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Father, 20, Dies After Getting 'Little Cut' On His Lip, Leaving Behind 2 Kids And Pregnant Partner: Reports
A 20-year-old father of two has reportedly died after a bacterial infection on his lip spread to his brain.
On Sunday, Nov. 24, Lockie Seddon, of Gippsland, Australia, died just days after he contracted a golden staph infection, per news.Com.Au, the Herald Sun and the Daily Mail Australia.
According to news.Com.Au, Seddon shares sons Mason, 3, and Jax, 2, with partner Claire, 22 — who is currently pregnant with their baby girl.
A GoFundMe page set up to help Seddon's mother, Tam, and his partner Claire, said, "Everyone who knew Lockie loved him, he leaves behind many broken hearts, also amazing memories."
"Tam lost her son, Claire lost her soul mate suddenly. Lockie was only 20, a young father to 2 beautiful boys, and a baby girl on the way," the description added. "He was a loving and doting father, he loved [Claire] and their children with all his heart. He leaves behind a distraught mother, father and a [devastated] brother."
Lockie Seddon.GoFundMe
The page has been set up to help raise funds so that Seddon's family can give him the "send off he deserves."
"Lockie was larger then life, a huge and proud mumas boy, cheeky and quirky," the description added.
Per the Mayo Clinic, "Staph infections are caused by staphylococcus bacteria. These types of germs are commonly found on the skin or in the nose of many healthy people. Most of the time, these bacteria cause no problems or cause relatively minor skin infections."
"Staph infections can turn deadly if the bacteria invade deeper into your body, entering your bloodstream, joints, bones, lungs or heart. A growing number of otherwise healthy people are developing life-threatening staph infections," the post added.
Seddon's aunt, Danielle Sherer — who set up the GoFundMe page — told news.Com.Au that the young father had developed a "small cold sore-like spot" on his lip in the days before his death, which he thought looked "weird" so he went to get it checked out.
After waking up in extreme pain, he was taken to a local hospital before being placed in an induced coma and airlifted to the Royal Melbourne Hospital. However, the publication said he "never woke up."
"The doctors said there were no signs missed and there was nothing anyone could have done, It was already too late," Sherer told the publication.
A stock photo of Staphylococcus aureus bacteria.CAVALLINI JAMES/BSIP/Universal Images Group via Getty
Seddon's aunt added to the Daily Mail Australia, "It just started with a little cut on his lip and the GP said it's like a bite or something."
"He was healthy one day, right? Had a little thing on his lip, and the next day, that was it," Sherer added to the outlet.
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Sherer told news.Com.Au that Seddon's kids were his "entire life."
"He was a very cheeky young man and a really hands-on dad. You could just tell how much his boys loved him," she told the outlet. "They would wrestle and playfight, they just adored him. It breaks my heart that they will never have that again."
"When Claire fell pregnant, we all couldn't believe that they finally got their little girl. He was over the moon," Sherer added. "We just can't believe this has happened."
The GoFundMe page has raised just over $2,900 (just over $4,500 AUD) as of Monday, Dec. 2.
Researchers Discover Genes Behind Antibiotic Resistance In Deadly Superbug Infections
Australian researchers have uncovered new genetic insights into Staphylococcus aureus, revealing what makes the bacterium so dangerous when it enters the blood.
While common, Staphylococcus aureus infections -- known as Golden staph -- can be life-threatening if the bacteria enter the bloodstream, causing sepsis. Golden staph is notorious for its ability to become resistant to antibiotics, making it hard to treat, which can lead to adverse health outcomes for patients infected with a drug-resistant form of the bacteria.
In one of the most comprehensive studies of its kind, published in Cell Reports, researchers, led by the Peter Doherty Institute for Infection and Immunity (Doherty Institute), analysed the unique genetic profiles of more than 1,300 Golden staph strains.
By combining this data with patient and antibiotic information, the researchers found that, while patient factors are critical in determining mortality risks, specific genes are linked to antibiotic resistance, along with the bacteria's ability to linger in the blood, evading antibiotics and the immune system.
University of Melbourne Dr Stefano Giulieri, a Clinician-Researcher at the Doherty Institute and first author of the paper, said the findings highlighted the diagnostic power of integrating clinical and genomic data.
"To the best of our knowledge, this is one of the first times that the method we used, called a genome-wide association study (GWAS), has been applied to delve into the role of bacterial genomes, host factors and antibiotics on the course of staphylococcal sepsis," said Dr Giulieri.
"In GWAS, scientists scan the genome of a big collection of bacteria to look for tiny changes (mutations) that show up more often in strains with a certain characteristic, such as antibiotic resistance. Mutations with a strong statistical link are precious clues to figure out how bacteria acquire attributes that are important for patient outcomes.
"Our study uncovered a deeper understanding of the intricate genetic dynamics underlying severe Golden staph infections. It highlights the potential of combining bacterial whole-genome sequencing, clinical data and sophisticated statistical genomics to discover clinically relevant bacterial factors that influence infection outcomes."
University of Melbourne Professor Ben Howden, Director of the Microbiological Diagnostic Unit (MDU) Public Health Laboratory at the Doherty Institute and co-senior author of the paper, said that this work represents a significant advancement in medical research as it reshapes our strategies against complex health challenges like Golden staph infections.
