FEVERISH EARTH: EXPLORING HEATSTROKE AND THE RISE OF INFECTIOUS DISEASES

By: Fadlika Harinda, Tiara Kumala Putri, Adhella Menur

Theories about climate change and early observations of the greenhouse effect on Earth began emerging around 1820. In 1938, an engineer and little-known amateur scientist named Guy Callen-dar became the first ‘doctor’ to diagnose the Earth’s fever. He analyzed records from 147 weather stations worldwide and discovered that average global temperatures had risen by 0.3°C over the previous 50 years. Calendar proposed that industry carbon dioxide (CO₂) emissions were responsible for this warming. Yet, his findings were largely ignored at the time, as most scientists doubted that human activities could significantly influence a system as vast as the Earth’s climate. Today, we know Callendar was right: the Earth’s fever won’t go away, and the degrees keep climbing.

In 2015, in response to the increasing urgency of climate change, 195 nations signed the Paris Agreement. This landmark treaty aims to keep Earth’s temperature rise “well below 2°C above pre-industrial levels” and ideally limit it to 1.5°C. The “pre-industrial” period refers to 1850–1900, when reliable observations of global surface temperatures first became available, and before widespread fossil fuel use. Although a 1.5°C increase might sound modest, climate scientists agree it marks a critical threshold. Beyond it, the impacts of climate change become significantly more severe for both human societies and natural ecosystems. Alarmingly, these changes may be inevitable, as global temperatures between 2023 and 2024 were the highest on record, exceeding 1.5°C above pre-industrial levels. According to the World Meteorological Organization (WMO), temperatures could reach as high as 1.9°C above pre-industrial levels by 2028. While natural phenomena like El Niño and volcanic eruptions contribute to the warming, the primary driver is human-induced greenhouse gas emissions.

Climate change is associated with negative impacts on physical, mental, and community health and well-being through the increasing frequency and intensity of extreme weather events such as extreme heat, prolonged heat waves, and abnormal rainfall. It is also driving a rise in infectious and vector-borne diseases, reduced air and water quality, food insecurity, and declining biodiversity. Moreover, it is projected to worsen heat-related illnesses and mortality, presenting unprecedented challenges to public health systems. Heat-related illnesses often affect elderly individuals, whose ability to adapt to heat stress has diminished, as well as those who are chronically ill, frail, pregnant, or unable to care for themselves, such as infants and toddlers. Additionally, outdoor and manual laborers, athletes, and individuals in poverty without access to cooling systems are at heightened risk. In this edition, we’ll explore heat stroke, the most serious heat-related illness, and examine how Earth’s “fever” is driving the spread of infectious diseases.

Uncovering heat stroke

Heat stroke is a severe, potentially life-threatening form of heat illness. It is a clinical constellation of symptoms that include a severe elevation in body temperature, typically, but not always, greater than 40°C, with central nervous system dysfunction. Determining where the patient falls on the heat illness continuum is crucial. The signs and symptoms of heat exhaustion, such as cramping, fatigue, dizziness, nausea, vomiting, and headache, may overlap. However, when progression to end-organ damage occurs, it becomes heat injury. What differentiates heat stroke from heat injury is the presence of neurological impairment. Patients typically present with hyperthermia, hypotension, hyperventilation, and tachycardia, often accompanied by altered mental status, seizures, and in severe cases, coma. The mortality rate for heat stroke ranges from 20-65%, and 7-20% of survivors may suffer permanent neurological damage.

There are two types of heat stroke depending on the heat source. The classic non-exertional heat stroke emanated from a poor heat-dissipation system during environmental passive heat exposure. Meanwhile, the heat source for exertional heat stroke is due mainly to endogenous heat, i.e., excessive metabolic heat production during physical exercise that overwhelms the physiological heat-loss system.

As the Earth’s fever rises, the likelihood of heat-related hospitalizations and mortality increases. Clinicians and researchers should be concerned about heat stroke, as it can affect a broad range of individuals, including healthy populations. For years, much of the focus has been on the thermo-lytic effects of heat, also known as the heat toxicity pathway, where high temperatures directly cause cellular and organ damage, leading to heat stroke.

And now, the potential link between heat stroke and endotoxemia, first discussed by Brock-Utne et al. in 1988 after observing exhausted runners following a long-distance race, has shed light on the concept of ‘heat sepsis,’ expanding our understanding of heat stroke mechanisms.

