A list of antibiotic resistant bacteria is provided below. These bacteria have shown antibiotic resistance (or antimicrobial resistance).
According to a 2015 CDC report, C. difficile caused almost 500,000 infections in the United States per year. 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 five years.
C. difficile colitis is most strongly associated with fluoroquinolones, , , and clindamycin.
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. Geographically dispersed outbreaks of C. difficile strains resistant to fluoroquinolone antibiotics, such as ciprofloxacin and levofloxacin, were also reported in North America in 2005.
Mycobacterium tuberculosis is an obligate pathogen that has evolved to ensure its persistence in human populations. 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. 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. 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.
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. M. tuberculosis lack the opportunity to interact with other bacteria in order to share plasmids.
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. 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. An alternative five-day treatment with azithromycin showed no development of antimicrobial resistance. 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. 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. Tetracyclines, including doxycycline, have a low clinical eradication rate for M. genitalium infections. A few cases have been described where doxycycline, azithromycin and moxifloxacin had all failed, but pristinamycin was still able to eradicate the infection.
Vancomycin non-susceptible isolates of Staph aureus have been isolated in Asia and the United States. A study performed in 1992 demonstrated that Vancomycin resistance could be transferred from Enterococcus faecalis/faecium to Staph aureus through the transfer of the VanA and VanB genes.
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. 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.
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. 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. 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 DNA methylation 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. Resistance to polymyxins first appear in 2011. An easier way for this resistance to spread, a plasmid known as MCR-1 was discovered in 2015.
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 Iraq War 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.
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