Scientists working at the Department of Molecular & Biomedical Sciences, University of Maine, Orono, Maine, USA, have discovered a phenomenon that, if you're gullible enough to be a creationist, which admittedly would make it unlikely that you'd be reading, let alone understanding, this blog, must look like the putative intelligent [sic] designer has lost the plot.
The discovery is that when two particular organism occur together to produce a polymicrobial disease, one of the organisms will work against the other. In the presence of an antibiotic, it will not only prevent the other organism developing resistance, but will remove it from the infection site.
The two organisms are the fungus, Candida albicans and the bacterium, Pseudomonas aeruginosa, both of which are opportunistic pathogens that can be found in similar sites of infection such as in burn wounds and most importantly in the lungs of cystic fibrosis and mechanically ventilated patients.
As the University of Maine news release explains:
More detail is given in the abstract tho the team's open access paper published in the journal Infection and Immunity:Polymicrobial infections are challenging to treat not only because of the lack of understanding of how invading microorganisms interact but also because we don’t know how these interactions affect treatment efficacy. Our work demonstrates that polymicrobial interactions can indeed affect treatment efficacy and, most importantly, it highlights the importance of nutrient availability in the environment — such as iron in our study — and how it modulates treatment efficacy.Pathogens don’t always work against drug treatments. Sometimes, they can strengthen them, according to a new University of Maine study.
Siham Hattab, lead author
PhD candidate.
Department of Molecular and Biomolecular Sciences. University of Maine, Orono, Maine, USA
Diseases caused by a combination of bacteria, viruses, fungi and parasites — also known as polymicrobial infections — are challenging to treat because scientists don’t fully understand how pathogens interact during infection and how these interactions impact the drugs used to treat them.
In a study published in the journal Infection and Immunity, researchers in the Molecular & Biomedical Sciences Department looked at two pathogens that often occur at similar sites, particularly in cystic fibrosis and mechanically ventilated patients: Candida albicans and Pseudomonas aeruginosa.
Candida is the fourth most common hospital-acquired pathogen, and is particularly difficult to treat. It is targeted by a number of antifungal agents, but some only slow it rather than kill it outright. Meanwhile, P. aeruginosa infects 90% of all adult cystic fibrosis patients. Combined, C. albicans and P. aeruginosa cause more serious disease in cystic fibrosis and ventilated patients.
We are really excited to have revealed that sometimes drugs against fungal infection can work even better in a more ‘real-world’ situation than in the test tube. There is still a lot to learn about how pathogens interact during infection, and it will be interesting to see how the bacteria manage to work with the drugs to target CandidaThe researchers investigated the effectiveness of an antifungal drug, fluconazole, in the test tube and during infection of the zebrafish with both pathogens. Fluconazole is known to slow fungal growth, but Candida can become tolerant to the drug and not only survive, but also develop tolerance that leads to failed therapy and, potentially, death.
Robert Wheeler, senior author
Associate professor of microbiology
Department of Molecular & Biomedical Sciences
University of Maine, Orono, Maine, USA.
What the study found was promising. The results showed that P. aeruginosa works with fluconazole to eliminate drug tolerance and clear the C. albicans infection in the culture and the zebrafish.
What’s more, the bacteria also enhance the drug’s ability against a second pathogenic Candida species that tends to be more resistant to the drug.
The increased effectiveness of the drug suggests to the researchers that there is still much more to learn about how current drugs work when targeting these dangerous and complex polymicrobial infections.
ABSTRACTThe evolutionary explanation for opportunistic organisms that cause these infections, the development of drug resistance, and the competition for resources, is obvious to anyone who understands even the basics of evolutionary biology, but what is not obvious is how this can be explained as the work of an intelligence.
Polymicrobial infections are challenging to treat because we don’t fully understand how pathogens interact during infection and how these interactions affect drug efficacy. Candida albicans and Pseudomonas aeruginosa are opportunistic pathogens that can be found in similar sites of infection such as in burn wounds and most importantly in the lungs of CF and mechanically ventilated patients. C. albicans is particularly difficult to treat because of the paucity of antifungal agents, some of which lack fungicidal activity. In this study, we investigated the efficacy of anti-fungal treatment during C. albicans-P. aeruginosa coculture in vitro and co-infection in the mucosal zebrafish infection model analogous to the lung. We find that P. aeruginosa enhances the activity of fluconazole (FLC), an anti-fungal drug that is fungistatic in vitro, to promote both clearance of C. albicans during co-infection in vivo and fungal killing in vitro. This synergy between FLC treatment and bacterial antagonism is partly due to iron piracy, as it is reduced upon iron supplementation and knockout of bacterial siderophores. Our work demonstrates that FLC has enhanced activity in clinically relevant contexts and highlights the need to understand antimicrobial effectiveness in the complex environment of the host with its associated microbial communities.
Hattab, Siham; Dagher, Anna-Maria; Wheeler, Robert T.; Noverr, Mairi C.(2022)
Pseudomonas Synergizes with Fluconazole against Candida during Treatment of Polymicrobial Infection
Infection and Immunity; e00626-21, DOI:10.1128/iai.00626-21
Copyright: © 2022 The authors / American Society for Microbiology
Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Firstly, what is the sense of creating pathogenic parasites in the first place and then designing one to fight the other when they try to co-exist? If the purpose of both organisms is to make sick people sicker - and, because that is what they do we can be sure that any omniscient designer who designed them, designed them for that purpose - then why create one so it reduces the ability of the other to do what they were designed to do?
Like most things in the world of ID creationism, none of it makes any sense when examined in detail. The reason for that is also obvious - the is no intelligence involved in the design of these organisms. The whole thing is the result of a natural process in which planning, intelligence and morality play no part.
Competition between bacteria and fungi led to Fleming discovering penicillin, of course, and indeed, numerous front line antibiotics were first discovered as antibacterial agents secreted by fungi. That reverse competition by bacteria can occur is a natural outcome of the same processes that led to fungal synthesis of antibacterial agents. In short, if a new feature works to enhance the reproductive fitness of an organism, evolution will select for it.
ReplyDeleteMind you, it's quite an eye opener to see Pseudomonas aeruginosa acting as a therapeutic agent in this setting! If this turns out to be clinically useful, this will be another victory for evolutionary medicine!
Though I'm more familiar with evolutionary medicine being applied to cancer (one of my correspondents has published papers in this field), seeing it deliver new ways of tackling the complications of cystic fibrosis will be a source of much delight.