S. Aubiotics : The Evolution Of Antibiotic Resistance Genes

Infections caused by antibiotic-resistant strains often occur in epidemic waves initiated by one or a few successful clones. Methicillin-resistant S. aureus (MRSA) is prominently featured during these epidemics. Historically associated with hospitals and other healthcare settings, MRSA now has emerged as a widespread cause of community infections. The majority of Staphylococcus aureus strains are now resistant to penicillin and methicillin (MRSA). Golden staph is creating headlines across the world, the superbug is becoming unstoppable. According to government statistics “one in five cases were resistant to antibiotics” (Alexander, 2017). Scientist are trying to eradicate golden staph with antibiotics, however they are adapting rapidly. Scientists are yet to identify how exactly the bacteria keeps adapting. Antibiotics attack infections by meddling with the bacterial ribosome, which is the part of the cell that makes proteins. If a cell cannot make protein, it dies. “The way the antibiotic works is it throws a spanner in the works. The drug comes in and jams up the machine so the cell can't make protein anymore. “Antibiotic-resistant bacteria find a way to apply oil and restart the machined Belousoff's team compared the cell structure of resistant and non-resistant strains of golden staph under an electron microscope to learn that the latter infections had developed a mutation several

The main hospital strains are already partially or fully resistant to the effects of commonly used antibiotics. Resistance is also emerging to last resort drugs like vancomycin. The more virulent community strains of MRSA are infiltrating hospitals while the more resistant hospital strain is leaking into the community. The history of MRSA as described in Superbug shows how quickly bacteria can evolve when we add a strong selective force like antibiotics. Around the world, species of bacteria are becoming “superbugs” that are resistant to conventional treatments. Pharmaceutical companies are cutting research on new antibiotics in favor of more profitable investments. We are quickly running out of options for treating multi-drug resistant bacteria. As we move toward a “post-antibiotic” world, there are valuable lessons to be found in the history of MRSA, one of the first superbugs. Students in Emerging Diseases should read Superbug to learn about the complex emergence of

Before the discovery of penicillin, infection with S. aureus had a fatality rate of approximately 70%. After penicillins discovery and development, treatment of S. aureus infections became routine resulting in the death rate falling to 25%.5 However, penicillin use provided an inadvertent selection pressure which resulted in the bacteria mutating and becoming resistant to its effects. The penicillin-resistant S. aureus strains produced enzymes known as penicillinases which break penicillin down. In 1959, the antibiotic methicillin was developed to battle penicillin-resistant S. aureus infections. At first it was effective, but with increasing use of methicillin S. aureus once again acquired resistance through the process of natural selection

Staphylococcus aureus is a leading cause of human bacterial infections worldwide1, and following the discovery and widespread utilization of antibiotics, S. aureus has evolved to become resistant to a number of antimicrobial treatments. Most notably, Methicillin-resistant Staphylococcus aureus (MRSA) strains have acquired the mecA gene, encoding the penicillin binding protein (PBP2a), which confers resistance to oxacillin and all β-lactam antibiotics 2. These characteristics, combined with other virulence factors, have made MRSA infections difficult to treat, and lead to MRSA being recognized as a significant cause of morbidity and mortality 3. MRSA is also the leading cause of nosocomial infections4–6, contributing significantly to increased healthcare costs 7. CDC estimated in 2008 that MRSA was responsible for 89,785 cases of disease, causing 15,249 deaths in the US8.

Methicillin-resistant Staphylococcus aureus (MRSA) is a major cause of hospital-acquired infections that are becoming increasingly difficult to treat because of emerging resistance to all current antibiotics. Infections are created by pathogens, or microbes that create diseases. There are different types of microbes including: bacteria, viruses, fungi and parasites. Some microbes are beneficial to the human body, however, there are pathogens that are deadly and require antibiotics. Antibiotics are antimicrobials that were developed to destroy microbes. Penicillin, the first commercialized antibiotic, was discovered in 1928 by Alexander Fleming.(Enright, Robinson, Randle, 2002) While it wasn’t distributed among the general public until 1945, it was widely used in World War II for surgical and wound infections among the Allied Forces. Methicillin was introduced in 1959 to treat infections caused by penicillin-resistant Staphylococcus aureus. In 1961, there were reports from the United Kingdom of S. aureus isolates that had acquired resistance to methicillin (methicillin-resistant S. aureus, MRSA).(Enright, Robinson, Randle, 2002)

Methicillin-Resistant Staphylococcus aureus (MRSA), a pathogen that causes many complicated health infections in our body. It’s a type of s. aureus bacteria that can produced by process of resistance to many antibiotics such as dicloxacillin, oxacillin, and methicillin. Why is MRSA so dangerous? Its natural ability is to continue transforming in ways to prevent from antibiotic from being completely successful in the batter against MRSA. The US had spent billions of dollar every year into research in order to prevent it from further spreading. In order to do so, we must step up to advance our technology and knowledge to be able to defeat the bacterial warfare. This research will discuss the prevalence and different factors of the disease, it

According to the Centers for Disease Control and Prevention (as cited in Upshaw-Owens & Bailey, 2012) MRSA-related infections have risen from 2% of S.aureus infections in 1974 to 64% in 2004. In the United States 46% of S.aureus cases are Methicillin resistant. The rise in infection rates is alarming and

