KATHMANDU – The number of cases of Japanese encephalitis (JE) infection has reached 33, up from 13 some 10 days ago. Along with the new cases, the number of deaths and districts reporting outbreaks of the deadly virus have also risen—three deaths and 18 districts.
Health ministry’s data show the case fatality rate among infected people is over nine percent, and the rise in the spread of the infection clearly indicates that the country is again witnessing a resurgence of the deadly disease, which has killed and infected thousands of people in the past. The unvaccinated make up most of those infected and dead.
Experts warn that without vaccination, these vulnerable populations are at high risk, and the government has yet to take decisive action to contain the outbreak.
“Vaccination is a proven and effective method to contain the spread of the JE virus,” said Dr Yasho Vardhan Pradhan, former director general at the Department of Health Services. “As the country has again witnessed a resurgence of the JE outbreak, vaccination is the only way to save lives and prevent permanent neurologic, cognitive and behavioural sequelae.”
JE is a viral brain infection endemic to Asia and parts of the Western Pacific. According to the World Health Organisation, it is a mosquito-borne flavivirus belonging to the same family as dengue, Zika, yellow fever, and West Nile viruses. The virus kills a third of those who fall ill and leaves up to half of the survivors with severe lifelong disabilities, according to the UN health body.
Last year, 23 people succumbed to the disease, including one in the Kathmandu Valley, and over 80 people were infected. Doctors say the actual number of cases could be much higher, as tests were carried out only on hospitalised patients with severe symptoms.
This year, Morang, Bara, Jhapa, Saptari, Siraha, Sarlahi, Parsa, Nawalparasi West, Sindhuli, Bardia, and Chitwan districts have reported JE cases. Five provinces—Koshi, Madhesh, Bagmati, Gandaki and Lumbini have reported JE infection.
Data show that mortality rate among people above 15 years of age is higher compared to those below 15, which indicates that those not receiving JE vaccine are at high risk of infection.
Experts say the unvaccinated population is at high risk of deaths and complications of JE infection. However, health authorities do not have immediate plans to vaccinate the unvaccinated population.
“We have capacity and human resources, but we currently don’t have the vaccine,” said Dr Abhiyan Gautam, chief of the Immunisation Section at the Family Welfare Division under the Department of Health Services. “We don’t have a budget to buy the vaccine. We have also requested our development partners, but there is no response.”
Gautam said various preventive measures, including awareness drives, environment management for vector control, and case management training for doctors in health facilities, have been taken in disease-hit districts. However, the rise in the number of infections in Tarai districts shows that those measures are not very effective.
Health Ministry officials admit that JE is the number one killer among vector-borne diseases, and vaccination could help control the spread of infections. They said that their attempts to convince development partners, including the World Health Organisation, to support a mass JE vaccination campaign have not succeeded over the past year.
“Despite knowing how dangerous the JE virus is, we are not able to do much to administer a vaccine to the unvaccinated population,” said Dr Bibek Kumar Lal, director at the Family Welfare Division, under the Department of Health Services. “We held multiple rounds of meetings with development partners and requested help for the vaccine, but could not convince them.”
In 2005, JE killed nearly 2,000 people in Nepal—mostly children from Tarai districts. Nepal started administering the JE vaccine in 2006, eight years before the World Health Organisation officially issued prequalification certification, due to the high rates of infection and deaths from the virus at the time.
In the first phase, all populations of the highly affected four districts—Banke, Bardiya, Dang, and Kailali—reveived the JE vaccine. Later, the vaccination programme was expanded to 19 other affected districts, and children under 15 were inoculated.
The government integrated the JE vaccine into routine immunisation in 2015. Still, people continue to die and dozens get infected by the deadly virus every year.
Public health experts say this is the right time to vaccinate all those at risk. Even if the vaccine does not help in outbreak management, it provides immunity against future infections, according to them.
“Every year, the Health Ministry could spend only around 60 percent of the allocated budget, so budget should not be an issue to save the lives of the population,” said Pradhan, who is also an immunisation expert. “Along with vaccination, authorities must take other measures to prevent further spread of the deadly disease.”
Doctors say complications from JE infection can cause permanent injuries to the brain and the nervous system. The disease has no cure, so treatment focuses on managing symptoms. However, safe and effective vaccines have been developed to prevent infection.
