This article was written by Safoura Derakhshan PhD, Shahin Najar Peerayeh PhD, and Bita Bakhshi PhD. These men currently work at Tarbiat Modares University and specialize in bacteriology. This article focused on the resistance patterns of Klebsiella Pneumoniae-- the relationship between virulence genes and antibiotic resistance. K. Pneumoniae is a gram negative opportunistic pathogen encapsulated in a polysaccharide capsule. K. Pneumoniae is frequently responsible for nosocomial infections. Typically K. Pneumoniae affects the respiratory tract but can also be found in urinary tract infections, wounds or in the blood stream. In recent years, multidrug resistant strains have been isolated from nosocomial infections. Bacteria have many ways to gain resistance. Plasmids are circular DNA strands separate from the host DNA. They are able to replicate independently of the host and are an important factor in horizontal gene transfer. Plasmids often encode resistance genes or other virulence factors. Transposable elements are another way bacteria can acquire resistance. Transposable elements are DNA sequences that have the ability to insert themselves into host DNA or plasmids. The transposing of a plasmid gene to the host can result in permanent genetic resistance. Integrons are mobile genetic structures with DNA genes that encode for an integrase site and attachment site. Integrons are able to acquire and incorporate gene cassettes which often contain resistance
The development of antibiotics was an important advancement in 20th century medicine. Previously deadly infectious diseases are now routinely treated with antibiotics. Moreover, for modern-day medical procedures such as chemotherapy treatment to be successful, antibiotic use is necessary. For these reasons, the prospect of bacteria developing widespread resistance to antibiotics is a major concern as it would render many modern-day medical therapies unviable.
In June of 2011, a woman entered the National Institutes of Health Research Hospital in Bethesda Maryland with a serious, but fairly routine infection; however the subsequent events were to prove anything but routine. The woman was suffering from an infection caused by an antibiotic-resistant organism, but it was a new strain, never before encountered. About a month after she was treated and discharged, another patient came down with the same infection, and then more and more. After many unsuccessful attempts to isolate the cause of the infections, the NIH eventually used a new technology, known as "Whole Genome Sequencing," to isolate the pattern of infection and bring it under control. (Melissa Block, Eddie Cornish) This process is a new way to quickly isolate and sequence the entire genome of a particular organism, which the NIH used to help identify the pattern of infection. Of the 17 other patients who contracted the infection, six died, but it was learned that the pathogen can be transmitted in ways never before seen. (Melissa Block, Eddie Cornish)
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
Klebsiella pneumoniae (contributing the ‘K’ in the ESKAPE acronym) is a strain of bacteria that has recently developed resistance against a class of β-Lactam antibiotics developed from thienamycin (a naturally derived product, discovered in 1976, of Streptomyces cattleya) known as carbapenems. K. pneumoniae is a Gram-negative bacterium compromised of straight rods 1-2 μm in length and contains lipolysaccarides (LPS) in its outer
Klebsiella pneumoniae is a gram-negative bacilli bacterium 0.3-1.0um in diameter and 0.6-6.0 um in length. Cells are capsulated and arranged in pairs or in short chains. K. pneumoniae can cause different types of healthcare associated infections that include pneumonia, blood, and wound infections along with meningitis. K. pneumoniae is normally found in the intestines of human stool. Infections are most common with people who require ventilators, intravenous catheters or patients taking long courses of antibiotics. The primary portal of entry is through the respiratory tract to cause pneumonia or through the blood to cause bacteremia. People with healthy immune systems usually do not get k. pneumoniae infections but should
Antimicrobial resistance is a growing problem in modern healthcare around the world. Multidrug resistant (MDR) strains of pathogenic bacteria, which are quickly becoming more common, pose a serious risk to patients. One of the most common species of bacteria that cause problems in healthcare today is Klebsiella pneumoniae. Today K. pneumoniae can be responsible for community acquired infections, but is most commonly observed as a major cause of hospital acquired infections which can be fatal. K. pneumoniae has been observed to develop resistance to antibiotics more easily than most bacteria through the production of new enzymes to break them down. As new resistance mechanisms develop, fewer and fewer treatments are available for infections by K. pneumoniae. Although some treatments still remain, few new ones are being explored, thus the best option is to control the development and spread of antimicrobial resistance.
