Why is Delta such a worry? It’s more infectious, probably causes more severe disease, and challenges our vaccines


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Michael Toole, Burnet InstituteWhile Australians may be focused on the havoc the Delta variant is wreaking on our shores, Delta is in fact driving waves of COVID infections all around the world.

With the World Health Organization (WHO) warning Delta will rapidly become the dominant strain, let’s take a look at this variant in a global context.

The rise and rise of Delta

The Delta variant (B.1.617.2) emerged quietly in the Indian state of Maharashtra in October 2020. It barely caused a ripple at a time when India was reporting around 40,000 to 80,000 cases a day, most being the Alpha variant (B.1.1.7) first found in the United Kingdom.

That changed in April when India experienced a massive wave of infections peaking at close to 400,000 daily cases in mid-May. The Delta variant rapidly emerged as the dominant strain in India.

The WHO designated Delta as a variant of concern on May 11, making it the fourth such variant.

The Delta variant rapidly spread around the world and has been identified in at least 98 countries to date. It’s now the dominant strain in countries as diverse as the UK, Russia, Indonesia, Vietnam, Australia and Fiji. And it’s on the rise.

In the United States, Delta made up one in five COVID cases in the two weeks up to June 19, compared to just 2.8% in the two weeks up to May 22.

Meanwhile, the most recent Public Health England weekly update reported an increase of 35,204 Delta cases since the previous week. More than 90% of sequenced cases were the Delta variant.

In just two months, Delta has replaced Alpha as the dominant strain of SARS-CoV-2 in the UK. The increase is primarily in younger age groups, a large proportion of whom are unvaccinated.

2 key mutations

Scientists have identified more than 20 mutations in the Delta variant, but two may be crucial in helping it transmit more effectively than earlier strains. This is why early reports from India called it a “double mutant”.

The first is the L452R mutation, which is also found in the Epsilon variant, designated by the WHO as a variant of interest. This mutation increases the spike protein’s ability to bind to human cells, thereby increasing its infectiousness.

Preliminary studies also suggest this mutation may aid the virus in evading the neutralising antibodies produced by both vaccines and previous infection.

A woman wearing a mask crosses the street in New York.
Evidence shows the Delta variant is more infectious. We can understand why by looking at its mutations.
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The second is a novel T478K mutation. This mutation is located in the region of the SARS-CoV-2 spike protein which interacts with the human ACE2 receptor, which facilitates viral entry into lung cells.

The recently described Delta Plus variant carries the K417N mutation too. This mutation is also found in the Beta variant, against which COVID vaccines may be less effective.




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What’s the ‘Delta plus’ variant? And can it escape vaccines? An expert explains


One good thing about the Delta variant is the fact researchers can rapidly track it because its genome contains a marker the previously dominant Alpha variant lacks.

This marker — known as the “S gene target” — can be seen in the results of PCR tests used to detect COVID-19. So researchers can use positive S-target hits as a proxy to quickly map the spread of Delta, without needing to sequence samples fully.

Why is Delta a worry?

The most feared consequences of any variant of concern relate to infectiousness, severity of disease, and immunity conferred by previous infection and vaccines.

WHO estimates Delta is 55% more transmissible than the Alpha variant, which was itself around 50% more transmissible than the original Wuhan virus.

That translates to Delta’s effective reproductive rate (the number of people on average a person with the virus will infect, in the absence of controls such as vaccination) being five or higher. This compares to two to three for the original strain.

There has been some speculation the Delta variant reduces the so-called “serial interval”; the period of time between an index case being infected and their household contacts testing positive. However, in a pre-print study (a study which hasn’t yet been peer-reviewed), researchers in Singapore found the serial interval of household transmission was no shorter for Delta than for previous strains.

One study from Scotland, where the Delta variant is predominating, found Delta cases led to 85% higher hospital admissions than other strains. Most of these cases, however, were unvaccinated.

The same study found two doses of Pfizer offered 92% protection against symptomatic infection for Alpha and 79% for Delta. Protection from the AstraZeneca vaccine was substantial but reduced: 73% for Alpha versus 60% for Delta.

A study by Public Health England found a single dose of either vaccine was only 33% effective against symptomatic disease compared to 50% against the Alpha variant. So having a second dose is extremely important.

In a pre-print article, Moderna revealed their mRNA vaccine protected against Delta infection, although the antibody response was reduced compared to the original strain. This may affect how long immunity lasts.




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A global challenge to controlling the pandemic

The Delta variant is more transmissible, probably causes more severe disease, and current vaccines don’t work as well against it.

WHO warns low-income countries are most vulnerable to Delta as their vaccination rates are so low. New cases in Africa increased by 33% over the week to June 29, with COVID-19 deaths jumping 42%.

There has never been a time when accelerating the vaccine rollout across the world has been as urgent as it is now.

WHO chief Tedros Adhanom Gebreyesus has warned that in addition to vaccination, public health measures such as strong surveillance, isolation and clinical care remain key. Further, tackling the Delta variant will require continued mask use, physical distancing and keeping indoor areas well ventilated.The Conversation

Michael Toole, Professor of International Health, Burnet Institute

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

Taking one for the team: 6 ways our cells can die and help fight infectious disease


White blood cells dying.

Georgia Atkin-Smith, La Trobe University and Ivan Poon, La Trobe UniversityWe have all heard of COVID-19, the flu and bacterial infections. But what is actually happening to our cells when we contract these diseases? Many of our body’s cells don’t live to tell the tale. But cell death isn’t necessarily a bad thing — in fact, the death of infected cells can provide a sacrificial mechanism to stop pathogens in their tracks before they can spread through our body.

