Cats carry diseases that can be deadly to humans, and it’s costing Australia $6 billion every year

Rotiv Artic/Unsplash

Sarah Legge, Australian National University; Chris Dickman, University of Sydney; Jaana Dielenberg, The University of Queensland; John Read; John Woinarski, Charles Darwin University; Pat Taggart, and Tida Nou, The University of Queensland

Toxoplasmosis, cat roundworm and cat scratch disease are caused by pathogens that depend on cats — pets or feral — for part of their life cycle. But these diseases can be passed to humans, sometimes with severe health consequences.

In our study published today in the journal Wildlife Research, we looked at the rates of these diseases in Australia, their health effects, and the costs to our economy.

Professor Sarah Legge discusses the key findings of the study.

Based on findings from a large number of Australian and international studies, Australian hospital data and information from the Australian Bureau of Statistics, we estimate many thousands of people in Australia fall ill or sustain a minor injury as a result of cat-dependent diseases each year.

Our estimations suggest more than 8,500 Australians are hospitalised and about 550 die annually from causes linked to these diseases.

We calculated the economic cost of these pathogens in Australia at more than A$6 billion per year based on the costs of medical care for affected people, lost income from time off work, and other related expenses.

Toxoplasmosis

Toxoplasmosis is an illness caused by the parasite Toxoplasma gondii. It’s the most serious cat-dependent disease.

Newly infected cats shed millions of T. gondii oocysts (like tiny eggs) in their poo and these can survive many months in the environment.

Humans become infected when they ingest these oocysts, which are in the soil and dust in places where cats have defecated, especially sandpits, vegetable gardens or kitty litter.

Humans can also become infected from eating undercooked meat, if those farm animals have come into contact with cat-shed oocysts.

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Up to one-third of people globally are infected with T. gondii, most without knowing it. Australian studies have reported infection rates between 22% and 66%.

Once infected, about 10% of people develop illness; the other 90% have no symptoms.

Based on overall infection rates and Australia’s population size, we estimate there are more than 125,000 new infections in Australia each year.

Of these, around 12,500 people get sick, mostly with non-specific, flu-like symptoms that resolve within a couple of weeks; 650 require hospitalisation, and 50 die, with these more serious cases often experiencing brain swelling and neurological symptoms.

People with compromised immune systems, such as those with cancer or HIV, are at highest risk.

Toxoplasmosis is caused by the parasite Toxoplasma gondii.
Yale Rosen/Flickr

Pregnant women who become infected for the first time can miscarry, or their babies may be born with congenital deformities.

Based on reported and estimated T. gondii infection rates in newborns, about 240 infected babies are born in Australia each year.

More than 20%, or about 50 of these babies, will have symptoms that require life-long care, including impaired vision or hearing, and intellectual disabilities. Another 90 babies will develop symptoms, usually related to vision or hearing, later in life.

Toxoplasmosis carries unique risks for pregnant women.
Freestocks/Unsplash

Long-term impacts of latent infection

Even if the initial infection causes little illness, the T. gondii parasite stays with us for life, encased in a cyst, often in the brain. These “latent” infections may affect our mental health and behaviour, such as delaying our reaction times.

Many studies have found people with T. gondii infection are more likely to have a car accident. A review of several studies found if there were no T. gondii infections, car accident rates would theoretically be 17% lower.

T. gondii infections also appear more common in people with mental health disorders such as schizophrenia, and in people who attempt suicide. Reviews across many studies suggest that without T. gondii infections, there could be 10% fewer suicides and 21% fewer schizophrenia diagnoses.

There’s still debate over whether the parasite causes car accidents and mental health disorders, or whether the association is explained by another shared factor. But it is possible T. gondii infection is a risk factor for these issues, in the same way smoking is a risk factor for heart attacks.

Scientists are still discovering how T. gondii influences the brain, but studies on rodents suggest it may involve changed brain chemistry or inflammation.

Putting it all together

If we accept T. gondii infections do increase the risk of car accidents, suicides and schizophrenia, then considering the incidence of these accidents and health issues in Australia, without T. gondii, we estimate we could potentially avoid:

• 200 deaths and 6,500 hospitalisations due to car accidents

• 300 suicides and 4,500 suicide attempts

• 800 schizophrenia diagnoses each year.

Combining deaths from car accidents and suicide with the 50 deaths from acute toxoplasmosis, we reach a total of 550 deaths related to T. gondii infection per year.

The hospitalisation total for T. gondii includes 650 for acute toxoplasmosis, 50 for congenitally infected babies, 6,500 for car accidents, and 800 for schizophrenia. We didn’t include hospitalisations for suicide attempts, as we didn’t have statistics on that. So this could be a conservative estimate, notwithstanding the fact there are other factors involved in car accidents and mental health issues.

Cat scratch and roundworm

Cat scratch disease is a bacterial infection (Bartonella henselae) that people can contract if bitten or scratched by an infected cat.

Typical symptoms include sores, fevers, aches and swollen glands. But more serious symptoms, such as inflammation of heart tissue, cysts in the organs and loss of vision, can also occur.

Prevalence figures are not available in Australia, but based on rates in the United States and Europe, where cat ownership patterns and cat infection rates are similar, we estimate at least 2,700 Australians get sick annually from cat scratch disease, and 270 are hospitalised.

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Cat roundworm is a parasitic infection (Toxocara cati) that people and other animals can contract by accidentally consuming the parasite’s egg, which infected cats shed in their poo.

Most cat roundworm infections cause mild symptoms, but the migration of the larvae through the body can cause tissue damage, which can be serious if it occurs in a place like the eye or heart.

An adult cat round worm.
Beentree/Wikimedia commons, CC BY

What can we do?

Some 700,000 feral cats and another 2.7 million pet cats roam our towns and suburbs acting as reservoirs of these diseases.

There are no human vaccines for these diseases. Treatment for T. gondii infection in cats isn’t considered useful because cats usually shed the oocysts without the owner even realising the cat has the parasite. Cats can be treated to rid them of roundworm, but treatment for B. henselae (the bacteria that causes cat scratch) may not be effective.

But if you’re a cat owner, there are some things you can do. Keeping pet cats indoors or in a securely contained outdoor area could reduce the chance your pet will contract or pass on a disease-causing pathogen.

