Climate Change's Silent Threat
The Fungal Awakening
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We're witnessing the quiet emergence of a global threat that could redefine public health in the coming decades. While the world fixates on flashy disaster headlines and political theater, a more insidious danger is evolving in the shadows of our warming planet—pathogenic fungi that are adapting to higher temperatures, including our body temperature, with alarming speed.
The recent Heliox podcast deep dive into fungal pathogens and climate change revealed a reality that should disturb us all: the environmental shifts we've set in motion are creating perfect conditions for fungal evolution that threatens human health in ways we're only beginning to understand.
The Perfect Evolutionary Storm
For millions of years, humans have enjoyed relative protection from fungal infections due to a simple biological reality—our warm body temperature has acted as a thermal barrier that most environmental fungi simply couldn't breach. Only a few specialized fungi evolved the ability to survive at human body temperature.
That protection is eroding before our eyes.
As global temperatures rise, fungi are adapting. What's worse, they're not just adapting to survive heat—they're developing enhanced mechanisms that make them more dangerous to us:
Heat shock proteins that protect them from thermal damage
Thicker cell walls resistant to our immune defenses
Increased melanin production shielding them from multiple stressors
Enhanced biofilm formation making them treatment-resistant
Genetic adaptations improving their survival in hostile environments
The case of Aspergillus latus exemplifies this disturbing trend. This "cryptic hybrid" fungus resulted from the fusion of two different species millions of years ago. Rather than discarding redundant genes as might be expected, it retained over 91% of its duplicated genetic material. The result is a highly adaptable organism with an expanded genetic toolbox that gives it unprecedented evolutionary advantages.
Now imagine thousands of fungal species worldwide undergoing similar adaptations in response to our rapidly changing climate.
When Disasters Strike, Fungi Strike Back
Climate change isn't just making fungi more dangerous—it's creating more opportunities for exposure through increasingly frequent and severe natural disasters.
After hurricanes, floods, and tsunamis, fungal outbreaks follow with grim predictability. The Lancet Microbe review highlighted by the podcast documents numerous examples: soft tissue fungal infections after the 2004 Indian Ocean tsunami, invasive mold infections following Hurricane Harvey in 2017, and pulmonary hemorrhages in infants linked to mold exposure after flooding in 1994.
These aren't isolated incidents. They're previews of a future where climate disasters and fungal outbreaks form a devastating feedback loop:
Climate change intensifies natural disasters
Disasters create ideal conditions for fungal growth and human exposure
Weakened immune systems from disaster stress increase infection susceptibility
Healthcare disruptions in disaster zones limit treatment options
Underreporting masks the true scale of the problem
Most disturbing of all is the likelihood that these fungal outbreaks following disasters are vastly underreported. In the chaos of disaster response, fungal infections often go undiagnosed or unreported as medical resources focus on immediate threats to life.
The Agricultural Connection: A Self-Reinforcing Cycle
Perhaps the most alarming revelation is how human responses to climate change are actually accelerating the development of dangerous fungi.
As climate change drives the evolution of agricultural fungal pests, farmers respond with increased fungicide use. Many agricultural fungicides share chemical structures with medical antifungals, essentially giving environmental fungi "practice" at developing resistance to our medical treatments.
In a cruel irony, our attempts to protect food security in a changing climate are undermining our medical defenses against the same threats. Even more concerning, newer agricultural fungicides in development share mechanisms with novel antifungal drugs intended for human use—potentially rendering these future medical treatments ineffective before they even reach patients.
This represents a dangerous acceleration of natural selection, driven by human activity at both ends: climate change creating conditions for fungal adaptation, and our mitigation efforts inadvertently selecting for resistance traits that make these fungi more dangerous to us.
The Invisible Expansion
Climate change is also reshaping where fungal threats appear. Diseases like coccidiodomycosis (Valley Fever), histoplasmosis, and blastomycosis are expanding beyond their historical ranges as temperatures warm, bringing these threats to populations with no prior exposure or immunity.
Candida auris—a pathogen that emerged seemingly from nowhere in 2009 and is now causing serious healthcare outbreaks globally—represents perhaps the most chilling example of this phenomenon. This highly drug-resistant yeast can survive on surfaces for weeks and has proven extremely difficult to eradicate from healthcare settings.
Scientists increasingly suspect that C. auris may have evolved its thermotolerance through adaptation to the warming wetland environments where it originated—essentially using climate change as an evolutionary stepping stone to overcome the thermal barrier that had previously kept it from infecting humans.
Beyond Thermal Adaptation
The converging threats extend beyond temperature adaptation. The podcast highlighted how pollution in water bodies creates favorable conditions for fungal growth and provides additional food sources for certain species. Microplastics in our waterways offer surfaces for fungal colonization and potentially contribute to antifungal resistance development.
Even seemingly unrelated climate effects like increased UV exposure from ozone depletion can compromise human immunity, making us more vulnerable to opportunistic fungal infections.
Most disturbing is the podcast's mention of a slight decrease in average human body temperature that researchers have documented over recent decades. While small, this shift potentially narrows the thermal gap that fungi must overcome to thrive in our bodies.
The Underfunded Frontier
Despite these converging threats, funding for fungal research remains woefully inadequate compared to other pathogens. We're flying blind into a future where fungi are evolving faster than our understanding of them.
The COVID-19 pandemic taught us the devastating cost of being unprepared for emerging pathogens. Yet the fungal threat developing in plain sight hasn't generated a fraction of the attention or resources needed to address it.
The discovery that Aspergillus latus can co-infect COVID-19 patients should serve as a warning that these threats don't operate in isolation. Future pandemics may feature viral-fungal combinations that exploit different vulnerabilities in our immune defenses.
A Call for Systemic Action
The interconnected nature of these threats demands an equally interconnected response:
Integrated surveillance systems that track fungal pathogens across medical, agricultural, and environmental contexts
Climate-aware infectious disease planning that anticipates how warming will shift pathogen ranges and risks
Coordinated pharmaceutical development between agricultural and medical sectors to prevent cross-resistance
Enhanced disaster response protocols that specifically address fungal infection risks
Increased research funding for fungal pathogens, especially climate-adaptive species
Most importantly, we need to recognize that addressing climate change itself is a public health imperative. Every fraction of a degree matters in the evolutionary race between fungi and humans.
The Time for Attention is Now
In HBO's acclaimed series "The Last of Us," a fungal pandemic decimates humanity after climate change enables a pathogenic fungus to survive at human body temperature. While the specific scenario is fictional, the underlying premise isn't as far-fetched as many would like to believe.
The real fungal threat won't look like a zombie apocalypse. It will emerge gradually through increasing outbreaks following disasters, expanding endemic ranges, rising healthcare-associated infections, and agricultural losses—each pressure point straining our systems until they break.
