Tag: disease

Cull ‘cannot save’ Tasmanian devil

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Culling does not effectively control the contagious cancer threatening the Tasmanian devil, a new study suggests.

The researchers modelled the effect of removing sick animals on the disease’s prevalence in a small population.

The study, in the Journal of Applied Ecology, seems to confirm findings in wild trials, that selective culling of sick animals is ineffectual at stopping the spread of the disease.

All trial culls of the devils have now been stopped.

Culling has been used to control infectious diseases in a range of species from deer to badgers, wolves to domestic cattle.

Despite proving successful in controlling the diseases of livestock, such as foot and mouth, culling wild animals is controversial because of the lack of evidence that it works.

In fact, cases exists where culling wild animals has made the problem worse.

But, hoping to save the Tasmanian devil, Sarcophilus harrisii, from the facial cancer that has wiped out more than 90% of individuals in some areas, conservation biologists have trialled a cull since 2004.

Costly cull

As part of the trial cull, researchers have trapped and euthanised sick animals two to five times a year from an isolated population in the south-east of Tasmania.

Each year, the project costs more than $200,000 (£122,000). Critics say this money could otherwise be spent on captive breeding programmes.

To assess the impact of the cull, Australian researchers Nick Beeton from University of Tasmania and Hamish McCallum from Griffith University created a computer model in which they simulated the effects of the cull.

“We found the removal rate required to suppress disease was higher than that which would be feasible in the field,” explained Mr Beeton.

In the field, biologists find that 20% of the population is never captured and could be acting as a reservoir for the disease.

Unless all the devils are trapped and inspected, including the “trap-shy” ones, continuous culling is unlikely to be an effective disease control, the researchers write.

Mr Beeton told BBC News: “The disease suppression trial was ended as this paper was being written.”

“Our research demonstrates that we must be flexible and be prepared to change strategy as new information comes to light,” he added.

“It’s much better to do a study like this, than spend a lot of money on a huge culling programme and then find that it hasn’t worked,” said geneticist Elizabeth Murchison from the Welcome Trust Sanger Institute in Hinxton, UK, who studies the devil cancer.

She added that by confirming that culling does not work, conservationists can then focus their efforts on alternative strategies, such as the captive breeding programme and developing a vaccine against the cancer.

The transmissible facial cancer

  • Devil Facial Tumour Disease (DFTD) is spread by biting during aggressive encounters
  • The living cancer exists as contagious clone cells; highly unusual for a cancer. There is only one other transmissible cancer known, which affects dog genitals
  • The devil’s immune system seems unable to detect the cancer
  • The disease forms tumours around the mouth interfering with feeding, leading to death
  • The cancer originally arose in Schwann cells – cells which wrap themselves around nerve tissue
  • First seen in 1996, the cancer has badly hit Tasmanian devil populations

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Bed bugs protect their sperm from bacteria

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Bed bugs protect their sperm against sexually transmitted infections by producing germ-busting ejaculates, scientists have found.

Bacteria covering bed bugs’ bodies are transmitted to the female, along with the sperm, during mating.

The new work shows that without the protection of antibacterial agents in the bug’s ejaculate, 40% of sperm die.

The results were presented at the 13th Congress of the European Society for Evolutionary Biology.

Bed bugs, and the related bat bugs that live in African caves, are renowned for their bizarre sex lives.

‘Traumatic insemination’

Males, instead of penetrating the female’s vagina, pierce her underside and deposit sperm inside the female, where it swims through the insect’s blood system to the ovaries to fertilise the eggs.

Female bed bugs protect themselves against the diseases that males transmit with a structure on their bellies that guides the penis into a mass of germ-fighting cells.

Males, it seems, have also evolved a way to fend off the effects of sexually transmitted infections, evolutionary biologist Oliver Otti from the University of Sheffield, UK, told conference attendees in Germany.

Suspecting that males load their ejaculates with proteins that protect sperm, Dr Otti carefully extracted sperm from a number of male bed bugs, being sure not to mix it with the seminal fluid that usually makes up the rest of the ejaculate.

