antibiotic

Honey Could Be The Next Antibiotic:

From sea bacteria to veterinary pain medications, scientists have been looking everywhere for a solution to antibiotic-resistant bacteria. But a new study finds that the solution may be right inside their kitchen cabinets. Honey, which has already shown some promise in treating wounds, may also be useful for fighting infections.

In a way, it makes sense. If honey can help treat wounds and prevent infection on the outside, then it could probably fight infections on the inside too. “The unique property of honey lies in its ability to fight infection on multiple levels, making it more difficult for bacteria to develop resistance,” said study leader Dr. Susan M. Meschwitz,. Her findings were presented recently at the National Meeting of the American Chemical Council.

Honey commits a multi-pronged attack on bacteria, as it uses hydrogen peroxide, acidity, osmotic effect, high sugar concentration, and polyphenols to kill bacterial cells. Together, these antibacterial properties make it difficult for the bacteria to adapt. Osmotic effect works particularly well due to honey’s high sugar concentration, which sucks water out of the bacterial cells, dehydrating them, and leading to death.

Honey also inhibits a bacterial cell’s ability to communicate with other bacterial cells, known as quorum sensing. This renders them unable to form communities, and therefore unable to attack in large numbers, where they would normally be stronger. Meanwhile, polyphenols, or antioxidants, such as caffeic acid, p-coumaric, and ellagic acid contain antimicrobial properties. “We have separated and identified the various antioxidant polyphenol compounds,” Meschwitz said in the release. “In our antibacterial studies, we have been testing honey’s activity against E. coli, Staphylococcus aureus, and Pseudomonas aeruginosa.”

Bacterial resistance, Meschwitz says, occurs when bacteria adapt to the antibiotics that are supposed to inhibit their growth processes. As their DNA adapts, they become immune to the antibiotic’s effect, and therefore become even more dangerous. It has been said that if we continue using antibiotics unsparingly, previously eradicated diseases will come back and wreak havoc. In an effort to reduce unnecessary antibiotic use, which occurs in doctor’s offices as well as industrial farms, both the health care community and the nation’s regulators have been taking action, and calling for reduced use.

source: Medical daily

 

New antibiotic discovered for multi-resistant tuberculosis

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Researchers from EPFL (Swiss Federal Institute of Technology in Lausanne) and the AN Bach Institute in Moscow have discovered a new and extremely promising antibiotic for tuberculosis, especially effective against multi-resistant strains of the disease, which are on the rise in Eastern Europe. The drug, developed as a European FP7 project, has proven very effective against the disease.

In an article published in EMBO Molecular Medicine, the researchers show that, when combined with other drugs, the new antibiotic, called ‘PBTZ169’, can take down even the most resistant strains of tuberculosis bacteria.

Following the publication, the researchers formed the IM4TB Foundation on their campus. Supported by EPFL, the foundation aims to bring the new treatment to the market. This unusual step was taken because traditionally, technology transfer from academia to the pharmaceutical industry doesn’t work well with tuberculosis: development costs are too high and the affected countries are often barely able to maintain their own healthcare infrastructures.

With the IM4TB Foundation, EPFL intends to pick up the slack in the limitations of the industrial model. “The development of antibiotics is increasingly expensive and the countries most affected by tuberculosis are still emergent,” says Benoit Lechartier, co-author of the PBTZ169 study. “The recent closure of the AstraZeneca research centre in India illustrates the extent to which it is difficult for the pharmaceutical industry to invest in infectious diseases.”

Human trials in 2015

Located on the EPFL campus, the IM4TB Foundation plans to move onto human trials within a year, in collaboration with the University of Lausanne Hospitals (CHUV).

PBTZ169 shows much promise. It attacks the bacterium’s strong point – the cell wall, which forms an impenetrable shield against antibiotics and the patient’s immune system. “Our molecule makes the bacterium literally burst open,” explains Stewart Cole, director of the study and head of EPFL’s Global Health Institute.

A cheap but formidable weapon against resistant strains

The researchers showed that PBTZ169 is extremely effective in tri-therapy, where it is combined with a standard drug, pyrazinamide, and a more recent one, bedaquiline – and both these drugs have already been approved by the EU and the FDA for multi-resistant strains. “This could be the winning strategy,” says Cole. “These molecules attack different targets in the bacterium. By combining them, we drastically reduce the risk that it will mutate into more resistant forms.”

As a treatment, PBTZ169 has many advantages. It is not expensive to produce, since it is relatively easy to synthesize. Initial tests have shown good compatibility with other anti-tuberculosis treatments and it is expected to be equally compatible with antiretrovirals used to treat AIDS, as HIV-positive individuals are particularly vulnerable to tuberculosis, and cases of cross-infection are on the rise.

This molecule is the culmination of many years of research. The preliminary versions were formidable in the laboratory, where they decimated bacteria in culture. However, their effectiveness in vivo was limited. New technologies like structural biology enabled researchers to redesign the molecule so that it could be more rapidly absorbed. “Thus we were able to improve its pharmacodynamics,” explains Cole. “Tuberculosis is often wrongly considered a disease of the past, but in order to fight it, we needed to employ 21st century technologies.”

More than 1.5 million deaths per year

Tuberculosis still kills more than 1.5 million people every year. It is uncommon in Europe, although certain countries such as the Ukraine are experiencing a resurgence of patients infected with multi-resistant strains. The EU is leading a programme that aims to eliminate the disease. The research team at EPFL that developed PBTZ169 received funding from the Seventh Framework Programme (FP7) of the European Commission, in the framework of an international collaboration.

Source: India Medical Times

How superbugs develop antibiotic resistance

A team of researchers used quantitative models of bacterial growth to discover the bizarre way by which antibiotic resistance allows bacteria to multiply in the presence of antibiotics.

According to UC San Diego biophysicists understanding how bacteria harbouring antibiotic resistance grow in the presence of antibiotics is critical for predicting the spread and evolution of drug resistance.

In the study, the researchers found that the expression of antibiotic resistance genes in strains of the model bacterium E. coli depends on a complex relationship between the bacterial colony’s growth status and the effectiveness of the resistance mechanism.

According to Terry Hwa, a professor of physics and biology who headed the research, the interaction between drug and drug-resistance is complex because the degree of drug resistance expressed in a bacterium depends on its state of growth, which in turn depends on the efficacy of drug, with the latter depending on the expression of drug resistance itself.

For a class of common drugs, the researchers realized that this chain of circular relations acted effectively to promote the efficacy of drug resistance for an intermediate range of drug doses.

The use of predictive quantitative models was instrumental in guiding the researchers to formulate critical experiments to dissect this complexity. In their experiments, E. coli cells possessing varying degrees of resistance to an antibiotic were grown in carefully controlled environments kept at different drug doses in “microfluidic” devices-which permitted the researchers to manipulate tiny amounts of fluid and allowed them to continuously observe the individual cells.

Hwa and his team found a range of drug doses for which genetically identical bacterial cells exhibited drastically different behaviours: while a substantial fraction of cells stopped growing despite carrying the resistance gene, other cells continued to grow at a high rate.

This phenomenon, called “growth bistability,” occurred as quantitatively predicted by the researchers’ mathematical models, in terms of both the dependence on the drug dose, which is set by the environment, and on the degree of drug resistance a strain possesses, which is set by the genetic makeup of the strain and is subject to change during evolution.

“Exposing this behavior generates insight into the evolution of drug resistance,” says Hwa. “With this model we can chart how resistance is picked up and evaluate quantitatively the efficacy of a drug.”

The study is published in the journal Science.

Source: ANI