If cats are always kept indoors they have a low risk of catching and spreading the disease.
Jaana Dielenberg, Author provided

Cats should be kept out of veggie gardens and children’s sandpits. Washing hands after handling kitty litter and gardening, and washing vegetables thoroughly, can also reduce the risk of transmission.

As T. gondii can be contracted from infected meat, cooking meat well before eating, and not feeding raw meat to pets, can also help.

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The urban feral cat resevoir could be reduced by preventing access to food sources such as farm sites, rubbish bins and tips. We could do this with improved waste management and fencing.

People shouldn’t feed feral cats, as this can lead to cat colony formation, where infection rates are also higher.

Pet cats should also be desexed to prevent unwanted litters that end up as free-roaming ferals.

These steps would cost us and our pet cats little, but could prevent unnecessary impacts on our health and well-being.

Sarah Legge, Professor, Australian National University; Chris Dickman, Professor in Terrestrial Ecology, University of Sydney; Jaana Dielenberg, University Fellow, Charles Darwin University. Science Communication Manager, The University of Queensland; John Read, Associate Lecturer, Ecology and Environmental Sciences; John Woinarski, Professor (conservation biology), Charles Darwin University; Pat Taggart, Adjunct Fellow, and Tida Nou, Project officer, The University of Queensland

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

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Social distancing works – just ask lobsters, ants and vampire bats

Caribbean spiny lobsters normally live in groups, but healthy lobsters avoid members of their own species if they are infected with a deadly virus.
Humberto Ramirez/Getty Images

Dana Hawley, Virginia Tech and Julia Buck, University of North Carolina Wilmington

Social distancing to combat COVID-19 is profoundly impacting society, leaving many people wondering whether it will actually work. As disease ecologists, we know that nature has an answer.

Animals as diverse as monkeys, lobsters, insects and birds can detect and avoid sick members of their species. Why have so many types of animals evolved such sophisticated behaviors in response to disease? Because social distancing helps them survive.

In evolutionary terms, animals that effectively socially distance during an outbreak improve their chances of staying healthy and going on to produce more offspring, which also will socially distance when confronted with disease.

We study the diverse ways in which animals use behaviors to avoid infection, and why behaviors matter for disease spread. While animals have evolved a variety of behaviors that limit infection, the ubiquity of social distancing in group-living animals tells us that this strategy has been favored again and again in animals faced with high risk of contagious disease.

What can we learn about social distancing from other animals, and how are their actions like and unlike what humans are doing now?

Feed the sick, but protect the queen

Social insects are some of the most extreme practitioners of social distancing in nature. Many types of ants live in tight quarters with hundreds or even thousands of close relatives. Much like our day care centers, college dormitories and nursing homes, these colonies can create optimal conditions for spreading contagious diseases.

In response to this risk, ants have evolved the ability to socially distance. When a contagious disease sweeps through their society, both sick and healthy ants rapidly change their behavior in ways that slow disease transmission. Sick ants self-isolate, and healthy ants reduce their interaction with other ants when disease is present in the colony.

Healthy ants even “close rank” around the most vulnerable colony members – the queens and nurses – by keeping them isolated from the foragers that are most likely to introduce germs from outside. Overall, these measures are highly effective at limiting disease spread and keeping colony members alive.

Many other types of animals also choose exactly who to socially distance from, and conversely, when to put themselves at risk. For example, mandrills – a type of monkey – continue to care for sick family members even as they actively avoid sick individuals to whom they are not related. In an evolutionary sense, caring for a sick family member may allow an animal to pass on its genes through that family member’s offspring.

Mandrills live in large groups in the rainforests of equatorial Africa. They will often groom other group members, but actively avoid sick mandrills unless they are close family members.
Eric Kilby/Wikipedia, CC BY-SA

Further, some animals maintain essential social interactions in the face of sickness while foregoing less critical ones. For example, vampire bats continue to provide food for their sick groupmates, but avoid grooming them. This minimizes contagion risk while still preserving forms of social support that are most essential to keeping sick family members alive, such as food sharing.

These nuanced forms of social distancing minimize costs of disease while maintaining the benefits of social living. It should come as no surprise that evolution favors them in many types of animals.

Altruism makes us human

Human behavior in the presence of disease also bears the signature of evolution. This indicates that our hominid ancestors faced many of the same pressures from contagious disease that we are facing today.

Like social ants, we are protecting the most vulnerable members of our society from COVID-19 infection by ensuring that older individuals and those with pre-existing conditions stay away from potentially contagious people. Like monkeys and bats, we also practice nuanced social distancing, reducing non-essential social contacts while still providing essential care for sick family members.

A black garden ant queen (upper left), surrounded by adult ants, larvae (left), eggs (middle) and a cocoon (right).
Pan weterynarz/Wikipedia, CC BY-SA

There also are important differences. For example, in addition to caring for sick family members, humans sometimes increase their own risk by caring for unrelated individuals, such as friends and neighbors. And health care workers go further, actively seeking out and helping precisely those who many of us carefully avoid.

Altruism isn’t the only behavior that distinguishes human response to disease outbreaks. Other animals must rely on subtle cues to detect illness among group members, but we have cutting-edge technologies that make it possible to detect pathogens rapidly and then isolate and treat sick individuals. And humans can communicate health threats globally in an instant, which allows us to proactively institute behaviors that mitigate disease. That’s a huge evolutionary advantage.

Finally, thanks to virtual platforms, humans can maintain social connections without direct physical contact. This means that unlike other animals, we can practice physical rather than social distancing, which lets us preserve some of the important benefits of group living while minimizing disease risk.

Worth the disruption

The evidence from nature is clear: Social distancing is an effective tool for reducing disease spread. It is also a tool that can be implemented more rapidly and more universally than almost any other. Unlike vaccination and medication, behavioral changes don’t require development or testing.

However, social distancing can also incur significant and sometimes unsustainable costs. Some highly social animals, like banded mongooses, do not avoid group members even when they are visibly sick; the evolutionary costs of social distancing from their relatives may simply be too high. As we are currently experiencing, social distancing also imposes severe costs of many kinds in human societies, and these costs are often borne disproportionately by the most vulnerable people.

Given that social distancing can be costly, why do so many animals do it? In short, because behaviors that protect us from disease ultimately allow us to enjoy social living – a lifestyle that offers myriad benefits, but also carries risks. By implementing social distancing when it’s necessary, humans and other animals can continue to reap the diverse benefits of social living in the long term, while minimizing the costs of potentially deadly diseases when they arise.

