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Showing posts with label antibiotic resistance. Show all posts
Showing posts with label antibiotic resistance. Show all posts

Thursday, April 4, 2013

Bacterial Infection? ...Have a dose of virus.

            When you go to a hospital, you typically expect it to make you better, not get you sicker. Unfortunately, hospitals are filled with bacteria, many of which ‘prey’ on patients with weakened immune systems and preexisting health issues. One such bacterium is klebsiella, a genus of Enterobacteriaceae. This bacteria is estimated to cause nearly 8% of all nosocomial (hospital-acquired) infections each year (Podschun, 1998). Klebsiella pneumoniae is normally found growing in places such as the mouth and on skin, but it can create health issues if it enters the lungs, causing inflammation, hemorrhaging, and necrosis of lung tissue. It is especially dangerous if bacteria have developed antibiotic resistance, as an increasing number of hospital-acquired infections have done.
            This resistance is coded for in plasmids (small, circular, transferrable bits of DNA) that the bacteria pick up. A common protein that causes antibiotic resistance is beta-lactamase. This enzyme, breaks open the beta-lactam ring in antibiotic molecules containing this structure, thereby deactivating them. Penicillin is one such beta-lactam-based antibiotic. It is widely used to treat bacterial infections, and resistant bacterial strains are a large reason for concern. While there are other antibiotics that can be used, some of these bacteria have extended-spectrum beta-lactamase genes, which makes them even more efficient at denaturing a wider range of beta-lactam antibiotics. In poorer areas, where less common antibiotics are harder to come by, this is even more of an issue. In 2003, over half of the antibiotics in use were beta-lactam compounds (Elander, 2003).
            These infections add time to hospital stays. Not only is this an inconvenience, but it is also an economic drain on the hospitalized individual. These types of infection are also prominent in intensive care units, where patients are already suffering from depressed immune systems, and an added infection without the help of antibiotics can kill a patient.
            For this reason, the search for alternate antimicrobials is a high priority. Bacteriophages (viruses that only infect bacteria) hold great promise in this area, but to be effective, they must be able to infect a wide host of bacteria. There are four types of host resistance mechanisms to bacteriophage infection: adsorption inhibition, blocking of DNA injection, restriction-modification, and abortive infection (Weinbauer, 2004). The host restriction system is one of the best-studied parts of this system. In “Characterizing the biology of novel lytic bacteriophages infecting multidrug resistant Klebsiella pneumoniae,” Kesik-Szeloch et al. culture and screen a number of bacteriophages for the pathogenicity in Klebsiella, and their abilities to resist host restriction-modification mechanisms.

Tuesday, November 15, 2011

Solving the Puzzle of the Super Bug


Solving the Puzzle of the Super Bug


"We have applied the latest genome sequencing technology to show that Staph can readily become vancomycin (antibiotic) resistant by acquiring a single mutation in its DNA. When the bacteria mutate, they are reprogramming themselves, changing their cell walls to resist the action of our antibiotics"-Dr. Stinear.
 
                The treatment of mild to serious infections from Staphylococcus aureus (Golden Staph) is severely hindered by the development of antibiotic resistance. This antimicrobial resistance is a major public health threat which is further worsened by the development of strains of Staph bacteria with resistance to strong antibiotics such as vancomycin and daptomycin, which are considered last line antimicrobials. Patients in hospitals are more susceptible to staph infections because their immune systems are already compromised.  In hospitals around the world, infections with methicillin-resistant Staph aureus (MRSA) continue to cause a significant number of unnecessary deaths.  Therefore developing treatments to fight staph resistant strains as well as reduce the number of cases in hospitals is a major topic of study.  Recently research has added a new piece to the puzzle of elucidating the mechanism by which Staph evades the immune response to develop resistance to these last-line antibiotics.  
Frighteningly so, a small number of clones of staph account for the large number of hospital acquired infections.  In Australia, multi-locus sequence type (MLST) 239 termed ST239 comprises the major clone MRSA and has been infecting patients for over 30 years.  Unfortunately this clone is resistant to almost all antibiotic types therefore the current treatment for such an infection is the strong antibiotic vancomycin. Generally speaking, vancomycin is only prescribed after treatment with other antibiotics has failed; therefore it is administered as a last resort. However, recently strains have evolved to develop a low resistance to this antibiotic as well.  These strains partially resistant to vancomycin are named vancomycin-intermediate S. aureus (VISA).  The genetics of these strains that enable them to resist vancomycin antibiotics are the topic of a recently published study in the journal PLoS Pathogens titled Evolution of Multidrug Resistance during Staphylococcus aureus Infection Involves Mutation of the Essential Two Component Regulator WalkR.