Your DNA Could Make You Resistant To Certain Bacteria

Scientists have already had some inklings of the relationship between genes and infectious diseases—for example, people with the genetic mutation for cystic fibrosis don’t usually get typhoid, which is caused by bacteria. Bacteria and viruses, in turn, can also affect your genes.

For this study, the researchers wanted to see if genes affected a person’s likelihood of contracting a common bacterial infection. The researchers infected 30 participants with E. coli bacteria, a common cause of diarrhea. For the next eight days, the researchers watched for symptoms—six participants basically showed no symptoms, while another six were debilitated by the infection—and then drew their blood.

The researchers were checking the blood for gene expression. While every cell might have thousands of genes, only a select few are activated at any given time, turned on throughout the process of development or by external factors like smoking and diet.

Bacteria, it seems, can also modify gene expression—when the researchers compared the gene expression of participants with severe symptoms and those with few symptoms, they found significant differences in the expression of 29 genes related to immune function. It seems that certain genes were turned on when the bacteria were present, making the participants more immune. They anticipate that those variations could help predict which patients will react strongly to an E. coli infection.

What’s not clear, though, is if the participants with few symptoms had mutations in those particular genes, or if those genes reacted more strongly to the presence of the bacteria. To answer that question and to further confirm their findings, the researchers hope to perform similar experiments with other types of bacteria and viruses, paying special attention to those 29 genes they suspect play a role in disease resistance. If they’re right, it’s possible that someday, treatments for infectious diseases might rely more on epigenetics, activating infection-resistant genes so that patients suffer less.

Dead After Claim of Gastro on Pacific Jewel Cruise Ship

One woman has died and several people are said to be unwell after what a family member said was an outbreak of gastroenteritis on a cruise ship off the coast of Queensland.

The P&O Pacific Jewel cruise ship left from Sydney on September 6 for a 10-night “Barrier Reef Discovery” cruise. P&O said there had not been a gastro outbreak on the ship.

Margaret Carlson boarded with her daughter and teenage grandson. It was the 79-year-old’s seventh cruise in 10 years after her husband passed away, and she was looking forward to the journey after being upgraded to a luxury cabin.

She soon began showing signs of gastro and was told by medical staff that she had probably brought the bug onto the ship with her, her family says. Her daughter and grandson also fell ill after boarding the ship.

On Saturday afternoon, when the ship was docked at Yorkeys Knob in Cairns, Mrs Carlson’s family discovered she had died in her room.

Police were called to inspect the scene and determined she had died of natural causes several hours earlier. An autopsy will be performed.

Mrs Carlson’s daughter Vanessa D’Souza, 41, said her mother’s death was sudden and extremely upsetting.

“I keep getting these bunches of flowers at home and I just want to scream because I’m like, ‘Oh, these flowers are beautiful and mum would love them’, but she’s not here,” Ms D’Souza said.

“My first priority was to let people know, because I thought you would not want to send your mother or grandmother on that [ship].”

Ms D’Souza has been in contact with her sister, who will remain on the ship until it arrives back in Sydney on Friday, where it will dock briefly before leaving again with fresh passengers.

A P&O spokesperson acknowledged the death but denied there was a gastro outbreak.

“An elderly passenger sadly passed away on Saturday on Pacific Jewel and our thoughts are with her family,” the spokesperson said. “There is no reported gastro outbreak onboard the ship.”

Queensland Health said it had not been informed of gastro on a cruise ship. Gastroenteritis is not a “notifiable” condition, meaning there is no obligation to report such an outbreak.

One passenger was medically evacuated from the ship by helicopter on Monday for reasons which could not be divulged.

Ms D’Souza said most of the passengers on board “can’t wait to get off”.

“We’d like some answers,” she said. “Is there really some issue with hygiene, or is there something going wrong?”

Mrs Carlson lived on her own in a house in Terrigal on the NSW central coast, where she had lived for 18 years. She had osteoporosis, but remained mobile by using a walking frame, and on her last check-up appeared to be in good health.

Queensland Police confirmed a 79-year-old woman died on a cruise ship that was docked at Cairns on Saturday. Officers will prepare a report for the Coroner.

Alcohol Hand Sanitizers Will Keep You Healthy And Safe

Over the last week, there has been some coverage by the major media outlets on a document released by the United States Food and Drug Administration (FDA). The federal agency has asked for more data on the safety and efficacy of hand sanitizers. Although this may appear to sound an alarm, there is no reason for concern. After all, the FDA even says within the text of the document that, “The proposed rule does not require any consumer hand sanitizer products to be removed from the market at this time”, and that this rule “does not mean these products are unsafe or ineffective.”