The JE virus is transmitted to humans through the bite of infected Culex mosquitoes. Pigs and ducks are considered natural reservoirs of the virus.
Doctors advise avoiding mosquito bites, such as by using mosquito repellents, wearing long-sleeved clothes, and getting vaccinated if one lives in or travels to disease-endemic areas. They also stress the importance of awareness and timely treatment to prevent infections and deaths.
An estimated 12.5 million people are thought to be at high risk of JE infection in Nepal.
Drugs such as Ozempic, Wegovy and Mounjaro (known as semaglutide and tirzepatide) have changed the way clinicians manage diabetes and obesity around the world.
Collectively known as GLP-1 agonists, these drugs mimic the hormone GLP-1. This limits both hunger and interest in food, helping users lose weight, and helps control blood sugar levels.
But two new studies published today show that people taking these drugs may have a small increased risk of serious eye conditions and vision loss.
Related: Ozempic-Like Drugs ‘Tentatively’ Linked With Sudden Vision Loss Risk
Here’s what you need to know if you’re taking or considering these medications.
What damage can occur?
Non-arteritic anterior ischaemic optic neuropathy, or NAION, is a rare but devastating eye condition that occurs when blood flow to the optic nerve is suddenly reduced or blocked. It’s also called an “eye stroke”.
The exact cause of NAION remains unclear and there are no current treatments available. People with diabetes are at increased risk of developing NAION.
Unlike other eye conditions that develop gradually, NAION causes a sudden, painless loss of vision. Patients typically notice the condition when they wake up and discover they’ve lost vision in one eye.
Vision tends to worsen over a couple of weeks and slowly stabilises. Recovery of vision is variable, but around 70% of people do not experience improvement in their vision.
What has previous research shown?
A previous study from 2024 found participants prescribed semaglutide for diabetes were four times more likely to develop NAION. For those taking it for weight loss, the risk was almost eight times higher.
In June, the European Medicines Agency concluded NAION represented a “very rare” side effect of semaglutide medications: a one in 10,000 chance. In a first for medicines regulators, the agency now requires product labels to include NAION as a documented risk.
However the recent studies suggest the risks may be lower than we first thought.
In addition to NAION, there is also evidence to suggest GLP-1 drugs can worsen diabetic eye disease, also known as diabetic retinopathy. This occurs when high blood sugar levels damage the small blood vessels in the retina, which can lead to vision loss.
Image of the retina, with blood vessels near the optic nerve. (olaaf/Getty Images Signature/Canva)
It may sound counter-intuitive, but rapid blood sugar reductions can also destabilise the fragile blood vessels in the retina and lead to bleeding.
What do the new studies say?
Two newly published studies investigated people with type 2 diabetes living in the United States over two years. The studies looked at the medical records of 159,000 to 185,000 people.
One study found semaglutide or tirzepatide was associated with a more modest risk of developing NAION than previously thought. Of 159,000 people with type 2 diabetes who were taking these drugs, 35 people (0.04%) developed NAION, compared with 19 patients (0.02%) in the comparison group.
The researchers also found an increased risk of developing “other optic nerve disorders”. However, it’s unclear what kind of optic nerve disorders this includes, as the medical record codes used didn’t specify.
Counter to this, the second study did not find an increased risk of NAION among those taking GLP-1 drugs.
However, the researchers found a small increase in the number of people developing diabetic retinopathy in those prescribed GLP-1 drugs.
But overall, participants on GLP-1 drugs experienced fewer sight-threatening complications related to their diabetic retinopathy and required less invasive eye treatments compared to the group taking other diabetes medications.
Further studies are still needed to understand how GLP-1 drugs can lead to eye complications. A current, five-year clinical trial is studying the long-term effects of semaglutides and diabetic eye disease in 1,500 people, which should tell us more about the ocular risks in the future.
What does this mean for people taking GLP-1 drugs?
NAION is a serious condition. But we need to strike a balance between these (and other) risks and the benefits of GLP-1 medications in diabetes care, obesity treatment, reducing heart attack risks and extending lives.
The key lies in informed decision-making and identifying different levels of risk.
People with multiple NAION risk factors – such as sleep apnoea, high blood pressure and diabetes – should undergo careful consideration with their treating doctor before starting these medications.
