Infectious bacteria hibernate to evade antibiotics

Researchers have discovered a surprising tactic of pathogenic bacteria when being attacked by antibiotics: hibernation.

Almost all pathogenic bacteria develop a small number of antibiotic-tolerant variants. This means that a significant fraction of bacteria survive courses of antibiotics.

While it is no secret that pathogenic bacteria are able to develop antibiotic resistant variants, a less well-appreciated fact is that a small number of bacteria, including some of nature's nastiest pathogens, can resist antibiotics and escape antibiotic treatments without relying on variants.

How's that? Researchers at the University of Copenhagen now have an answer. They have found examples of a small portion of pathogenic bacteria hiding out in a dormant, hibernation-like state, until the danger posed to them by antibiotics passes. When safe, they awaken and resume their regular functions.

The bacterium's stop growth mechanism

Antibiotics usually target a bacteria cell's ability to grow, which means that a hibernating bacterium is exempt from attack.

"A bacterium in hibernation is not resistant. It is temporarily tolerant because it stops growing, which allows it to survive the effects of an antibiotic," says Professor Gerdes.

Genetically, hibernating bacteria share the same characteristics as other bacteria in a given population, an E. coli population for example. So, for now, there are no clear rules as to why certain bacteria survive antibiotics by going dormant while others do not.

The researchers used a new method to study what happens in the disease-causing cells that go dormant and hide in the body.

Enzyme catalyzes hibernation

The researchers found an enzyme in dormant bacteria that is responsible for catalyzing hibernation, which allows the bacteria to avoid being attacked.

"The discovery of this enzyme is a good foundation for the future development of a substance capable of combatting dormant bacteria cells," says Professor Gerdes.

The road ahead will not be easy and will require many years of hard work, expertise and research funding to develop new antibiotics. For Gerdes, it obvious that Denmark ought to play a leading role in this area of research.

The enzyme triggers a 'survival program' that almost all disease-causing bacteria deploy to survive in the wild and resist antibiotics in the body. Developing an antibiotic that targets this general programme would be a major advance.

https://www.sciencedaily.com/releases/2018/09/180925110025.htm

Source: University of Copenhagen

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Acute flaccid myelitis: A mystery disease

Acute flaccid myelitis, or AFM, is not a new syndrome or disease. The classical cause of the syndrome is infection with the poliomyelitis virus. Of course, there has been no poliomyelitis originating in the United States since 1979. Sporadic cases of nonpolio AFM have been recognized in the U.S. for many years after the eradication of polio, but it was not until 2014, when there was a surge of cases in the U.S., that it reached the national consciousness and was given the name “acute flaccid myelitis” rather than “polio-like syndrome,” “acute flaccid paralysis” or other names that had been previously attached to the syndrome.

The CDC’s criteria for a confirmed diagnosis of AFM include acute onset of flaccid limb weakness in one or more limbs with confirmation by MRI of a spinal cord lesion largely restricted to gray matter and spanning one or more vertebral segments. If there is no MRI confirmation available, the case is considered probable, provided there is cerebrospinal fluid (CSF) showing pleocytosis (white blood cell count [WBC] > 5 cells/mm3). There was no official tracking of cases of AFM in the U.S. before 2014; however, from August through December of that year, there was a national outbreak of the disease that resulted in 120 cases. As of Feb. 15 — including those 120 cases from 2014 — there has been a total of 552 AFM cases confirmed after review by the CDC. The agency is attempting to collect retrospective MRI data to determine the annual number of yearly cases before 2014.

Epidemiology in the US

AFM causes disease primarily in children. More than 90% of cases have been aged younger than 18 years, and most of these have been aged 2 to 8 years. The majority of cases occur during August through October. The male-to-female ratio has been about 60:40. A very interesting observation is that larger outbreaks of AFM have occurred in alternate years from 2014 to 2018. For example, there were 120 cases in 2014, 22 cases in 2015, 149 cases in 2016, 35 cases in 2017 and 215 cases in 2018. This last number will probably increase because records are still under review.

The 2014 outbreak occurred against a backdrop of a large national outbreak of human enterovirus D68 (EV-D68) infection in children. EV-D68 (one of more than 100 nonpolio enteroviruses) was first described in 1962, but case clusters were not recognized until about 2008, when reports of respiratory infection, some severe, caused by EV-D68 came in from around the world. In 2014, EV-D68 was demonstrated in respiratory specimens of 20 of the 120 cases of AFM, and non-D68 enteroviruses were found in 21 of the cases. Cases of AFM associated with EV-D68 were also reported during the 2016 U.S. outbreak and from multiple other countries as well.