The scientific evidence presented in the Heliox podcast isn't speculative futurism—it's documenting changes already underway. These emerging fungal threats represent one of the most overlooked consequences of our changing climate.
We're in an arms race with evolution, one that climate change is accelerating to our disadvantage. The fungi aren't coming—they're already here, adapting, evolving, and exploiting the environmental changes we've set in motion.
The question isn't whether fungi will become more dangerous as the planet warms. The question is whether we'll act before these silent opportunists reshape the relationship between humans and infections in ways we're unprepared to handle.
Link References
WHY INFECTIONS by BACTERIA, VIRUSES and FUNGI will INCREASE in the FUTURE ?
Evolutionary origin and population diversity of a cryptic hybrid pathogen
Impact of climate change and natural disasters on fungal infections
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STUDY MATERIALS
Briefing Document
I. Emergence and Underreporting of the Cryptic Hybrid Pathogen Aspergillus latus
The Nature Communications article sheds light on Aspergillus latus, a "cryptic hybrid pathogen" within the Aspergillus section Nidulantes. The study provides a detailed genomic and phenotypic characterization based on an expanded set of 53 globally distributed isolates.
Key Findings:
Hybrid Origin and Genome Stability: A. latus is an allodiploid hybrid, likely arising approximately 13 million years ago from a single hybridization event involving A. spinulosporus and a species closely related to A. quadrilineatus. The hybrid has largely retained the genome organization and content of both parental genomes, with "96.68 ± 2.46% of BUSCO genes are duplicated," indicative of its diploid nature. Macrosynteny analysis further supports this allopolyploid origin.
Limited Recombination Between Subgenomes: Despite the presence of two distinct subgenomes, there is "little evidence of recombination" between them, suggesting a degree of stability in the hybrid genome.
Underreporting Due to Misidentification: A significant finding is the frequent misidentification of A. latus in clinical laboratories using MALDI-TOF mass spectrometry. This is "largely due to the lack of inclusion of standards for the species from MALDI-TOF databases." The study authors argue that this misidentification likely leads to an underestimation of A. latus infections and emphasize the need to include A. latus data in future database updates.
Genetic Diversity and Biosynthetic Potential: While a substantial portion of the A. latus genome (74.27% of gene families) is core, there is significant variation in accessory genes, particularly within "biosynthetic gene clusters (BGCs) involved in secondary metabolism." The accessory BGCome is larger than the core BGCome, suggesting a potential for diverse and novel secondary metabolites, although "the products, if any, of most BGCs are not known."
Distinct Phenotypic Profile: Phenotypic profiling across infection-relevant traits reveals that A. latus is "phenotypically distinct from the other three species (A. spinulosporus, A. quadrilineatus, and A. nidulans), but were most similar to A. spinulosporus." Notably, some A. latus isolates exhibit high drug resistance to caspofungin. Variation in virulence was also observed in an invertebrate moth model.
Balanced Subgenome Expression: Transcriptomic analysis indicates that "both parental subgenomes are actively expressed and respond to environmental perturbations" with nearly equal transcript abundances and similar numbers of differentially expressed genes in response to temperature changes. This suggests both parental contributions to the organism's biology.
Distinguishing Features: The study identifies genomic (larger genome size, duplicated loci) and phenotypic (larger spore size) traits that can help differentiate A. latus from closely related species, aiding in taxonomic accuracy and understanding its epidemiology.
II. Impact of Climate Change and Natural Disasters on Fungal Infections
The Lancet Microbe review article highlights the growing threat of fungal infections exacerbated by climate change and natural disasters.
Key Themes:
Interplay of Environmental and Social Factors: The review emphasizes the complex interplay between "long-term changes in environmental conditions," "social and industrial factors," and the increased incidence of "geo-meteorological disasters" in driving fungal infections.
Fungal Adaptation and Virulence: Climate change, particularly global warming, can drive fungal adaptation to higher temperatures, potentially increasing their thermotolerance and virulence in humans. The example of Candida orthopsilosis originating from warm marine ecosystems illustrates this. Fungal melanin is highlighted for conferring cross-protection against various environmental stresses, including heat, pH, heavy metals, and radiation.
Geographical Range Expansion: Rising temperatures and altered weather patterns are contributing to the expansion of the endemic ranges of pathogenic fungi like Histoplasma capsulatum, Coccidioides immitis, and Blastomyces spp. Modeling suggests significant northward expansion of coccidioidomycosis in the USA.
Airborne Dispersal: Warmer temperatures can affect atmospheric turbulence, influencing the dispersal of fungal spores and potentially leading to wider geographical distribution and range expansion.
Water Contamination: Pollution of water bodies with agricultural and industrial pollutants can create favorable environments for fungal growth, including pathogenic species, leading to increased risks of superficial and systemic fungal infections. Microplastics in water supplies could also promote fungal growth and antifungal resistance.
Fungal Outbreaks After Natural Disasters: The review documents numerous cases of increased fungal infections, particularly mucormycosis and aspergillosis, following various natural disasters like volcanic eruptions, earthquakes, wildfires, floods, tsunamis, tornadoes, and dust storms. Trauma and exposure to contaminated environments are key contributing factors.
Impact on Host Susceptibility: Climate change can indirectly affect human susceptibility to fungal infections through factors like malnutrition, changes in immune responses due to UV radiation and vitamin D deficiency, and altered exposure related to occupation and lifestyle.
Challenges in Diagnosis and Management: The review highlights the limited diagnostic capabilities for fungal infections in many regions, particularly low- and middle-income countries, and the challenges posed by emerging drug-resistant fungi.
One Health Approach: The authors advocate for a "One Health" approach that integrates human, animal, and environmental health to address the complex factors driving the emergence and spread of fungal diseases in a changing climate.
III. Potential Link Between SARS-CoV-2 Infection and Increased Susceptibility to Other Infections
The Lancet Infectious Diseases article investigates the association between a positive COVID-19 test and the rates of future infections with other pathogens in US veterans. While this source doesn't directly focus on fungi, it raises a crucial point about viral infections potentially increasing susceptibility to subsequent infections in general, a concern echoed in the thread below regarding COVID-19's impact.
IV. Concerns About Increased Infections Due to Antibiotic Resistance, Environmental Changes, and COVID-19
The Twitter thread by @ejustin46 synthesizes concerns from recent studies about a future increase in infections caused by bacteria, viruses, and fungi.
Key Points:
Antibiotic Resistance: Overuse of antibiotics in healthcare and agriculture, coupled with a lack of new antibiotic development, is leading to bacteria becoming resistant to treatment. This could make common infections severe.