People with risk factors for NAION should discuss their use of GLP-1 medications with their doctor. (David Petrus Ibars/Getty Images)
“Crowded” optic nerve heads are also a risk factor for NAION. This is an anatomical feature where blood vessels at the optic nerve head are tightly packed together. People with crowded optic nerve heads should also undergo careful consideration before starting GLP-1 medications.
Although NAION can strike without warning, regular comprehensive eye examinations with your optometrist or ophthalmologist still serve important purposes.
They can detect other drug-related eye problems, including worsening diabetic retinopathy, and can identify patients with crowded optic nerve heads. It’s also important to tell them if you are taking GLP-1 medications so they can keep a close watch on your eye health.
Emerging research also suggests that improving your heart health might help reduce risks of developing NAION. This includes proper management of high blood pressure, diabetes and cholesterol – all conditions that compromise the small blood vessels feeding the optic nerve.
Studies also show patients with heart conditions who better adhere to their medication prescriptions have lower risks of NAION than those who don’t.
Doctors should discuss NAION risks during prescribing decisions and work with eye care providers to monitor regularly for diabetic eye disease. Patients need clear instructions to seek immediate medical attention for sudden vision loss and the need for regular eye examinations.
Aggressive treatment of sleep apnoea and other heart conditions may also help reduce NAION risks. But for now, there remains an ongoing need for more research to understand how GLP-1 medications can affect the eye.
Flora Hui, Research Fellow, Centre for Eye Research Australia and Honorary Fellow, Department of Surgery (Ophthalmology), The University of Melbourne and Pete A Williams, Ulla and Ingemar Dahlberg Professor in Vision Science, Research Group Leader, Karolinska Institutet
This article is republished from The Conversation under a Creative Commons license. Read the original article.
A research team at McMaster University has discovered a new drug class that could someday lead to breakthrough treatments for dangerous fungal infections.
The new molecules, dubbed coniotins, were isolated from a plant-dwelling fungus called Coniochaeta hoffmannii – the samples ofwhich were collected from the McMaster greenhouse, located on the university’s campus.
Detailed recently in the journal Nature Communications, the discovery responds to a critical need for new antifungal medicines.
There is a huge, growing clinical need for new drugs that target fungal infections. Unlike antibiotics, of which there are dozens of different classes approved for use in clinics, there are really only three classes of antifungals on the market right now.”
Gerry Wright, a professor of biochemistry and biomedical sciences at McMaster and principal investigator on the new study
The reason for such a limited arsenal, Wright says, is two-fold.
First, although disease-causing fungi are microscopic like bacteria and viruses, they’re actually more closely related to humans than they are to other microbes – “so things that kill fungi tend to kill us too,” he says. This makes finding antifungals that are safe for human consumption a real challenge.
And then there’s the historical lack of urgency. Wright says that most fungi cannot withstand our internal body temperature, and usually die off before they can cause serious infection. It’s why fungal infections typically occur on us instead of in us – think athlete’s foot, for example. Because our bodies can generally handle these pathogens naturally, Wright says there’s been little incentive for pharmaceutical companies to invest in antifungal R&D – until recently.
“Discovery remains a challenge today, but the level of urgency has changed dramatically over the past 15 years or so,” he says. “In 2009, a novel fungal pathogen called Candida auris emerged all over the world, and this fungus thrives at higher temperatures – and it can be extremely drug-resistant, too.”
C. auris is particularly problematic for individuals with compromised immune systems, like cancer patients undergoing chemotherapy. It can infect the lungs, the bloodstream, and the nervous system, and can be fatal. For these reasons, C. auris sits atop the World Health Organization’s list of priority fungal pathogens.
It’s a good thing then that the Wright Lab’s new molecule exhibits potent activity against C. auris.
Indeed, the research team showed that coniotins not only attack C. auris and several other fungal pathogens, but do so without harming human cells.
The new molecules function unlike any other antifungal on the market. Where most target proteins and membranes, coniotins instead bind to the fungal cell wall.
Wright, a member of the Michael G. DeGroote Institute for Infectious Disease Research at McMaster, likens the cell wall to the candy coating on an M&M – a protective shell that provides structural integrity for what’s inside. Disturbing this structure, as coniotins do, fundamentally changes how well the organism can survive.
Xufei Chen, a postdoctoral fellow in Wright’s lab and first-author on the new paper, identified the new drug class through a process called prefractionation, which allows scientists to tease specific molecules out from complex chemical mixtures.