He then mixed the sperm with a “soup” of micro-organisms that he had collected from the outer skin of the bed bugs.

To half of these samples he added lysozyme, a bacteria-killing enzyme known to be active in bed bugs, and saw that 40% more sperm survived in its presence.

Females didn’t gain any protection from these introduced bacteria-busting enzymes, he explained; the presence of lysozyme in the ejaculate seemed to be purely to protect sperm.

But other work by Dr Otti’s colleague Michael Siva-Jothy, who is also based at the University of Sheffield, shows that females protect themselves from the infections introduced during sex with their own lysozymes.

In fact, females ramp up their lysozyme activity just before they are about to feed. Dr Siva-Jothy explained that this is probably because in the bed bug world, feeding is generally always followed by mating.

“Wounding is a very frequent event during and after copulation, and generally genitals are not that clean, ” Dr Otti told BBC News.

He explained that the research that has focused on human sexual transmitted diseases has tended to ignore the microbes that coexist with us on our skin; these microbes are likely also transferred during sex.

“It is not clear what the cost of having them around is,” Dr Otti added.

The advantage of studying bed bugs, he said, is that we share many components of our immune system. As a result, scientists can learn much from manipulating the bugs’ sex lives to study the consequences on lifespan and offspring production – some of these trade-offs could be relevant to humans.

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Insects use antibacterial secretions to protect young

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Scientists have confirmed that so-called burying beetles coat their young’s food with an antibacterial substance to guarantee their survival.

Burying beetles lay their eggs on the carcasses of small animals, such as birds and rodents.

The researchers show that without the anti-microbial secretions the young fail to gain weight and die.

The results were presented the 13th Congress of the European Society for Evolutionary Biology.

Most animals try to do the best for their young, but burying beetles, in the genus Nicrophorus, which are found in temperate regions in Europe and North America, are truly doting parents.

As a prospective parent, burying beetles find a dead animal, such as a mouse or bird, and roll the carcass into a ball.

They then bury the carcass, hiding it from predators that might eat it or fancy it for a nursery for their own young – no small feat for a beetle that is only 15mm long.

The beetles then lay their eggs in the flesh of the animal and wait to welcome their young into the world.

But a buried carcass is not going to stay fresh for very long, and the bacterial communities that colonise it are likely to threaten the beetle’s developing larvae.

Germ-free

So burying beetles use secretions from their anal glands to coat the fur or feathers with substances that guarantee the carcass stays germ-free and fresh for longer.

Now scientists from the University of Manchester have worked out what makes these secretions so good at killing germs.

The researchers extracted secretions from the anal glands of a species of burying beetle called Nicrophorus vespilloides, and showed that when this substance was added to bacterial cells, they were destroyed.

Evolutionary biologists Andres Arce, who led the study, and his colleagues, suspecting that they were dealing with a enzyme that “chops up microbial cell walls”, investigated and confirmed that the secretions were rich in lysozymes.

These are anti-microbial enzymes, and a common component of animals’ immune systems.

Lysozymes are also secreted in mammals’ breast milk and in human tears.

The team showed that larva raised in the absence of either their parents secretions were 40% more likely to die before adulthood.

Dr Arce explained that for a non-social insect, these burying beetles are already known to show quite substantial levels of parental care.

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Spermless mosquitoes hold promise to stop malaria

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Scientists have created spermless mosquitoes in an effort to curb the spread of malaria.

Experts say that this is an important first step toward releasing sterile males into the wild to reduce the size of mosquito populations.

Malaria kills around one million people worldwide every year, and in Africa alone, accounts for 20% of all childhood deaths.

The work is reported in Proceedings of the National Academy of Sciences.

Insect sterilisation isn’t new: scientists have attempted to control the sleeping sickness-carrying tsetse fly by exposing them to radiation to render them sterile.