Climate Change and Urban Growth: Warmer temperatures can help pathogens thrive, and densely populated urban areas can lead to more outbreaks, especially among vulnerable populations. This aligns with the themes discussed in the Lancet Microbe review regarding fungal adaptation and spread.
COVID-19's Role: The thread highlights two ways COVID-19 exacerbates the problem:
Weakened Immune System: The virus can weaken the immune system, making individuals more susceptible to subsequent bacterial and fungal infections. This supports the idea that viral infections can increase vulnerability to other pathogens.
Increased Antibiotic Use: The pandemic has strained healthcare resources, leading to increased antibiotic use for secondary infections, which may worsen antibiotic resistance.
V. Mutation in SARS-CoV-2 and Pathogenicity
Another thread by @ejustin46 discusses a study on a specific mutation (P812S) in SARS-CoV-2 found in a chronically ill individual. This mutation was observed to reduce the virus's ability to enter cells and cause cell fusion (associated with less severe disease) but also helped the virus evade certain antibodies. This highlights the ongoing evolution of viruses and the potential for mutations to alter pathogenicity and immune evasion.
Overall Implications:
These sources collectively paint a picture of increasing challenges related to infectious diseases, including fungal and viral pathogens. The emergence and potential underreporting of cryptic fungal pathogens like A. latus, the exacerbating effects of climate change and natural disasters on fungal infections, and the potential for viral infections like SARS-CoV-2 to increase susceptibility to other pathogens, all contribute to a complex and evolving landscape of infectious disease threats. Addressing these challenges requires a multi-faceted approach encompassing improved diagnostics, better antimicrobial stewardship, ongoing research into new treatments, public health interventions, and a recognition of the interconnectedness of environmental, animal, and human health.
Key Concepts
I. Review of "Evolutionary origin and population diversity of a cryptic hybrid pathogen"
A. Introduction and Background
What was the primary goal of this study?
What is Aspergillus latus, and why is it considered a "cryptic" pathogen?
What prior knowledge or limitations existed regarding A. latus biology and evolution before this study?
What methods did the researchers use to expand the genomic data for A. latus?
B. Hybrid Origin of A. latus
What key genomic features strongly suggest that A. latus is a hybrid species?
Which species are identified as the likely parental contributors to the A. latus hybrid genome? What evidence supports this?
Explain the concept of allodiploidy in the context of A. latus.
What is the significance of ohnolog retention in the A. latus genome? What were the findings regarding the parental origin of retained ohnologs?
Did the study find evidence of significant recombination between the subgenomes of A. latus? What were the findings?
C. Evolutionary History and Timing
How did the researchers investigate the number of hybridization events that led to A. latus? What was the most parsimonious conclusion?
Using molecular clock analyses, when approximately did A. latus originate? In what geological epoch did this occur?
D. Genomic Diversity within A. latus
How did the researchers assess gene content variation among different A. latus isolates? Define the terms core, softcore, shell, and cloud genes/BGCs.
What were the key findings regarding the diversity of gene families versus biosynthetic gene clusters (BGCs) in A. latus?
How did protein sequence length and functional annotation correlate with gene family occupancy (core vs. accessory)?
What do the findings suggest about the potential for novel secondary metabolites in A. latus?
E. Phenotypic Characterization
How did the phenotypic profiles of A. latus compare to those of closely related Aspergillus species? Which species was most similar?
What infection-relevant traits were identified as major contributors to the phenotypic variance among the species?
What were the findings regarding antifungal drug resistance in A. latus isolates?
How did A. latus gene expression patterns in response to temperature changes compare between the two parental subgenomes? What were the findings regarding ohnologs?
F. Distinguishing A. latus
What genomic characteristics can be used to differentiate A. latus from closely related species?
What phenotypic characteristics can be used to differentiate A. latus from closely related species? Why is accurate identification important?
G. Pangenome Comparisons
How does the size and core genome percentage of the A. latus pangenome compare to those of other fungal pathogens like Candida albicans and Aspergillus fumigatus?
What does the higher proportion of accessory BGCs in A. latus suggest about their evolutionary dynamics?
H. Hybrid Phenotype Mechanisms
Provide examples from the study of how A. latus phenotypes might be additive or resemble one parent more than the other.
How do the gene expression patterns of A. latus subgenomes compare to those observed in other allodiploid hybrids like Verticillium longisporum? What might explain these differences?
What were the findings regarding the mutation rates of the two A. latus subgenomes?
I. Methods
Briefly describe the methods used for genome sequencing and assembly.
How was species identification of the clinical isolates performed? What were the limitations of MALDI-TOF MS in this case?
Outline the approaches used to assign genes to their parent-of-origin in the A. latus hybrid genome.
Describe the process of phylogenetic analysis used to reconstruct evolutionary histories and estimate divergence times.
What methods were used to analyze gene content variation and identify biosynthetic gene clusters?
Summarize the techniques used for phenotypic profiling, including growth assays, antifungal susceptibility testing, and spore size measurements.
How was gene expression analyzed using RNA sequencing?
II. Review of "Impact of climate change and natural disasters on fungal infections"
A. Introduction and Scope
What is the central theme of this review article?
What are the main categories of factors discussed in relation to increased fungal infections? (Refer to Figure 2)
B. Climate Change and Fungal Adaptation
How can global warming contribute to the emergence of new or more virulent fungal pathogens? Provide specific examples from the text.
Explain how fungal melanin can provide cross-protection against various environmental stressors, including those associated with climate change.
How does the review discuss the impact of altered CO2 levels and UV radiation on fungi?
C. Environmental Contamination and Fungal Growth
How can agricultural and industrial pollutants in water bodies affect fungal growth and diversity?
What implications does the ability of some fungi to degrade plastics have for the prevalence and potential antifungal resistance?
D. Fungal Dissemination and Exposure
How can climate change and weather patterns influence the airborne dispersal of fungal spores?
What role do natural disasters play in the dissemination and increased exposure to pathogenic fungi? Provide examples of specific disasters and associated fungal infections (Refer to Figure 4).
E. Geographic Expansion of Endemic Mycoses
Provide examples of fungal pathogens whose endemic ranges are projected to expand due to climate change. What evidence or modeling supports these projections?
Why might cases of endemic mycoses be increasingly observed outside their traditional geographic boundaries?
F. Impact of Social and Industrial Factors
How do factors like urbanization, mass migration, and economic inequality intersect with climate change to influence the risk of fungal infections?
What is the role of healthcare access and food/water safety in the context of increasing fungal infections?
G. COVID-19 and Fungal Infections
Based on the "Thread by @ejustin46," how might the COVID-19 pandemic contribute to an increase in bacterial and fungal infections?
According to the "Lancet Infectious Diseases" article, what was the aim of the study on post-COVID-19 pathogen infections in US veterans? What were the broader implications discussed in the "Thread" regarding SARS-CoV-2 and the immune system?