Over the years, researchers have realised there are many ways for our cells to die. Our genetics contain a comprehensive “licence to die”, with the route to cell death dictated by both the type of the cell and the pathogen. Let’s check some out:

The dancing death

In the time it takes you to read this sentence, ten million cells in your body will have died, through a type of death called apoptosis. This term, coined in 1972 by Australian pathologist John Kerr, comes from the Greek phrase for “leaves falling from a tree”.

Apoptosis is the most common form of cell death, and has also been nicknamed the “dance of death”, because of the extraordinary shape changes exhibited by the cells under a microscope as they sacrifice themselves.

For example, apoptotic cells dying from radiation or infection with influenza A virus (aka, the flu) generate large, bubble-like structures on their surface called blebs, before shooting out long beaded necklace-like protrusions and finally shattering into pieces.

The death of flu-infected cells is suggested to both aid and limit viral spread. Nevertheless, it’s a spectacular event to witness (and an excellent reminder to get your flu shot this winter).

White blood cell blebbing and dying.

Out with a bang

Vaccinia virus is used worldwide to vaccinate against smallpox. In fact, it was the very first vaccine, developed in 1796 by Edward Jenner.

We now also know that vaccinia virus can make our cells more sensitive to a particular type of cell death, caused by a molecule called TNF. This can help prevent the disease spreading by killing off infected cells before the virus has a chance to replicate.

Many of our cells have a roughly spherical or balloon-like shape, encapsulated by a protective layer called the cell membrane. Just like bursting a balloon with a pin, puncture to the cell membrane marks the point of no return.

This process occurs during necroptosis — an explosive type of cell death in which proteins inside the cell punch holes in the membrane. The cell pops and dies, shutting down the machinery needed for viral replication.

The spider web of death

When they aren’t busy haunting our nightmares, spiders can be found weaving silken masterpieces of extraordinary detail and strength. The web of a golden orb weaving spider, for example, is strong enough to entangle small birds.

On a smaller but equally impressive scale, our immune system contains specialised cells called neutrophils that can weave a deadly web of their own and entrap bacteria. Neutrophils gallantly sacrifice themselves in the process of casting their web, in a type of cell death perhaps fittingly called NETosis.

When infected with bacteria such as Streptococcus pneumoniae, which causes pneumonia and meningitis, neutrophils eject a specialised web made from their own DNA. These webs can entangle nearby bacteria to prevent their escape until other immune cell reinforcements arrive to clear the infection. Sometimes, proteins found in these webs can also kill the bacteria – quite an impressive defence mechanism!

Cartoon illustrating different forms of cell death
There are a surprising number of ways cells can lay down their lives for the greater good.
Author provided

The last meal

Just as our bodies are compartmentalised into organs such as the stomach, liver or heart, our individual cells also have specialised compartments. One of the cell’s “stomachs” (a structure called the “autophagosome”) engulfs and digests cellular contents such as damaged molecules through the process of autophagy.

However, in some circumstances, the machinery that drives this Pac-Man-style action can also facilitate the cell’s demise. Coincidentally, the bacteria Helicobacter pylori can infect cells of the human stomach lining, called epithelial cells, which can cause ulcers and gastritis. The cells can respond with a process called autophagic cell death, in which the induction of autophagy causes the cell to die.

A fiery death

Pyromania, derived from the Greek word pyr, meaning fire, is an obsessive desire to set things ablaze. Some of our immune cells also have the ability to self-immolate and cause inflammation as part of our response to infection.

Since its relatively recent discovery in 2001, this type of cell death, called pyroptosis, has become a hot topic (sorry) among cell biologists, and is often facilitated by a molecular complex called the inflammasome.




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In 2021, understanding pyroptosis is more important than ever, as it has been linked to infection with SARS-CoV-2 infection, the virus that causes COVID-19.

Activation of the factors that cause pyroptosis may help explain the excessive inflammation seen in patients with severe COVID-19. And this could potentially offer a new way to combat the disease.

Overdosing on iron and fat

There’s no doubt the key to a long and healthy life is a balanced diet and exercise. However, sometimes we can’t resist the urge to devour a burger and fries with ice cream for dessert. With enough hard work, we can burn it off again. But for individual cells, overindulging can be fatal.

Too much iron and/or harmful types of fat molecules can cause cells to die by ferroptosis. Cells infected with Mycobacterium tuberculosis, the bacterium that causes TB, can increase their iron content and cause ferrototic cell death! Pass the salad, thanks.




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The survival of the human body is a fine balancing act between cell growth and cell death. Understanding our cells’ complex “licence to die” could give us new ways to combat disease.The Conversation

Georgia Atkin-Smith, Research scientist, La Trobe University and Ivan Poon, Associate Professor, Biochemistry, La Trobe University

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

Clear evidence for a link between pro-inflammatory diets and 27 chronic diseases. Here’s how you can eat better


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Meghan Hockey, Deakin University and Wolfgang Marx, Deakin UniversityAlmost half of all Australians live with a chronic disease, which contribute to some 90% of deaths.

It’s no secret our diet can have a major impact on our health. But our new umbrella review, published this week in Advances in Nutrition, provides compelling evidence that pro-inflammatory diets increase the risk of 27 chronic diseases and premature death. An umbrella review is a review of multiple reviews, and is among the highest levels of evidence.

What’s more, reducing inflammation by eating better could cut our risk of developing certain chronic diseases.




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Clear evidence

A pro-inflammatory diet is one that, over the long-term, may lead to increased inflammation in the body. Such a diet often includes high amounts of commercially baked goods, fried foods and fatty meats, and at the same time is low in fruits, vegetables and other healthy foods.

We reviewed and pooled data from 15 meta-analyses, which is a type of study that summarises data from lots of individual studies. All up, we looked at 38 health outcomes from four million people from across the world.

