New treatment for tuberculosis

In search of new strategies against life-threatening tuberculosis infections, a team from the Technical University of Munich (TUM), as well as Harvard University and Texas A&M University in the USA have found a new ally. They discovered a substance that interferes with the mycomembrane formation of the bacterium. It is effective even in low concentrations and when combined with known antibiotics their effectiveness is improved by up to 100-fold.

Among the greatest challenges when treating life-threatening tuberculosis infections is the increasing resistance to antibiotics. But the pathogen itself also makes the life of doctors difficult: its dense mycomembrane hampers the effect of many medications. The mycomembrane of the tuberculosis pathogen Mycobacterium tuberculosis consists of a lipid double layer that encapsulates the cell wall, forming an exterior barrier.

 Structural hallmarks are mycolic acids, branched beta-hydroxy fatty acids with two long hydrocarbon chains. The team hypothesizes that similarly structured beta lactones could "mask" themselves as mycolic acid to enter the mycolic acid metabolic pathways and then block the decisive enzymes. In the context of an extensive search, the interdisciplinary team of scientists hit the bullseye with the beta lactone EZ120. It does indeed inhibit the biosynthesis of the mycomembrane and kills mycobacteria effectively.

Using enzyme assays and mass spectroscopy investigations, Dr. Johannes Lehmann, a researcher at the Chair of Organic Chemistry II at TU Munich, demonstrated during his doctoral work that the new inhibitor blocks especially the enzymes Pks13 and Ag85, which play a key role in the development of mycomembranes. EZ120 is effective even in low doses, easily passes the mycomembrane and exhibits only low toxicity to human cells.

The combined application of this substance with known antibiotics showed a synergistic effect leading to significantly increased effectiveness."Vancomycin, a common antibiotic, and EZ120 work together very well. When used together, the dose can be reduced over 100-fold. Disrupting the mycomembrane enables antibiotics to enter the bacteria more easily. This is a new mode of action and might be a starting point for novel tuberculosis therapies.
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Managing antibiotics can not reverse the resistance

Researchers have discovered that reducing the use of antibiotics will not be enough to reverse the growing prevalence of antibiotic resistance for some types of bacteria. Besides passing along the genes bestowing antibiotic resistance to their offspring, many bacteria can also swap genes among themselves through a process called conjugation.

The bacteria tested by researchers have fast conjugation rate, even if you don't use antibiotics the resistance can be maintained. Most resistance to antibiotics arises and spreads through natural selection. Some bacteria have genes that help them survive around of antibiotics, they quickly parent the next generation and pass on those genes.

Many of these genes, however, come at a cost. For example, a mutation may allow a bacterium to build a thicker membrane to survive a particular antibiotic, but that mutation might also make it more difficult for the cell to reproduce. Without the selective pressure of antibiotics killing off the competition, bacteria with this mutation should disappear over time.

The results indicate that for bacteria that swap resistance genes simply managing the amount of antibiotics being used will not turn the tide on the growing problem of resistance. To make any headway, drugs will also be needed that stop the sharing of genes and decrease the rate at which they are passed on through reproduction. One of the drugs is a benign natural product and FDA-approved antipsychotic.
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Bacterium delays wound healing

Pseudomonas aeruginosa and its variants are associated with delays in wound healing. The bacterium is present on the skin that causes poor wound healing in certain conditions.
Damage to a receptor that allows the body to recognise the bacteria is associated with a change in the balance of the community of bacteria present normally on the skin.

The shift in balance has an enormous impact on the ability of the wound to heal. The bacterium has previously been associated with wound infections, and such infection is a major complication of skin wounds that fail to heal. The research was carried out using mice that were previously shown to heal poorly. The mice lack the receptor Nod2 that recognises bacterial components and has been shown to regulate the host response to bacteria.

Researchers discovered that mice lacking Nod2 had more Pseudomonas aeruginosa than normal mice, which is associated with delayed wound healing. The bacteria also caused normal mice to heal poorly. The team says the findings are also applicable to humans as Pseudomonas aeruginosa is associated with infected wounds that heal poorly in people.

There is an urgent need to understand the bacterial communities in our skin and why so many of us will develop wounds that do not heal. Wounds can be caused by a multitude of factors from trauma to bed sores, but infection is a complication that can lead to life-threatening illness. Many people are struggling with wounds that heal poorly, but this new study suggests that the types of bacteria present may be responsible for failure to heal, which is important for treatment management.
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Antibiotics drug resistance gonorrhoea

Gonorrhoea is sexually-transmitted infection that is difficult to treat. It can be transmitted through vaginal, anal and oral intercourse.

The bacterium that causes gonorrhea can be contacted by touching an infected area or person. The bacteria that cause gonorrhoea resist different antibiotics.

 Gonorrhoea can infect the genitals, rectum and throat. Common complications of gonorrhoea are abdominal pain, pelvic inflammatory disease, ectopic pregnancy and risk of HIV and infertility.

Pregnant women can infect their babies through child birth and it will leads to blindness. The United Nations health agency advises doctors to prescribe two antibiotics- ceftriaxone and azithromycin for gonorrhoea. It can be prevented by consistent and correct use of condom.
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How gonorrhea manipulates female reproductive tract

The bacterium that causes gonorrhea breaks links between cell in female reproductive tract and infects the tract.

Gonorrhea is one of the common sexually transmitted diseases caused when Neisseria gonorrhoeae bacteria infect the protective inner lining of human genital tissue.

Common symptoms of gonorrhea in women are: vagina discharge, burning with urination and vagina bleeding between period.

Liang-Chun Wang of the University of Maryland, College Park and colleagues infected human endocervix tissue with Neisseria gonorrhoeae, and used molecular and imaging methods to check the infection mechanism.

Scientists discovered that Neisseria gonorrhoeae caused disruption of cellular connections and cell shedding by encouraging activation and accumulation of a human protein called non-muscle myosin II.