In 1961, soon after the introduction of methicillin, the first β-lactamase-resistant penicillin, strains of Staphylococcus aureus that were resistant to methicillin were identified in the United Kingdom. From the 1960s into the early 1970s, MRSA infections in Europe were limited largely to hospital outbreaks caused predominantly by S. aureus phage type 83A (subsequently identified to be sequence type 250; this so-called “archaic clone” gradually became infrequent and was replaced in the 1970s and 1980s by five prevalent clonal lineages, although many MRSA backgrounds existed between the 1960s and 2000. The terms Community-Acquired Methicillin Resistant Staphylococcus aureus (CA-MRSA) and hospital acquired Methicillin Resistant Staphylococcus aureus (HA-MRSA) have been used to call attention both to the genotypic differences of certain MRSA isolates as well as to the epidemiological and clinical features of the

Methicillin-resistant Staphylococcus aureus (MRSA) bacteria are resistant to all beta-lactam antibiotics such as methicillin, penicillin, oxacillin, and amoxicillin. Sometimes called a “super-bug” because of its ability to resist so many of our antibiotics. MRSA can be fatal and according to the CDC, of the over 80,000 invasive MRSA infections every year, 11,285 related deaths occur. Methicillin-resistant Staphylococcus aureus (MRSA) has become the bacteria of this decade.

Staphylococcus aureus is a bacterium that infects of the skin of an animal that creates horrific pain to the host. The name is broken down into three parts in Latin. “Staphyle” meaning “a bunch of grapes”, coccus which means “spherical bacterium” and aureus which best means “golden or gold-colored.” This name came about in Latin because when looked at under a microscope, the bacteria are all clumped together like grapes on a vine and the color is gold. (Harper n.d.) This bacterium is Gram-positive meaning that within the walls of the cell, peptidoglycan exceptionally thick. (Bruckner 2012) (PHAC 2012) A different strain of this bacterium called MRSA (Methicillin-Resistant Staphylococcus aureus) is a bigger problem because it is unaffected by a type of penicillin, Methicillin. The first known sighting this particular resistant strain was first documented in 1961 by British scientists in England. (NiAID NIH 2008) Penicillin is used to create antibiotics because it in a way interferes with the cell wall of the strain and weakens it causing it to loose structure and die. By a strain becoming resistant, it learns the make-up of the antibiotic to change itself for the best chance of survival. (Tufts EDU 2014)

Staphylococcus aureus is a gram-positive coccal bacterium that is a member of the Firmicutes, and is frequently found in the nose, respiratory tract, and on the skin. It is often positive for catalase and nitrate reduction. Although S. aureus is not always pathogenic, it is a common cause of skin infections such as abscesses, respiratory infections such as sinusitis, and food poisoning. Pathogenic strains often promote infections by producing potent protein toxins, and expressing cell-surface proteins that bind and inactivate antibodies. The emergence of antibiotic-resistant strains of S. aureus such as Methicillin-resistant S. aureus (MRSA) is a worldwide problem in clinical medicine.

Staphylococcus aureus is a pathogen of more importance due to rise in resistance to antibiotic (Lowy, 1998).It is different from the CoNS (e.g. S. epidermidis), and more venomous despite their phylogenic similarity (Waldvogel, 1990; Projan and Novick, 1997). CoNS when grown on solid media form translucent white color colonies (Howard and Kloos, 1987). Genome databases to date the staphylococcus aureus have been completed for 7 strains, MRSA, 8325, MSSA COL, MW2, N315, and Mu50. S. aureus genome average size is 2.8Mb (Kuroda et al., 2001). S. aureus cell wall is 20-40 nm thick a hard protective coat, which is generally unstructured in appearance (Shockman and Barrett, 1983). Under the cell wall is the cytoplasm that is enclosed by the cytoplasmic

Staphylococcus aureus is bacteria species characterized by its golden color and round shape (Lowy, 1998). The bacteria can cause small skin infections or severe infections in vital organs. Infections are most common in the hospital setting. S. aureus has developed resistance to antibiotics in the form of methicillin-resistant S. aureus (MRSA), which displays strong virulent factors and exemplifies the need for novel medications to treat bacterial infections. Current research has examined several options for potential drug treatments as well as vaccine development. Advances in genetic sequencing techniques may help to characterize S. aureus strains to better understand outbreaks and transmission of the bacteria. The impact of S. aureus on human health inspires future research on treatments, especially for antibiotic resistance strains.

First of all, what causes S. aureus to survive is the genetic discovery that was made. An experiment was done with several different strains of S. aureus to see similarities and differences. Genetic variation among strains that had the most abundant disease causing clonal lineages of S. aureus, with 332 ORFs absent in one strain compared to a reference strain COL was identified. Also 2,198 (78%) of the 2,817 ORFs represented on the DNA microarray were present in all S. aureus strains tested. The results suggested that these genes were essential for S. aureus cell maintenance. Some of these 2,198 genes encoded known virulence factors. This gave reason to suggest these genes were a critical role for these proteins in staphylococcal survival and pathogenesis. (Fitz 2001)

A., Conly, J. M., Lau, V., Elsayed, S., Louie, T., Hutchins, W., Zhang, Z. (2006). Novel Multiplex PCR Assay for Detection of the Staphylococcal Virulence Marker Panton-Valentine Leukocidin Genes and Simultaneous Discrimination of Methicillin-Susceptible from -Resistant Staphylococci. Journal of Clinical Microbiology. 44:1141-1144