We found strong evidence for a link between pro-inflammatory diets and heart attacks, premature death and certain cancers including bowel cancer, pancreatic cancer, respiratory cancers and oral cancers. There was also evidence pro-inflammatory diets were linked with depression.




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By bringing together data from populations all over the world, we were able to provide a comprehensive and reliable overview of the research to date. We also looked at the strength of the evidence of studies and found that for most outcomes, evidence was limited, highlighting the need for more research.

Because of the type of study we did, we were unable to determine cause and effect, so we can’t conclusively say pro-inflammatory diets cause these chronic diseases yet. But we found clear evidence a pro-inflammatory diet is linked with an increased risk of developing certain chronic diseases and premature death.

Fried crumbed veal with chips
Dietary patterns that contain lots of calorie-dense, ultra-processed foods can contribute to inflammation and increase your risk of certain chronic diseases.
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But what is inflammation, and what role does our diet play?

Inflammation is part of our body’s natural defence processes. It’s our immune system’s response to an irritant, be that an infection or injury, and is often a welcome sign our body is working to protect us. For example, swelling when you roll your ankle delivers resources to help repair the damage.

But when inflammation can’t be turned off, this process may start to work against us.

Persistent low levels of inflammation (known as chronic inflammation) can be problematic and is linked to premature death and conditions including coronary heart disease and depression, to name a few.

We can detect whether chronic inflammation exists by a simple blood test that looks at levels of inflammatory markers in the blood. Our diet is one factor that influences levels of these inflammatory markers, among many.

Take the “Western diet”, for example, which consists of calorie-dense, ultra-processed foods and is low in fruits, vegetables and other plant-foods. This type of dietary pattern has been linked to higher levels of inflammation.

Conversely, healthy dietary patterns have been linked to lower inflammatory markers. This includes the Mediterranean diet, which is high in fruits, vegetables, legumes, olive oil and oily fish, and low in ultra-processed, refined foods.




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The potential for diets to be pro- or anti-inflammatory can be measured using a tool known as the Dietary Inflammatory Index.

The index takes into account a number of nutrients, compounds, and foods that have been identified in research as having either anti- or pro-inflammatory properties.

Using foods to fight inflammation

Despite promising marketing claims you might see online, there’s no magic supplement or superfood to combat all our inflammation woes.

Instead, you should focus on improving your overall diet quality, rather than on a single food or nutrient. This is because many nutrients and foods interact with one another and can work together to improve inflammation.

Two pieces of salmon with lemon wedge
A Mediterranean diet full of oily fish, fruit, vegetables and legumes has been linked with lower levels of inflammation.
Shutterstock

As for what to eat?

  1. Load up your plate with a wide variety of plant foods such as fruits, vegetables, wholegrains and legumes, like chickpeas and lentils. These foods are high in anti-inflammatory nutrients, such as fibre and a range of vitamins. They also contain unique “phytochemicals”, such as polyphenols which are plant compounds that have potential antioxidant and anti-inflammatory effects
  2. Flavour your food liberally with herbs and spices, and sip on tea and coffee regularly. These are also great sources of polyphenols
  3. Enjoy oily fish regularly, such as salmon, sardines and mackerel, which are rich in anti-inflammatory omega-3 fatty acids
  4. Reduce your intake of foods that may fuel inflammation. These include foods high in trans and saturated fats, found in commercially baked goods, fried foods and fatty meats.



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Given almost half of us live with a chronic disease, and many more are likely at risk, adopting an anti-inflammatory diet could be very beneficial for your health, and may help you live longer too.The Conversation

Meghan Hockey, PhD Candidate, Accredited Practising Dietitian, Deakin University and Wolfgang Marx, Postdoctoral research fellow, Deakin University

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

From STIs to malaria, here are six disease trends we should heed during the pandemic


Stuart Ralph, University of Melbourne and Jacqueline Coombe, University of Melbourne

The number of COVID-19 deaths globally – more than 750,000 – is now greater than the amount of people who succumb to malaria most years.

Meanwhile, national statistics show lockdown restrictions in Australia have potentially helped reduce the number of flu cases.

So while the pandemic continues to have a huge impact on global health, here are some of the known and likely impacts the virus is having on six other major health challenges.

The results might surprise you.

1. Sexually transmitted infections

Some dating apps such as Tinder and Bumble report an increase in online activity, but is this translating to an increase of meet-ups for sexual activity despite the lockdown?

Researchers from the University of Melbourne are investigating these and other questions in a survey examining the sexual and reproductive health impacts of COVID-19.

Although this research is ongoing, preliminary analysis suggests a decline in sexual activity among those without cohabitating partners during lockdown, and an increase in solo sex activities such as masturbation and using sex toys.

Adult stores have also reported a jump in sales during the lockdown.




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While early reports suggest a possible decline in STIs during the lockdown period, with the resumption of normal life across most of Australia, it’s unclear if this trend will continue.

The shopfront of an adult shop.
Adult shops report a sales jump during lockdown.
Flickr/OZinOH, CC BY-NC

2. Respiratory infections

Each year the flu kills 2,000-3,000 Australians. The measures people are taking to limit COVID-19, such as increased physical distancing, good hand hygiene and face masks, are already having a clear benefit on limiting flu spread.




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Deaths from flu in the first half of 2020 were down to just 36, compared with 430 in the same period last year.

While we might expect similar reductions in other respiratory infections, the World Health Organization has major concerns about tuberculosis (TB). Well over a million people worldwide die each year from TB, and extensive detection and tracing programs are key to reducing deaths.

These TB control programs have already been impacted by the pandemic and the WHO predicts an extra 1.4 million people could die as a result over the next five years.

