Infection and Drug Resistance | Volume 15 - Dove Press Open ...
New Bacteriophage-based Rapid Test Could Identify Bacteria Causing UTIs Within Hours
It may take a few days for conventional tests to determine which bacteria has caused infection in a particular patient. Doctors prescribe antibiotics to manage the infection for the time being without necessarily knowing how effective they are against the particular bacteria causing the infection.
However, this new test allows for the faster detection of the infection-causing bacteria first, avoiding the need for unnecessary antibiotic use to treat UTIs.
For this test, the scientists genetically modified phages to allow harmful bacteria to emit light signals. Following this, they were easily able to detect harmful bacteria in urine samples in less than four hours.
Through this test, doctors would be able to quickly prescribe the right medication to treat an infection caused by a specific bacterium type.
Sniper-like phagesOne of the most significant benefits of phages is that they function like snipers, targeting just specific bacteria.
To make the most of this feature, the researchers modified the genetic composition of the phages to boost their ability to destroy bacteria.
The phages were genetically modified in such a way that they not only infected their target but also created additional phages and bacteriocin proteins. These proteins are extremely effective in killing bacteria, especially those that have developed phage resistance.
"Once they are released, these bacteria-killing proteins are particularly effective against bacterial strains that have altered parts of their surface in such a way that the phages no longer recognize them. This double-barrelled attack makes the treatment more effective," explained the medical writer, Vanessa Bleich in a statement.
Here's What Happens If You Don't Wash Your Pillowcase—and It's Disgusting
Your sheets have a dirty little secret. Here's just how nasty those unwashed pillowcases can get.
Be honest, how often do you wash your sheets? Sure, experts say that it's recommended to wash your bedding at least once every two weeks. But are you actually doing it that often? And are your pillowcases included? If you just whispered no, then it may be time to toss a load into the wash—especially when you consider how much bacteria can collect on your pillow in just one week alone. Here's what you need to know.
The dirty truth about your pillowcase
Don't wait until your pillows are stained yellow. According to a recent study conducted by mattress company Amerisleep, after one week of sleeping on the same pillow, your pillowcase can collect between 3 and 5 million colony-forming units (CFUs) of bacteria per square inch. That is 17,000 times the amount of bacteria found on the average toilet seat. Yes, you read that right.
If you find yourself washing your bedding only once a month, your pillowcase can collect almost 12 million CFUs per square inch. That means your face is touching 39 times the amount of bacteria that's found in your pet's food and water bowl.
The bacteria is gross, but is it unsafe?The type of bacteria found on the tested pillowcases was a point of concern. In the study, Amerisleep found four main strains of bacteria: gram-positive rods, gram-negative rods, gram-positive cocci and bacilli.
Gram-negative rods were the most common bacteria found on dirty pillowcases, making up 41% of the detected CFUs. This type of bacteria is a common cause of certain infections, including pneumonia, and can even cause antibiotic resistance, according to the Centers for Disease Control and Prevention. Bacilli was also found on the dirty pillowcases and is a typical suspect for bouts of food poisoning and other infections.
Keep in mind that not every pillowcase is the same; it all depends on the person's health and hygiene. If you're generally healthy and clean your face regularly, your pillowcase will have fewer bacteria than the average one found in Amerisleep's study, but that's still a large number. Regardless, it's probably wise to change and wash your pillowcases often.
How to wash your pillowcases
Your clothes are washed after each wear, but pillowcases? People tend to forget those. For a cleaner—and healthier!—sleep in your bed, here are some laundry tips to thoroughly wash away the bacteria on your pillowcases.
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How Bacteria Can Colonize Skin And Accelerate Eczema Growth
Eczema, the most common form of atopic dermatitis, is a non-contagious skin condition characterized by patches of dry, itchy skin.
The condition affects about 30% of the population in the United States.
While there is no cure for eczema, medications do exist to manage its symptoms. These include as topical corticosteroids and emollients and sometimes topical immunosuppressants.
Eczema is thought to arise from a mix of environmental and genetic factors. Irritants found in soaps and surface cleaners, for example, can trigger the immune system, which then causes inflammation that may present as an eczema flare-up.
People with eczema may have reduced filaggrin production due to variants in the gene the encodes for this protein. Filaggrin plays an important role in strengthening the skin.
Bacteria can enter breaks in the skin of people with eczema, where they can grow and multiply. The immune system may try to control this colonization by increasing inflammation, leading to more skin damage and itchiness.