"By revealing the genes responsible for antibiotic resistance in Golden staph, our GWAS is pointing the scientific community to clearer targets for the development of effective solutions to treat Golden staph bloodstream infections," said Professor Howden.
"This knowledge has the potential to shape and enhance our ability to tackle these persistent infections. As bacterial genomes become increasingly available in the clinical routine, we inch closer to customised therapeutic strategies, where treatments will be tailored to the unique genetic makeup of the infecting strain, rather that treating everyone in the same way."
Funding: This research was funded by the National Health and Medical Research Council (NHMRC) and the University of Melbourne.
New Tool Uncovers 'elegant' Mechanism Responsible For Antibiotic Tolerance In Golden Staph
An international team of researchers, including those from UNSW's School of Biotechnology & Biomolecular Sciences, have applied a promising new tool -- CLASH -- to capture hundreds of undiscovered mechanisms of gene regulation in a strain of multi-drug resistant Staphylococcus aureus (MRSA).
The 500 mechanisms uncovered by the new tool were based on the mRNA of S. Aureus. Normally serving merely as instructions for making proteins, these newly revealed mRNAs were controlling other genes in S. Aureus through direct interactions -- regulating the bacteria's very own genetic information and antibiotic tolerance.
Among those RNAs found was a mechanism that thickens the bacteria's cell wall -- a change commonly seen in clinical strains of MRSA that are tolerant to last-line antibiotics -- potentially identifying new targets for antibiotic treatment. Their work has been published in Nature Communications.
"Before our study, only three other mRNAs had been shown to regulate bacterial RNA," says co-author Associate Professor Jai Tree. "It's relatively rare. But looking at our CLASH data was the real surprise. We found that in Staphylococcus aureus, there was evidence for 543 regulatory mRNAs interactions."
"This is a shift from our current understanding of gene regulation in bacteria."
This system of adaptation in S. Aureus has remained undetected due to a lack of tools for broadly capturing RNA interactions. In other disease-causing bacteria, related techniques rely on the presence of particular proteins, proteins that don't seem to function in S. Aureus.
If mRNA can be compared to copied pages from a recipe book, the regulatory mRNAs in S. Aureus have eschewed the chef and begun dictating the pace and production of their own meals.
"When a gene (DNA) is transcribed into RNA, a little bit of extra sequence is transcribed from either side -- like the aglets of a shoelace -- these are termed the 'untranslated regions' or UTRs," says A/Prof Tree. "It's these UTRs of mRNAs in S. Aureus that are performing a regulatory role.
"And where a typical UTR is 40 to 50 bases long, we found that around one-third of the UTRs in S. Aureus are 100 bases long -- which is long. This likely adds an entirely new layer of gene regulation."
The particular strain of S. Aureus used in this study was taken from a patient with MRSA septicaemia who was treated for 42 days with our 'last-line of defence' and most effective antibiotic: vancomycin. Since S. Aureus do not acquire vancmycin tolerance extraneously from other S. Aureus but evolve it through a series of mutations, the researchers analysed this strain using CLASH to understand how they were becoming vancomycin tolerant.
"One of the mRNA UTRs we discovered was a regulatory RNA that promotes an enzyme involved in cell wall thickening. It's this thickening that is consistent with vancomycin-tolerant S. Aureus," says A/Prof Tree.
"We found evidence of over 500 mRNA-mRNA interactions occuring in S. Aureus -- information uncovered by CLASH that allows us to ascribe functions to many regulatory RNAs in S. Aureus - often for the first time.
"The 'superbug', multi-drug resistant Staphylococcus aureus, is a major problem in both healthcare and community settings," says A/Prof. Tree. "Treatment options for MRSA septicaemia -- infections that enter the blood -- are limited to last-line antibiotics, and the treatment of choice is vancomycin.
"Vancomycin is an antibiotic that blocks assembly of a new cell wall in S. Aureus. If the bacterium can't make a new cell wall during division, it explodes. Those S. Aureus tolerant to vancomycin have thicker cell walls, likely limiting antibiotic at the site of cell wall synthesis."
By revealing one of the mechanims of vancomycin tolerance in S.Aureus, the once hidden line of defence is made visible for our offensive, 're-sensitising' resistant S. Aureus to vancomycin again.
"There has been renewed interest in using 'antisense RNA' that can be delivered into the bacterial cell, penetrating the cell wall and binding RNAs within the cell. In this way, we might be able to co-administer an antisense RNA with vancomycin -- the antisense RNA would make MRSA sensitive and the vancomycin would kill the cell," says A/Prof Tree.
While the functions of some mRNAs in S. Aureus have been ascribed, there remains a lot of work to do -- especially given the varied mechanisms behind vancomycin-tolerance S. Aureus.
"The next steps are to understand if [the regulatory RNA we've already isolated] is required for a broad spectrum of other, clinical strains of vancomycin-tolerant S. Aureus. These are genetically heterogenous isolates and one of the difficulties has been the multitude of methods of becoming vancomycin tolerant.
"So we would like to understand if targeting the regulatory RNA would be a useful approach for many different vancomycin tolerant strains. Although we don't know exactly what all the mRNAs are doing, our next step is to identify the really important ones."
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