The last three decades of evidence suggested that endotoxemia and sepsis may have important roles independently from the heat stress itself in heat stroke pathophysiology. Suggested that heat-related sepsis precedes the thermolytic effects generated by heat, such as heat toxicity, during the development of heat stroke. This evidence and information presented on the mechanisms of heat stroke apply to heat stroke in general without differentiating between the two forms. Learning this model will hopefully lead to a better understanding of how heat stroke develops and will give a wider opportunity to prevent fatal events.

The dual-pathway model of heat stroke introduces novel concepts, suggesting that heat stroke is triggered by two independent pathways, activated in sequence. The first pathway to start with is heat sepsis, in which endotoxemia, systemic inflammation, and the sepsis response are the underlying’ pathophysiological pathways. In this pathway, heat contributes to the induction of change in gut permeability and the promotion of gram‐negative bacteria and lipopolysaccharides (LPS) translocation to the circulatory space. In immune-competent individuals, LPS in the circulation is removed by monocytes, LPS‐specific antibodies, and high-density lipoproteins. When the immune system is under suppression, the LPS clearance is compromised, leading to endotoxemia of LPS accumulation until it reaches the systemic inflammatory response threshold and turns into sepsis.

This pathway is then followed by the second pathway which is known as the heat toxicity pathway. During this pathophysiological process, heat initiates cellular disintegration, thus damaging the structure and body organs. It is postulated that the heat sepsis pathway preceding the heat toxicity pathway started when the core body temperature (Tc) entered 40oC and transitioned to when the Tc reached around 42oC. Further mechanism of the proposed heat sepsis is seen in figure 3. In this model, the immune system state acts as a switch between heat tolerance and intolerance. Examples of immune-suppressing circumstances are also suggested in the figure.

The management of heat stroke involves ensuring proper airway protection, breathing, and circulation (the ABCs). After stabilizing these critical functions, rapid cooling becomes the primary treatment. Thus, if we find someone with heat stroke symptoms, we must cool down the core body through whatever means. For instance, put the body in a pool of cool water or under a cool shower; spray the body using a garden hose or sponge with cool water; fan the body with cool water mist; place ice packs or cool wet towels on the neck, armpits, and groin; cover the body with cool damp bedsheets; and offer chilled water if the person is con-scious enough or begin CPR if the person shows no consciousness with a missing pulse and breath. In all cases, the person should be transported to a hospital as quickly as possible for emergency medical care. The target core temperature is typically below 39°C, with a preferred range between 38.0°C and 38.5°C, to reduce the risk of further clinical deterioration and prevent end-organ damage. Anticipating SIRS and sepsis in heat stroke cases and immediate intervention should be the standard of care (e.g., antibiotics, fresh frozen plasma, cryoprecipitate, or platelet concentrates to treat DIC). Pharmaceutical and nutraceutical approaches to boost the immune system and cleanse the gut of bacteria might improve heat tolerance. Further research is needed to optimize the management of heat stroke and refine treatment protocols.

Hotter Earth and infectious diseases

The relationship between climatic factors and infectious diseases is complex, involving multiple interactions. A warming and increasingly unstable climate, characterized by more frequent and intense heat waves, abnormal precipitation, and droughts, is playing a growing role in driving the global emergence, resurgence, and redistribution of infectious diseases. It affects pathogen abundance, survival, and virulence, as well as human behavior and host susceptibility. Furthermore, droughts and heat waves may increase the risk of wildfires and accelerate the melting of ice and frozen ground (permafrost) in polar regions, damaging ecosystems both on land and at the poles. These poor habitat conditions can force animals to move into human settlements, potentially increasing the risk of pathogen exposure and disease outbreaks.

Vector-borne infectious diseases are caused by pathogens transmitted by arthropods, with mosquitoes, fleas, and ticks being the primary vectors. The effect of global warming on these diseases is indirect but significant. High temperatures and humidity alter the geographical distribution of vectors, creating favorable conditions for their survival and faster reproduction. This, in turn, can accelerate the spread and transmission of infectious diseases. Mosquitoes are prevalent vectors in tropical and subtropical regions. They transmit diseases by biting their hosts and turning previously non-infectious individuals into infectious ones. High temperatures could have activated the mosquito breeding season early and reduced the extrinsic incubation period. As the temperature continues to rise, mosquitoes in low-latitude regions may find new habitats in mid or high-latitude regions and in areas of high altitude, leading to geographical expansion or shift of diseases. Aedes aegypti, the primary mosquito vector for several arboviral diseases such as dengue, chikungunya, yellow fever, and Zika, has experienced global expansion due to rising global temperatures along with increased population movement through air travel and urbanization.