Social distancing can be profoundly disruptive to our society, but it can also stop a disease outbreak in its tracks. Just ask ants.

[You need to understand the coronavirus pandemic, and we can help. Read The Conversation’s newsletter.]

Dana Hawley, Professor of Biological Sciences, Virginia Tech and Julia Buck, Assistant Professor of Biology, University of North Carolina Wilmington

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

Explainer: what is Murray Valley encephalitis virus?

Ana Ramírez, James Cook University; Andrew Francis van den Hurk, The University of Queensland; Cameron Webb, University of Sydney, and Scott Ritchie, James Cook University

Western Australian health authorities recently issued warnings about Murray Valley encephalitis, a serious disease that can spread by the bite of an infected mosquito and cause inflammation of the brain.

Thankfully, no human cases have been reported this wet season. The virus that causes the disease was detected in chickens in the Kimberley region. These “sentinel chickens” act as an early warning system for potential disease outbreaks.

What is Murray Valley encephalitis virus?

Murray Valley encephalitis virus is named after the Murray Valley in southeastern Australia. The virus was first isolated from patients who died from encephalitis during an outbreak there in 1951.

The virus is a member of the Flavivirus family and is closely related to Japanese encephalitis virus, a major cause of encephalitis in Asia.

Murray Valley encephalitis virus is found in northern Australia circulating between mosquitoes, especially Culex annulirostris, and water birds. Occasionally the virus spreads to southern regions, as mosquitoes come into contact with infected birds that have migrated from northern regions.

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How serious is the illness?

After being transmitted by an infected mosquito, the virus incubates for around two weeks.

Most people infected don’t develop symptoms. But, if you’re unlucky, you could develop symptoms ranging from fever and headache to paralysis, encephalitis and coma.

Around 40% of people who develop symptoms won’t fully recover and about 25% die. Generally, one or two human cases are reported in Australia per year.

Since the 1950s, there have been sporadic outbreaks of Murray Valley encephalitis, most notably in 1974 and 2011. The 1974 outbreak was Australia-wide, resulting in 58 cases and 12 deaths.

It’s likely the virus has been causing disease since at least the early 1900s when epidemics of encephalitis were attributed to a mysterious illness called Australian X disease.

Traditional monitoring of mosquito-borne diseases relies on the collection of mosquitoes using specially designed traps baited with carbon dioxide.
Cameron Webb

Early warning system

Given the severity of Murray Valley encephalitis, health authorities rely on early warning systems to guide their responses.

One of the most valuable surveillance tools to date have been chooks because the virus circulates between birds and mosquitoes. Flocks of chickens are placed in areas with past evidence of virus circulation and where mosquitoes are buzzing about.

Chickens are highly susceptible to infection so blood samples are routinely taken and analysed to determine evidence of virus infection. If a chicken tests positive, the virus has been active in an area.

The good news is that even if the chickens have been bitten, they don’t get sick.

Mosquitoes can also be collected in the field using a variety of traps. Captured mosquitoes are counted, grouped by species and tested to see if they’re carrying the virus.

This method is very sensitive: it can identify as little as one infected mosquito in a group of 1,000. But processing is labour-intensive.

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How can technology help track the virus?

Novel approaches are allowing scientists to more effectively detect viruses in mosquito populations.

Mosquitoes feed on more than just blood. They also need a sugar fix from time to time, usually plant nectar. When they feed on sugary substances, they eject small amounts of virus in their saliva.

This led researchers to develop traps that contain special cards coated in honey. When the mosquitoes feed on the cards, they spit out virus, which specific tests can then detect.

We are also investigating whether mosquito poo could be used to enhance the sugar-based surveillance system. Mosquitoes spit only tiny amounts of virus, whereas they poo a lot (300 times more than they spit).

This mosquito poo can contain a treasure trove of genetic material, including viruses. But we’re still working out the best way to collect the poo.

Mosquito poo, shown here after mosquitoes have fed on coloured honey, can be used to detect viruses like Murray Valley encephalitis.
Dagmar Meyer

Staying safe from Murray Valley encephalitis

There is no vaccine or specific treatment for the virus. Avoiding mosquito bites is the only way to protect yourself from the virus. You can do this by:

• wearing protective clothing when outdoors

• avoiding being outdoors when the mosquitoes that transmit the virus are most active (dawn and dusk)

• using repellents, mosquito coils, insect screens and mosquito nets

• following public health advisories for your area.

The virus is very rare and your chances of contracting the disease are extremely low, but not being bitten is the best defence.

Ana Ramírez, PhD candidate, James Cook University; Andrew Francis van den Hurk, Medical Entomologist, The University of Queensland; Cameron Webb, Clinical Lecturer and Principal Hospital Scientist, University of Sydney, and Scott Ritchie, Professorial Research Fellow, James Cook University

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

Why naming all our mozzies is important for fighting disease

And you can be…Susan.
from http://www.shutterstock.com

Bryan Lessard, CSIRO

Notorious for spreading diseases like malaria and Zika virus overseas, mosquitoes contribute to thousands of cases of human disease in Australia each year. But only half of Australia’s approximately 400 different species of mosquitoes have been scientifically named and described. So how are scientists able to tell the unnamed species apart?

Climate change means population change

Mosquito populations and our ability to predict disease outbreaks are likely to change in the future. As climates change, disease-carrying mozzies who love the heat may spread further south into populated cities.

As human populations continue to grow in Australia, they will interact with different communities of wild animals that act as disease reservoirs, as well as different mosquito species that may be capable of carrying these diseases. The expansion of agricultural and urban water storages will also create new homes for mosquito larvae to mature, allowing mosquitoes to spread further throughout the country.

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Mosquito larvae need a body of water to mature in.
James Gathany, CDC

Agents of disease

Mosquitoes like the native Common Banded Mosquito (Culex annulirostris) are known to spread human diseases such as Ross River virus, Barmah Forest virus, Dengue fever and Murray Valley encephalitis.

It’s not the adult mosquito itself that causes the disease, but the viruses and other microbes that accumulate in the mosquito’s saliva and are injected into the bloodstream of the unsuspecting victim during feeding.

The mosquitoes that bite humans are female, requiring the proteins in blood to ripen their eggs and reach sexual maturity. Male mosquitoes, and females of some species, are completely vegetarian, opting to drink nectar from flowers, and are useful pollinators.

