R-Type Pyocin Essay

If a pillbug curls into a ball, it can be concluded that it feels threatened.

Antibiotic resistant infections are not only increasing, but intensifying exponentially. Even worse, there are few drugs readily available to diminish the swelling number of contagions; a sparse and meager quantity of combatants to tackle the vehement and aggressive pathogenic bacterium. These microscopic organisms, though infinitesimal, cause gigantic problems and wreak extra havoc when they attack the drugs prescribed to destroy and eradicate them, and survive. In culmination, they are more resilient, more powerful than ever before. Many of these superbugs are stronger and more alive, violently destroying the immune system of the body that has become their habitat, instead of ultimately dying. The tiny,

S. pyogenes infections may vary from mild to life-threatening with a plethora of symptoms due to the many types of infections it causes. This bacterium is responsible for the diseases of pharyngitis, rheumatic fever, impetigo, erysipelas, cellulitis, necrotizing fasciitis, acute poststreptococcal glomerulonephritis, and toxic shock syndrome, just to name a few. Each of these infections has its own unique set of symptoms as will be explored in depth below.

Staphylococcus aureus (S. aureus) is a spherical bacteria which is known to produce a cytotoxin called Panton-Valentine leucocidin (PLV) which destroys leukocytes, and kills tissue (Lina et al., 1999). Five percent of strains of Staphylococcus are known to produce the disease-causing toxin (Lina et al., 1999), but though the amount of PLV-producing strains is somewhat small, the strains which produce PLV are apparently resistant to vancomycin, an antibiotic commonly used to treat staph infections (CDC, 2002). The first recorded case of S. aureus resistance to vancomycin was a reduction in sensitivity to the antibiotic observed in Japan, and has since spread to the United States (CDC, 2002). The most common source of infection of these drug-resistant bacteria are actually in hospitals, wherein the patients are exposed to the bacteria and subsequently infected (CDC, 2002).

Three of the four quadrants were labeled S, P, T, for streptomycin, penicillin, and tetracycline. One quadrant was left blank for the control (Figure 1.1) Having a control of no antibiotic was used to show the growth of the bacteria when it is uninhibited by antibiotics. Then, Escherichia coli K12 from VWR (catalog #470179-082) and Staphylococcus aureus from VWR (catalog #470179-208) were evenly swabbed across the surface of the agar plate with a cotton swab; ten plates, contained E. coli and the other ten plates contained S. aureus. Then, Streptomycin (10 μg/mL), Penicillin (10 U = ~10 μg/mL), and Tetracycline (30 μg/mL) were obtained and placed into the middle of their respective quadrants. After this, the agar plates were stacked into two stacks of five, for each bacteria, were wrapped with parafilm, and were incubated at 37°C for 48 hours (Figure 1.2). After 48 hours, the plates were moved to a refrigerator at 4°C, until they were taken out of the fridge approximately a week after the stacks of agar plates had initially been placed in the incubator. The diameters of the zones of inhibition were then measured with a ruler and recorded to the nearest millimeter. After measuring the zones of inhibition, a gram-staining technique was used to illustrate the difference in cell wall structure between S. aureus and E. coli. First, a small sample of each species of bacteria was transferred with a loop from the agar plate onto two different areas on a microscope slide that had previously been washed, wiped with alcohol, and dried. Then a drop of water was added to each bacterial sample, was smeared into a thin layer, then allowed to air dry. Once the bacterial samples were dry, the slide was held at one end and was passed through a Bunsen burner flame with the smeared-bacteria samples facing up.

The effectiveness of disease treatment is often presented by the challenge of antimicrobial resistance. Cystic Fibrosis (CF) for example, is a pulmonary infection characterized by the poly-microbial growth of bacteria within biofilms, in the pulmonary tract of humans. For children suffering from CF, Staphylococcus aureus (S. aureus) initially colonizes their airways, which with age, becomes replaced by Pseudomonas Aeruginosa (P. aeruginosa). The eradication of P. aeruginosa by antibiotics fails in 10-40% of CF patients. In the article, it was proven that there existed an interaction between the staphylococcal protein A (SpA) from S. aureus filtrates (SaF, a bacterial supernatant of S. aureus), and an exopolysaccharide (Psl) of P. aeruginosa. This interaction lead to the aggregation and increased resistance to tobramycin¬ – an antibiotic used to eradicate P. aeruginosa, to prevent chronic colonization of the bacteria. The study conducted involved 7 samples of P. aeruginosa that were taken from individuals who underwent successful eradication treatment, and 7 samples from individuals who still had persistent isolates. These P. aeruginosa samples were cultured for 24 hours in media. When SaF was added to the overnight preformed biofilms, the eradicated isolates were not affected by the SaF; however, the persistent isolates showed significant reduction is surface coverage due to densely packed cellular aggregation, without affecting the biomass or viability of persistent isolates. The