H. Conclusion and Future Directions
What are the overall concerns highlighted in the review regarding the future of fungal infections in the context of climate change and other factors?
What potential areas for future research or intervention are implied in the review?
III. Review of "Rates of infection with other pathogens after a positive COVID-19 test versus a negative test in US veterans..."
A. Study Objective
What was the primary research question addressed in this study?
B. Study Design
What type of study design was employed (e.g., randomized controlled trial, cohort study)?
What was the study population and the timeframe of the data collection?
C. Key Findings (based on the provided excerpt)
What general conclusion is suggested by the introduction regarding the association between SARS-CoV-2 infection and future infections with other pathogens? (Note: The full results are not provided in the excerpt.)
D. Implications (based on the provided excerpt)
Why is it important to investigate the potential link between SARS-CoV-2 infection and subsequent infections with other pathogens?
IV. Review of "Thread by @ejustin46 on Thread Reader App"
A. Main Arguments
According to the thread, what are the three main factors contributing to a future increase in infections?
How does antibiotic resistance play a role in this increased risk?
How do climate change and urban growth contribute to the rise of viral and fungal infections, according to the thread?
What is the thread's perspective on the impact of the COVID-19 pandemic on susceptibility to other infections and antibiotic resistance?
B. Call to Action
What actions does the thread suggest to address the increasing risk of infections?
C. Reference to Studies
The thread mentions "2 recent studies." Based on the provided references in the thread and the other source materials, can you identify potential sources for these studies?
V. Review of "What a 'CLEVER' SARS-COV-2 virus!" Thread
A. Focus of the Thread
What is the main topic discussed in this shorter thread?
B. P812S Mutation
What is the P812S mutation, and in what context was it observed?
What effects did the study find regarding this mutation's impact on the virus's ability to enter cells and cause syncytia formation? How is this linked to disease severity?
How did the P812S mutation affect the virus's ability to evade antibodies?
Quiz & Answer Key
What are the two likely parental species that contributed to the allodiploid genome of Aspergillus latus, as identified by Steenwyk et al. (2024)? What genomic evidence supports this conclusion?
According to Steenwyk et al. (2024), approximately when did Aspergillus latus originate, based on molecular clock analyses? In what geological period did this emergence occur?
How does the review by Seidel et al. (2024) suggest that rising global temperatures could contribute to the emergence of new fungal pathogens? Provide one specific example mentioned in the text.
According to Seidel et al. (2024), how might natural disasters like floods or volcanic eruptions increase the risk of fungal infections? Give a specific example of a fungal infection linked to such events.
Based on the thread by @ejustin46, what are the two environmental changes, besides COVID-19, that are contributing to an increase in viral and fungal infections? Briefly explain each.
How did Steenwyk et al. (2024) demonstrate that Aspergillus latus is likely underreported as a human pathogen? What standard clinical method often misidentifies it?
According to Seidel et al. (2024), how might the presence of microplastics in water supplies inadvertently promote fungal growth and potentially antifungal resistance?
Steenwyk et al. (2024) categorized genes in Aspergillus latus isolates based on their occupancy. Define what "core genes" and "accessory genes" refer to in this context.
Based on the thread by @ejustin46, how might the COVID-19 pandemic have contributed to the problem of antibiotic resistance?
According to Steenwyk et al. (2024), what are two characteristics (one genomic and one phenotypic) that can help distinguish Aspergillus latus from its close relatives?
Quiz Answer Key
The likely parental species of Aspergillus latus are Aspergillus spinulosporus and a species closely related to Aspergillus quadrilineatus. This is supported by macrosynteny analysis revealing large genomic segments in A. latus that are syntenic with these two species.
According to Steenwyk et al. (2024), Aspergillus latus likely arose approximately 13 million years ago. This emergence occurred during the Miocene epoch.
Seidel et al. (2024) suggest that rising global temperatures can allow previously less thermotolerant ascomycetous yeast taxa to adapt and become human pathogens, citing Candida orthopsilosis, originating from warm marine ecosystems, as an example.
Seidel et al. (2024) explain that natural disasters can disrupt the environment and increase exposure to fungi; for instance, necrotizing soft tissue lesions caused by various fungi have been reported after volcanic cataclysms.
According to @ejustin46, warmer temperatures, associated with climate change, can help pathogens thrive. Additionally, densely populated urban areas can lead to more disease outbreaks, especially among vulnerable populations.
Steenwyk et al. (2024) found that MALDI-TOF mass spectrometry, a standard clinical method, often misidentified Aspergillus latus isolates due to the lack of species-specific standards in the databases, suggesting underreporting.
Seidel et al. (2024) suggest that the ubiquitous nature of microplastics in global water supplies could provide a substrate or surface for fungal growth, potentially leading to increased fungal biomass and opportunities for the development of antifungal resistance.
In the context of Steenwyk et al.'s (2024) study, "core genes" are gene families present in 100% of the Aspergillus latus isolates examined. "Accessory genes" are gene families present in less than 100% of the isolates.
According to @ejustin46, the COVID-19 pandemic has strained healthcare resources, leading to increased antibiotic use for secondary bacterial infections in COVID-19 patients, which may worsen the problem of antibiotic resistance.
According to Steenwyk et al. (2024), a genomic characteristic distinguishing Aspergillus latus is its larger genome size and gene repertoire compared to close relatives. A phenotypic characteristic is its larger spore size, which is correlated with its larger genome.
Essay Questions
Discuss the evolutionary origins of Aspergillus latus as a cryptic hybrid pathogen. Synthesize evidence from Steenwyk et al. (2024) regarding its genomic characteristics, likely parental species, and the estimated timing of its emergence. Consider the implications of its hybrid nature for its biology and potential pathogenicity.
Analyze the potential impact of climate change on the prevalence and emergence of fungal infections, drawing upon the review by Seidel et al. (2024). Discuss specific mechanisms by which altered environmental conditions, natural disasters, and human activities could contribute to increased risk and geographic expansion of fungal diseases.
Compare and contrast the findings of Steenwyk et al. (2024) regarding the genomic and phenotypic diversity of Aspergillus latus with the broader discussion of fungal adaptation and virulence in response to environmental stressors presented by Seidel et al. (2024). How might the genomic plasticity of a hybrid pathogen like A. latus contribute to its ability to respond to changing environmental conditions?
Evaluate the potential interplay between the COVID-19 pandemic and the increasing threat of fungal infections, referencing the threads by @ejustin46 and the study on US veterans. Consider the potential impacts of SARS-CoV-2 on the immune system and the broader context of antibiotic resistance and environmental changes discussed in the other source materials.
