Refuting Creationism - How A Common Bacterium Became A Dangerous Pathogen - By Evolution, Naturally

Pseudomonas aeruginosa

Pseudomonas aeruginosa

Scientists map how deadly bacteria evolved to become epidemic | University of Cambridge

Aficionados of creationism's putative intelligent designer will doubtless be thrilled to discover the imaginative lengths it's gone to to ensure as many people get sick as possible with its cleverly designed bacterium, Pseudomonas aeruginosa, which has gradually been modified over the last 200 years to make it more effective and more resistant to the antibiotics medical science has developed to protect us. There is even a strain specially 'designed' to infect children with cystic fibrosis, just to add to their suffering.

Since these modifications involve genetic mutations which improve the bacterium's ability to love and replicate, we can dismiss the scientific gibberish Michael J Behe invented to explain parasites away as 'devolutionary' and due to 'genetic entropy, since even Michael J Behe would be hard pressed to explain how an advantageous mutation can be less perfect that what went before it. Something better can't be less perfect than something less good, unless you invoke a private definition of 'perfect' that means something which can be bettered.

So, what are these changes in this dangerous pathogen that makes it a problem for people with other health conditions?

Tell me all about the bacterium, Pseudomonas aeruginosa, and what makes it so dangerous to people with underlying respiratory diseases. Overview of Pseudomonas aeruginosa

Pseudomonas aeruginosa is a Gram-negative, rod-shaped bacterium known for its versatility and adaptability. It is ubiquitous in the environment, found in soil, water, and on surfaces in hospitals and other settings. This bacterium is an opportunistic pathogen, meaning it typically affects individuals with weakened immune systems or underlying health conditions. Characteristics

• Gram-Negative: The cell wall structure of P. aeruginosa includes an outer membrane that contributes to its resistance to many antibiotics.
• Motility: It possesses flagella, which allows it to move and colonize new areas.
• Biofilm Formation: P. aeruginosa can form biofilms, which are protective layers that shield bacterial communities from the immune system and antibiotics.
• Pigment Production: It produces pigments like pyocyanin and pyoverdine, which can be involved in iron acquisition and can contribute to its pathogenicity.

Virulence Factors

P. aeruginosa has several virulence factors that make it particularly dangerous:

1. Exotoxins: Toxins such as Exotoxin A inhibit protein synthesis in host cells, leading to cell death.
2. Enzymes: Enzymes like elastase and alkaline protease degrade host tissues and evade immune responses.
3. Efflux Pumps: These pumps expel antibiotics out of the bacterial cell, contributing to antibiotic resistance.
4. Quorum Sensing: This communication system regulates gene expression related to virulence and biofilm formation.

Pathogenesis in Respiratory Diseases

P. aeruginosa is particularly dangerous to individuals with underlying respiratory diseases, such as:

1. Cystic Fibrosis (CF):
   • In CF patients, thick mucus in the lungs creates an ideal environment for P. aeruginosa colonization.
   • The bacteria form biofilms within the mucus, making it difficult to eradicate with antibiotics.
   • Chronic infection leads to persistent inflammation, lung tissue damage, and a decline in lung function.
2. Chronic Obstructive Pulmonary Disease (COPD):
   • COPD patients have damaged airways and impaired mucus clearance, facilitating bacterial colonization.
   • Infections can exacerbate COPD symptoms, leading to increased frequency of hospitalizations and a decline in overall health.
3. Ventilator-Associated Pneumonia (VAP):
   • Patients on mechanical ventilation are at high risk of P. aeruginosa infections due to compromised airway defenses.
   • VAP caused by P. aeruginosa is associated with high morbidity and mortality rates.

Antibiotic Resistance

P. aeruginosa is notorious for its multi-drug resistance, making infections challenging to treat:

• Intrinsic Resistance: Natural resistance to many antibiotics due to the impermeable outer membrane and efflux pumps.
• Acquired Resistance: Gains resistance through horizontal gene transfer and mutations.
• Adaptive Resistance: Ability to develop resistance in response to environmental pressures, including antibiotic exposure.

Clinical Management

Treatment of P. aeruginosa infections involves:

1. Antibiotics:
   • Combination therapy with antibiotics like beta-lactams, aminoglycosides, and fluoroquinolones.
   • Carbapenems are often reserved for multi-drug resistant strains.
2. Antibiotic Stewardship:
   • Careful selection and optimization of antibiotic use to prevent the development of resistance.
3. Adjunct Therapies:
   • Aerosolized antibiotics for lung infections.
   • Agents targeting biofilm disruption.
4. Monitoring and Supportive Care:
   • Regular monitoring of lung function in patients with chronic respiratory diseases.
   • Supportive care to manage symptoms and improve quality of life.

Prevention

Preventing P. aeruginosa infections, especially in hospital settings, involves:

• Infection Control Measures: Rigorous hand hygiene, sterilization of equipment, and isolation of infected patients.
• Environmental Controls: Monitoring water sources and surfaces for contamination.
• Vaccination: Ongoing research into developing effective vaccines against P. aeruginosa.