3. Insect-borne diseases

Staying home should stop you inhaling someone else’s cough or sneeze, but it probably won’t stop you being bitten by a mosquito.

More than 700,000 people die each year from diseases spread by biting insects, such as malaria, dengue, sleeping sickness and yellow fever.




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There are already signs dengue cases are growing in Southeast Asia in the wake of reduced control measures brought by COVID-19.

Monash University’s Scott O’Neill, director of the World Mosquito Program and dengue expert, predicts we’re facing a perfect storm in which fragile health systems manage outbreaks of two diseases at once.

In the case of malaria, the WHO estimates deaths in many parts of the world could double this year, killing hundreds of thousands more people if insecticide-treated net campaigns are interrupted because of COVID-19.

A mosquito
Disease-carrying bugs are still biting.
Shutterstock/mycteria

4. Non-communicable diseases

In wealthy countries such as Australia, non-communicable diseases such as cancer, heart disease and stroke are some of the main causes of death and disability. Death from some of these can be reduced by appropriate screening and primary healthcare interventions.




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If people delay going to their doctor to monitor blood pressure or put off routine cancer testing (and reports so far suggest this is happening), we will inevitably see more illness and deaths from these causes.

Cancer Australia has launched a campaign, Cancer Won’t Wait, to remind people to continue to participate in national screening campaigns for breast, cervical and bowel cancers and not to put off seeking medical attention for danger signs of cancer.

In countries that have relatively good control of COVID-19, increases in these non-communicable diseases are likely to far exceed the deaths directly caused by COVID-19.

5. Alcohol and substance abuse

If social media posts are anything to go by, people could be drinking more frequently and in higher volume than normal during the pandemic.

According to a poll commissioned by the Foundation for Alcohol Research and Education, one in five Australian households are buying more alcohol than normal during the pandemic.

Alcohol contributed to more than 1,000 deaths in Australia in 2017 alone, and heavier drinking during the pandemic would exacerbate this pattern.




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Experts also worry about possible longer-term behavioural changes in drinking at home.

The health impacts of abuse of other substances such as heroin or cocaine during the pandemic remains contentious. Limits on transport and movement are already impacting both the trafficking and use of illicit drugs, but users might replace scarce drugs with other equally hazardous substances.

6. Mental health

Mental health disorders have some of the heaviest global health burdens of any type of illness. The social, economic and health impacts of COVID-19 will have huge consequences for mental health for many around the world.

Mental health support services have already reported a surge in calls, while hospitals have seen an increase in presentations of young people after self harm. Australia has launched a National Mental Health and Wellbeing Pandemic Response Plan backed by an initial A$48.1 million.

The Victorian government announced an additional A$60 million for mental health services but much more will likely be needed to avert a crisis in this area.




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As ‘lockdown fatigue’ sets in, the toll on mental health will require an urgent response


What’s the verdict?

Although some infectious diseases that are normally spread directly from person to person are already reducing their transmission because of our response to COVID-19, many other diseases will get much worse during and after the pandemic.

Although we can’t ease up our efforts to control the spread of COVID-19, taking our eye off other ongoing illnesses will mean even worse health and economic outcomes. It’s crucial to maintain our focus on prevention, control and elimination for the many other health challenges that impact Australia, and the world.The Conversation

Stuart Ralph, Associate Professor and malaria researcher, University of Melbourne and Jacqueline Coombe, Research Officer, Melbourne School Of Population And Global Health, University of Melbourne

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

We’ve discovered how these deadly bacteria use a common sugar to spread through the body. It could help us stop them



CDC/Antibiotic Resistance Coordination and Strategy Unit. Medical Illustrator: Meredith Newlove

Vikrant Minhas, University of Adelaide

Although bacteria are single-celled and microscopically small, they still need energy to survive, just like us. One of the most efficient ways of acquiring energy for bacteria is through sweet, soluble carbohydrates: sugars.

In fact, the keen ability of the deadly bacteria Streptococcus pneumoniae to use the plant-derived sugar raffinose may explain how it spreads through the human body.

S. pneumoniae is a bacteria that can quickly develop antibiotic resistance. Each year it causes millions of infections and about one million deaths. Its “ecological niche”, which refers to the natural position of a species within an ecosystem, is our noses and throats, where it doesn’t cause disease.

But from there, S. pneumoniae can spread into the lungs, blood and brain, or more locally into the ear, to cause diseases such as pneumonia, bacteremia, meningitis and otitis media (middle ear inflammation).

Unfortunately, S. pneumoniae is a genetically diverse pathogen, which means it has many different strains. This complicates research efforts to identify how the bacteria spreads into specific sites of the body.

New research published today in Nature Communications Biology by my colleagues and I circumvented these genetic diversity issues by studying closely related strains of S. pneumoniae. We discovered a difference in a gene between two bacterial strains that regulated their use of raffinose, and this resulted in one being more likely to spread and cause disease.




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Sickly sweet, sugars and bacterial disease

In our previous research, two closely related strains of S. pneumoniae were isolated, one from the blood of a patient and another from the ear. Their sequenced genomes were aligned to pick out differences that may impact how they spread to different parts of the body, and hence how they cause disease.

We found a difference in the regulating gene rafR which is responsible for raffinose uptake. This difference allowed the bacteria in the blood sample to use raffinose more efficiently than in the ear sample.

When infecting mice lungs with S. pneumoniae through their nose, we found the blood sample remained in the lungs, causing invasive disease. However, the ear sample was cleared from the lungs, and was unable to cause disease.

Remarkably, swapping the rafR gene between the strains switched their ability to use raffinose, and the way the disease progressed in each case reversed too. This confirmed the rafR gene was indeed playing a large role in causing disease.