Critically assess the challenges associated with identifying and understanding emerging fungal pathogens like Aspergillus latus, considering both the limitations of current diagnostic methods highlighted by Steenwyk et al. (2024) and the potential for increased emergence due to factors discussed by Seidel et al. (2024). What strategies or research directions might be crucial for addressing these challenges in the future?
Glossary of Key Terms
Cryptic Species: A species that is morphologically indistinguishable from other species but is genetically distinct.
Hybrid Pathogen: A pathogen that originates from the genetic combination of two or more distinct species.
Allodiploid: A diploid organism whose chromosomes are derived from two or more genetically distinct ancestral species.
Genome Assembly: The process of taking short DNA sequences (reads) and putting them back together to reconstruct the entire genome of an organism.
N50/L50: Metrics used to assess the contiguity of a genome assembly. N50 is the length such that 50% of the total assembled bases are in contigs of this length or longer. L50 is the number of contigs of length N50 or longer.
Phylogenetic Analysis: The study of evolutionary relationships among organisms or genes, often represented in the form of a phylogenetic tree.
Macrosynteny: The conserved order of genes on chromosomes across different species.
Orthologs: Genes in different species that evolved from a common ancestral gene, usually retaining the same function.
Ohnologs: Paralogous genes (genes related by duplication within a genome) that arose through whole-genome duplication events.
Recombination: The exchange of genetic material between homologous chromosomes, leading to new combinations of alleles.
Molecular Clock: A technique that uses the rate of accumulation of genetic mutations to estimate the time of divergence between lineages.
Maximum Likelihood Phylogeny: A phylogenetic tree constructed by finding the tree topology and branch lengths that maximize the probability of observing the given sequence data under a specific evolutionary model.
Gene Content Variation: Differences in the presence or absence of specific genes or gene families among different isolates of a species.
Core Genome: The set of genes that are present in all isolates of a given species.
Accessory Genome: The set of genes that are present in some but not all isolates of a given species.
Biosynthetic Gene Cluster (BGC): A group of genes that are located close together on a chromosome and are involved in the synthesis of a specific secondary metabolite.
Phenotypic Profile: The observable characteristics or traits of an organism, resulting from the interaction of its genotype with the environment.
Transcriptomic Analysis: The study of the complete set of RNA transcripts in an organism or a cell, providing insights into gene expression.
Subgenome: In a hybrid organism, the set of chromosomes or genes inherited from one of the parental species.
RNA Sequencing (RNA-seq): A sequencing technique used to determine the transcriptome of an organism.
Differentially Expressed Genes: Genes that show significantly different levels of RNA transcript abundance between different conditions or groups.
Pangenome: The entire set of genes found across all strains within a species, including the core and accessory genomes.
Thermotolerant: Able to withstand or grow at high temperatures.
Endemic Mycosis: A fungal disease that is consistently present in a specific geographic region.
Spore Dispersal: The movement of fungal spores away from the parent organism.
Antifungal Resistance: The ability of a fungus to grow in the presence of an antifungal drug that would normally inhibit its growth.
Post-acute Sequelae of SARS-CoV-2 (PASC) / Long COVID: A wide range of persistent health problems that can occur after SARS-CoV-2 infection.
Antibiotic Resistance: The ability of bacteria to survive and multiply in the presence of an antibiotic drug.
Syncytia: Large cells formed by the fusion of multiple smaller cells, observed in some viral infections.
Mutation: A change in the DNA sequence of an organism.
Timeline of Main Events
Pre-History - Miocene Epoch (Approximately 13-13.9 Million Years Ago):
Aspergillus latus likely arose through a single hybridization event between the ancestors of Aspergillus spinulosporus and a close relative of Aspergillus quadrilineatus.
Ongoing - Throughout the Study Period (Specific dates vary by experiment):
Researchers collect a substantially expanded set of 53 globally distributed isolates from Aspergillus section Nidulantes, including 50 clinical isolates and three type strains (A. latus, A. spinulosporus, A. quadrilineatus).
High-quality genome assemblies are generated for these isolates using long- and/or short-read sequencing technologies (Oxford Nanopore and Illumina).
Molecular phylogenetic analyses using β-tubulin and calmodulin loci confirm the species of the clinical isolates: A. latus (30), A. spinulosporus (8), A. quadrilineatus (1), and A. nidulans (11). One previously published A. latus strain is included.
MALDI-TOF mass spectrometry, a standard clinical identification method, is shown to frequently misidentify A. latus due to a lack of species-specific standards in the databases.
Genomic analysis of A. latus reveals it is an allodiploid hybrid with approximately twice the genome size and gene number compared to closely related species, retaining the genome organization and content of both parental genomes.
Macrosynteny analysis supports the allopolyploid origin of A. latus, showing large genomic segments syntenic with A. spinulosporus and A. quadrilineatus.
Analysis shows little evidence of recombination between the two subgenomes of A. latus across a broad sampling of isolates.
Relaxed molecular clock analyses estimate the origin of A. latus to be approximately 13.1-13.9 million years ago during the Miocene.
Gene content variation analysis in A. latus identifies core, softcore, shell, and cloud gene families and biosynthetic gene clusters (BGCs), revealing higher diversity in accessory BGCs compared to core BGCs.
Extensive phenotyping of infection-relevant traits (growth under stress, antifungal susceptibility, spore size, etc.) demonstrates that A. latus has a distinct phenotypic profile compared to its close relatives.
Invertebrate moth model (Galleria mellonella) experiments show variation in virulence among the Aspergillus species.
Secondary metabolite profiling reveals variation between and within Aspergillus species, including sterigmatocystin production.
Transcriptomic analysis of A. latus clinical isolate CI 1908 shows that both parental subgenomes are actively expressed and respond to temperature perturbations with similar numbers of differentially expressed genes, including conserved and subgenome-specific responses in ohnologs.
Genomic (genome size, gene repertoire, two distinct loci in single-locus phylogenies) and phenotypic (larger spore size) traits are identified that can help distinguish A. latus from its close relatives.
Comparison of the A. latus pangenome to Candida albicans and Aspergillus fumigatus reveals intermediate levels of core gene family conservation but a less diverse BGCome than A. fumigatus.
November 2021 - December 2023 (From Separate Source):
A retrospective cohort study is conducted on US veterans to assess the association between a positive COVID-19 test and the rates of future infections with other pathogens. (Note: This event is from a separate source focusing on COVID-19 and its long-term effects on susceptibility to other infections, not directly related to the A. latus study but relevant to the broader context of emerging infections.)
April 3, Year Unknown (From Separate Source - Twitter Thread):
A Twitter thread discusses the increasing threat of bacterial, viral, and fungal infections in the future.
The thread highlights antibiotic resistance due to overuse in healthcare and agriculture.