The impetus behind the FDA announcement is a decades-long journey merging consumer products and government regulation to ensure public safety. The basis of this regulatory action is what is known as a monograph. It’s an official standard regarding a specific chemical or group of chemicals and is used to certify a product containing these chemicals – also known as active ingredients – is safe when used appropriately.

Back in the 1960s, the FDA expanded the scope of monographs to include non-prescription medications, also known as Over The Counter (OTC) drugs. This was not an easy task, however, as the number of products ranged into the hundreds of thousands. But the agency was undeterred and in 1972, the official OTC Drug Review was initiated in the hopes of developing monographs for every drug on pharmacy – and now grocery – shelves.

As one might expect, the process was not quick and final monographs didn’t appear until at least ten years later. But slowly the number grew and included categories such as anti-acne products, toothpaste, antiperspirants, dandruff products, antacids, sunscreens, and cough, cold and allergy remedies. Today, there is a searchable list of monographs for anyone wishing to learn more about a particular product.

Though nearly forty years have passed since the monograph endeavor was started, some are still in in the review process. One of these focuses on what officially are called topical antimicrobial drug products – most of us simply call them hand sanitizers. The journey has been long but the final document is slated to be published in the government’s official rules and regulations publication, the Federal Register, in 2019. This particular monograph is the reason for last week’s announcement.

The last time the FDA conducted an official review of these products was back in 1994 when a Tentative Final Monograph was released. Back then, a list of questions regarding safety and effectiveness. Over the last 22 years, there has been a significant amount of research performed to address these issues but there hasn’t been a formal rule requesting this information. Now the FDA officially wants to know what science is out there.

Much of the data gained over the last few decades has focused on alcohol-based hand sanitizers. After all, more people are using these products and some major health organizations such as the World Health Organization recommend them to reduce infection spread. As a result, the amount of information collected on the safety and effectiveness of these products has grown tremendously.

In terms of effectiveness, alcohol hand sanitizers have proven in hundreds of scientific articles to be useful in keeping people safe. All that’s required is a concentration between 62 and 70% alcohol – ethyl alcohol to be exact – and 15 seconds on contact time and the majority of pathogenic threats will be killed. This includes bacteria, viruses, and fungi. It’s why this product is considered by the United States Centers for Disease Control and Prevention (CDC) to be the best option to prevent infectious disease spread when running water and soap are not available.

As for safety, there is more than enough information to show the safety of alcohol hand sanitizers. Even the FDA agrees as the only data gap is long term daily use. Thankfully, researchers have shown continual use of alcohol hand sanitizers (30 times an hour over 12 hours) leads to the same absorption as drinking a non-alcoholic beverage like fruit juice.

In essence, the recent FDA announcement is an administrative formality heading towards the 2019 publication of the Final Monograph. Over the coming months, the information found in the scientific literature will be put forth to the regulatory body such that they can begin to fill in the gaps. Come 2019, when this monograph will be finalized, one can be sure the agency will find ethyl alcohol, to be an integral part of hygiene and hand sanitizers will be given the regulatory endorsement to complement the overwhelming public approval.

Why Does Hair Turn Gray

ytHave you ever watched someone try to cover up gray hair by dyeing it? Or maybe you wonder why your granddad has a full head of silver hair when in old pictures it used to be dark brown? Getting gray, silver, or white hair is a natural part of growing older, and here’s why.

Each hair on our heads is made up of two parts:

  1. a shaft — the colored part we see growing out of our heads
  2. a root — the bottom part, which keeps the hair anchored under the scalp

The root of every strand of hair is surrounded by a tube of tissue under the skin that is called the hair follicle (say: FAHL-ih-kul). Each hair follicle contains a certain number of pigment cells. These pigment cells continuously produce a chemical called melanin (say: MEL-uh-nin) that gives the growing shaft of hair its color of brown, blonde, red, and anything in between.

Melanin is the same stuff that makes our skin’s color fair or darker. It also helps determine whether a person will burn or tan in the sun. The dark or light color of someone’s hair depends on how much melanin each hair contains.

As we get older, the pigment cells in our hair follicles gradually die. When there are fewer pigment cells in a hair follicle, that strand of hair will no longer contain as much melanin and will become a more transparent color — like gray, silver, or white — as it grows. As people continue to get older, fewer pigment cells will be around to produce melanin. Eventually, the hair will look completely gray.

People can get gray hair at any age. Some people go gray at a young age — as early as when they are in high school or college — whereas others may be in their 30s or 40s before they see that first gray hair. How early we get gray hair is determined by our genes. This means that most of us will start having gray hairs around the same age that our parents or grandparents first did.

