A Superbug is a bacterium that can live in the human body and has the ability to withstand all forms of antibiotic medication. Superbugs are becoming increasingly significant in modern medicine as they are becoming more and more resistant to antibiotics. Antibiotics were discovered in 1928 by Alexander Fleming (Walsh and McManus, 2000). This resulted in a huge movement forward in medical history and even greatened human life expectancy. Since then antibiotics have been widely used and abused, people began to treat everything with this ‘miracle’ drug. If antibiotics are continually used as bacteria grows exponentially more resistant to them then eventually society will fall back into an era without the readily
Certain E. Coli strains are also known to show resistance to bacteria killing antibiotics. This resistance is due to the plasmids, or small round DNA molecules, in the bacteria that carry the resistant genes. R Plasmids (resistance plasmids) are widely studied and bestow resistance to factors that inhibit growth of the organism. R plasmids code for proteins that can
The article “The End of Antibiotics” discusses a 57 year old man that was dying and how doctors could only sit by while his condition deteriorated. This man was not shot or stabbed, he was infected with antibiotic resistant bacteria that was slowly killing him. He died months later after being bombarded with antibiotics in the form of capsules, tablets, and IVs (Begley par.1). This is the unsettling power that superbugs like this one has over modern day medicine. A superbug is a bacteria that has evolved its cellular structure to resist antibiotics. Dr. Richard Wenzel of the University of Iowa stated, “Only a few years after penicillin came into wide use with World War II, strains of staph had emerged
The TEM-1 type of Beta-lactamase is the most common -lactamase enzyme found in E. coli. More importantly, this enzyme is highly interactive with antibiotics by inhibiting antibiotics from accomplishing their purpose of: halting the synthesis of bacteria cell walls to cease the spread and existence of the bacteria. This makes TEM type
There are a few antibiotics that are affected in this case which include cephalosporin and also include penicillin (Munoz-Price & Jacoby, 2015). There are a few different ESBL’s which include TEM, SHV, CTX-M, OXA, and many others (Munoz-Price & Jacoby, 2015). All of the strains will be treated slightly differently due to the different chemical makeup (Munoz-Price & Jacoby, 2015). In order to determine the presence of ESBLs, lab tests can be used such as disk diffusion and pyrosequencing ((Munoz-Price & Jacoby, 2015). Every patient has a different level of risk for becoming contaminated with ESBLs such as the differing lengths in hospital stay, as well as whether the patient has a PICC line (Munoz-Price & Jacoby, 2015). Another risk factor for the patient may be that they were previously in a nursing home (Munoz-Price & Jacoby, 2015). With the patient being elderly, the chances that they may have been in a nursing home are
The Infectious Diseases Society of America (IDSA) has recently noted several model antibiotic-resistant bacteria strains with redesigned capabilities in pathogenesis, transmission and resistance. These several strains, Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter species, have been given the acronym-based title of the ESKAPE Pathogens. These strains of bacteria compromise one of the biggest threats faced by physicians today not because of the infectious and devastating illnesses they lead to, but because of their ability to resist antibiotics in the healthcare setting. Failure for industries, academia and government to cooperate and develop research/development operations has left healthcare providers one-step behind in the fight against these new brands of infectious diseases. A lack of research/development operations has left the healthcare industry with antiquated antibiotics no longer capable of targeting and eradicating these microorganisms in human systems.
β-lactam antibiotics (beta-lactam antibiotics) are a class of broad-spectrum antibiotics, consisting of all antibiotic agents that contain a beta-lactam ring in their molecular structures. They kill bacteria by generally inhibiting their cell wall synthesis. They are mainly active against gram positive bacterias but many gram negative bacteria are also susceptible to amoxicillin. Staphylococcus aureus being a gram positive bacteria are highly susceptible to amoxillin.
(Centers for Disease Control and Prevention, 17 April 2015, para. 7). If your doctor has ever given, or will give you antibiotics, the misuse, the wrong dosage, and even the wrongful prescription of antibiotics, such as for a virus, can eventually contribute to making a superbug, again according to the CDC (Centers for Disease Control and Prevention, 1 February 2017, para. 2-5). There are already many instances of superbugs taking people’s lives. For example, just this January 2017, the CDC reported that a Washoe County resident in Reno, Nevada died in late September 2016 because she had an infection from a superbug that could not be cured by every available antibiotic in the United States (Centers for Disease Control and Prevention, 1 August 2017, para. 1-5). Posted on the Infectious Diseases Society of America website in 2007 by her mother was the story of how Rebecca Lohsen, a 17-year-old high school student and swimmer from New Jersey, died from an MRSA infection, an infection resulting from a superbug (Infectious Diseases Society of America, September 2007, para. 1). On that same website, posted by her parents, a 19-year-old college student, Meredith LittleJohn, died to a superbug after spending time in an intensive care unit in a hospital (Infectious Diseases Society of America, n.d., para. 1-3). And the list of those affected goes way on. So as we can see, superbugs are definitely a threatening and real issue that can affect almost anyone.