Conclusion

Pseudomonas aeruginosa's adaptability, virulence factors, and resistance mechanisms make it a formidable pathogen, particularly dangerous for individuals with underlying respiratory conditions. Effective management requires a combination of antibiotic therapy, infection control measures, and ongoing research to develop new treatments and preventive strategies.

To understand this better an international team led by scientists at the University of Cambridge, examined DNA data from almost 10,000 samples taken from infected individuals, animals, and environments around the world, to create phylogenetic trees – ‘family trees’ – that show how the bacteria from the samples are related to each other, and so discover how they have evolved over the past 200 years.

Their findings are published in the journal Science, sadly copyright protected, but available online, however the structured abstract contains a lot of detail. The research is also explained in a Cambridge University press release:

Scientists map how deadly bacteria evolved to become epidemic

Pseudomonas aeruginosa – an environmental bacteria that can cause devastating multidrug-resistant infections, particularly in people with underlying lung conditions – evolved rapidly and then spread globally over the last 200 years, probably driven by changes in human behaviour, a new study has found.

P. aeruginosa is responsible for over 500,000 deaths per year around the world, of which over 300,000 are associated with antimicrobial resistance (AMR). People with conditions such as COPD (smoking-related lung damage), cystic fibrosis (CF), and non-CF bronchiectasis, are particularly susceptible.

How P. aeruginosa evolved from an environmental organism into a specialised human pathogen was not previously known. To investigate this, an international team led by scientists at the University of Cambridge examined DNA data from almost 10,000 samples taken from infected individuals, animals, and environments around the world. Their results are published today in Science

By mapping the data, the team was able to create phylogenetic trees – ‘family trees’ – that show how the bacteria from the samples are related to each other. Remarkably, they found that almost seven in ten infections are caused by just 21 genetic clones, or ‘branches’ of the family tree, that have rapidly evolved (by acquiring new genes from neighbouring bacteria) and then spread globally over the last 200 years. This spread occurred most likely as a result of people beginning to live in densely-populated areas, where air pollution made our lungs more susceptible to infection and where there were more opportunities for infections to spread.

These epidemic clones have an intrinsic preference for infecting particular types of patients, with some favouring CF patients and other non-CF individuals. It turns out that the bacteria can exploit a previously unknown immune defect in people with CF, allowing them to survive within macrophages. Macrophages are cells that ‘eat’ invading organisms, breaking them down and preventing the infection from spreading. But a previously-unknown flaw in the immune systems of CF patients means that once the macrophage ‘swallows’ P. aeruginosa, it is unable to get rid of it.

Having infected the lungs, these bacteria then evolve in different ways to become even more specialised for a particular lung environment. The result is that certain clones can be transmitted within CF patients and other clones within non-CF patients, but almost never between CF and non-CF patient groups.

Our research on Pseudomonas has taught us new things about the biology of cystic fibrosis and revealed important ways we might be able to improve immunity against invading bacteria in this and potentially other conditions.

From a clinical perspective, this study has revealed important information about Pseudomonas. The focus has always been on how easily this infection can spread between CF patients, but we’ve shown that it can spread with worrying ease between other patients, too. This has very important consequences for infection control in hospitals, where it’s not uncommon for an infected individual to be on an open ward with someone potentially very vulnerable.

We are incredibly lucky at Royal Papworth Hospital where we have single rooms and have developed and evaluated a new air-handling system to reduce the amount of airborne bacteria and protect all patients.

Professor Andres Floto, senior author
Director of the UK Cystic Fibrosis Innovation Hub
University of Cambridge, Cambridge, UK
And Royal Papworth Hospital NHS Foundation Trust.

It’s remarkable to see the speed with which these bacteria evolve and can become epidemic and how they can specialise for a particular lung environment. We really need systematic, pro-active screening of all at risk patient groups to detect and hopefully prevent the emergence of more epidemic clones.

Dr Aaron Weimann, first author
Victor Phillip Dahdaleh Heart & Lung Research Institute
University of Cambridge, Cambridge, UK.

Structured Abstract

INTRODUCTION
The major human bacterial pathogen Pseudomonas aeruginosa causes multidrug-resistant infections, particularly in people with underlying immunodeficiencies or inflammatory lung diseases such as cystic fibrosis (CF). However, it remains unclear how P. aeruginosa has evolved into a highly adapted, globally disseminated pathogen.

RATIONALE
We therefore sought to understand the pathogenic evolution of P. aeruginosa by combining population-level genomic exploration with transcriptomic and phenotypic studies.