“Since the golden age of antibiotic discovery, progress has slowed, due primarily to the frequent rediscovery of known compounds,” she says. “To address this, we implemented a prefractionation screening approach to target overlooked or masked metabolites. By integrating mass spectrometry, metabolomics, and computational analysis, I was able to discover this previously hidden molecule.”
Using this same process, Wright’s lab recently discovered a new class of antibiotics. They have also used prefractionation to identify several other new drug candidates, which remain under study.
“What’s really amazing is that we’ve only screened about five percent of the chemical library that we’ve built here at McMaster,” Wright says. “We have an immense, largely unexplored chemical space at our fingertips, and a cost-effective way to reduce the rediscovery of known compounds. Who knows what else is in there?”
Wright’s team is eager to move coniotins along the development pathway. The next steps, he says, include producing it at scale through fermentation, and formulating the new drug class so that it may eventually be suitable intravenous (IV) delivery.
Source:
Journal reference:
Chen, X., et al. (2025). Coniontins, lipopetaibiotics active against Candida auris identified from a microbial natural product fractionation library. Nature Communications. doi.org/10.1038/s41467-025-62630-z.
Groundbreaking research led by a Swansea University academic has revealed a synthetic glycosystem – a sugar-coated polymer nanoparticle – that can block Covid-19 from infecting human cells, reducing infection rates by nearly 99%.
The glycosystem is a specially designed particle that mimics natural sugars found on human cells. These sugars, known as polysialosides, are made of repeating units of sialic acid – structures that viruses often target to begin infection. By copying this structure, the synthetic molecule acts as a decoy, binding to the virus’s spike protein and preventing it from attaching to real cells.
Unlike vaccines, which trigger immune responses, this molecule acts as a physical shield, offering a novel approach to infection prevention.
Using advanced lab techniques to measure molecular interactions and simulate virus binding, researchers found that the glycosystem binds to the virus 500 times more strongly than a similar compound containing sulphates but no sugars. It was also effective at very low doses and worked against both the original SARS-CoV-2 strain and the more infectious D614G variant.
Tests on human lung cells showed a 98.6% reduction in infection when the molecule was present. Crucially, the research highlighted that its effectiveness stems not just from its charge, but from its precise sugar structure – giving this glycosystem its powerful infection-blocking capability.
The discovery is the result of collaboration between Swansea University, Freie Universität Berlin, and Charité – Universitätsmedizin Berlin.
As the main corresponding author and research supervisor, Dr Sumati Bhatia, Senior Lecturer in Chemistry at Swansea University, said: “Leading this research, alongside our international partners, has been incredibly rewarding. It opens a new direction for using glycosystems as a therapeutic strategy against SARS-CoV-2 and could lay the foundation for a new class of antiviral therapies to protect those most at risk.”
The team is now preparing for further biological testing in high-containment laboratories to assess the molecule’s effectiveness against multiple virus strains.
This breakthrough could pave the way for antiviral nasal sprays, surface disinfectants, and treatments to protect vulnerable groups, offering a new line of defense against Covid-19 and future pandemics.
Source:
Journal reference:
Khatri, V., et al. (2025). Polysialosides Outperform Sulfated Analogs for Binding with SARS-CoV-2. Small. doi.org/10.1002/smll.202500719.
Iron deficiency alert: Are you and your family getting enough? Why this nutrient matters more than you think.
If your child fusses, gets irritable, or struggles to sleep, or if you’re a parent running on empty, iron deficiency could be the missing piece of the puzzle.
With 25 years as a clinical dietitian, Dr Libby Weaver knows how often families overlook this vital nutrient. In her new book, Fix Iron First, she explains why iron plays a crucial role in growing bodies and brains, how deficiency appears differently at each stage of childhood and adolescence, and why mums especially need to watch their iron levels.
We sat down with Dr Libby to explore the key signs, challenges, and solutions every parent needs to know.
Iron deficiency in families: What every parent needs to know
Why did you feel now was the right time to write Fix Iron First?
I actually set out to write about something else entirely. But 62,000 words in – 11,000 of which were about iron – I felt compelled to shift focus. Iron has always been front of mind throughout my 25+ years of clinical practice, and I’ve long believed it’s under-appreciated for far more than just energy.