Streptococcus pneumoniae imaged with a scanning electron microscope. This bacteria is a major cause of pneumonia. When present in the nose or throat (its ‘ecological niche’) it benefits from the human body without harming it.
Debbie Marshall, CC BY-SA

In our most recent work, we wanted to figure out how this sugar-regulating gene was so profoundly impacting disease progression.

Using a cutting-edge sequencing technique during live mice infections, we discovered the difference in the rafR gene altered how both the mice and the bacteria responded to infection. Notably, strains containing the rafR from the ear sample resulted in more neutrophils, an important immune cell, at the site of infection.

In experiments where neutrophils were depleted in the lungs, the ear sample was not cleared, and the risk of disease was more. This research highlights how this single difference in the gene increased neutrophil levels during infection, preventing S. pneumoniae from causing invasive disease.

Potential research impacts

Raffinose is mainly found in vegetables, grains and legumes. It’s not known whether the human body ever has high enough levels of it to dramatically impact the likelihood of disease. It may be a carbohydrate similar in structure to raffinose is activating the raffinose regulator rafR instead.

Nonetheless, our research provides insight into how S. pneumoniae causes disease. As we understand what enables this deadly bacteria’s spread through the body, more paths will open up to stopping it.

If this raffinose phenomenon proves to be widespread across S. pneumoniae strains, blocking their ability to use raffinose may prevent them from surviving in, and thus invading, the lungs.

This illustration depicts a gram stained specimen under a microscope, with a number of Streptococcus pneumoniae bacteria (the small black dashes).
CDC

Treatments that prevent S. pneumoniae from spreading around the body may be better for preventing disease compared to simply inhibiting or killing the bacteria, as is current practice.

S. pneumoniae can stay in our nose and throats, where it does not cause disease. It plays an import role in this ecosystem. When this bacteria is killed, other deadly bacteria may take its place and spread to sites such as the lungs to cause disease.

The risk in failing to find new treatments

S. pneumoniae’s ability to rapidly develop antibiotic resistance has led the World Health Organisation and US Centres for Disease Control and Prevention to list it as a priority pathogen.

Though vaccines are available, they’re far from perfect and fail to cover all the different strains of S. pneumoniae. If new treatments and vaccines aren’t created soon, the already deadly impact of this bacteria may increase.

Despite the known dangers, research into discovering new antibiotics has been slow. Many treatments in the pipeline don’t provide much benefit over existing antibiotics. Also, effective new treatments usually aren’t implemented widely, and are instead used as a back up in case all else fails. This greatly reduces their profitability, which in turn decreases incentives to make them.

In a worst case scenario, antibiotic-resistant bacteria could kill up to ten million people each year by 2050. To avoid such catastrophe, more research is needed on how bacteria cause disease. And with this knowledge we may be able to lessen the likelihood of future pandemics.




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The Conversation


Vikrant Minhas, PhD candidate, University of Adelaide

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

Mobile phones are covered in germs. Disinfecting them daily could help stop diseases spreading



shutterstock.

Lotti Tajouri, Bond University; Mariana Campos, Murdoch University; Rashed Alghafri, Bond University, and Simon McKirdy, Murdoch University

There are billions of mobile phones in use around the globe. They are present on every single continent, in every single country and in every single city.

We reviewed the research on how mobile phones carry infectious pathogens such as bacteria and viruses, and we believe they are likely to be “Trojan horses” that contribute to community transmission in epidemics and pandemics.

This transfer of pathogens on mobile phones poses a serious health concern. The risk is that infectious pathogens may be spreading via phones within the community, in workplaces including medical and food-handling settings, and in public transport, cruise ships and aeroplanes.

Currently mobile phones are largely neglected from a biosecurity perspective, but they are likely to assist the spread of viruses such as influenza and SARS-CoV-2, the novel coronavirus responsible for the COVID-19 pandemic.




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What the research shows

We reviewed all the studies we could find in peer-reviewed journals that analysed microbes found on mobile phones. Our conclusions are published in the Journal of Travel Medicine and Infectious Disease.

There were 56 studies that met our criteria, conducted in 24 countries around the world between 2005 and 2019.

Most of the studies looked at bacteria found on phones, and several also looked at fungi. Overall, the studies found an average of 68% of mobile phones were contaminated. This number is likely to be lower than the real value, as most of the studies aimed to identify only bacteria and, in many cases, only specific types of bacteria.

The studies were all completed before the advent of SARS-CoV-2, so none of them could test for it. Testing for viruses is laborious, and we could find only one study that did test for them (specifically for RNA viruses, a group that includes SARS-CoV-2 and other coronaviruses).

Some studies compared the phones of healthcare workers and those of the general public. They found no significant differences between levels of contamination.

What this means for health and biosecurity

Contaminated mobile phones pose a real biosecurity risk, allowing pathogens to cross borders easily.

Viruses can live on surfaces from hours to days to weeks. If a person is infected with SARS-CoV-2, it is very likely their mobile phone will be contaminated. The virus may then spread from the phone to further individuals by direct or indirect contact.

Mobile phones and other touchscreen systems – such as at airport check-in counters and in-flight entertainment screens – may have contributed to the rapid spread of COVID-19 around the globe.

Why phones are so often contaminated

Phones are almost ideal carriers of disease. We speak into them regularly, depositing microbes via droplets. We often have them with us while we eat, leading to the deposit of nutrients that help microbes thrive. Many people use them in bathrooms and on the toilet, leading to faecal contamination via the plume effect.

And although phones are exposed to microbes, most of us carry them almost everywhere: at home, at work, while shopping, on holidays. They often provide a temperature-controlled environment that helps pathogens survive, as they are carried in pockets or handbags and are rarely switched off.