The life cycle of a mosquito.
from http://www.shutterstock.com

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Common Australian mosquitoes can’t spread Zika

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The name game

Mosquitoes belong to the fly family Culicidae and are an important part of our biodiversity. There are more than 3,680 known species of mosquitoes in the world. Taxonomists, scientists who classify organisms, have been able to formally name more than 230 species in Australia.

The classification of Australian mosquitoes tapered off in the 1980s with the publication of the last volume of The Culicidae of the Australasian Region and passing of Dr Elizabeth Marks who was the most important contributor to our understanding of Australian mosquitoes.

She left behind 171 unique species with code numbers like “Culex sp No. 32”, but unfortunately these new species were never formally described and remained unnamed after her death. This isn’t uncommon in biodiversity research, as biologists estimate that we’ve only named 25% of life on earth during a time when there is an alarming decline in the taxonomic workforce.

Dr Marks’ unnamed species are still held in Australian entomology collections, like CSIRO’s Australian National Insect Collection, Museum Victoria and the Queensland Museum. Although all the major disease-carrying species of mosquitoes are known in the world, several of Marks’ undescribed Australian species are blood feeding and may have the capacity to transmit diseases.

How do we tell mozzies apart?

Naming, describing and establishing the correct classification of Australia’s mosquitoes is the first step to understanding their role in disease transmission. This is difficult work as adults are small and fragile, and important diagnostic features that are used to tell species apart, like antennae, legs and even tiny scales, are easily lost or damaged.

CSIRO scientists, with support from the Australian Biological Resources Study, Government of Western Australia Department of Health, and University of Queensland, have been tasked with naming Australia’s undescribed mosquitoes. New species will be named and described based on the appearance of the adults and infant larval stages which are commonly intercepted by mozzie surveillance officers. New identification tools will also be created so others can quickly and reliably identify the Australian species.

A 100 year old specimen of the native Common Banded Mosquito Culex annulirostris, capable of spreading Murray Valley encephalitis virus, one of 12 million specimens held in CSIRO’s Australian National Insect Collection in Canberra.
CSIRO/Dr Bryan Lessard

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Scientists are now able to extract DNA and sequence the entire mitochondrial genome from very old museum specimens. CSIRO are using these next generation techniques to generate a reliable DNA reference database of Australian mosquitoes to be used by other researchers and mozzie surveillance officers to accurately identify specimens and diagnose new species. CSIRO are also digitising museum specimens to unlock distribution data and establish the geographical boundaries for the Australian species.

By naming and describing new species, we will gain a more complete picture of our mosquito fauna, and its role in disease transmission. This will make us better prepared to manage our mosquitoes and human health in the future as the climate changes and our growing human population moves into new areas of Australia.

Bryan Lessard, Postdoctoral Research Fellow, CSIRO

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

Mozzie repellent clothing might stop some bites but you’ll still need a cream or spray

Clothes can offer some protection.
John Jones/Flickr, CC BY

Cameron Webb, University of Sydney

A range of shirts, pants, socks and accessories sold in specialist camping and fishing retailers claim to protect against mosquito bites for various periods.

In regions experiencing a high risk of mosquito-borne disease, insecticide treated school uniforms have been used to help provide extra protection for students.

During the 2016 outbreak of Zika virus in South America, some countries issued insecticide-treated uniforms to athletes travelling to the Olympic Games.

Some academics have even suggested fashion designers be encouraged to design attractive and innovative “mosquito-proof” clothing.

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But while the technology has promise, commercially available mosquito-repellent clothing isn’t the answer to all our mozzie problems.

Some items of clothing might offer some protection from mosquito bites, but it’s unclear if they offer enough protection to reduce the risk of disease. And you’ll still need to use repellent on those uncovered body parts.

First came mosquito-proof beds

Bed nets have been used to create a barrier between people and biting mosquitoes for centuries. This was long before we discovered mosquitoes transmitted pathogens that cause fatal and debilitating diseases such as malaria. Preventing nuisance-biting and buzzing was reason alone to sleep under netting.

Bed nets have turned out to be a valuable tool in reducing malaria in many parts of the world. And they offer better protection if you add insecticides.

The insecticide of choice is usually permethrin. This and other closely related synthetic pyrethroids are commonly used for pest control and have been assessed as safe for use by the United States Environmental Protection Authority, the Australian Pesticides and Veterinary Medicines Authority and other regulatory bodies.

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New technologies have also allowed for the development of long-lasting insecticidal bed nets, offering extended protection against mosquito bites, perhaps up to three years, even with repeated washing.

Mosquito repellent clothing

Innovations in clothing that prevent insect bites have primarily come from the United States military. Mosquito-borne disease is a major concern for military around the globe. Much research funding has been invested in strategies to provide the best protection for personnel.

Traditional insect repellents, such as DEET or picaridin, are applied to the skin to prevent mosquitoes from landing and biting.

While permethrin will repel some mosquitoes, treated clothing most effectively works by killing the mosquitoes landing and trying to bite through the fabric.

Clothing treated with permethrin has been shown to protect against mosquitoes and ticks, as well as other biting insects and mites. For these studies, clothing was generally soaked in solutions or sprayed with insecticides to ensure adequate protection.

Clothing made from insecticide impregnated fabrics may help reduce mosquito bites.
Cameron Webb (NSW Health Pathology)

Fabrics factory-treated with insecticides, as used by many military forces, are purported to provide more effective protection. But while some studies suggest clothing made from these fabrics provide protection even after multiple washes, others suggest the “factory-treated” fabrics don’t provide greater levels of protection than “do it yourself” versions.

Overall, the current evidence suggests insecticide-treated clothing may reduce the number of mosquito bites you get, but it doesn’t offer full protection.

More research is needed to determine if insecticide-treated clothing can prevent or reduce rates of mosquito-borne disease.

Better labelling and regulation

All products that claim to provide protection from insect bites must be registered with the Australian Pesticides and Veterinary Medicines Authority. This includes sprays, creams and roll-on formulations of repellents.

Anything labelled as “insect repelling”, including insecticide treated clothing, requires registration. Clothing marketed as simply “protective” (such as hats with netting) doesn’t. This approach reflects the requirements of the US EPA.

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If you’re shopping for insect-repellent clothing, check the label to see if it states that it is registered by the APVMA. You should see a registration number and the insecticide used in the fabric clearly displayed on the clothing’s tag.