It’s essential for mood, with low levels linked to anxiety and depression. It’s vital for thyroid function, detoxification and countless biochemical processes. It is the most common nutritional deficiency in the world, particularly among women across the menstruation years, pregnant women, teenage girls, athletes, and sadly a growing number of toddlers and children. Yet, it’s not getting the attention it needs to alleviate the unnecessary suffering it causes – other nutrients have become ‘trendier’ and we’re missing iron deficiency. There are very few systems in the body that aren’t impacted by low iron – and that’s a conversation we need to bring to the forefront.
Parents often sense something’s “off” with their child – fussy eating, poor sleep, emotional outbursts – but don’t think to check iron. Why is it such a key piece of the puzzle?
Iron is vital for growing bodies and developing brains. It’s needed for oxygen transport, energy production, immunity and the production of mood-regulating neurotransmitters like dopamine (motivation) and GABA (calming).
It’s becoming increasingly common for women to go through pregnancy iron deficient, which means many babies are born with low iron stores. Breastmilk contains virtually no iron, and while formulas tend to be fortified, calcium can block iron absorption. A baby born to term has accumulated iron in the liver over the third trimester of gestation and also draws from its mother – and if those are low, the baby’s reserves may not last the 6 months they are supposed to before complementary foods are started.
Premature birth and low birth weight are other factors that contribute to inadequate iron stores at birth. Couple this with a lack of awareness around babies from 7-12 months of age requiring 11mg of iron per day, and how important it is to introduce iron-rich foods as soon as solids are started and you can see how easily iron deficiency can develop in those early months. The Kids Research Institute found that one-third of one-year-olds and up to two-thirds of three-year-olds in WA have low iron. It’s likely similar elsewhere in Australia – and that’s deeply concerning.
Iron is the “most common nutritional deficiency in the world, particularly among women across the menstruation years, pregnant women, teenage girls, athletes, and sadly a growing number of toddlers and children”. (Image: Getty Images)
It can be hard to tell the difference between behavioural or developmental concerns and something biological like low iron. What early signs should parents look out for?
Iron deficiency isn’t the only cause of developmental or behavioural issues – but it’s one that’s often missed. When I worked as a dietitian, I saw many children whose symptoms pointed to low iron, even without a blood test. A pattern often emerged, usually with three or more of the following:
Has a pale face (can have an almost translucent appearance if the deficiency is severe), sometimes with visible veins on their face or a bluish tint in the whites of their eyes
Has a poor appetite or is a very selective eater
Avoids meat, even when offered regularly
Has a tendency to be irritable, easily agitated or restless
Has trouble concentrating or staying focused
Has a rapid heart rate at times when it’s not warranted
Experiences shortness of breath quite easily with activity
Might have times of irregular, rapid breathing (body trying to transport more oxygen)
Shows slower physical growth or developmental progress
Has pale gums or inner eyelids when gently pulled down
Drinks more than 500 ml of cow’s milk daily (this can interfere with iron absorption and/or crowd out iron-rich foods)
Gets frequent colds, infections or is often unwell
Has a tendency to have cold hands and/or feet, unrelated to the weather
Eats or craves non-food items like dirt, clay, sand, ice, paper or paint (a condition known as pica; this is more common in very young children)
Delayed puberty (teenage boys).
How does iron deficiency show up differently in toddlers, school-aged children, and teens?
While the symptoms often overlap, they can present differently with age.
Toddlers: Look for fussy eating, recurrent infections, easily agitated/irritated and sleep issues.
School-aged children: Trouble concentrating and continued picky eating may become more noticeable or pronounced. One UWA study found that 1 in 4 children with ADHD-like symptoms had a history of iron deficiency.
Teens: Moodiness, anxiety and irritability may be chalked up to hormones – but it’s worth asking whether low iron could be contributing. Heavy periods are a common cause in teen girls.
Sleep issues have so many causes – how does low iron affect a child’s ability to fall or stay asleep?
Iron plays a critical role in the production of melatonin, the primary hormone that allows us to fall asleep and stay asleep. Without adequate iron available, melatonin production can be compromised leading to poor sleep quality. Low iron is also a driver of restless legs and sleep-disordered breathing in children. If a child has trouble settling at night, frequently wakes or seems tired despite sleeping, checking iron status is a worthwhile starting point.