The small, circular DNA molecules that exist apart from the chromosomes in most bacterial species are called plasmids. Plasmids are not needed for the survival of the host bacterial, but some plasmids can carry genes that makes bacteria ampicillin resistant like pUC18 or
Klebsiella pneumoniae, is a gram negative bacillus bacteria, that is nonmobile, encapsulated, bacteria that is hard to treat because of the Multi drug Klebsiella pneumoniae strand that is already grown past antibiotic control (Evaluation 1). To obtain a good view of this bacteria you would do a gram stain to determine if positive or negative,
One of the four ways that bacteria can increase their genetic diversity is by conjugation. This is a process by which a bacterium can transfer genetic material to another bacterium of different mating type, through direct contact. During conjugation one bacterium is going to be the receptor of the genetic material while the other is going to be the donor. The donor bacterium is going to grow a tube-like structure called a pilus, which is going to be used to contact the other bacterium and to transfer the genetic material. Usually these genetic material is going to have the form of plasmid, which are small circular pieces of non-chromosomal DNA. Another method that bacteria have developed in order to acquire different DNA is transformation. These is a process by which some bacteria can get pieces of DNA from the external environment, under certain circumstances. Transformation occur naturally in Bacillus, and some Streptococcus and Staphylococcus species. The third means by which bacteria obtain new DNA is by the acquisition of plasmids. These plasmids can travel between bacteria of the same or different species, and the act like parasitic pieces of DNA that infect bacteria. Usually these plasmids are not required for the normal function of bacteria and is often expel by them, unless it contains material beneficial
In this last situation, resistant genes become embedded in small units of DNA, called transpons, which can easily move into other DNA molecules. Making matters worse, many bacteria have specialized transpons called integrons, which act like flypaper when catching new genes (3).
My best bacterial friend has genes that has antibiotic resistance that I must have. There are many different ways for me to get ahold of them or transferred into my genes. One way to receive the gene is by the use of a plasmid. A plasmid is circular piece of replicating dna that is separate from chromosomal dna. In order to manipulate the plasmids, i will need to mutate them by using restriction enzymes, PCR, and ligation. Being able to use restriction enzymes to cut portions of genomes and have them inserted into a plasmid, make it easy for mutations (mutagenesis) to occur. Also, PCR can enable mutagenesis. Each plasmid is mapped out with information that includes the restriction enzyme sites and the origins of their replications. I could
I selected a presentation on Antimicrobial Resistance given by Dame Sally Davies, England’s Chief Medical Officer, for the Royal Institution of Great Britain. This review will focus on the first five minutes of the lecture (https://www.youtube.com/watch?v=2H_Ox1vVnTc, 0:10-5:35).
Mobile genetic elements have the ability to encode bacterial pathogenicity, metabolic functions, and resistance factors. Genes that encode other toxins known as phage encoded, and plasmid encoded Gram negative, and Gram positive organisms have the ability to spread among a population. Gene transfer by plasmid and phage encoded microorganisms may play a role in the creation of new pathogenic variants. Other virulence factors can be found on the chromosome, and can function as virulence blocks. Specific areas on these genes are known as pathogenicity islands.These islands show us that genetic elements that effect bacterial virulence and the genetic flexibility of certain bacterium. They may be involved in the process of microbial evolution.
Elements belonging to KPC transposon Tn4401, including tnpA, tnpR, ISKpn6, and ISKpn7 (14), were identified by PCR and sequencing on both KPC-3–encoding plasmids originating from Kpn1 and Eco2. These genetic determinants were absent in the susceptible Eco1. These data suggest that Eco1 has acquired pKpQIL from Kpn1 in the patient’s gut, leading to the formation of Eco2. Although acquisition of the plasmid increased MICs for imipenem, meropenem, and ertapenem considerably, it did not confer full resistance (Appendix Table) presumably due to copy number of the plasmid or the expression level of blaKPC-3 in E. coli. Curing of pKpQIL from Eco2 was performed by sequential transfers at an elevated temperature (42°C). The cured strain, which lacked the KPC-encoding plasmid, showed full susceptibility to all antimicrobial drugs tested, similar to the Eco1 strain isolated from the patient’s gut flora.
The discovery of transformation by Frederick Griffith in Streptococcus pneumonia has played an important role in how we are now able to introduce plasmid DNA molecules into cells. Transformation is the uptake of DNA molecules released from the donor cell by the recipient cell. It is one of the three ways bacteria are able to exchange genetic material. In Griffith’s experiment he introduced mice to two different forms of S. pneumonia, one smooth, pathogenic and encapsulated and the other rough, nonpathogenic and noncapsulated (Snustad, 193). The mice were injected with live rough strain and heat killed smooth strain. The deaths of the mice lead Griffith to conclude that some genes of the killed smooth strain were transformed to the rough strain and the bacteria became encapsulated and pathogenic, therefore leading to the death of the mice (Snustad, 193).