The United States Department of Agriculture last week reported that a pig on a backyard farm in Oregon was infected with bird flu.

As the bird flu situation has evolved, we’ve heard about the A/H5N1 strain of the virus infecting a range of animals, including a variety of birds, wild animals and dairy cattle.

Fortunately, we haven’t seen any sustained spread between humans at this stage. But the detection of the virus in a pig marks a worrying development in the trajectory of this virus.

How did we get here?

The most concerning type of bird flu currently circulating is clade 2.3.4.4b of A/H5N1, a strain of influenza A.

Since 2020, A/H5N1 2.3.4.4b has spread to a vast range of birds, wild animals and farm animals that have never been infected with bird flu before.

While Europe is a hotspot for A/H5N1, attention is currently focused on the US. Dairy cattle were infected for the first time in 2024, with more than 400 herds affected across at least 14 US states.

Bird flu has enormous impacts on farming and commercial food production, because infected poultry flocks have to be culled, and infected cows can result in contaminated diary products. That said, pasteurisation should make milk safe to drink.

While farmers have suffered major losses due to H5N1 bird flu, it also has the potential to mutate to cause a human pandemic.

Birds and humans have different types of receptors in their respiratory tract that flu viruses attach to, like a lock (receptors) and key (virus). The attachment of the virus allows it to invade a cell and the body and cause illness. Avian flu viruses are adapted to birds, and spread easily among birds, but not in humans.

So far, human cases have mainly occurred in people who have been in close contact with infected farm animals or birds. In the US, most have been farm workers.

The concern is that the virus will mutate and adapt to humans. One of the key steps for this to happen would be a shift in the virus’ affinity from the bird receptors to those found in the human respiratory tract. In other words, if the virus’ “key” mutated to better fit with the human “lock”.

A recent study of a sample of A/H5N1 2.3.4.4b from an infected human had worrying findings, identifying mutations in the virus with the potential to increase transmission between human hosts.

Why are pigs a problem?

A human pandemic strain of influenza can arise in several ways. One involves close contact between humans and animals infected with their own specific flu viruses, creating opportunities for genetic mixing between avian and human viruses.

Pigs are the ideal genetic mixing vessel to generate a human pandemic influenza strain, because they have receptors in their respiratory tracts which both avian and human flu viruses can bind to.

This means pigs can be infected with a bird flu virus and a human flu virus at the same time. These viruses can exchange genetic material to mutate and become easily transmissible in humans.

Interestingly, in the past pigs were less susceptible to A/H5N1 viruses. However, the virus has recently mutated to infect pigs more readily.

In the recent case in Oregon, A/H5N1 was detected in a pig on a non-commercial farm after an outbreak occurred among the poultry housed on the same farm. This strain of A/H5N1 was from wild birds, not the one that is widespread in US dairy cows.

The infection of a pig is a warning. If the virus enters commercial piggeries, it would create a far greater level of risk of a pandemic, especially as the US goes into winter, when human seasonal flu starts to rise.

How can we mitigate the risk?

Surveillance is key to early detection of a possible pandemic. This includes comprehensive testing and reporting of infections in birds and animals, alongside financial compensation and support measures for farmers to encourage timely reporting.

Strengthening global influenza surveillance is crucial, as unusual spikes in pneumonia and severe respiratory illnesses could signal a human pandemic. Our EPIWATCH system looks for early warnings of such activity, which can speed up vaccine development.

If a cluster of human cases occurs, and influenza A is detected, further testing (called subtyping) is essential to ascertain whether it’s a seasonal strain, an avian strain from a spillover event, or a novel pandemic strain.

Early identification can prevent a pandemic. Any delay in identifying an emerging pandemic strain enables the virus to spread widely across international borders.

Australia’s first human case of A/H5N1 occurred in a child who acquired the infection while travelling in India, and was hospitalised with illness in March 2024. At the time, testing revealed Influenza A (which could be seasonal flu or avian flu), but subtyping to identify A/H5N1 was delayed.

This kind of delay can be costly if a human-transmissible A/H5N1 arises and is assumed to be seasonal flu because the test is positive for influenza A. Only about 5% of tests positive for influenza A are subtyped further in Australia and most countries.

In light of the current situation, there should be a low threshold for subtyping influenza A strains in humans. Rapid tests which can distinguish between seasonal and H5 influenza A are emerging, and should form part of governments’ pandemic preparedness.

A higher risk than ever before

The US Centers for Disease Control and Prevention states that the current risk posed by H5N1 to the general public remains low.

But with H5N1 now able to infect pigs, and showing worrying mutations for human adaptation, the level of risk has increased. Given the virus is so widespread in animals and birds, the statistical probability of a pandemic arising is higher than ever before.

The good news is, we are better prepared for an influenza pandemic than other pandemics, because vaccines can be made in the same way as seasonal flu vaccines. As soon as the genome of a pandemic influenza virus is known, the vaccines can be updated to match it.