“Iron plays a critical role in the production of melatonin, the primary hormone that allows us to fall asleep and stay asleep.” (Image: Getty Images)
We often link iron to tiredness, but how else can it affect a child’s brain development, learning, or emotional regulation?
We tend to associate iron with energy – but its role in brain development and emotional wellbeing is just as critical. A study published in the British Medical Journal highlights a consistent global finding: children who experience severe, chronic iron deficiency in infancy tend to have poorer cognitive performance and lower achievement in school.
The authors suggest this is because iron is essential during key windows of brain growth and development – and that a deficiency during these critical periods may lead to lasting changes that are difficult to reverse. While socioeconomic and psychosocial factors also play a role, the biological impact of low iron during early development is profound and well-documented.
Teen girls are especially at risk. What signs might suggest low iron, especially when mood swings and fatigue are often blamed on hormones or school stress?
It’s true that teenage girls face a perfect storm when it comes to iron deficiency. The combination of the onset of menstruation, rapid growth, increased academic and social demands – and often limited iron intake – can easily tip the balance.
The challenge is that many of the early signs of low iron overlap with what’s often considered “normal” teen behaviour: tiredness, mood swings, low motivation, anxiety, trouble focusing. But if these signs persist or intensify, it’s worth taking a closer look. A simple blood test can offer clarity, and addressing low iron can dramatically improve energy, focus, mood and overall resilience during these important developmental years.
Many mums assume it’s normal to feel foggy, exhausted, and flat. How can iron deficiency impact their ability to cope and parent?
Motherhood is demanding at the best of times — emotionally, mentally and physically. However, there’s a point where “normal” fatigue may actually signal something deeper, like iron deficiency.
Iron is essential for more than just energy. It plays a crucial role in brain function, mood regulation, immune health and even your ability to handle stress. When iron levels are low, mothers may experience not just physical exhaustion, but also mental fog, low mood, irritability and a shorter fuse – all of which can make day-to-day parenting feel overwhelming. Tasks that once felt manageable can start to feel insurmountable. The constant decision-making, emotional labour and multitasking that parenting requires becomes harder to sustain. You might feel less patient, less present and less like yourself.
Because these symptoms often creep in slowly, many women accept them as part of life – especially after having children. Yet, they’re not just a natural consequence of motherhood. Often, they’re a signal from the body that something needs attention. And when iron levels are restored, many women describe it as “getting themselves back”. That renewed energy, mental clarity and emotional steadiness can make a profound difference – not just in how they feel, but in how they parent and connect with their family.
How serious can iron deficiency become if left untreated, not just in mums, but across the whole family?
Iron deficiency may start quietly, but if left unaddressed, it can have serious consequences for every member of the family. Remember, it doesn’t just affect energy levels – it impacts mood, concentration, immunity, sleep, thyroid hormone production, physical development and emotional regulation. Over time, the effects can ripple through family life in subtle but significant ways.
Left untreated long-term, iron deficiency can progress to iron deficiency anaemia – a more severe form where red blood cell production is compromised. This can lead to heart palpitations, breathlessness, dizziness, and in some cases, more serious complications like heart strain or complications in pregnancy. Because the symptoms can be so varied – from foggy thinking and fussy eating to frequent infections or emotional agitation – it’s easy to miss the common thread. But when iron deficiency is identified and treated appropriately, the changes can be life-changing. And in the grand scheme of things, it’s a simple fix. For many families, it’s not just about correcting a nutrient gap – it’s about reclaiming wellbeing, resilience and quality of life.
Fix Iron First is “for anyone who has ever felt persistently tired, anxious, low in mood, or disconnected from their spark – and not known why.” (Image: Supplied)
Finally, if there’s one takeaway you hope parents get from this book, what would it be?
You don’t have to accept feeling tired, foggy, forgetful or flat as just part of modern life – or part of being a parent. Yes, there will be sleep-deprived nights and seasons that stretch you physically and emotionally. But if you’re not bouncing back… if exhaustion, low mood or mental fatigue have become your norm… please don’t dismiss it as “just the way it is now”.
Your body is always communicating with you. When you tune in and listen with curiosity and compassion, you may uncover something simple – yet powerful – like iron deficiency, quietly affecting your energy, focus, emotions and resilience. My hope is that Fix Iron First helps you join the dots. That it gives you the insight and confidence to ask the right questions, seek the right tests and advocate for your wellbeing – and your family’s. Because when your iron is truly restored, it can change everything.