Source: Infectious Disease News, March 2019

Donald Kaye, MD, MACP

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When 8-year olds look like 80: Researchers describe mechanism behind premature aging disease

Progeria, a premature aging disease, is the research focus of Roland Foisner's team at the Max F. Perutz Laboratories of the University of Vienna and the Medical University of Vienna. Children suffering from progeria die at an average age of 14 to 15 years, often from heart attacks and strokes. So far, there is no cure for the disease, and though researchers identified the abnormal protein behind the disease -- progerin -- the exact way in which it causes the accelerated aging remains elusive. In their latest publication in Genes & Development, Roland Foisner and his group describe a yet unknown mechanism behind progeria that may provide new approaches for therapy.

Children suffering from progeria are born normal, but from age one to two their disease starts to resemble premature aging in some aspects. So by the time they reach their teens they have typical age-related conditions such as brittle bones, stiff joints and severe cardiovascular disease. In the end many die from strokes and heart attacks before reaching their twenties. Presently, there is no cure for progeria. Patients can be treated with drugs called FTIs (farnesyltransferase inhibitors), which were initially developed to treat cancer. These drugs improve some aspects of the disease, such as bone structure, arterial stiffness, and increase estimated lifespan by at least 1.6 years.

Progerin: the protein behind the aging disease progeria

Progerin, a protein present in very high concentration in progeria cells, is known to be responsible for many of the characteristics of the disease. It is a mutant version of lamin A, a protein crucial for the stability of the nucleus and involved in many essential nuclear functions. How progerin exerts its effects exactly is the reseach interest of Roland Foisner and his team at the Max F. Perutz Laboratories -- a joint venture of the University of Vienna and the Medical University of Vienna. They investigate the molecular functions of nuclear lamins and their mutated forms such as progerin and associated diseases.

"A few years ago, we and others found that progeria cells have much less LAP2α than normal cells. LAP2α is a protein that interacts with lamin A to regulate cell proliferation, the process that produces new cells. Interestingly, LAP2α levels also decrease during normal aging," explains Roland Foisner, Deputy Director of the Department of Medical Biochemistry of the Medical University of Vienna. Supported by an Innovator Award from The Progeria Research Foundation, senior postdoc Thomas Dechat and PhD student Sandra Vidak in collaboration with Tom Misteli from the NIH National Cancer Institute (USA) developed a cell line that allows studying the molecular mechanisms behind progeria in the lab.

See more: https://www.sciencedaily.com/releases/2015/10/151007033313.htm

Source: Medical University of Vienna

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Theme : Treating Diseases with Advanced Techniques

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Fighting deadly drug resistant bacteria in intestines with new antibiotic

A new antibiotic developed by a Flinders University researcher is being heralded as a breakthrough in the war against a drug resistant superbug.

Bacteria are winning the fight against antibiotics as they evolve to fight off traditional treatments, threatening decades of advancements in modern medicine, with predictions they will kill over 10 million people by 2050.

The scientific development of new, effective and safe antibiotics is crucial in addressing the ever-growing threat posed by drug resistant bacteria around the world.

Clostridium difficile infection (CDI) is a potentially deadly infection in the large intestine most common in people who need to take antibiotics for a long period of time, particularly in Australia's ageing population.

Dr Ramiz Boulos, adjunct research associate at Flinders University and CEO of Boulos & Cooper Pharmaceuticsals, says the fact CDI is becoming resistant to traditional antibiotics is alarming and highlights the need to develop more effective treatments.

"Cases of CDI disease are rising and the strains are becoming more lethal. If there is an imbalance in your intestines it can begin to grow and release toxins that attack the lining of the intestines which leads to symptoms," says Dr Boulos.

Over the past ten years, various strains of C. difficile have emerged, and are associated with outbreaks of severe infections worldwide. One particular strain is easily transmitted between people and has been responsible for large outbreaks in hospitals in the United States and Europe.

"It's concerning when you consider CDI is one of the most common infections acquired during hospital visits in the Western hemisphere, and the most likely cause of diarrhea for patients and staff in hospitals."

But when doses of a new antibiotic called Ramizol were given to hamsters infected with a lethal dose of the bacteria, a significant proportion of hamsters survived the infection.

In a recent safety study in rats evaluating the effect of repeated exposure of the antibiotic, no rats experienced serious side effects or changes in weight.

"Our research indicates Ramizol is an extremely well-tolerated antibiotic in rats, with good microbiology and antioxidant properties. It also has high chemical stability and is scalable because of the low cost of manufacturing, which could make it a viable treatment option."

Forty-eight rats were given a high dose of a new class of antibiotic for 14 days to assess its safety.

See more: https://www.sciencedaily.com/releases/2019/01/190118122954.htm

Source: Flinders University