Treatment Of Infectious Diseases And Drug Development Against Antibiotic Resistant Pseudomonas

Unlike many environmental bacteria, Pseudomonas aeruginosa has a remarkable capacity to cause disease in susceptible hosts. It has the ability to adapt to and thrive in many ecological niches, from water and soil to plant and animal tissues. The bacterium is capable of utilizing a wide range of organic compounds as food sources, thus giving it an exceptional ability to

“Bacterial illness is a result of complex interactions between bacteria and the host. During evolution, humans developed many ways to protect themselves against bacterial pathogens. On the other hand, bacteria have developed strategies to evade, subvert or circumvent these defenses” (Sousa, 2003) “One of the most important characteristics of bacterial pathogenicity is the various strategies developed by prokaryotic organisms to use host molecules for their own benefit” (Sousa, 2003). “To accomplish this, bacteria have evolved elaborate control mechanisms to turn genes on and off, varying the transcriptional activator or

“The Last Resort,” by Maryn McKenna is an article about antibiotic resistance. It explains the increase of carbapenem-resistant Enterobacteriaceae also known as CREs which are a class of antibiotic-resistant bacteria. CREs have been described as “a risk as serious as terrorism”(McKenna, 2013, p.394). CREs can cause bladder, lung, and blood infections that can develop into life-threatening septic shock. Unfortunately, it kills half of the people who contract it. This bacteria is resistant even to carbapenems, which are considered drugs of last resort because of the serious health risks in taking them. “Antibiotics have been falling to resistance for almost as long as people have been using them; Alexander Fleming, who discovered penicillin, warned about the possibility when he accepted his Nobel prize in 1945”(McKenna, 2013, p.394). Although CREs was first discovered almost 15 years ago, it did not become a public-health priority until just recently. The North Carolinan strain of Klebsiella produced an enzyme called Klebsiella pneumoniae carbapenemase or KPC for short. It broke down carbapenems which made the strongest antibiotic now resistant. “Physicians find themselves caught between using bad drugs or using no drugs at all”(McKenna, 2013,

Pseudomonas aeruginosa is a key opportunistic pathogen characterized by high-level antibiotic resistance and biofilm formation (1).Biofilm is a structured community of bacterial cells enclosed in a self-produced polymeric matrix adherent to an inert or living surface. Biofilmproducing organisms are more antimicrobial resistant than organisms without biofilm. In some extreme cases, the concentrations of antimicrobials required to kill biofilm positive organisms can be three- to four-fold higher than for biofilm negative bacteria, depending on the species and drug combination (2). Biofilms have great importance for public health as they are the main cause of nosocomial infections, especially implant-based and chronic infections (3). Antibiotic resistance in biofilms is due to a combination of many factors that act together to result in a level of resistance that is much higher than that of planktonic bacteria (4,5).

The number of bacteria (CFU/ml) in each serum and saline sample will be Serratia in serum, Pseudomonas in serum, Serratia in saline, and Pseudomonas in saline. We will count if it is 30-300 colonies which it shows me that there is 92, 65, 293, and 150. In Serratia in serum, it is 9.2 x 10^2 CFU/ml. In Pseudomonas in serum, it is 6.5 x 10^7 CFC/ml. In Serratia in saline, it is 2.93 x 10^8 CFU/ml. In Pseudomonas in saline, it is 1.50 x 10^8 CFU/ml.

Pseudomonas Aeruginosa is a bacteria often found in the environment. It is the most common nosocomial infection affecting people with weak immune systems. Pseudomonas infections are usually spread by medical equipment which are not properly cleaned and by the hands of the medical workers. It can be prevented by washing your hands correctly and by conducting environment screening. They are typically treated with antibiotics. However, they are becoming multi-drug resistant.

The identification of the unknown began with a gram-negative result during the gram stain testing; gram-negative results are pink in color, because the structure of the cell does not hold Gram’s crystal violet stain as well as gram-positive bacteria does. Gram-positive bacteria are purple in color, compared to the pink in the gram-negative cells because of the safranin. The unknown, Pseudomonas aeruginosa, was a gram-negative aerobe, which was the first piece of evidence used to narrow down to the identification of the unknown. The morphology of the unknown was short rods organized in pairs, and they were about 1 micrometer wide and 3 micrometers long. It also showed true motility, which

Pseudomonas aeruginosa is a motile, rod-shaped, gram-negative organism. It is an opportunistic, nosocomial pathogen. P. aeruginosa is reported to affect around 3700 to 4000 people per year. Although P. aeruginosa is ubiquitous in the environment in things such as soil, water, and plants, it is also commonly acquired in hospitals; especially in intensive care units. It rarely occurs in a healthy person. The infection occurs in people who are already hospitalized or have a weak immune system. An example includes, how a patient who is receiving chemotherapy for cancer, has an increased risk of contracting the infection. It can be contracted through simply breathing it in through breathing machines. If it affects the lungs, it will cause pneumonia. Pneumonia is associated with difficulty of breathing.