While some products will be registered, there are still some concerns about how the efficacy of mosquito bite protection is assessed.

There is likely to be growing demand for these types of products and experts are calling for internationally accepted guidelines to test these products. Similar guidelines exist for topical repellents.

Finally, keep in mind that while various forms of insecticide-treated clothing will help reduce the number of mosquito bites, they won’t provide a halo of bite-free protection around your whole body.

Remember to apply a topical insect repellent to exposed areas of skin, such as hands and face, to ensure you’re adequately protected from mosquito bites.

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.

Lord of the forest: New Zealand’s most sacred tree is under threat from disease, but response is slow

Tāne Mahuta is New Zealand’s most sacred tree, but its days will be numbered if it is infected with kauri dieback disease.
from http://www.shutterstock.com, CC BY-SA

Matthew Hall, Victoria University of Wellington

Tāne Mahuta is Aotearoa New Zealand’s largest living being – but the 45m tall, 2,500-year-old kauri tree is under severe threat from a devastating disease.

Nearly a decade after the discovery of kauri dieback disease, it is continuing to spread largely unchecked through the northern part of the North Island. Thousands of kauri trees have likely been infected and are now dead or dying. The Waipoua forest, home of Tāne Mahuta and many other majestic kauri, is reported to be one of the worst affected areas.

For Māori, who trace their whakapapa (lineage) to the origins of the earth, Tāne Mahuta is kin. The threat of losing this tree should electrify the fight against kauri dieback.

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Call to close the forest

Named after Tāne, the son of Ranginui the sky father and Papatūanuku the earth mother, Tāne Mahuta is a highly revered taonga, or treasure. In Māori mythology, it was Tāne who brought trees and birds to earth.

The loss of this ancestor, with a presence that has been known to move some to tears, is incalculable.

Kauri dieback has been recorded metres from this ancient tree, despite the best efforts of a prevention programme that has been in place since 2009. Much of the focus of the programme has been on encouraging behaviour change by forest users (following paths, washing boots) and upgrading tracks (from mud to boardwalks). A new national pest management plan proposes more of the same.

As part of a prevention programme to limit the spread of kauri dieback, visitors to kauri forests are encouraged to spray their shoes with a disinfectant.
Eli Duke/WIkimedia Commons, CC BY-SA

Signs remind visitors in the Waitākere Ranges about precautions against the spread of kauri dieback disease.
from Wikimedia Commons, CC BY-SA

In my view, the most notable, and frustrating, aspect of this programme is the significant resistance to close kauri forest tracks to people, who, along with wild pigs, are one of the major vectors of the disease.

Te Kawerau ā Maki, a Māori tribal group with mana whenua (customary authority) over the land of the Waitākere forest in the Auckland region, have maintained a consistent stance that the only way to protect kauri forests is to close them to humans. In November 2017, they placed a rāhui (temporary closure) over the entire forest area, severely frustrated by the lack of effective action to control kauri dieback by Auckland Council.

A rāhui is not legally enforceable, and it was largely ignored by forest users who continued to enter and spread the disease. Eventually, six months later, Auckland Council voted to close the majority of tracks, but Te Kawerau ā Maki have viewed this as too little, and possibly too late.

Keeping the forest open

In a similar laggardly vein, the Department of Conservation has only just put forward a proposal to close or partially close 24 kauri forest tracks. This proposal is currently going through a consultation process, which seems inappropriate when dealing with an immediate biosecurity crisis.

The proposal does not include the Waipoua forest and the track that leads to Tāne Mahuta, or to other significant kauri such as Te Matua Ngahere. The department says:

the decision to propose track closures is not taken lightly, but has been considered in situations where there is high kauri dieback risk, low visitor use, high upgrade and ongoing maintenance costs, and a similar experience provided in the vicinity.

Tāne mahuta draws hundreds of thousands of tourists to the Waipoua forest area. This, combined with the fact that forest tracks are generally in good condition has led to the decision to keep the forest open. For now, the tangata whenua (local Māori with authority over land) support it.

Tāne Mahuta draws hundreds of thousands of visitors to the kauri forests in the north of New Zealand.
from http://www.shutterstock.com, CC BY-SA

Relinquishing our claims

Although we know that our human presence in kauri forests will lead to the certain death of the trees, many people still wish to venture into the forests, to walk or to hunt, regardless of the consequences.

Whether conscious or not, the value assessment here must be that the right of kauri trees to live and flourish is of lesser value than some fleeting recreation on a weekend afternoon. As people kept blindly tramping into the Waitākere forest, infection rates increased from 8% to 19% in just five years.

What I find most disturbing here is that government agencies tasked with preserving the “intrinsic values” of native species are prepared to let this happen for pragmatic and economic reasons. This is one of those situations where competing values can’t be balanced.

The life and flourishing of kauri must be prioritised above all else, whatever the economic or recreational hit. This means letting go of our claim to kauri trees as “natural and recreational resources” and acknowledging them for what they are – our living, spiritual, intelligent kin.

Kauri or kiwifruit

Pragmatically, our assistance to kauri also necessitates that we re-assess the value we place on the survival of kauri from an economic perspective.

Funding of less than NZ$2 million per year for the kauri dieback programme pales in comparison to the magnitude of the response to recent agricultural biosecurity threats.

In 2010, a huge response to the incursion of a microbial pathogen (Pseudomonas syringae pv. actinidiae, or Psa) in kiwifruit vines saw a NZ$50 million fund created to fight the disease.

In 2015, after a single Queensland fruit fly was caught in a trap in February, a large coordinated response, with local, restrictive biosecurity control orders in place, resulted in eradication in October, at a cost of NZ$13.6 million.

With such funds, it would be much easier to enforce the closure of kauri forests, until more long-term measures, such as improving genetic resistance, become possible.

At the end of last year, Minister for Forestry Shane Jones was quoted expressing a similar opinion, following the government’s announcement that it would attempt to eradicate the cow disease Mycoplasma bovis.

If it’s possible for us to move swiftly and cull diseased cows and stop the transport of potentially diseased cows off private farms, we need a similar level of vigour in safeguarding areas where our kauri are still strong.

For the survival of Tāne Mahuta, we should close off kauri forests immediately and boost funding for the implementation of the dieback management programme.

Matthew Hall, Associate Director, Research Services, Victoria University of Wellington

This article was originally published on The Conversation. Read the original article.