A similar approach has been successfully used against the potatoes weevil in Japan and the tropical screwworm that attacks cattle.

Frail fly

However, exposing mosquitoes to radiation has tended to leave male mosquitoes frail, and unable to compete in the frenzied mating aerobatics that Anopheles gambiae – the world’s most efficient malaria vector – enjoys.

Now scientists have developed an alternative route to mosquito sterility.

Entomologist Flaminia Catteruccia from Imperial College London enlisted the help of her graduate student Janis Thailayil in the search for how to make male mosquitoes sterile but leave them otherwise unharmed.

Mr Thailayil injected 10,000 mosquito embryos with tiny fragments of RNA designed to turn off a gene – called zpg – that is essential for normal sperm development.

After months of laborious work, the researchers created around 100 spermless mosquitoes, and showed that females were just as willing to mate with these males as with fertile ones.

Dr Catteruccia explains that female mosquitoes mate only once in their lives. If scientists can trick them into thinking that they have successfully mated, then they will continue to lay their eggs without knowing that they have not been fertilised.

“You [could] in principle release large numbers of sterile males over many generations… and eventually all the females will have mated with the sterile males and…you can really reduce the number of mosquitoes,” explained Dr Catteruccia.

This would gradually reduce the number of hatching mosquitoes. And hopefully help eradicate what many consider to be the single most dangerous insect species for mankind.

However, Dr Catterucci warns that this is only a proof of principle. The method her team used to create the spermless males would be far too labour-intensive to flood wild populations with enough spermless males to have any effect on their numbers.

However, knowing that females don’t notice whether they are receiving sperm or not is still an important step, she said.

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Researchers switch on genes with blue pulse

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Scientists have developed a technique that could be used to deliver precise doses of hormones to people who don’t make them naturally.

To do this, they rewired kidney cells with light-sensitive molecules from the eye, they reported in the journal Science.

When pulsed with blue light, these cells churned out proteins on demand.

Ultimately, this technique could avoid the need for people with diabetes to inject themselves regularly.

“When I speak to diabetes patients they say that if you could take away always having to inject themselves it would really increase their quality of life,” said lead author Martin Fussenegger, a bioengineer of the Swiss Federal Institute of Technology, Zurich.

Dr Fussenegger thought he saw a solution in his own field of optogenetics. Optogenetics, as the name suggests, uses light to control the behaviour cells.

To get a cell to respond to light you first have to rejigger it so it has a light-sensitive molecule on its surface. Dr Fussenegger coaxed kidney cells to express melanopsin, a molecule usually found in animals’ eyes.

Blue genes

He then placed these cells into diabetic mice. Along with the cells he placed an optic fibre, down which he could pulse blue light to expose the cells at his command.

In the dark, these cells behaved as usual; In the light, however, genes in the cell were switched on and the cell pumped out a protein required for the breakdown of sugars in the blood, helping the mice to control their glucose levels.

He hopes that cells like these could ultimately be implanted into people, and exposed to light – either through the skin or down a optic fibre – to release proteins that would help treat diabetes.

The new technique is a proof of principle. He told BBC News that it was not limited to treating diabetes; this technology could be usedto switch on genes to produce many different proteins in people who do not make them naturally, or are not making enough of them to be healthy.

Light switch

“I think this is a phenomenal research tool,” said James Collins, a synthetic biologist at Howard Hughes Medical Institute, Maryland, US, who was not involved in the work.

Dr Collins explained that as we move into an age of regenerative medicine, and begin to think of how we use stem cells to produce different tissues in the body, one of the challenges will be to work out which genes are needed to produce certain tissues and cells.

This new technique allows researchers to switch genes on and off to determine which are essential to make a specific tissues.

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Superbug Gene Found

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superbuggene_lgA gene that causes bacteria to become resistant to antibiotics has been found in drinking water in New Delhi, India. NDM-1 is commonly found in Escherichia coli but can spread to other bacteria thanks to their ability to swap DNA. The gene confers resistance to antibiotics, including potent, last-resort drugs called carbapenems.

