Malevolent Designer News - How A Deadly Superbug Is 'Designed' To Make Us Sick

Staphylococcus aureus

CDC

Scanning electron micrograph of methicillin-resistant Staphylococcus aureus (MRSA) bacteria being engulfed by an immune cell known as a neutrophil.

Credit: National Institute of Allergy and Infectious Diseases, National Institutes of Health

Researchers discover genes behind antibiotic resistance in deadly superbug infections | Doherty Website

Scientists based at the Docherty Institute, Melbourne University, Victoria, Australia have discovered just how devious any designer of the deadly super bug, Staphylococcus aureus, also known as Golden staph, would need to have been to come up with such a clever way to make us sick and die.

Curiously, for people who purport to worship the putative designer of all living things, creationists would have us believe that the designer is just such a mendacious malevolence, rather than have us believe that a natural process such as evolution by natural selection is responsible for parasites and the way they evade our immune systems - also, so creationists claim, designed by the same designer, making it look like a bumbling incompetent amnesiac than a supremely intelligent deity.

First, a brief background on S. aureus and MRSA:

Tell me all about Staphylococcus aures and MRSA, please.

Staphylococcus aureus (S. aureus) is a bacterium commonly found on the skin and in the nasal passages of healthy individuals. While it is usually harmless in these locations, it can cause a wide range of infections when it enters the body through wounds, surgical incisions, or other means. Some of these infections can be minor, such as skin infections like boils or impetigo, while others can be more serious, causing conditions like pneumonia, bloodstream infections, or endocarditis. Methicillin-Resistant Staphylococcus aureus (MRSA) is a specific strain of S. aureus that has developed resistance to multiple antibiotics, including methicillin and other beta-lactam antibiotics like penicillin. This resistance makes MRSA infections more challenging to treat compared to regular S. aureus infections. Here are some key points about MRSA:

1. Antibiotic Resistance: MRSA is resistant to beta-lactam antibiotics, which are commonly used to treat bacterial infections. This resistance is due to the presence of a specific gene called mecA or mecC, which encodes for a modified penicillin-binding protein that makes the bacteria resistant to these drugs.
2. Transmission: MRSA can be transmitted through direct skin-to-skin contact, sharing personal items like towels or razors, or contact with contaminated surfaces. It is often associated with healthcare settings (healthcare-associated MRSA or HA-MRSA) but can also infect individuals in the community (community-associated MRSA or CA-MRSA).
3. Clinical Manifestations: MRSA infections can manifest in various ways, including skin and soft tissue infections (such as abscesses, cellulitis, or wound infections), respiratory infections (pneumonia), bone and joint infections, bloodstream infections (bacteremia), and infections of the heart valves (endocarditis).
4. Symptoms: The symptoms of MRSA infections can vary depending on the site of infection but may include fever, pain, swelling, redness, and pus at the site of infection. In severe cases, MRSA infections can lead to systemic symptoms and complications.
5. Diagnosis: Diagnosis of MRSA typically involves taking a sample from the infected site, such as a wound or blood, and testing it in a laboratory to identify the bacteria and determine its antibiotic susceptibility.
6. Treatment: MRSA infections are treated with antibiotics other than beta-lactams, such as vancomycin, daptomycin, or linezolid. The choice of antibiotic depends on the severity and location of the infection, as well as the results of antibiotic susceptibility testing.
7. Prevention: Preventing MRSA infections involves good hygiene practices, including regular handwashing, keeping wounds clean and covered, not sharing personal items that come into contact with the skin, and practicing good infection control measures in healthcare settings.

It's important to note that while MRSA is a concerning bacterium due to its antibiotic resistance, not all strains of S. aureus are MRSA. Additionally, not all S. aureus infections are caused by MRSA, and many S. aureus infections can still be treated with antibiotics like penicillin. Proper diagnosis and treatment by healthcare professionals are crucial for managing MRSA infections and preventing their spread.

What the scientists discovered is the genetic basis for antibiotic resistance, which easily arises in S. aureus, to give us the Methicillin Resistant, or Multi-Resistant Staphylococcus aureus (MRSA) which is a major problem in hospitals and care homes. This is explained in a news release from the Docherty Institute:

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.

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.

Stefano G. Giulieri, co-senior author
Department of Microbiology and Immunology
The Doherty Institute for Infection and Immunity
The University of Melbourne, Melbourne, VIC, Australia

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.

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.

Professor Benjamin P. Howden, co-senior author
Department of Microbiology and Immunology
The Doherty Institute for Infection and Immunity
The University of Melbourne, Melbourne, VIC, Australia

The researchers have published their findings, open access, in Cell:

Highlights

• Low heritability of clinical outcomes in a large-scale bacterial GWAS of S. aureus sepsis
• Vancomycin resistance had high heritability and contributed to infection severity
• Novel pathoadaptive mutations linked to vancomycin resistance and duration of bacteremia

Summary

Outcomes of severe bacterial infections are determined by the interplay between host, pathogen, and treatments. While human genomics has provided insights into host factors impacting Staphylococcus aureus infections, comparatively little is known about S. aureus genotypes and disease severity. Building on the hypothesis that bacterial pathoadaptation is a key outcome driver, we developed a genome-wide association study (GWAS) framework to identify adaptive mutations associated with treatment failure and mortality in S. aureus bacteremia (1,358 episodes). Our research highlights the potential of vancomycin-selected mutations and vancomycin minimum inhibitory concentration (MIC) as key explanatory variables to predict infection severity. The contribution of bacterial variation was much lower for clinical outcomes (heritability <5%); however, GWASs allowed us to identify additional, MIC-independent candidate pathogenesis loci. Using supervised machine learning, we were able to quantify the predictive potential of these adaptive signatures. Our statistical genomics framework provides a powerful means to capture adaptive mutations impacting severe bacterial infections.

Graphical abstract

The same old, as yet unanswered question for creationist devotees of the putative designer of these organisms: Why do you prefer to have your supposedly omnibenevolent creator god portrayed as a pestilential sadist, rather than have people understand how they are the result of a god-free, mindless evolutionary process?

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