Some tropical frogs may be developing resistance to a deadly fungal disease – but now salamanders are at risk

Panamanian golden frogs (Atelopus zeteki) are listed as critically endangered, and may be extinct in the wild.
Jeff Kubina, CC BY-SA

Louise Rollins-Smith, Vanderbilt University

My office is filled with colorful images of frogs, toads and salamanders from around the world, some of which I have collected over 40 years as an immunologist and microbiologist, studying amphibian immunity and diseases. These jewels of nature are mostly silent working members of many aquatic ecosystems.

The exception to the silence is when male frogs and toads call to entice females to mate. These noisy creatures are often wonderful little ventriloquists. They can be calling barely inches from your nose, and yet blend so completely into the environment that they are unseen. I have seen tropical frogs in Panama and native frogs of Tennessee perform this trick, seemingly mocking my attempts to capture them.

My current research is focused on interactions between amphibians and two novel chytrid pathogens that are linked to global amphibian declines. One, Batrachochytrium dendrobatidis ( abbreviated as Bd), has caused mass frog dieoffs around the world. Recently my lab group contributed to a study showing that some species of amphibians in Panama that had declined due to Bd infections are recovering. Although the pathogen has not changed, these species appear to have developed better skin defenses than members of the same species had when Bd first appeared.

This is very good news, but those who love amphibians need to remain vigilant and continue to monitor these recovering populations. A second reason for concern is the discovery of a closely related chytrid, Batrachochytrium salamandrivorans (Bsal), which seems to be more harmful to salamanders and newts.

Amphibian chytrid fungus has been detected in at least 52 countries and 516 species worldwide.
USDA Forest Service

Global frog decline

More than a decade ago, an epidemic of a deadly disease called chytridiomycosis swept through amphibian populations in Panama. The infection was caused by a chytrid fungus, Batrachochytrium dendrobatidis. Scientists from a number of universities, working with the Smithsonian Tropical Research Institute in Panama, reported that chytridiomycosis was moving predictably from west to east from Costa Rica across Panama toward Colombia.

I was part of an international group of scientists, funded by the National Science Foundation, who were trying to understand the disease and whether amphibians had effective immune defenses against the fungus. Two members of my lab group traveled to Panama yearly from 2004 through 2008, and were able to look at skin secretions from multiple frog species before and after the epidemic of chytridiomycosis hit.

Many amphibians have granular glands in their skin that synthesize and sequester antimicrobial peptides (AMPs) and other defensive molecules. When the animal is alarmed or injured, the defensive molecules are released to cleanse and protect the skin.

Through mechanisms that remain a mystery, we observed that these skin defenses seemed to improve after the pathogen entered the amphibian communities. Still, many frog populations in this area suffered severe declines. A global assessment published in 2004 showed that 43 percent of amphibian species were declining and 32 percent of species were threatened.

In Panama, Smithsonian scientists operate the largest amphibian conservation facility of its kind in the world.

Signs of resistance

In 2012-2013, my colleagues ventured to some of the same sites in Panama at which amphibians had disappeared. To our great delight, some of the species were partially recovering, at least enough so that they could be found and sampled again.

We wanted to know whether this was happening because the pathogen had become less virulent, or for some other reason, including the possibility that the frogs were developing more effective responses. To find out, we analyzed multiple measures of Bd‘s virulence, including its ability to infect frogs that had never been exposed to it; its rate of growth in culture; whether it had undergone genetic changes that would show loss of some possible virulence characteristics; and its ability to inhibit frogs’ immune cells.

As our group recently reported, we found that the pathogen had not changed. However, we were able to show that for some species, frog skin secretions we collected from frogs in populations that had persisted were better able to inhibit the fungus in a culture system than those from frogs that had never been exposed to the fungus.

The prospect that some frog species in some places in Panama are recovering in spite of the continuing presence of this virulent pathogen is fantastic news, but it is too soon to celebrate. The recovery process is very slow, and scientists need to continue monitoring the frogs and learn more about their immune defenses. Protecting their habitat, which is threatened by deforestation and water pollution, will also be a key factor for the long-term survival of these unique amphibian species in Panama.

If Bsal fungus spreads to North America, it could wipe out species like this Northern Slimy Salamander (Plethodon glutinosus).
Marshal Hedin, CC BY

Salamanders (and frogs) at risk

On a global scale, Bd is not the only threat. A second pathogenic chytrid fungus called Batrachochytrium salamandrivorans (abbreviated as Bsal) was recently identified in Europe, and has decimated some salamander populations in the Netherlands and Belgium. This sister species probably was accidentally imported into Europe from Asia, and seems to be a greater threat to salamanders than to frogs or toads.

Bsal has not yet been detected in North America. I am part of a new consortium of scientists that has formed a Bsal task force to study whether it could become invasive here, and which species might be most adversely affected.

In January 2016 the U.S. Fish and Wildlife Service listed 201 salamander species as potentially injurious to wildlife because of their their potential to introduce Bsal into the United States. This step made it illegal to import or ship any of these species between the continental United States, the District of Columbia, Hawaii, the Commonwealth of Puerto Rico or any possession of the United States.

The Bsal task force is currently developing a strategic plan that lists the most urgent research needs to prevent accidental introduction and monitor vulnerable populations. In October 2017 a group of scientists and conservation organizations urged the U.S. government to suspend all imports of frogs and salamanders to the United States.

In short, it is too early to relax. There also are many other potential stressors of amphibian populations including climate change, decreasing habitats and disease. Those of us who cherish amphibian diversity will continue to worry for some time to come.

Louise Rollins-Smith, Associate Professor of Pathology, Microbiology and Immunology, Vanderbilt University

This article was originally published on The Conversation. Read the original article.

11 billion pieces of plastic bring disease threat to coral reefs

A plastic bottle trapped on a coral reef.
Tane Sinclair-Taylor, Author provided

Joleah Lamb, Cornell University

There are more than 11 billion pieces of plastic debris on coral reefs across the Asia-Pacific, according to our new research, which also found that contact with plastic can make corals more than 20 times more susceptible to disease.

In our study, published today in Science, we examined more than 124,000 reef-building corals and found that 89% of corals with trapped plastic had visual signs of disease – a marked increase from the 4% chance of a coral having disease without plastic.

Globally, more than 275 million people live within 30km of coral reefs, relying on them for food, coastal protection, tourism income, and cultural value.