On top of this, we rarely clean or disinfect them. Our (unpublished) data suggests almost three-quarters of people have never cleaned their phone at all.




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What this means: clean your phone

While government agencies are providing guidelines on the core practices for effective hand hygiene, there is little focus on practices associated with the use of mobile phones or other touch screen devices.

People touch their mobile phones on average for three hours every day, with super-users touching phones more than 5,000 times a day. Unlike hands, mobile devices are not regularly washed.

We advise public health authorities to implement public awareness campaigns and other appropriate measures to encourage disinfection for mobile phones and other touch screen devices. Without this effort, the global public health campaign for hand washing could be less effective.

Our recommendation is that mobile phones and other touch screen devices should be decontaminated daily, using a 70% isopropyl alcohol spray or other disinfection method.

These decontamination processes should be enforced especially in key servicing industries, such as in food-handling businesses, schools, bars, cafes, aged-care facilities, cruise ships, airlines and airports, healthcare. We should do this all the time, but particularly during a serious disease outbreak like the current COVID-19 pandemic.The Conversation

Lotti Tajouri, Associate Professor, Biomedical Sciences, Bond University; Mariana Campos, Lecturer and researcher, Murdoch University; Rashed Alghafri, Honorary Adjunct Associate Professor, Bond University, and Simon McKirdy, Professor of Biosecurity, Murdoch University

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

Fix housing and you’ll reduce risks of coronavirus and other disease in remote Indigenous communities


Nina Lansbury Hall, The University of Queensland; Andrew Redmond, The University of Queensland; Paul Memmott, The University of Queensland, and Samuel Barnes, The University of Queensland

Remote Indigenous communities have taken swift and effective action to quarantine residents against the risks of COVID-19. Under a plan developed by the Aboriginal and Torres Strait Islander Advisory Group, entry to communities is restricted to essential visitors only. This is important, because crowded and malfunctioning housing in remote Indigenous communities heightens the risk of COVID-19 transmission. High rates of chronic disease mean COVID-19 outbreaks in Indigenous communities may cause high death rates.

The “old story” of housing, crowding and health continues to be overlooked. A partnership between the University of Queensland and Anyinginyi Health Aboriginal Corporation, in the Northern Territory’s (NT) Tennant Creek and Barkly region, re-opens this story. A new report from our work together is titled in Warumungu language as Piliyi Papulu Purrukaj-ji – “Good Housing to Prevent Sickness”. It reveals the simplicity of the solution: new housing and budgets for repairs and maintenance can improve human health.




Read more:
Coronavirus will devastate Aboriginal communities if we don’t act now


Infection risks rise in crowded housing

Rates of crowded households are much higher in remote communities (34%) than in urban areas (8%). Our research in the Barkly region, 500km north of Alice Springs, found up to 22 residents in some three-bedroom houses. In one crowded house, a kidney dialysis patient and seven family members had slept in the yard for over a year in order to access clinical care.

Many Indigenous Australians lease social housing because of barriers to individual land ownership in remote Australia. Repairs and maintenance are more expensive in remote areas and our research found waiting periods are long. One resident told us:

Houses [are] inspected two times a year by Department of Housing, but no repairs or maintenance. They inspect and write down faults but don’t fix. They say people will return, but it doesn’t happen.

Better ‘health hardware’ can prevent infections

The growing populations in communities are not matched by increased housing. Crowding is the inevitable result.

Crowded households place extra pressure on “health hardware”, the infrastructure that enables washing of bodies and clothing and other hygiene practices.




Read more:
Homelessness and overcrowding expose us all to coronavirus. Here’s what we can do to stop the spread


We interviewed residents who told us they lacked functioning bathrooms and washing machines and that toilets were blocked. One resident said:

Scabies has come up a lot this year because of lack of water. We’ve been running out of water in the tanks. There’s no electric pump … [so] we are bathing less …

[Also] sewerage is a problem at this house. It’s blocked … The toilet bubbles up and the water goes black and leaks out. We try to keep the kids away.

A lack of health hardware increases the transmission risk of preventable, hygiene-related infectious diseases like COVID-19. Anyinginyi clinicians report skin infections are more common than in urban areas, respiratory infections affect whole families in crowded houses, and they see daily cases of eye infections.

Data that we accessed from the clinic confirmed this situation. The highest infection diagnoses were skin infections (including boils, scabies and school sores), respiratory infections, and ear, nose and throat infections (especially middle ear infection).

These infections can have long-term consequences. Repeated skin sores and throat infections from Group A streptococcal bacteria can contribute to chronic life-threatening conditions such as kidney disease and rheumatic heart disease (RHD). Indigenous NT residents have among the highest rates of RHD in the world, and
Indigenous children in Central Australia have the highest rates of post-infection kidney disease (APSGN).




Read more:
The answer to Indigenous vulnerability to coronavirus: a more equitable public health agenda


Reviving a vision of healthy housing and people

Crowded and unrepaired housing persists, despite the National Indigenous Reform Agreement stating over ten years ago: “Children need to live in accommodation with adequate infrastructure conducive to good hygiene … and free of overcrowding.”

Indigenous housing programs, such as the National Partnership Agreement for Remote Indigenous Housing, have had varied success and sustainability in overcoming crowding and poor housing quality.

It is calculated about 5,500 new houses are required by 2028 to reduce the health impacts of crowding in remote communities. Earlier models still provide guidance for today’s efforts. For example, Whitlam-era efforts supported culturally appropriate housing design, while the ATSIC period of the 1990s introduced Indigenous-led housing management and culturally-specific adaptation of tenancy agreements.

Our report reasserts the call to action for both new housing and regular repairs and maintenance (with adequate budgets) of existing housing in remote communities. The lack of effective treatment or a vaccine for COVID-19 make hygiene and social distancing critical. Yet crowding and faulty home infrastructure make these measures difficult if not impossible.