Partially matched vaccines are already available, and some countries such as Finland are vaccinating high-risk farm workers.

C Raina MacIntyre, Professor of Global Biosecurity, NHMRC L3 Research Fellow, Head, Biosecurity Program, Kirby Institute, UNSW Sydney and Haley Stone, Research Associate, Biosecurity Program, Kirby Institute & CRUISE lab, Computer Science and Engineering, UNSW Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

What’s the difference? is a new editorial product that explains the similarities and differences between commonly confused health and medical terms, and why they matter.

Changes in thinking and memory as we age can occur for a variety of reasons. These changes are not always cause for concern. But when they begin to disrupt daily life, it could indicate the first signs of dementia.

Another term that can crop up when we’re talking about dementia is Alzheimer’s disease, or Alzheimer’s for short.

So what’s the difference?

What is dementia?

Dementia is an umbrella term used to describe a range of syndromes that result in changes in memory, thinking and/or behaviour due to degeneration in the brain.

To meet the criteria for dementia these changes must be sufficiently pronounced to interfere with usual activities and are present in at least two different aspects of thinking or memory.

For example, someone might have trouble remembering to pay bills and become lost in previously familiar areas.

It’s less-well known that dementia can also occur in children. This is due to progressive brain damage associated with more than 100 rare genetic disorders. This can result in similar cognitive changes as we see in adults.

So what’s Alzheimer’s then?

Alzheimer’s is the most common type of dementia, accounting for about 60-80% of cases.

So it’s not surprising many people use the terms dementia and Alzheimer’s interchangeably.

Changes in memory are the most common sign of Alzheimer’s and it’s what the public most often associates with it. For instance, someone with Alzheimer’s may have trouble recalling recent events or keeping track of what day or month it is.

We still don’t know exactly what causes Alzheimer’s. However, we do know it is associated with a build-up in the brain of two types of protein called amyloid-β and tau.

While we all have some amyloid-β, when too much builds up in the brain it clumps together, forming plaques in the spaces between cells. These plaques cause damage (inflammation) to surrounding brain cells and leads to disruption in tau. Tau forms part of the structure of brain cells but in Alzheimer’s tau proteins become “tangled”. This is toxic to the cells, causing them to die. A feedback loop is then thought to occur, triggering production of more amyloid-β and more abnormal tau, perpetuating damage to brain cells.

Alzheimer’s can also occur with other forms of dementia, such as vascular dementia. This combination is the most common example of a mixed dementia.

Vascular dementia

The second most common type of dementia is vascular dementia. This results from disrupted blood flow to the brain.

Because the changes in blood flow can occur throughout the brain, signs of vascular dementia can be more varied than the memory changes typically seen in Alzheimer’s.

For example, vascular dementia may present as general confusion, slowed thinking, or difficulty organising thoughts and actions.

Your risk of vascular dementia is greater if you have heart disease or high blood pressure.

Frontotemporal dementia

Some people may not realise that dementia can also affect behaviour and/or language. We see this in different forms of frontotemporal dementia.

The behavioural variant of frontotemporal dementia is the second most common form (after Alzheimer’s disease) of younger onset dementia (dementia in people under 65).

People living with this may have difficulties in interpreting and appropriately responding to social situations. For example, they may make uncharacteristically rude or offensive comments or invade people’s personal space.

Semantic dementia is also a type of frontotemporal dementia and results in difficulty with understanding the meaning of words and naming everyday objects.

Dementia with Lewy bodies

Dementia with Lewy bodies results from dysregulation of a different type of protein known as α-synuclein. We often see this in people with Parkinson’s disease.

So people with this type of dementia may have altered movement, such as a stooped posture, shuffling walk, and changes in handwriting. Other symptoms include changes in alertness, visual hallucinations and significant disruption to sleep.

Do I have dementia and if so, which type?

If you or someone close to you is concerned, the first thing to do is to speak to your GP. They will likely ask you some questions about your medical history and what changes you have noticed.

Sometimes it might not be clear if you have dementia when you first speak to your doctor. They may suggest you watch for changes or they may refer you to a specialist for further tests.

There is no single test to clearly show if you have dementia, or the type of dementia. A diagnosis comes after multiple tests, including brain scans, tests of memory and thinking, and consideration of how these changes impact your daily life.

Not knowing what is happening can be a challenging time so it is important to speak to someone about how you are feeling or to reach out to support services.

Dementia is diverse

As well as the different forms of dementia, everyone experiences dementia in different ways. For example, the speed dementia progresses varies a lot from person to person. Some people will continue to live well with dementia for some time while others may decline more quickly.

There is still significant stigma surrounding dementia. So by learning more about the various types of dementia and understanding differences in how dementia progresses we can all do our part to create a more dementia-friendly community.

The National Dementia Helpline (1800 100 500) provides information and support for people living with dementia and their carers. To learn more about dementia, you can take this free online course.

Nikki-Anne Wilson, Postdoctoral Research Fellow, Neuroscience Research Australia (NeuRA), UNSW Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.