How Climate Change is Unleashing Silent Fungal Threats
The same environmental changes that are reshaping our coastlines and weather patterns are also quietly transforming the world of fungal diseases, creating new health threats that transcend the boundaries between animals and humans.
In the complex tapestry of infectious diseases, a remarkable group of conditions exists at the intersection of animal health, human medicine, and environmental science—mycotic zoonoses. These are fungal diseases naturally transmitted between animals and humans, often through the environment we share. What makes them particularly fascinating, and concerning, is their characteristic known as "natural focality"—their tendency to persist in specific ecological niches where particular animal hosts, environmental conditions, and pathogenic fungi intersect 1 .
For decades, these diseases remained relatively stable within their natural boundaries. But now, climate change is rewriting these boundaries, altering the delicate ecological balance that has long contained these fungal threats. As global temperatures rise and weather patterns shift, the geographical ranges of fungal pathogens are expanding, exposing new populations to diseases once considered confined to specific regions 3 . This article explores the ecological criteria governing mycotic zoonoses and examines how our changing climate is rapidly transforming this landscape.
Diseases persist in specific ecological niches with particular hosts and environmental conditions 1 .
Rising temperatures and shifting weather patterns are expanding fungal geographic ranges 3 .
Fungal diseases naturally transmitted between animals and humans through shared environments.
The concept of natural focality provides a critical framework for understanding how mycotic zoonoses operate within ecosystems. Researchers have identified that these diseases depend on specific ecological criteria that allow them to persist in nature independent of human activity 1 .
Several interconnected factors determine whether a mycotic zoonosis will establish and maintain a natural focus:
Each fungal species has particular environmental requirements—specific soil types, humidity levels, temperature ranges, and organic substrates that enable its survival and propagation 1 .
Pathogenic fungi associate with vertebrate hosts that can be divided into at least six ecologically distinct groups, each playing different roles in maintaining the fungal life cycle 1 .
The presence of specific non-animal substrates (such as soil, decaying matter, or vegetation) is crucial for long-term fungal maintenance or active propagation in the environment 1 .
These may include direct contact with infected animals, inhalation of spores from contaminated environments, or indirect transmission through various environmental components 5 .
This complex interplay means that mycotic zoonoses are not randomly distributed across landscapes but are instead tightly linked to specific ecological conditions that support their complete life cycle—from fungal growth and sporulation to animal infection and environmental persistence.
Anthropogenic climate change, primarily driven by greenhouse gas emissions, is dramatically reshaping the epidemiology of fungal infections 3 . Several climate-related factors are disrupting the established rules of natural focality:
Dimorphic fungi, once confined to specific geographic regions, are particularly susceptible to climate-induced environmental shifts 3 . These fungi, which exist in mold form in the environment but transform into yeast-like structures at human body temperature, are expanding their territories in response to changing conditions:
| Fungal Species | Historical Distribution | Recent Geographic Expansion | Climate Change Impacts |
|---|---|---|---|
| Coccidioides species 3 | Arid regions of southwestern US, Mexico, parts of Central & South America | Missouri, Washington State (US), Portugal | Warmer temperatures, shifting precipitation, dust storms, wildfire smoke |
| Blastomyces dermatitidis complex 3 | North America (Mississippi & Ohio River valleys, Great Lakes regions) | Expanding in Canada (Ontario, Quebec, Manitoba, Saskatchewan); cases in Tunisia, South Africa, Zimbabwe, India | Seasonal patterns, drought-associated, influenced by climate extremes |
| Histoplasma capsulatum 3 | Globally distributed with high prevalence in specific river basins in North & South America | Northward expansion in North America; cases in northern Italy, Neuquén (Argentina), Turkey | Rising temperatures contributing to emergence of more virulent, thermally tolerant strains |
Perhaps one of the most significant climate-related developments is the evolution of increased thermotolerance in fungal pathogens 3 . Fungi that traditionally could not withstand mammalian body temperatures are now adapting to warmer environments, potentially crossing what was once a significant thermal barrier to human infection 3 .
Candida auris presents a striking example of this phenomenon. This globally disseminated pathogen demonstrates exceptional thermal and salt tolerance compared to other Candida species, enabling it to survive in extreme environments characterized by high temperatures and salinity 3 . Notably, C. auris emerged nearly simultaneously across three different continents—a pattern scientists suspect may be linked to climate adaptation 3 .
Understanding how fungal pathogens cause disease under different conditions requires sophisticated experimental models. Research on mucormycosis provides an excellent example of how scientists study these complex interactions in controlled settings.