The climate crisis is driving a sharp rise in dengue fever cases across the Pacific islands, experts say, as infections hit their highest level in a decade and several countries declare emergencies.
Pacific Island countries and territories have reported 16,502 confirmed cases and 17 deaths since the start of 2025, according to the Pacific Syndromic Surveillance System (PSSS), which collaborates with the World Health Organization (WHO) and other agencies. Infections across the region are at the highest level since 2016, the WHO said. Fiji, Samoa and Tonga are among the worst affected.
Dr Paula Vivili, deputy director general of the Pacific Community (SPC) said historically dengue outbreaks were seasonal.
“However, due to climate change, transmission seasons are lengthening, and some areas are experiencing year-round dengue risk,” Vivili said.
Dengue fever, a viral illness spread by Aedes mosquitoes, causes high fever, severe headache, joint and muscle pain, rash, and in severe cases, can be fatal. Rising temperatures, rainfall and increased humidity are creating ideal breeding conditions for Aedes mosquitoes, even in areas previously unsuitable for transmission.
“Dengue is one of the first real disease-related phenomena that we can lay at the foot of climate change,” said Dr Joel Kaufman, epidemiologist and director of the Center for Exposures, Diseases, Genomics and Environment at the University of Washington.
“Rainfall raises the waterline over mosquito eggs laid just above the surface, which then hatch – that’s part of the natural breeding cycle. Heavy rains can also increase stagnant water sources, creating more opportunities for mosquitoes to breed,” said Kaufman.
Kaufman warned these outbreaks point to a wider public health challenge.
“It is in the vanguard of what will certainly be many types of human disease that become more common and more serious as the planet warms.”
Since declaring an outbreak in April,Samoa has confirmed six dengue-related deaths, including two siblings, and more than 5,600 cases. This year Fiji has recorded eight deaths and 10,969 cases. Tonga has reported over 800 cases and three deaths, since declaring an outbreak in February.
These outbreaks underscore the region’s vulnerability to climate-sensitive diseases, which are expected to intensify as global temperatures rise.
Pacific Island countries produce just 0.03% of global greenhouse gas emissions, according to the Intergovernmental Panel on Climate Change (IPCC), but face some of the most severe climate-related health threats, including vector-borne diseases.
Recent months have brought extreme rainfall to parts of the Pacific including Palau, Papua New Guinea and Solomon Islands, while severe drought has gripped parts of the Marshall Islands, Papua New Guinea, Nauru and Fiji, according to the New Zealand National Institute of Water and Atmospheric Research (NIWA). Forecasts show these contrasts will continue into October.
Although higher rainfall has been attributed to ideal conditions for mosquito breeding, Kaufman said that extreme weather events can also increase transmission of mosquito-borne diseases.Seriously dry or very dry conditions were recorded across large parts of the Pacific in the first half of the year, according to NIWA.
“We might have thought the dryness would reduce mosquito-borne infections, but it seems that’s not what happens. Instead, there’s an acceleration of transmission.”
Across the Pacific, national responses have varied. Samoa, Cook Islands and American Samoa have declared emergencies. The Cook Islands has conducted island-wide clean-ups, intensified surveillance and targeted spraying. Tonga has worked with the WHO to bolster its outbreak response in its worst-hit islands, while Tuvalu has turned to social media and health campaigns to promote preventive measures. Samoa has held school clean-ups and boosted public health messaging. New Zealand has sent a clinical team and NZ$300,000 ($178,000) worth of medical supplies to Samoa, alongside on-the-ground personnel and ongoing coordination with Samoan health officials.
But experts say these measures are being undermined by inadequate surveillance.
“Current disease surveillance systems are rarely sufficient to manage dengue, as evidenced by the continual growth of dengue in the region, and more generally globally,” said Dr Bobby Reiner, disease ecologist at the Institute for Health Metrics and Evaluation at the University of Washington.
Mosquito control tools are methods used to reduce the population of Aedes mosquitoes that spread dengue, such as removing breeding sites, applying larvicides, or spraying insecticides. They can also include biological controls, personal protection measures, and community clean-up campaigns to prevent mosquito bites and transmission.
Still, Reiner said many mosquito control tools have never been proven to reduce transmission, with most responses reactive and often “wastefully chasing the outbreak, applying effort too late”.