Indigenous Australians living on remote country urgently need additional and functional housing. This may begin to provide the long-term gains described to us by an experienced Aboriginal health worker:

When … [decades ago] houses were built, I noticed immediately a drop in the scabies … You could see the mental change, could see the difference in families. Kids are healthier and happier. I’ve seen this repeated in other communities once housing was given – the change.


Trisha Narurla Frank contributed to the writing of this article, and other staff from Anyinginyi Health Aboriginal Corporation provided their input and consent for the sharing of these findings.The Conversation

Nina Lansbury Hall, Senior Lecturer, School of Public Health, The University of Queensland; Andrew Redmond, Senior Lecturer, School of Medicine, The University of Queensland; Paul Memmott, Professor, School of Architecture, and Director, Aboriginal Environments Research Centre (AERC), The University of Queensland, and Samuel Barnes, Research Assistant, School of Public Health, The University of Queensland

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

What is a rare disease? It’s not as simple as it sounds



Shutterstock

Yvonne Zurynski, Macquarie University

If you have a rare disease, you may be the only person in Australia with that condition.

You may not know, however, that being diagnosed with a rare disease means you are part of a community of up to two million Australians with one of these conditions. And more than 300 million people globally.




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Today, health minister Greg Hunt announced Australia will have its first National Strategic Action Plan for rare diseases.

This action plan will harness the power of rare disease advocates, patients and families, clinicians, researchers, peak bodies, industry and government to improve care for people with rare diseases.

What is a rare disease?

A rare disease is one that is very uncommon. The most widely accepted definition stipulates a rare disease affects fewer than five in 10,000 people.

Rare diseases are serious, complex, usually chronic, often life-limiting and most have no cure.

We know of about 7,000 different rare diseases, most with a genetic origin. Many begin in childhood.

Rare diseases are often progressive — they get worse over time — and can be associated with physical or intellectual disability.

Examples of rare diseases are uncommon childhood cancers such as hepatoblastoma (a cancer of the liver), and other better-known conditions like cystic fibrosis and phenylketonuria (a birth defect that causes an amino acid called phenylalanine to build up in the body, and untreated can lead to intellectual disability, seizures and behavioural problems). Both are symptomatic from birth. Huntington’s disease is another, but only shows symptoms in adulthood, even though it’s inherited.




Read more:
Explainer: what is cystic fibrosis and how is it treated?


What makes a rare disease so difficult to diagnose and manage?

For a person living with a rare disease, and the people around them, the journey to obtaining a diagnosis and receiving treatment can be difficult, complex, worrying, confusing and isolating.

Rare diseases are difficult to diagnose because individually they occur so infrequently, and symptoms can be very complex. My research and another Australian study show it can take years to get the final correct diagnosis. Most health professionals have never diagnosed or cared for a person with osteogenesis imperfecta, Fabry disease or any other of the 7,000 rare diseases.

Added to this, the onset of symptoms for a rare disease can occur anywhere between birth and adulthood, and diagnostic tests are lacking or difficult to access.

Rare diseases are often genetic.
Shutterstock

But diagnosis is only part of the puzzle. People with rare diseases typically need complex care from large teams of health professionals because with many rare diseases, several body systems are affected. Also, given the often-progressive nature of the condition, care needs can change — sometimes dramatically — over time.

Important questions also arise around life expectancy and what the risks would be if the person with a rare disease was to start a family. Would their children inherit the disease? Genetic counsellors can help with these sorts of questions.




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No matter how you fund it, medical research is a good investment


Further, care is costly to families and to the health system. The cost of providing hospital care to just one child with a rare lung disorder who eventually needed a lung transplant amounted to almost A$1 million before the child’s ninth birthday.

The market for drugs for rare diseases, often called “orphan drugs”, is small. Although governments incentivise the pharmaceutical industry to develop orphan drugs, there are no effective drug treatments for most rare diseases.

In recognition that rare cancers and rare diseases traditionally lose out to more common diseases in terms of research, additional targeted funding has recently been allocated to boost research in Australia. In 2019 the NHMRC and the Medical Research Future Fund pledged A$15 million over five years for rare cancers, rare diseases and unmet need.

While a positive step, we are still lagging behind other countries. The United States, for example, spent US$3.5 billion (A$5.3 billion) on rare disease research in 2011.

Rare diseases commonly progress over time.
Shutterstock

What does the future look like?

The action plan recognises people with a rare disease and their right to equitable access to health and support services, timely and accurate diagnosis and the best available treatments. It aims to increase rare disease awareness and education, enhance care and support, and drive research and data collection.

Its roll out should lead to better outcomes for people with rare diseases and less worry and frustration for families. For example, access to care coordinators or care navigators could help guide people and families through our often-fragmented health, disability and social care systems.




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Personalised medicine has obvious benefits but has anyone thought about the issues?


Recent advances in personalised medicine, where a person’s specific genomic make-up could be used to tailor specific medicines for that person’s particular disease, holds much promise for people with rare diseases in the future.

Genetic testing for critically ill babies and children is already resulting in faster diagnosis and treatment of rare diseases.

The action plan aims to build on and support the sustainability of these important developments.

If you or a family member has a rare disease, and you’d like more information, the Rare Voices Australia website is a good place to start.

Nicole Millis, CEO of Rare Voices Australia, co-authored this article.The Conversation

Yvonne Zurynski, Associate Professor of Health System Sustainability, Australian Institute of Health Innovation, Macquarie University

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

Does your mental state affect recovery from illness and disease? We asked five experts



A positive mindset can affect some aspects of disease, but grief is normal and to be expected.
from http://www.shutterstock.com

Alexandra Hansen, The Conversation

Many of those who’ve suffered from illness or disease would have received the advice to “stay positive”. Is this sage advice that can truly have a positive effect on health, or an added burden for someone who is already suffering – the need to also feel good about it?