Fleas are vectors that infect both domestic and wild animals. Flea species such as Ctenocephalides canis and Ctenocephalides felis, commonly found on domestic animals, act as vectors for the bacterium Rickettsia typhi, which causes murine typhus. Fleas can survive in a wide range of environmental conditions, and warm temperatures and high humidity favor their proliferation. Ticks are poikilo-thermic animals that cannot regulate their body temperature, so the ambient temperature greatly influences their body temperature. Some diseases transmitted by ticks include encephalitis, babesiosis, Lyme disease, Crimean-Congo hemorrhagic fever, spotted fever, and various rickettsioses. Global warming causes an increase in extreme temperatures, heat waves, and longer summers and springs, with shorter winters, creating conditions that favor the survival of ticks.

Positive associations between hot temperature and all-cause or bacterial diarrhea have been observed, while negative associations have been noted with viral diarrhea, particularly rotavirus-associated gastroenteritis. Drought can increase the risk of diarrhea by concentrating pathogens in water sources. The changing climate and increased drought may jeopardize access to adequate water, sanitation, and hygiene (WASH) practices, leading to heightened diarrhea risk. Salmonella is climate-sensitive, with higher temperatures linked to increased incidence due to faster bacterial replication. In contrast, Campylobacter, which cannot replicate outside the host, is less directly influenced by warm weather. Instead, its seasonal variation may be linked to human behaviors, such as riskier food production, consumption patterns, or other seasonal factors.

growth, increase infection rates, and expand the geographical distribution of bacteria. This also raises the frequency of infections in healthcare settings and enhances the likelihood of horizontal gene transfer, leading to the emergence of drug-resistant infections.

Furthermore, due to global warming, Alas-ka’s entire ecosystem is changing, with winter temperatures rising by nearly 4°C over the past 60 years. Sea ice is breaking up earlier, and new pathogens are emerging. Viruses and bacteria can survive for millennia when frozen, and there is little understanding of what might be released as policy soils and glaciers melt. It could be seen as a ‘Pandora’s box,’ given the vast reservoir of pathogens accumulated over time and the possibility that many of these may be novel to humans. In the past five years, the European Space Agency has discovered hundreds of ancient, antibiotic-resistant microorganisms in Alaskan permafrost. Similarly, Chinese hunters have isolated 33 previously unknown viruses, dating back at least 11,000 years, from Tibetan glaciers and ice samples in Greenland and other regions. Finally, the changes brought by a feverish Earth are presenting numerous medical challenges and pandemic threats, and we must be prepared.

What should we do?

The Earth’s persistent and worsening ‘fever’ will continue to pose increasing risks to public health, both in the short and long term. To prevent heat-related illnesses, it’s important to stay cool indoors during the hottest parts of the day, wear loose-fitting, lightweight clothing, protect our body from sunburn by wearing a hat and sunscreen, and stay hydrated. It’s also important to improve gut health by increasing high fibre intake, limiting consumption of ultra-processed foods, incorporating probiotics into our diet, managing stress, and getting enough sleep. Try to schedule exercise or physical labor for cooler times of the day, such as early morning or evening, and gradually increase the time spent working or exercising in the heat to allow our body to acclimate. With the rise of infectious diseases in the context of global warming, we can take proactive measures to protect ourselves: maintain good hygiene, wash hands regularly, stay current with vaccinations (including for our pets), handle food and water safely, use insect repellent, avoid contact with sick animals, and stay informed with global health news.

Mitigating climate change requires reducing the emission of heat-trapping greenhouse gases into the atmosphere. This means cutting emissions from major sources like power plants, factories, cars, and farms. Forests, oceans, and soils, which absorb and store these gases, are also crucial to the solution. While we rely on nations for high-level commitments to combat climate change and on scientists to develop clean energy and green technologies, there are actions individuals can take to reduce their personal carbon footprint and contribute to cooling the planet, such as saving energy at home and work; walk, bike, or use public transportation; reduce waste and plastic usage; reuse, repair, and recycle; consume more vegetables and reduce meat and dairy consumption; plant trees; switch to eco-friendly energy sources; choose products from companies that use resources responsibly; and, most importantly, speak up and raise awareness! Our everyday choices shape the future and can help cool our Earth!

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