Coli bacteria, and mix it with the plasmid. We can select the bacteria that are resistant by introducing ampicillin. Bacteria that are not resistant to ampicillin dies. The screening of the bacteria with the resistance occurs when the bla gene turns on to produce beta lactamase which will kill the antibiotic ampicillin. After this, we can get the plasmid into the bacterial cell through the process of horizontal gene transfer through transformation. This can be done by a cold treatment in an ionic solution, then a heat shock where it increases membrane fluidity to take up the plasmid into the bacteria cell. In order to know if the EPAS1-TD gene product was produced by the bacteria, we have to perform a Western Blot. We do this by extracting the protein and run it through gel electrophoresis to separate the proteins by their size. We then label the proteins with the colored probe based on their size. We can detect the EPAS1-TD gene being produced based on the colored
Among the 213 ESBL positive isolates, 66 also tested positive for AmpC β-lactamase. Of those, 16 (24.2%) isolates were proved to be ESBL only by FEP/CLA combined disc test. Thus 16 isolates would have been missed by using only CLSI recommended method (Table
The incidence of neonatal septicemia caused by Gram negative bacilli (GNB) has increased in the past decade and it is often associated with higher mortality rate.(3) The emergence of multi-drug resistant among gram negative bacilli specifically Extended spectrum β-lactamase (ESBL) producing GNB deserves particular concerns, as the treatment options available for multiple drug resistant (MDR) strain is often limited. Inappropriate initial antibiotics predispose these neonates to severe sepsis and poor outcome (4). Sepsis related mortality is largely preventable with prevention of sepsis, timely recognition, and rational antimicrobial therapy (5).
Ceftazidime is a third generation cephalosporin antibiotic used to treat a number of bacterial infections, particularly Pseudomonas and other Gram negatives, and its activity relies on binding of essential penicillin-binding proteins (PBPs) (1). Despite its effectiveness against certain bacteria, there have been reports of rapidly increasing incidences of antibacterial resistance to ceftazidime caused by extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae (2). Recently, a new beta-lactam/beta-lactamase inhibitor combination, ceftazidime-avibactam (AVYCAZ) has shown to have “in vitro activity against Enterobacteriaceae in the presence of some beta-lactamases and extended-spectrum beta-lactamases” and is FDA-approved for treating complicated intra-abdominal infections as well as complicated urinary tract infections (1). Due to the resistance frequency of inpatient Enterobacteriaceae isolates at the University of Washington Medical Center (4), susceptibility testing of Ceftazidime and Ceftazidime-Avibactam are crucial to ensure antibiotic treatment efficacy and to take action to reduce the spread of multi-drug resistant bacteria in a hospital setting.
How do β-lactam antibiotics work to fight against gram-positive bacteria? Transpeptidases are known for being sensitive to penicillin because their activity is inhibited by beta-lactam antibiotics. Transpeptidase is an enzyme that catalyzes the transpeptidation reaction (“Transpeptidase”). Transpeptidation, the chemical reaction conversion amino acid residue or a peptide residue is transferred from one amino compound to another (“Transpeptidation”). Once penicillin binds the PBP it is resilient to many forms of detachment, but can be removed by destroying the PBP through high
The excessive and frequent use of antibiotics in medical treatment largely contributed to the development of antibiotic resistance (Sengupta, 2013). But, bacteria that have never been exposed to antibiotics also exhibit antibiotic resistance showing that it is an ancient and natural phenomenon (Bhullar et al, 2012). Antibiotic resistance can result due to intrinsic qualities of the bacteria or it can be acquired through genetic methods such as mutations or horizontal gene transfer through plasmids. Antibiotics kill susceptible bacteria but are ineffective against resistant bacteria, this creates selective pressure, which allows the resistant bacteria to grow and multiply. This leads to the development of highly resistant pathogenic