RESULTS
We analyzed a global collection of 9829 isolates of P. aeruginosa, identifying 21 major clones, which we call “epidemic” clones. These epidemic clones caused most clinical P. aeruginosa infections worldwide, were widely distributed across the phylogenetic tree, and had all spread globally. We estimate that these epidemic clones emerged from ancestral locations distributed around the world and then expanded nonsynchronously between the late 17th and late 20th centuries, potentially driven by changes in human population density, migration patterns, and/or air pollution. Using pan-genome analysis, we identified significant differences between epidemic and sporadic isolate genomes in the acquisition of genes involved in specific cellular processes such as transcriptional control (see figure).

We found that epidemic clones appeared to have intrinsic preferences for CF or non-CF individuals, and we discovered a clear expression signature of genes positively and negatively associated with CF affinity. We found that high-CF-affinity clones were better able to survive within CF macrophages, in part mediated by expression of the stringent response modulator DksA1, suggesting that enhanced host innate immune evasion might explain the intrinsic success at infecting CF patients of certain epidemic clones (see figure).

Examining the recent mutation history of individual clones to understand how epidemic clones of P. aeruginosa have adapted to the human host through multiple rounds of within-patient evolution, we identified 224 of 5641 genes that had a higher total mutational burden than expected by chance, which we call “pathoadaptive” genes.

We found that the products of these pathoadaptive genes were tightly interconnected, indicating their likely coordinated functional roles. Many genes were more frequently mutated in either CF or non-CF isolates, suggesting that distinct functional programs were being modified as part of host-specific adaptation (see figure). Pathoadaptive genes were frequently associated with changes in transmissibility and/or host-specific adaptation, thereby potentially driving host specialization. In support of this notion, we found strong evidence of cross-infection either between CF patients or between non-CF patients, but very little CF to non-CF transmission (see figure).

CONCLUSION
Our findings describe the key sequential steps involved in the evolution of P. aeruginosa from an environmental organism to a major human pathogen. These steps include saltatory evolution caused by horizontal gene transfer generating epidemic clones, varying intrinsic host affinities of these clones (linked to specific transcriptional changes enabling survival within macrophages), and multiple rounds of convergent, host-specific adaptation, eventually resulting in the loss of their ability to transmit between different patient groups. Our work thus highlights the importance of global surveillance and cross-infection prevention in averting the emergence of future epidemic clones.

Host-specific evolution of P. aeruginosa.
Shown are key steps in the pathogenic evolution of P. aeruginosa: (1) Environmental clones with epidemic potential are created through horizontal gene transfer, as revealed by comparative pan-genome graph analysis; (2) intrinsic, transcriptionally driven varying preference of emerging clones for CF hosts is associated with an increased ability to survive within CF macrophages; (3) distinct trajectories of subsequent evolution of isolates infecting CF versus non-CF patients are mediated by mutations in 224 pathoadaptive genes, which influence transmissibility and/or host-specific adaptation; and (4) as a result of host specialization, transmission is constrained between CF and non-CF patients. [Top panel created with BioRender.com]

Abstract
The major human bacterial pathogen Pseudomonas aeruginosa causes multidrug-resistant infections in people with underlying immunodeficiencies or structural lung diseases such as cystic fibrosis (CF). We show that a few environmental isolates, driven by horizontal gene acquisition, have become dominant epidemic clones that have sequentially emerged and spread through global transmission networks over the past 200 years. These clones demonstrate varying intrinsic propensities for infecting CF or non-CF individuals (linked to specific transcriptional changes enabling survival within macrophages); have undergone multiple rounds of convergent, host-specific adaptation; and have eventually lost their ability to transmit between different patient groups. Our findings thus explain the pathogenic evolution of P. aeruginosa and highlight the importance of global surveillance and cross-infection prevention in averting the emergence of future epidemic clones.

Aaron Weimann et al.
Evolution and host-specific adaptation of Pseudomonas aeruginosa. Science 385, eadi0908 (2024). DOI:10.1126/science.adi0908

© 2024 The Authors, published by American Association for the Advancement of Science.
Reprinted with kind permission under license #5823260211605

The grown-up, scientific explanation of these changes over time is, of course, simply explained by the Theory of Evolution. These scientists have no doubt about that. They also discovered that the pathogen acquired new genetic information (something creationists are told is impossible) by horizontal gene transfer from other bacteria.

They think the major environmental drivers of this evolution has been industrial pollution with smoke and dust particles causing underlying respiratory diseases that create conditions for opportunistic parasites such as P. aeruginosa to exploit, so any mutations that have improved their ability to exploit these new opportunities will tend to produce more offspring better able to infect patients who are already sick.

Additionally, as medical science has progressed, more people are living longer with chronic conditions such as cystic fibrosis and are frequently admitted to hospitals where these nosocomial organisms tend to be concentrated and acquire antibiotic resistance.

Curiously, since they also claim their putative 'intelligent' [sic] designer is also the reputed omnibenevolent god of the Bible and Qur'an, creationists would prefer us to think this same god is responsible for these pestilential organisms, rather than accept that they evolved naturally without the intervention of supernatural magic.

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