Climate change and urban growth are mentioned as contributors to rising viral and fungal infections.
The COVID-19 pandemic is noted to have potentially weakened immune systems and increased antibiotic use, further exacerbating the problem.
March 19, 2024 (Publication Date of Review Article):
A review article is published discussing the impact of climate change and natural disasters on fungal infections.
The review covers how environmental stressors can drive fungal adaptation and virulence.
It addresses the role of pollution, global warming, altered weather patterns, and natural disasters in the emergence and spread of fungal pathogens.
The article notes the expansion of the geographic range of endemic mycoses due to climate change.
It also discusses fungal outbreaks linked to specific natural disasters like volcanic eruptions, earthquakes, wildfires, floods, tsunamis, tornadoes, and hurricanes.
April 1, 2025 (Publication Date of COVID-19 Study):
A study is published in The Lancet Infectious Diseases detailing the findings of the retrospective cohort study on US veterans, examining the increased risk of other infections after COVID-19. (Note: This is a future date relative to the other sources.)
Cast of Characters
Principle Researchers (Authors of the A. latus study):
Jacob L. Steenwyk: One of the lead researchers, involved in conceptualization, methodology, validation, formal analysis, investigation, resources, data curation, writing, visualization, supervision, and funding acquisition. Held a scientific advisory position for WittGen Biotechnologies during part of the project and is an advisor for ForensisGroup Incorporated.
Sonja Knowles: Involved in methodology, validation, formal analysis, investigation, and data curation.
Rafael W. Bastos: Involved in methodology, validation, formal analysis, investigation, and data curation. Affiliated with the Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Brazil, and the Institute of Marine Science and Technology, Shandong University, China.
Charu Balamurugan: Involved in validation and formal analysis.
David Rinker: Involved in validation and formal analysis.
Matthew E. Mead: Involved in methodology, validation, and investigation.
Christopher D. Roberts: Involved in validation and formal analysis.
Huzefa A. Raja: Involved in methodology, validation, formal analysis, investigation, and data curation.
Yuanning Li: Involved in methodology, validation, investigation, and data curation. Affiliated with the Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Ludwig Maximilian University, Munich, Germany.
Ana Cristina Colabardini: Involved in validation and investigation.
Patrícia Alves de Castro: Involved in validation, formal analysis, and investigation.
Thaila Fernanda dos Reis: Involved in validation, formal analysis, and investigation.
Adiyantara Gumilang: Involved in formal analysis and investigation.
María Almagro-Molto: Involved in validation and formal analysis.
Alexandre Alanio: Involved in validation and formal analysis.
Dea Garcia-Hermoso: Involved in validation and formal analysis.
Endrews Delbaje: Involved in validation, formal analysis, investigation, and data curation.
Laís Pontes: Involved in validation and formal analysis.
Camila Figueiredo Pinzan: Involved in validation and formal analysis.
Angélica Zaninelli Schreiber: Involved in validation and formal analysis. Her lab is supported by FAPESP grants.
David Canóvas: Involved in methodology, validation, investigation, and resources. His lab is supported by grants from MICIU/AEI and European Union NextGenerationEU/PRTR. Affiliated with the Department of Microbiology, Immunology and Transplantation, Katholieke Universiteit Leuven, Belgium.
Rafael Sanchez Luperini: Involved in methodology, validation, investigation, and resources.
Katrien Lagrou: Involved in methodology, validation, investigation, resources, data curation, writing, and supervision. Affiliated with the Department of Laboratory Medicine and National Reference Centre for Mycosis, University Hospitals Leuven, Belgium, and the Life and Health Sciences Research Institute (ICVS), University of Minho, Portugal.
Egídio Torrado: Involved in validation, investigation, and resources. Affiliated with South China Agricultural University, Guangzhou, China.
Fernando Rodrigues: Involved in methodology, validation, investigation, resources, and funding acquisition. His lab was supported by the European Union’s Horizon 2020 program. Affiliated with South China Agricultural University, Guangzhou, China.
Nicholas H. Oberlies: Involved in methodology, validation, investigation, resources, writing, and supervision.
Xiaofan Zhou: Involved in methodology, validation, investigation, resources, and writing.
Gustavo H. Goldman: One of the lead researchers, involved in conceptualization, methodology, validation, investigation, resources, data curation, writing, visualization, supervision, project administration, and funding acquisition. His lab is supported by FAPESP and CNPq grants from Brazil. Is a scientific consultant for Innovation Pharmaceuticals Inc.
Antonis Rokas: The other lead researcher, involved in conceptualization, methodology, validation, resources, data curation, writing, visualization, supervision, project administration, and funding acquisition. His lab is supported by grants from the National Science Foundation and the National Institutes of Health/National Institute of Allergy and Infectious Diseases. Is a scientific consultant for LifeMine Therapeutics, Inc.
Principle Researchers (Authors of the Climate Change and Fungal Infections Review):
Danila Seidel: Joint first author, contributed equally. Received speaker fees from Pfizer and Hikma Pharmaceuticals (outside the submitted work).
Sebastian Wurster: Joint first author, contributed equally.
Jeffrey D Jenks: Joint first author, contributed equally. Received research funding from Astellas, F2G, and Pfizer (outside the submitted work).
Hatim Sati: Provided crucial comments.
Jean-Pierre Gangneux: Provided crucial comments. Received speaker fees and travel support from Gilead, Mundipharma, Pfizer, and Shionogi (outside the submitted work).
Matthias Egger: Contributed to figures and provided crucial comments.
Ana Alastruey-Izquierdo: Provided crucial comments.
Nathan P Ford: Provided crucial comments.
Anuradha Chowdhary: Provided crucial comments. Fellow of the CIFAR Program Fungal Kingdom: Threats & Opportunities.
Rosanne Sprute: Contributed to figures and received speaker fees and travel support from Pfizer and Hikma (outside the submitted work).
Oliver Cornely: Provided crucial comments and contributed to figures. Reports numerous grants, contracts, consulting fees, honoraria, expert testimony, DSMB participation, patents, stocks, and other interests (detailed in declarations).
George R Thompson III: Provided crucial comments. Received research and consulting fees from various pharmaceutical companies and served on a DSMB for Pfizer (outside the submitted work).
Martin Hoenigl: Joint senior author, contributed equally. Received research funding from various pharmaceutical companies (outside the submitted work).
Dimitrios P Kontoyiannis: Joint senior author, contributed equally. Received honoraria, research support, and consultant fees from various pharmaceutical companies and is a member of data review committees (details in declarations).
Principle Researchers (Authors of the COVID-19 and Subsequent Infections Study):
Miao Cai: Involved in the study.
Evan Xu: Involved in the study.
Yan Xie: Involved in the study.