We asked five experts in various fields whether a positive mindset can affect outcomes for those suffering from illness and disease.

Five out of five experts said yes

However, they had some important caveats. It depends on the disease – for example, one expert said studies in cancer have not found positive thinking affects disease progression or the likelihood of early death.

And while our mental health can have powerful effects on our physical health, the perceived need to “stay positive” can be an added burden during a difficult time. So it’s also important to remember grief is normal.

Here are the experts’ detailed responses:


If you have a “yes or no” health question you’d like posed to Five Experts, email your suggestion to: alexandra.hansen@theconversation.edu.au


Erica Sloan is a member of the Scientific Advisory Board of Cygnal Therapeutics. Jayashri Kulkarni receives funding from the NHMRC.The Conversation

Alexandra Hansen, Chief of Staff, The Conversation

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

After the floods come the mosquitoes – but the disease risk is more difficult to predict


Cameron Webb, University of Sydney

We’re often warned to avoid mosquito bites after major flooding events. With more water around, there are likely to be more mosquitoes.

As flood waters recede around Townsville and clean-up efforts continue, the local population will be faced with this prospect over the coming weeks.

But whether a greater number of mosquitoes is likely to lead to an outbreak of mosquito-borne disease is tricky to predict. It depends on a number of factors, including the fate of other wildlife following a disaster of this kind.

Mozzies need water

Mosquitoes lay their eggs in and around water bodies. In the initial stages, baby mosquitoes (or “wrigglers”) need the water to complete their development. During the warmer months, it doesn’t take much longer than a week before they are grown and fly off looking for blood.

So the more water, the more mosquito eggs are laid, and the more mosquitoes end up buzzing about.

But outbreaks of disease carried by mosquitoes are dependent on more than just their presence. Mosquitoes rarely emerge from wetlands infected with pathogens. They typically need to pick them up from biting local wildlife, such as birds or mammals, before they can spread disease to people.




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Mosquitoes and extreme weather events

Historically, major inland flooding events have triggered significant outbreaks of mosquito-borne disease in Australia. These outbreaks have included epidemics of the potentially fatal Murray Valley encephalitis virus. In recent decades, Ross River virus has more commonly been the culprit.

A focal point of the current floods is the Ross River, which runs through Townsville. The Ross River virus was first identified from mosquitoes collected along this waterway. The disease it causes, known as Ross River fever, is diagnosed in around 5,000 Australians every year. The disease isn’t fatal but it can be seriously debilitating.

Following substantial rainfall, mosquito populations can dramatically increase. Carbon dioxide baited light traps are used by local authorities to monitor changes in mosquito populations.
Cameron Webb (NSW Health Pathology)

In recent years, major outbreaks of Ross River virus have occurred throughout the country. Above average rainfall is likely a driving factor as it boosts both the abundance and diversity of local mosquitoes.

Flooding across Victoria over the 2016-2017 summer produced exceptional increases in mosquitoes and resulted in the state’s largest outbreak of Ross River virus. There were almost 1,700 cases of Ross River virus disease reported there in 2017 compared to an average of around 300 cases annually over the previous 20 years.




Read more:
Explainer: what is Ross River virus?


Despite plagues of mosquitoes taking advantage of flood waters, outbreaks of disease don’t always follow.

Flooding resulting from hurricanes in North America has been associated with increased mosquito populations. After Hurricane Katrina hit Louisiana and Mississippi in 2005, there was no evidence of increased mosquito-borne disease. The impact of wind and rain is likely to have adversely impacted local mosquitoes and wildlife, subsequently reducing disease outbreak risk.

Applying insect repellent is worthwhile even if the risk of mosquito-borne disease isn’t known.
From shutterstock.com

Australian studies suggest there’s not always an association between flooding and Ross River virus outbreaks. Outbreaks can be triggered by flooding, but this is not always the case. Where and when the flooding occurs probably plays a major role in determining the likelihood of an outbreak.

The difficulty in predicting outbreaks of Ross River virus disease is that there can be complex biological, environmental and climatic drivers at work. Conditions may be conducive for large mosquito populations, but if the extreme weather events have displaced (or decimated) local wildlife populations, there may be a decreased chance of outbreak.

This may be why historically significant outbreaks of mosquito-borne disease have occurred in inland regions. Water can persist in these regions for longer than coastal areas. This provides opportunities not only for multiple mosquito generations, but also for increasing populations of water birds. These birds can be important carriers of pathogens such as the Murray Valley encephalitis virus.




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Giant mosquitoes flourish in floodwaters that hurricanes leave behind


In coastal regions like Townsville, where the main concern would be Ross River virus, flood waters may displace the wildlife that carry the virus, such as kangaroos and wallabies. For that reason, the flood waters may actually reduce the initial risk of outbreak.

Protect yourself

There is still much to learn about the ecology of wildlife and their role in driving outbreaks of disease. And with a fear of more frequent and severe extreme weather events in the future, it’s an important area of research.

Although it remains difficult to predict the likelihood of a disease outbreak, there are steps that can be taken to avoid mosquito bites. This will be useful even if just to reduce the nuisance of sustaining bites.

Cover up with long-sleeved shirts and long pants for a physical barrier against mosquito bites and use topical insect repellents containing DEET, picaridin, or oil of lemon eucalyptus. Be sure to apply an even coat on all exposed areas of skin for the longest lasting protection.The Conversation

Cameron Webb, Clinical Lecturer and Principal Hospital Scientist, University of Sydney

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