Clostridioides difficile Clostridioides difficile is a
nosocomial pathogen that causes diarrheal disease worldwide. 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. 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,
cephalosporins,
carbapenems, 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.
Enterococcus Multidrug-resistant
Enterococcus faecalis and
Enterococcus faecium are associated with
nosocomial infections. These strains include:
penicillin-resistant
Enterococcus,
vancomycin-resistant Enterococcus, and
linezolid-resistant
Enterococcus.
Mycobacterium tuberculosis Tuberculosis (TB) resistant to antibiotics is called
MDR TB (multidrug-resistant TB). Globally, MDR TB causes 150,000 deaths annually. The rise of the HIV/AIDS epidemic has contributed to this. 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. 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.
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. 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. Found on the
mucous 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. 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. 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.
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. 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. == Gram negative ==