Ziyad Al-Aly: The corresponding author of the study.
Other Individuals Mentioned:
DavidJoffe64: Mentioned in the Twitter thread for support.
Emmanuel (@ejustin46): Author of the Twitter thread discussing the future increase in infections.
FAQ
Environmental changes and the ongoing consequences of COVID-19 have a broad impact on infectious disease risks in several ways.
Environmental Changes:
•
Climate Change and Fungal Infections: Climate change is causing long-term shifts in temperatures and weather patterns, disrupting ecological systems and leading to shifts in the global distributions of pathogens. Many pathogenic fungi are adapting to rising Earth temperatures, becoming more thermotolerant, which enhances their fitness and virulence. This adaptation to higher temperatures might allow fungi to overcome the thermal barrier that previously prevented them from infecting humans and other mammals. For example, Candida auris shows heat tolerance and has adapted to human body temperatures.
•
Emergence and Spread of Fungal Pathogens: Climate change is creating conditions conducive to the emergence of new fungal pathogens and is priming fungi to adapt to previously inhospitable environments, such as polluted habitats and urban areas. This can lead to the geographical spread of some fungi to traditionally non-endemic areas. The term "endemic mycoses" is increasingly being recognized as a misnomer due to the expansion of these fungi outside their traditional ranges.
•
Impact of Pollution and Urbanization: Contamination of water sources with agricultural and industrial pollutants can increase the growth and diversity of fungi, including pathogenic species. Rapid urbanization contributes to increased local air and soil temperatures (the urban heat-island effect), which can exert evolutionary pressure on microorganisms, leading to greater fungal stress adaptation.
•
Natural Disasters and Fungal Outbreaks: Climate change is contributing to increases in the frequency and severity of natural disasters, which can trigger outbreaks of fungal diseases and increase the spread of fungal pathogens. Natural disasters can cause traumatic injuries that provide entry routes for fungal pathogens, lead to wound contamination, and overwhelm healthcare systems, increasing susceptibility to and hindering the treatment of fungal infections. Wildfires and flooding can also disperse fungal spores and create environments conducive to fungal growth.
•
Antifungal Resistance: The increased reliance on fungicides in agriculture due to climate change's impact on food security might contribute to the development of antifungal resistance in human fungal pathogens, posing a threat to both agriculture and human health.
Consequences of COVID-19:
•
Increased Susceptibility to Infections: A positive test for COVID-19 has been associated with increased rates of diagnosis of various infections in the 12 months following the acute illness, compared with a negative test. This includes bacterial, fungal, and viral infections, suggesting that SARS-CoV-2 infection might have long-term effects on the immune system, making individuals more susceptible to other pathogens. People with COVID-19 had increased test positivity rates for bacterial and viral infections, and those not hospitalized had significantly increased rates of outpatient diagnoses of infectious illnesses, including fungal infections, as well as hospital admissions for infectious illnesses.
•
Impact on Healthcare Resources and Antibiotic Use: The COVID-19 pandemic has strained healthcare resources, potentially leading to increased antibiotic use for secondary infections, which may worsen the problem of antibiotic resistance.
•
Aspergillus Co-infections: Aspergillus species, including the cryptic pathogen A. latus, have been identified as co-infections in COVID-19 patients, adding to the evidence that these fungi can establish co-infections with SARS-CoV-2.
In summary, environmental changes, particularly climate change, are altering fungal ecosystems, promoting the emergence and spread of fungal pathogens, and potentially contributing to antifungal resistance. Simultaneously, the COVID-19 pandemic appears to increase individuals' susceptibility to various infections, including fungal ones, highlighting the complex and interconnected nature of infectious disease risks in a changing world. Accurate identification of cryptic pathogens like A. latus becomes even more critical in this context.
Here are the key findings regarding rates of infection with other pathogens after a positive COVID-19 test:
•
Compared to participants with a negative COVID-19 test, individuals who had COVID-19 but did not require hospitalization had increased test positivity rates for bacterial infections (in blood, urine, and respiratory cultures) and viral diseases(including Epstein–Barr virus, herpes simplex virus reactivation, and respiratory viral infections).
•
People who tested positive for COVID-19 and were admitted to hospital also showed increased rates of bacterial infections in blood, respiratory, and urine samples, as well as viral infections in blood and respiratory samples.
•
Analyses of prespecified outcomes revealed that outpatients with a positive COVID-19 test had significantly increased rates of outpatient diagnosis of infectious illnesses (Risk Ratio [RR] 1.17 [95% CI 1.15–1.19]), including bacterial, fungal, and viral infections; outpatient respiratory infections (1.46 [1.43–1.50]); and admission to hospital for infectious illnesses (1.41 [1.37–1.45]), including for sepsis and respiratory infections.
•
The rates of these prespecified outcomes were generally higher among those who were admitted to hospital for COVID-19 during the acute phase.
•
When comparing those admitted to hospital for COVID-19 with those admitted for seasonal influenza, the COVID-19 group had higher rates of admission to hospital for infectious illnesses (RR 1.24 [1.10–1.40]), admission to hospital for sepsis (RR 1.35 [1.11–1.63]), and in-hospital use of antimicrobials (1.23 [1.10–1.37]).
The authors of this study concluded that a positive COVID-19 test was associated with an increased risk of being diagnosed with various infections in the subsequent 12 months. This finding supports the idea that SARS-CoV-2 infection may have long-term effects on the immune system, increasing susceptibility to other pathogens, as we discussed previously [95, from prior turn]. This highlights an important consequence of the COVID-19 pandemic in the broader context of infectious disease risks.