Pseudomonas aeruginosa (P. aeruginosa) is an important Gram-negative opportunistic pathogen that has the capability to create variable clinical infections including, but not limited to, wound infections, urinary tract infections (UTIs) and blood stream infections (BSI), particularly in hospitalized and immunocompromised patients (1, 2). P. aeruginosa was the second most common cause of hospital-acquired pneumonia, third and fifth common cause of hospital-acquired UTIs in USA and Europe, respectively (2- 4). It has been demonstrated that P. aeruginosa due to low permeability of outer membrane in combination with efflux pump overexpression is intrinsically resistant to a variety of antibiotics (5). Expression of Different classes of extended-spectrum

Virulence-associated proteins (Vaps) are a particular class of type-II TA systems characterized by a bi-cistronic locus encoding a proteolytically labile antitoxin (VapB), typically followed by a stable toxin (VapC). These proteins were first identified in connection with virulence plasmids in human pathogens, such as Salmonella Dublin (7), but have since been recognized as one of the most predominant forms of type-II toxins, particularly among the archaea (8). A central component of VapC toxin activity is a PIN-domain, occurring within the approximately 100-amino acid sequence, that displays divalent cation-dependent ribonucleolytic

Study of inhibiting the type III secretion system (T3SS) is important because T3SS helps gram-negative bacteria sense other eukaryotic organism and secrets proteins that help the bacteria infect other organisms. T3SS activity is often seen as a requirement for many pathogenic bacteria to infect their hosts cells – such bacteria include E. coli, Salmonella, Yersinia, and Chlamydia. Much like in the first paper, the researchers’s analysis of the biosynthetic pathway helped them identify the gene cluster that led to the production of the T3SS, giving more insight into how the mechanism worked and how to suppress

John Wesley is a 56 year old man who apart from taking warfarin for his chronic atrial fibrillation is not on any other medication. His International Normalised Ratio (INR) is monitored regularly so that it is around 2.5 (range 2.06-2.8). John goes to his GP with a lower urinary tract infection and is prescribed a 7 day course of cefixime, a 3rd generation cephalosporin. His GP tells John that he will need to come in the following week for a blood test for his INR.

The clinical question that guides the search for a quantitative article is: In hospitalized adults, does implementation of prevention control measures decrease antibiotic resistance?

In this study, they focused on finding a mechanistic way that S. aureus forms these ex-tremely large biofilms in synovial fluid by testing altered expressions of specific bacterial factors. They also tested the Agr gene and PSM’s roles in formation of biofilms. Quorum sensing is known to play a major role in the expression of virulence factors. Agr (a quorum sensing system) deletion causes unregulated and non-structured biolfilm production. PSMs are largely in control of Agr in the production of biofilms. The PSM operon promoter is directly bound to the AgrA re-sponse regulator of Agr. In S. aureus there are 4 loci that encode PSMs. The PSM-alpha locus en-codes for PSM-alpha 1 through 4 peptides, while the PSM-beta locus

RNA III is not only mechanism by which Agr controls target genes, recent studies show that AgrA also binds to the promoters controlling the expression of the phenol-soluble modulin alpha(PSMα) and beta (PSMβ) peptides, which also part of the staphylococcal peptide toxins family. It works by binding to the PSMα and PSMβ promoter sequences which upregulates the transcription of the operons. PSM has multiple roles in staphylococcal pathogenesis and contributes to a further extent to the pathogenic success virulent staphylococci, such as S.aureus. PSM, especially PSMα3 is a strongly pro-inflammatory, causes lysis of cells include leukocytes, erythrocytes, creates inflammatory responses and contributes to biofilm development. Due to the responsible for the biofilm formation and structuring, it also appears to play a role in commensal lifestyle of staphylococci where they promote growth and spreading of the bacteria on the epithelial cells. Lastly, the article points out that a potential correlation between quorum-sensing control of PSM genes