Gray hair is more noticeable in people with darker hair because it stands out, but people with naturally lighter hair are just as likely to go gray. From the time a person notices a few gray hairs, it may take more than 10 years for all of that person’s hair to turn gray.

Some people think that a big shock or trauma can turn a person’s hair white or gray overnight, but scientists don’t really believe that this happens.

A New Frontier For Statins

Up until recently, anyone suffering from high cholesterol had a fairly easy option to improve health. All they needed was a prescription for a group of chemicals known as statins. For decades, this was the go-to drug to cost-effectively keep low density lipoprotein (LDL) levels in check and prevent the onset of cardiovascular disease. Although this view has changed somewhat with the FDA providing advice on the potential risks associated with their use, the number of people taking these drugs continues to be high.

While the majority of research on statins appears to be focused solely on cholesterol, researchers have examined other potential benefits. Some include the formation of new blood vessels and an improvement in immune, bone and central nervous systems . But one of the most studied has been the antimicrobial effects of these drugs. For some reason, their inclusion seems to help the chances of infection prevention and control.

One of the first mention of statins as antimicrobials came out in 2001 when their use appeared to help reduce the mortality rate in people suffering from sepsis. The effect was so pronounced, the drugs were considered as potential therapy for this life-threatening disease. As the evidence grew, so did the experiments in the laboratory. In 2008, the effect of statins on one of the causes of sepsis, Staphylococcus aureus, was shown. It even had an effect on the antimicrobial resistant version, Methicillin Resistant Staphylococcus aureus (MRSA).

With the knowledge of the effects during the most critical infections, researchers sought to identify whether the drugs could help those who might not be at immediate risk. In 2014, the drug was even suggested to be an important part of cardiovascular disease reduction by simply preventing microbial-based inflammation. The reason stemmed from the ability of the drugs to stop the development of S. aureus colonies, biofilms, which is a critical step in the development of infections of the skin and the blood.

But S. aureus wasn’t the only target. Other studies have revealed the antimicrobial effects against pathogens such as Mycobacterium tuberculosis, the influenza virus, and the worm, Schistosoma mansoni. In each case, the drugs seemed to have a direct effect on the microbe to keep it from causing an infection or at least allowing it to worsen.

There is another potential protective mechanism against pathogens. This time, the target is yeast, particularly Candida. This particular species is known to cause both skin infections as well as the bloodborne infection called candidemia. Without immediate intervention, the latter can be life-threatening.

The first hints of yeast-blocking activity came in 2010 when statins appeared to help reduce the mortality rate. This was echoed in 2013, although the results were not conclusive. Though there was apparently some benefit, the actual contribution of the drug could not be determined.

Now there is evidence statins have the same anti-biofilm effect on yeast as they do on bacteria. Last week, a Brazilian team of researchers published their analysis of the effects of the drugs on Candida and another genus, Cryptococcus. Their results suggest the previous results were actually due to the drug and may offer hope for the development of novel therapies.

The group used 51 strains of Candida and 25 strains of Cryptococcus for the test. As for the statins, three were chosen, simvastatin, atorvastatin, and pravastatin. The team also included antifungal drugs such as amphotericin B, itraconazole and fluconazole to act both as individual controls and also as additive for combinatorial therapy.

The testing followed to particular paths. The first attempted to determine the effect of statins on individual cells, called planktonic. The second focused on the formation of biofilms. If all worked out well, the drugs on their own would both kill the yeast and consequently prevent biofilm formation. In case this didn’t work, the combination option was expected to be effective.

The results were somewhat surprising. Out of the three statins, simvastatin came out on top. It killed Candida planktonic cells and also prevented biofilm formation. The effect was solely due to the drug as combinations with antifungals had no improved effect. The authors suggested the drug prevented the yeast from being able to properly function by both causing defects in the outside membrane as well as the internal mitochondria.

When it came to Cryptococcus, the results were similar. The only difference was a noticeable synergy between simvastatin and amphotericin B. The authors believed this was due to the different routes of antimicrobial activity working together although an exact mechanism wasn’t elucidated.

The authors concluded simvastatin was by far the best potential antifungal statin and that further research would be well worth following. As to the reason why this particular drug was better than the other two, there was no explanation. Yet, the answer may be found in the original nature of the statins.

Although simvastatin, atorvastatin, and pravastatin are synthetic, they are based on a class of naturally-derived molecules found in fungus. Simvastatin is based on a molecule lovastatin derived from Aspergillus terreus. Pravastatin is a modification of a molecule from Penicillium citrinum. Both these species have the ability to fight off yeast in the wild and as a result the derived statins may still harbour the antifungal activity. As for atorvastatin, it a completely synthetic molecule developed through molecular modelling. As a result, the antimicrobial activity may not have been included in the final product.