Table of Contents with Timestamps
Contents for "Climate Change and Fungal Pathogens: A Hidden Threat"
00:00 - 00:15 | Introduction
Opening remarks and podcast format overview of Heliox: Where Evidence Meets Empathy
00:25 - 01:07 | Episode Topic Preview
Introduction to the connections between fungal pathogens, climate change, and natural disasters
01:07 - 01:56 | Research Overview
Discussion of the scientific papers being analyzed: Nature Communications study on Aspergillus latus and Lancet Microbe review on climate change impacts
01:57 - 03:00 | Deep Dive Goals
Outlining the learning objectives and connecting disparate research themes
03:00 - 04:16 | Aspergillus latus: The Hybrid Fungus
Explanation of allodiploid hybrid nature and genetic characteristics
04:16 - 05:03 | Genetic Detective Work
Analysis methods used to determine the hybrid origins of A. latus
05:03 - 06:10 | Evolutionary Stability
Discussion of gene retention and the ancient origins of A. latus (13.1-13.7 million years ago)
06:10 - 08:13 | Gene Distribution and Expression
Detailed breakdown of core genes versus accessory genes and biosynthetic gene clusters
08:13 - 11:00 | Temperature Responses
How the fungus's genes respond differently to temperature changes (30°C vs 37°C)
11:00 - 13:13 | Cryptic Pathogen and COVID-19 Connection
Difficulties in identifying A. latus and its potential role as a co-infection in COVID-19 patients
13:13 - 15:07 | Climate Change and Fungal Adaptation
Broader impacts of climate change on fungal pathogens and how they adapt to increasing temperatures
15:07 - 17:21 | Fungal Adaptation Mechanisms
Specific biological adaptations fungi use to survive in warmer environments
17:21 - 20:20 | Environmental Factors
Effects of pollution, microplastics, UV exposure, and agricultural fungicide use on fungal evolution
20:20 - 22:17 | Emerging Threats
New fungal pathogens and geographical shifts in established diseases due to climate change
22:17 - 25:57 | Natural Disasters and Fungal Outbreaks
How events like floods, hurricanes, and wildfires trigger fungal infections and specific historical examples
25:57 - 27:13 | Soil Ecosystems and Wildfires
Effects of wildfires on fungal communities and the emerging field of pyroaerobiology
27:13 - 28:22 | Conclusion and Key Takeaways
Summary of main insights on cryptic pathogens, climate change impacts, and public health implications
Index with Timestamps
Agricultural fungicides, 19:21, 19:38
Allodiploid hybrid, 03:10, 03:18, 03:24
Antifungal resistance, 18:40, 19:20, 19:31, 19:46, 19:53
Aspergillus fumigatus, 12:59, 19:46
Aspergillus latus, 01:29, 01:37, 03:06, 03:18, 03:24, 03:37, 05:43, 06:00, 06:44, 12:48
Aspergillus quadrilineatus, 04:31, 05:20, 09:33
Aspergillus spinulosporus, 04:31, 05:17, 09:33
Azole class, 19:39
Biofilms, 16:57
Biosynthetic gene clusters (BGCs), 07:41, 07:44, 07:49, 08:01, 08:31
BUSCO genes, 03:39, 03:42, 03:55, 05:13
Calcineurin signaling, 15:43, 15:49
Candida auris, 14:36, 21:14
Cell walls, 16:34
Climate change, 00:37, 00:42, 13:47, 13:54, 14:21, 15:08, 19:20, 19:22, 20:28, 22:23, 22:26
Codon usage bias, 09:38, 09:42
COVID-19, 02:19, 12:46, 12:49, 12:54, 13:01
Cryptococcus gaudii, 24:30
Cryptic pathogen, 01:29, 01:34, 11:52, 11:54, 12:03
Differential expression analysis, 10:09, 10:12
Endemic mycosis, 21:36
Food supply, 15:05, 15:10
Fungal adaptations, 15:24, 15:27, 15:34, 15:39, 16:34, 16:37, 16:42, 16:57
Fungal co-infections, 02:25, 13:01, 13:18
Glutathione metabolic process, 10:37, 10:42
Heat shock proteins (HSPs), 15:35, 15:39
HOG signaling, 15:43, 15:49
HSF signaling, 15:43, 15:49
Hurricane Harvey, 25:17, 25:23
Hurricane Katrina, 25:34, 25:37
Hurricane Sandy, 25:34, 25:37
Hybridization, 05:24, 05:29, 06:43, 06:48
Immune systems, 17:37, 23:21, 23:26
Indian Ocean tsunami, 25:06, 25:15
Macrosyntony analysis, 04:08, 04:11, 04:17
Melanin, 16:01, 16:02, 16:04, 16:06
Microplastics, 17:50, 17:59, 18:20, 18:26, 18:30
Morphogenesis, 16:49, 16:57
Natural disasters, 00:37, 00:42, 22:17, 22:23, 22:26, 22:33, 22:37, 22:48, 22:54, 23:18, 24:54
Onalogues, 05:30, 05:32, 05:51, 06:00, 10:27, 11:01, 11:05, 11:11
Phylogenomics, 05:03, 05:08
Ploidy, 16:34, 16:37
Pollution, 17:50, 17:59, 18:00, 18:08, 18:11, 18:16
Pyroaerobiology, 26:06, 26:09, 26:10, 26:17
Relaxed molecular clock analyses, 06:44, 06:48
Respiratory infections, 23:47, 23:49, 23:53, 23:56
Rhizopus aresis, 25:06
SARS-CoV-2, 13:01, 13:12
Soft tissue infections, 23:08, 23:11, 25:06
Spore dispersal, 23:41, 23:42, 23:42
Transcript abundances, 09:22, 09:26
Traumatic injuries, 22:54, 22:54, 22:56, 23:01
Tsunamis, 24:23, 24:24, 24:24, 25:06
UV exposure, 17:50, 17:59, 18:47, 18:49
Virulence, 17:34, 17:37
Waterborne microbes, 24:24, 24:27
Wildfires, 23:42, 23:47, 25:56, 25:57, 25:58, 26:03
Poll
Post-Episode Fact Check
Verified Information:
Aspergillus latus is correctly described as an allodiploid hybrid fungus with a doubled genome compared to related species.
The fungus originated between 13.7 and 13.1 million years ago, as confirmed by molecular clock analyses.
The genetic description of A. latus having approximately 96.68% of essential genes duplicated is accurate.
A. latus is correctly identified as having genetic material from Aspergillus spinulosporus and a relative of Aspergillus quadrilineatus.
The high retention rate of onalogs (91.63%) is correctly stated.
Accurate Climate Change Connections:
Climate change is accurately described as expanding the geographical range of endemic fungal diseases like coccidioidomycosis and histoplasmosis.
Candida auris is correctly identified as a pathogen that has demonstrated notable heat tolerance.
The connection between agricultural fungicide use and antifungal resistance in human medicine is accurately represented.
The adaptation mechanisms of fungi (heat shock proteins, melanin production, signaling pathways) are correctly described.
Natural Disaster Connections:
The link between natural disasters and fungal infections through traumatic injuries, immune suppression, and environmental changes is factually correct.
Specific examples cited (Rhizopus infections after Colombian volcanic eruption, invasive mold infections after Hurricane Harvey) are verified.
The concept of pyroaerobiology is accurately described as an emerging field studying microbial transport in wildfire smoke.
Minor Corrections/Clarifications:
The transcript refers to "Aspergillus lattice" at several points, but the correct scientific name is "Aspergillus latus."
While A. latus isolates were found in COVID-19 patients, research on this specific co-infection is still developing.
The hypothesis regarding tsunamis introducing Cryptococcus gattii to the Pacific Northwest following the 1964 Alaska earthquake remains a theory requiring additional evidence.
Note: This fact check confirms the scientific accuracy of the major claims while noting minor terminology corrections.
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