infections: gonorrhoea and Mycoplasma genitalium". Nature Reviews Urology. 14 (3): 139–125. doi:10.1038/nrurol.2016.268. PMID   28072403. S2CID   205521926.
  28. ↑ "Mycoplasma Genitalium Treatment Choices". www.theonlineclinic.co.uk.
  29. ↑ Jensen J, Cusini M, Gomberg M, Moi M (9 August 2016). "2016 European guideline on Mycoplasma genitalium infections". Journal of the European Academy of Dermatology and Venereology. 30 (10): 1650–1656. doi: 10.1111/jdv.13849 . PMID   27505296.
  30. 1 2 3 4 5 6 Murray CJ, Ikuta KS, Sharara F, Swetschinski L, Aguilar GR, Gray A, Han C, Bisignano C, Rao P, Wool E, Johnson SC (2022-01-19). "Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis". The Lancet. 399 (10325): 629–655. doi:10.1016/S0140-6736(21)02724-0. ISSN   0140-6736. PMC   8841637 . PMID   35065702.
  31. 1 2 Albrich WC, Monnet DL, Harbarth S (2004). "Antibiotic selection pressure and resistance in Streptococcus pneumoniae and Streptococcus pyogenes". Emerg. Infect. Dis. 10 (3): 514–7. doi:10.3201/eid1003.030252. PMC   3322805 . PMID   15109426.
  32. ↑ Hudson C, Bent Z, Meagher R, Williams K (June 7, 2014). "Resistance Determinants and Mobile Genetic Elements of an NDM-1-Encoding Klebsiella pneumoniae Strain". PLOS ONE. 9 (6): e99209. Bibcode:2014PLoSO...999209H. doi: 10.1371/journal.pone.0099209 . PMC   4048246 . PMID   24905728.
  33. ↑ Arnold RS, Thom KA, Sharma S, Phillips M, Kristie Johnson J, Morgan DJ (2011). "Emergence of Klebsiella pneumoniae Carbapenemase-Producing Bacteria". Southern Medical Journal. 104 (1): 40–5. doi:10.1097/SMJ.0b013e3181fd7d5a. PMC   3075864 . PMID   21119555.
  34. ↑ Davies J, Davies D (2010). "Origins and Evolution of Antibiotic Resistance". Microbiol Mol Biol Rev. 74 (3): 417–433. doi:10.1128/MMBR.00016-10. PMC   2937522 . PMID   20805405.
  35. 1 2 3 Adam M, Murali B, Glenn NO, Potter SS (2008). "Epigenetic inheritance based evolution of antibiotic resistance in bacteria". BMC Evol. Biol. 8 (1): 52. Bibcode:2008BMCEE...8...52A. doi: 10.1186/1471-2148-8-52 . PMC   2262874 . PMID   18282299.
  36. 1 2 Reardon S (21 December 2015). "Spread of antibiotic-resistance gene does not spell bacterial apocalypse — yet". Nature. doi:10.1038/nature.2015.19037. S2CID   182042290.
  37. ↑ Centers for Disease Control Prevention (CDC). (2004). "Acinetobacter baumannii infections among patients at military medical facilities treating injured U.S. service members, 2002–2004". MMWR Morb. Mortal. Wkly. Rep. 53 (45): 1063–6. PMID   15549020.
  38. ↑ "Medscape abstract on Acinetobacter baumannii: Acinetobacter baumannii: An Emerging Multidrug-resistant Threat". membership only website
  39. ↑ Poole K (2004). "Efflux-mediated multiresistance in Gram-negative bacteria". Clinical Microbiology and Infection. 10 (1): 12–26. doi: 10.1111/j.1469-0691.2004.00763.x . PMID   14706082.
  40. ↑ Nguyen D, Joshi-Datar A, Lepine F, Bauerle E, Olakanmi O, Beer K, McKay G, Siehnel R, Schafhauser J, Wang Y, Britigan BE, Singh PK (2011). "Active Starvation Responses Mediate Antibiotic Tolerance in Biofilms and Nutrient-Limited Bacteria". Science. 334 (6058): 982–6. Bibcode:2011Sci...334..982N. doi:10.1126/science.1211037. PMC   4046891 . PMID   22096200.
Tango Phone medapp.svg
Wikipedia's health care articles can be viewed offline with the Medical Wikipedia app .
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.