With coral reefs already under pressure from climate change and mass bleaching events, our findings reveal another significant threat to the world’s corals and the ecosystems and livelihoods they support.

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Read more:
This South Pacific island of rubbish shows why we need to quit our plastic habit

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In collaboration with numerous experts and underwater surveyors across Indonesia, Myanmar, Thailand and Australia, we collected data from 159 coral reefs between 2010 and 2014. In so doing, we collected one of the most extensive datasets of coral health in this region and plastic waste levels on coral reefs globally.

There is a huge disparity between global estimates of plastic waste entering the oceans and the amount that washes up on beaches or is found floating on the surface.

Our research provides one of the most comprehensive estimates of plastic waste on the seafloor, and its impact on one of the world’s most important ecosystems.

Plastic litter in a fishing village in Myanmar.
Kathryn Berry

The number of plastic items entangled on the reefs varied immensely among the different regions we surveyed – with the lowest levels found in Australia and the highest in Indonesia.

An estimated 80% of marine plastic debris originates from land. The variation of plastic we observed on reefs during our surveys corresponded to the estimated levels of plastic litter entering the ocean from the nearest coast. One-third of the reefs we surveyed had no derelict plastic waste, however others had up 26 pieces of plastic debris per 100 square metres.

We estimate that there are roughly 11.1 billion plastic items on coral reefs across the Asia-Pacific. What’s more, we forecast that this will increase 40% in the next seven years – equating to an estimated 15.7 billion plastic items by 2025.

This increase is set to happen much faster in developing countries than industrialised ones. According to our projections, between 2010 and 2025 the amount of plastic debris on Australian coral reefs will increase by only about 1%, whereas for Myanmar it will almost double.

How can plastic waste cause disease?

Although the mechanisms are not yet clear, the influence of plastic debris on disease development may differ among the three main global diseases we observed to increase when plastic was present.

Plastic debris can open wounds in coral tissues, potentially letting in pathogens such as Halofolliculina corallasia, the microbe that causes skeletal eroding band disease.

Plastic debris could also introduce pathogens directly. Polyvinyl chloride (PVC) – a very common plastic used in children’s toys, building materials like pipes, and many other products – have been found carrying a family of bacteria called Rhodobacterales, which are associated with a suite of coral diseases.

Similarly, polypropylene – which is used to make bottle caps and toothbrushes – can be colonised by Vibrio, a potential pathogen linked to a globally devastating group of coral diseases known as white syndromes.

Finally, plastic debris overtopping corals can block out light and create low-oxygen conditions that favour the growth of microorganisms linked to black band disease.

Plastic debris floating over corals.
Kathryn Berry

Structurally complex corals are eight times more likely to be affected by plastic, particularly branching and tabular species. This has potentially dire implications for the numerous marine species that shelter under or within these corals, and in turn the fisheries that depend on them.

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Read more:
Eight million tonnes of plastic are going into the ocean each year

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Our study shows that reducing the amount of plastic debris entering the ocean can directly prevent disease and death among corals.

Once corals are already infected, it is logistically difficult to treat the resulting diseases. By far the easiest way to tackle the problem is by reducing the amount of mismanaged plastic on land that finds its way into the ocean.

Joleah Lamb, Research fellow, Cornell University

This article was originally published on The Conversation. Read the original article.

Why we shouldn’t be too quick to blame migratory animals for global disease

Alice Risely, Deakin University; Bethany J Hoye, University of Wollongong, and Marcel Klaassen, Deakin University

Have you ever got on a flight and the person next to you started sneezing? With 37 million scheduled flights transporting people around the world each year, you might think that the viruses and other germs carried by travellers would be getting a free ride to new pastures, infecting people as they go.

Yet pathogenic microbes are surprisingly bad at expanding their range by hitching rides on planes. Microbes find it difficult to thrive when taken out of their ecological comfort zone; Bali might just be a tad too hot for a Tasmanian parasite to handle.

But humans aren’t the only species to go global with their parasites. Billions of animals have been flying, swimming and running around the globe every year on their seasonal migrations, long before the age of the aeroplane. The question is, are they picking up new pathogens on their journeys? And if they are, are they transporting them across the world?

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Read more: A tale of three mosquitoes: how a warming world could spread disease

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Migratory animals are the usual suspects for disease spread

With the rate of zoonotic diseases (pathogens that jump from animals to humans) on the rise, migratory animals have been under increasing suspicion of aiding the spread of devastating diseases such as bird flu, Lyme disease, and even Ebola.

These suspicions are bad for migrating animals, because they are often killed in large numbers when considered a disease threat. They are also bad for humans, because blaming animals may obscure other important factors in disease spread, such as animal trade. So what’s going on?

Despite the logical link between animal migration and the spread of their pathogens, there is in fact surprisingly little direct evidence that migrants frequently spread pathogens long distances.

This is because migratory animals are notoriously hard for scientists to track. Their movements make them difficult to test for infections over the vast areas that they occupy.

But other theories exist that explain the lack of direct evidence for migrants spreading pathogens. One is that, unlike humans who just have to jump on a plane, migratory animals must work exceptionally hard to travel. Flying from Australia to Siberia is no easy feat for a tiny migratory bird, nor is swimming between the poles for giant whales. Human athletes are less likely to finish a race if battling infections, and likewise, migrant animals may have to be at the peak of health if they are to survive such gruelling journeys. Sick travellers may succumb to infection before they, or their parasitic hitchhikers, reach their final destination.

Put simply, if a sick animal can’t migrate, then neither can its parasites.

On the other hand, migrants have been doing this for millennia. It is possible they have adapted to such challenges, keeping pace in the evolutionary arms race against pathogens and able to migrate even while infected. In this case, pathogens may be more successful at spreading around the world on the backs of their hosts. But which theory does the evidence support?

Sick animals can still spread disease

To try and get to the bottom of this question, we identified as many studies testing this hypothesis as we could, extracted their data, and combined them to look for any overarching patterns.

We found that infected migrants across species definitely felt the cost of being sick: they tended to be in poorer condition, didn’t travel as far, migrated later, and had lower chances of survival. However, infection affected these traits differently. Movement was hit hardest by infection, but survival was only weakly impacted. Infected migrants may not die as they migrate, but perhaps they restrict long-distance movements to save energy.