Understanding more about how bacteria spread into the skin of people with eczema and how it increases inflammation could aid the development of new drugs to treat the condition.
Recently, researchers investigated how the bacteria Staphylococcus aureus adapts to the skin of people with eczema. They reported that the bacteria develop mutations, which mean they no longer have a cellular capsule and can thus grow faster on the skin.
Medical News Today spoke with Dr. Alain Michon, the medical director of Project Skin MD Ottawa in Canada who was not involved in the study, about the findings.
"Targeted treatment of S.Aureus bacteria strains with capD mutations could be valuable not only to help treat acute episodes of eczema but also to prevent flare-ups and keep eczema under control," Michon said.
The recent study was published in the journal Cell Host & Microbe.
Previous research indicates that S. Aureus is often present on the skin of people with eczema.
The more of the bacteria they have, the more severe their eczema tends to be.
S. Aureus is thought to contribute to eczema pathology by secreting toxins and recruiting immune cells, something that further damages the skin barrier.
Up to 30% of people have S. Aureus in their nostrils.
While most infections are not serious, they can cause serious bloodstream infections, pneumonia, and bone and joint infections.
The researchers conducted this longitudinal study on 23 children in Mexico between 5 and 15 years old with moderate to severe eczema.
All the participants were being treated with standard care, including topical steroids, emollient moisturizers, and bleach baths.
The researchers took samples of skin microbes from the children once a month for three months and then again at nine months. Samples were taken from common eczema-affected sites such as the backs of knees and inside of elbows. They also took samples from forearms, which are usually not affected by the bacteria, and the nostrils.
The researchers then cultured S. Aureus cells from each site, yielding almost 1,500 unique colonies. This enabled them to observe how the bacertail cells evolved in greater detail.
Ultimately, they found that most participants had a single lineage of S. Aureus over the study period, meaning that new strains did not come in over time from the environment or other people. They noted, however, that each lineage mutated a lot during the study.
In particular, the researchers noted that many mutations occurred that reduced or eliminated function of a gene known as capD, which encodes for an enzyme necessary for synthesizing polysaccharide — a capsule-like coating that protects S. Aureus from immune cells.
Over the course of the study, the researchers found that capD mutations took over the entire S. Aureus microbiome population in a third of the participants.
In one child, the researchers had initially detected four different mutations of capD. However, by the end of the study, one of the variants became dominant and spread to the entire microbiome.
From further experiments, the researchers said they found that mutations in capD allowed the bacteria to grow faster than those with a regular capD gene.
Lastly, the researchers analyzed almost 300 publically available genomes of bacteria isolated from people with and without eczema.
They found that those with eczema were more likely to have S. Aureus variants that could not produce capsular polysaccharides than those without eczema.
Medical News Today spoke with Dr. J. Wes Ulm, a bioinformatic scientific resource analyst and biomedical data specialist at the National Institutes of Health who was not involved in the study, about how mutations that make S. Aureus more detectable by the immune system increase the spread of the bacteria – and eczema – on the skin.
Ulm noted that from a certain perspective, it may seem like a disadvantage for S. Aureus to become more easily detectable by the immune system. He continued to explain, however, that loss or reduction in capD expression could increase the bacteria's ability to grow and spread as energy that would otherwise be spent in making a productive capsule can be channeled directly into growth.
Furthermore, lacking a capsule would allow the bacterium to latch onto the skin surface more easily, increasing its efficiency in spreading throughout the skin.
"When the capD-deficient strain becomes more predominant on the [skin's] microbiome, its lack of capD makes it more easily detected and targetable by the immune system there," Ulm said. "And this, in turn, can enhance the immune response and magnify the inflammatory reaction giving rise to the characteristic rash and symptoms of eczema."
Michon said that the study's small sample size limits how far these findings may apply to other populations.
He added that some participants' microbiomes may have been altered in those who took antibiotics prior to and during the study, which may have affected the results.
Cameron K. Rokhsar, FAAD FAACS, a dermatologist and fellowship-trained cosmetic and laser surgeon in Manhattan and Long Island in New York who was not involved in the study, also noted other limitations.
"The limitation of these findings is that bacterial overgrowth is only part of the whole mystery," Rokhsar told Medical News Today. "The real issue with atopic dermatitis is the dysfunctional barrier particular to these patients. Putting patients on antibiotics help atopic dermatitis flares but does not cure eczema."
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