P. aeruginosa is a ubiquitous Gram-negative bacterium that thrives in moist environmental reservoirs such as in the soil, water and plants8, 9. P. aeruginosa is an opportunistic human pathogen that infects immunocompromised individuals, lending to its association with life-threatening illnesses10. In addition to pulmonary infections in CF patients, P. aeruginosa is frequently found in nosocomial infections11. As such, P. aeruginosa is recognized for its medical importance in clinical infections.

Potential synergistic interactions between antimicrobials have been investigated for years. Severe multidrug-resistant P. aeruginosa (MDR-Pa) infection, particularly in debilitated hosts, requires aggressive treatment, usually involving at least two antimicrobial agents. Combinations of agents that exhibit synergy or partial synergy actively could potentially

Escherichia Coli is a bacterium that inhabits the gastrointestinal tract of both humans and animals. E. coli isn’t always a harmful bacterium. Some are actually crucial to a healthy intestinal tract because this bacterium assists with the production of Vitamin K2 and stops pathogenic bacteria from interacting and establishing inside the intestines (Gould, 2010). A person maybe exposed to E. coli through water or food that maybe contaminated or from raw meat such as ground beef or raw vegetables. Lack of good hygiene is another way that E. coli infections can spread especially in places such as hospitals or day care centers. While a healthy adult with an E.coli infection will most likely recover within five to seven days, those who are at risk include young children, elderly and those with a weak immune system.

Antibiotics are inarguably one of the greatest advances in medical science of the past century. Although the first natural antibiotic Penicillin was not discovered until 1928 by Scottish biologist Alexander Flemming, evidence exists that certain plant and mold growths were used to treat infections in ancient Egypt, ancient India, and classical Greece (Forrest, 1982). In our modern world with the advent of synthetic chemistry synthetic antibiotics like Erithromycin and its derivative Azithromycin have been developed. Antibiotics have many uses including the treatment of bacterial and protozoan infection, in surgical operations and prophylactically to prevent the development of an infection. Through these applications, antibiotics have saved countless lives across the world and radically altered the field of medicine. Though a wonderful and potentially lifesaving tool, antibiotic use is not without its disadvantages. Mankind has perhaps been too lax in regulation and too liberal in application of antibiotics and growing antibiotic resistance is the price we must now pay. A recent study showed that perhaps 70% of bacterial infections acquired during hospital visits in the United States are resistant to at least one class of antibiotic (Leeb, 2004). Bacteria are not helpless and their genetic capabilities have allowed them to take advantage of society’s overuse of antibiotics, allowing them to develop

Antibiotics, composed of microorganisms such as streptomycin and penicillin, kill other infectious microorganisms in the human body. At one point, antibiotics were considered to have “basically wiped out infection in the United States”, but due to their overuse and evolutionary

While Shapiro et al. was not able to recommend antimicrobial prophylaxis with amoxicillin Nadelman et al. devised

Although a vaccine does exist, its cost and multiple doses needed to achieve immunity have limited its acceptability by the medical community [20, 21]. Antimicrobial therapy has been at the forefront of research in trying to identify if prophylactic treatment is necessary, what drug is most successful, and what dosing is most appropriate.

In the last fifty years, the most prominent and transformative medical advancement made was the discovery of antibiotics and disinfectants. On the contrary, with the uncovering of antibiotics came the repercussion of the progressively threatening antibiotic-resistant bacteria. Antibiotic-resistant bacteria or ‘superbugs’ formed due to the lack of care from the people to follow through with simple safety procedures in order to entirely get rid of bacterial illnesses and infections. Appropriate precautions are necessary and expectedly need to be taken, in order to minimize and possibly prohibit the formation, continual growth and limit the strength of resistance in the antibiotic-resistant superbugs, and most importantly to preserve medical advancements

Rather than trying to treat P. aeruginosa infections, stopping the infection from occurring in the first place may be a better strategy than treating with antibiotics that may not work. This bacterium can be spread to people by a variety of means by contact with contaminated inanimate or animate objects. In hospitals, P. aeruginosa can colonise equipment’s such as catheters, ventilators if they are not maintained properly or kept clean. Therefore, strict procedures and controls should be in place to make sure these are maintained especially when they are to be used on at risks patients who are more prone to infection. Another source in hospitals are water supply and sinks which provides a moist environment that is ideal for this bacteria to