Diabetes mellitus, particularly with ketoacidosis, is a major risk factor for rhino-orbital-cerebral mucormycosis. To study this relationship, researchers have developed precise protocols to replicate diabetic ketoacidosis in mouse models :
After a 4-8 hour fasting period, mice receive a single injection of streptozotocin (190-250 mg/kg), a compound toxic to insulin-producing pancreatic cells.
Following injection, animals receive drinking water with 10% sucrose for 24 hours to counter potential hypoglycemic shock.
Hyperglycemia and ketoacidosis typically develop over 7-10 days, monitored through measurements of blood glucose, blood pH, and urine ketones.
Once ketoacidosis is established, animals are inoculated with Mucorales sporangiospores via intranasal installation to simulate respiratory exposure.
Infected diabetic animals are compared with healthy controls and animals with other immune impairments to identify disease mechanisms specific to the diabetic state.
This experimental approach revealed crucial insights into species-dependent differences in virulence. Researchers discovered that Rhizopus species could establish infection in diabetic mice without additional immunosuppression, whereas infection with Lichtheimia species required the addition of cortisone acetate . This finding aligns with clinical observations that Rhizopus species are particularly associated with rhino-orbital-cerebral mucormycosis in patients with diabetes mellitus .
| Mucorales Species | Infection Establishment in Diabetic Mice | Additional Immunosuppression Required | Clinical Correlation |
|---|---|---|---|
| Rhizopus species | Consistent establishment | None | Strong association with rhino-orbital-cerebral mucormycosis in diabetic patients |
| Lichtheimia species | Limited or no establishment | Cortisone acetate required | Less frequently associated with diabetes-related cases |
These findings demonstrate the value of experimental models in unpacking the complex relationships between specific fungal pathogens, host metabolic states, and resulting disease patterns—relationships that are increasingly relevant as diabetes prevalence grows worldwide.
Advancing our understanding of mycotic zoonoses requires specialized reagents and methodologies. The field relies on several key approaches to investigate these environmentally persistent pathogens.
| Research Tool | Function and Application | Examples from Literature |
|---|---|---|
| Immunosuppressive Agents | Model specific human risk factors (neutropenia, corticosteroid use, diabetes) to study host-pathogen interactions | Cyclophosphamide (induces neutropenia), cortisone acetate (models corticosteroid immunosuppression), streptozotocin (induces diabetes) |
| Animal Models | Replicate human disease syndromes and test interventions in complex living systems | Mouse models of pulmonary mucormycosis, diabetic ketoacidosis models for rhino-orbital-cerebral disease |
| Environmental Sampling Methods 3 | Detect and quantify fungal pathogens in soil, air, and other environmental reservoirs | Soil sampling for Coccidioides, air sampling for Aspergillus spores, water sampling for Candida auris |
| Genomic Sequencing 3 6 | Track pathogen spread, evolution, and mechanisms of thermotolerance and antifungal resistance | Whole genome sequencing of C. auris isolates, phylogenetic analysis of expanding fungal populations |
| Ecological Niche Modeling 3 | Predict future geographic expansion under climate change scenarios | Models using temperature, precipitation, and soil data to forecast range shifts for dimorphic fungi |
Advanced sequencing technologies enable tracking of pathogen evolution and spread in response to environmental changes.
GIS and ecological niche modeling predict how fungal distributions will shift with climate change.
Animal models replicate human disease conditions to study pathogenesis and test interventions.
The study of mycotic zoonoses represents a paradigm of the "One Health" approach—the understanding that human, animal, and environmental health are inextricably linked 6 . As climate change continues to reshape our planet, the ecological criteria governing natural focality are becoming increasingly dynamic, with pathogens expanding beyond their historical boundaries and adapting to new environmental conditions 3 .
Addressing these emerging threats will require integrated strategies that cross traditional disciplinary lines. Enhanced disease surveillance, improved diagnostic capabilities, development of novel antifungal therapies, and targeted public health interventions will all be essential 3 . Perhaps most importantly, we must recognize that policies aimed at mitigating climate change and preserving ecosystem balance are, fundamentally, also health policies.
The hidden world of mycotic zoonoses reminds us that human health cannot be separated from the health of the animals and environments we share. As we move forward into a world of changing climates and evolving pathogens, this holistic perspective may prove to be our most valuable tool in maintaining the delicate balance between humans and the microscopic fungi with which we coexist.
Monitoring disease emergence, developing diagnostics and treatments
Surveillance in wildlife and domestic animals, understanding reservoir hosts
Monitoring ecological changes, preserving ecosystem balance