So pathogens seem to pose some costs on their migratory hosts, which would reduce the chances of migrants spreading pathogens, but perhaps not enough of a cost to eliminate the risk completely.

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Read more: Giant marsupials once migrated across an Australian Ice Age landscape

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But an important piece of the puzzle is still missing. In humans, travelling increases our risk of getting ill because we come into contact with new germs that our immune system has never encountered before. Are migrants also more susceptible to unfamiliar microbes as they travel to new locations, or have they adapted to this as well?

Guts of migrants resistant to microbial invasion

To investigate the susceptibility of migrants, we went in a different direction and decided to look at the gut bacteria of migratory shorebirds – grey, unassuming birds that forage on beaches or near water, and that undergo some of the longest and fastest migrations in the animal kingdom.

Most animals have hundreds of bacterial species living in their guts, which help break down nutrients and fight off potential pathogens. Every new microbe you ingest can only colonise your gut if the environmental conditions are to its liking, and competition with current residents isn’t too high. In some cases, it may thrive so much it becomes an infection.

The Red-necked stint is highly exposed to sediment microbes as it forages for the microscopic invertebrates that fuel its vast migrations.
Author provided

We found the migratory shorebirds we studied were exceptionally good at resisting invasion from ingested microbes, even after flying thousands of kilometres and putting their gut under extreme physiological strain. Birds that had just returned from migration (during which they stopped in many places in China, Japan, and South East Asia), didn’t carry any more species of bacteria than those that had stayed around the same location for a year.

Although these results need to be tested in other migratory species, our research suggests that, like human air traffic, pathogens might not get such an easy ride on their migratory hosts as we might assume. There is no doubt that migrants are involved in pathogen dispersal to some degree, but there is increasing evidence that we shouldn’t jump the gun when it comes to blaming migrants.

Alice Risely, PhD candidate in Ecology, Deakin University; Bethany J Hoye, Lecturer in Animal Ecology, University of Wollongong, and Marcel Klaassen, Alfred Deakin Professor and Chair in Ecology, Deakin University

This article was originally published on The Conversation. Read the original article.

We could reduce pest carp in Australian rivers using a disease that came from Israel

Susan Lawler, La Trobe University

Everyone wants to give Australian carp the herpes virus. That’s right, introduced carp are a serious pest species and research suggests that a viral control agent may be the most effective solution.

I love stories like this one, where groups that would normally disagree come together in an “unlikely coalition”. That is to say, fishers, conservationists, irrigators, scientists and farmers agree on the desirability of an environmental release of the carp-specific virus.

After all, it worked for rabbits. The release of the myxomatosis virus in the 1950s and the more recent release of calicivirus have permanently decreased rabbit numbers on our continent. Using viral pathogens to control vertebrate pests can be extremely effective because it does not require ongoing human intervention.

Like rabbits, carp were introduced to Australia deliberately. The first introductions in the 1800s did not cause problems, but a strain bred for European aquaculture escaped from farm dams near Mildura in the 1960s and spread throughout the Murray Darling Basin. The impact of carp on our rivers has been well documented, including increasing turbidity (making the water muddy), destroying aquatic vegetation, and contributing to the decline of native fish.

In other parts of the world, carp are an important food species, often raised in fish farms. When I worked on a kibbutz in Israel in 1980 we caught and sorted carp from geothermal pools near the Sea of Galilee. The fish were a desirable food item and water from the fish ponds was used to fertilise banana crops via drip irrigation. I admired the sustainable farming practice that was then ahead of its time.

Twenty years later while participating in a fish survey at Horseshoe Lagoon near Albury, I remember pulling dozens of giant carp out of our nets, lamenting the lack of native fish. Because we were not allowed to return the carp to the water due to its pest status, we had to kill each one, resulting in a large pile of stinky dead fish that nobody wanted to eat.

The only similarity between these two memories was the method of death: although it looks brutal and cruel, hitting carp on the back of the head with a heavy wooden stick dispatches them instantly and humanely. On those two occasions this peaceful vegetarian turned into a lethal killing machine.

Ironically, at about the time I was whacking pest carp in Australia, the carp industry in Israel was affected by a new disease. The koi herpesvirus, or Cyprinid herpesvirus 3 (CyHV-3) appeared in Israel in 1998 and was so contagious that it soon spread throughout Europe and Asia. The carp industry was devastated.

While this virus is bad news for carp farming, it could be good news for managing feral carp in Australia. With an expected mortality rate of 70-80%, CyHV-3 may be just what we need to curb the plague of carp in our rivers.

Of course, given our sometimes disastrous experience with biological control species, caution is warranted. That’s why scientists have spent the last eight years doing research to ensure that the herpes will not affect other species. Ken McColl is a leader of the team that has examined the host specificity of the virus in an Australian context.

The good news is that CyHV-3 has no impact on other native fish, yabbies and trout. It cannot infect mammals, amphibians or reptiles. In other words, it looks safe.

The bad news is that it will affect ornamental carp (koi) which are highly valued, so people who keep koi will need to monitor their water and food sources. I see this as something like vaccinating your pet rabbits against calicivirus, an inconvenient but reasonable impost given the benefit for the nation and our environment.

What happens now? There are a number of government organisations that are responsible for biosecurity. Getting approval to introduce a virus into our waterways will probably take a few years, so the research will continue as the Invasive Animals Cooperative Research Centre goes through the application process.

There is also research underway to identify locations suitable for early releases, and this is where members of the public can get involved. Hotspots for invasive fish species will be identified by gathering data from concerned citizens at a new website called Feral Fish Scan. Anyone interested in learning how to identify invasive fish and record observations of their local waterways can do so at this link.

Other conventional approaches to reducing carp are still underway, from the development of traps that target carp to better ways for Charlie Carp to turn those feral fish into fertiliser. But harvesting tons of carp and turning them into pellets will never reduce the impact of this noxious pest as effectively as a carp-specific disease.

This is why virtually everyone is excited about the possibility of giving herpes to Australian carp. And even though I think it sounds like a good idea, I am also grateful that we have robust regulations about biocontrol, because there was a time when cane toads seemed like a good idea, too.

We can wait a couple of years to ensure that we do not regret our decision, but then we may enjoy a great irony: a disease that caused huge financial losses overseas could save freshwater environments in Australia.

Susan Lawler, Senior Lecturer, Department of Ecology, Environment and Evolution, La Trobe University

This article was originally published on The Conversation. Read the original article.