India’s warm temperatures, over-crowding, and poor sanitation are likely to blame for the gene’s spread into the main water system from bacteria in people’s guts, write Timothy Walsh of Cardiff University in the United Kingdom and colleagues in a paper published online last week in The Lancet Infectious Diseases. The team, who found the gene in two out of 50 tap water samples and 51 of 171 samples taken from puddles and streams in the capital, say the gene could spread farther afield when tourists drink local water supplies and then return home.

NDM-1 has already been found in U.K. hospitals in bacteria infecting people who had medical treatment in India and those admitted with “traveler’s tummy.” The new finding raises concerns that resistant genes, so far found mainly in gut flora, are becoming widespread in natural environments, where they are highly mobile.

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Researchers Grow Protoeye in Dish

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It’s not quite Avatar, but a movie released today shows, in three dimensions, how a chaotic patch of cells grows into the beginnings of an eyeball. Even more impressive, this protoeye was grown in a laboratory dish. Scientists say the finding brings them closer to growing entire organs in the lab, including eyes that could replace those damaged by injury or disease.

In the past decade, researchers have made dramatic progress in understanding how eyes form. They have learned how to turn on and off essential genes and how to transform embryonic stem cells into retinal cells, which can be transplanted into mice to restore vision. But so far, growing an entire eyeball in the lab has eluded scientists, largely because they’ve been unable to recreate the “optic cup,” a chalice-shaped structure that becomes the back of the eye.

Now Yoshiki Sasai of the RIKEN Center for Developmental Biology in Kobe, Japan, and his colleagues have induced embryonic mouse stem cells to spontaneously form the optic cup in a dish. The key ingredient was a mixture of jellylike proteins, called Matrigel, which forms an enticing bed on which stem cells seem to prefer to lie before turning into the eye’s various structures.

In the movie, the cells—made to glow green—push out before inverting and forming two different layers: the first, the retinal cells, and the second, the neurons. This is the first demonstration that stem cells direct their own development in the eye, the team reports online today in Nature.

Knowing that stem cells can direct their own development is key if we want to grow organs without having to also grow the tissues that usually develop around them, says developmental biologist Jane Sowden of University College London, who was not involved in the study. She says that even though Sasai’s team hasn’t yet grown an entire eyeball in a dish, the work shows that it’s possible to grow specific eye structures, such as retinas, from stem cells in a great enough quantity that they could be used in therapy. If the researchers can get the technique to work with human stem cells, she says, it could help the one in 3000 people born with a form of blindness caused by damaged retinal cells and the many more who lose their sight because of age-related disease.

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Sensing Organ Rejection

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sensingorganrejection

Rejection hurts, but for organ transplant patients it’s more than an emotive issue—it can be a matter of life and death. Having waited months, sometimes years, for a donor and survived major surgery, transplant patients face an uphill battle to prevent their immune systems from rejecting their new organ. Now a new test in which a transplant patient’s blood is scanned for DNA from the donor organ can alert doctors if serious rejection has begun, allowing them to try to stop the process.

Approximately 40% of transplant patients experience at least one episode of acute rejection in the first year after they receive an organ. Catching any major immunological backlash early is key to minimizing its effects, especially because most rejection episodes are reversible with a large dose of immunosuppressant drugs. But patients typically must undergo regular biopsies of their new organ to monitor its health; the procedure is both painful and expensive, and biopsies also risk damaging the organ, explains cardiologist Hannah Valantine of Stanford University School of Medicine in Palo Alto, California. In 2009, Valantine developed a noninvasive rejection test that relies on monitoring a patient’s immune system. AlloMap became the first U.S Food and Drug Administration-approved test for heart transplants, but it still fails to catch about half of rejection events.

To capture the rest, Valantine recently headed back to the drawing board. This time she enlisted help from biophysicist Stephen Quake of Stanford. Together they designed a test that relies on the fact that a transplanted organ’s genome is distinct from that of its new host. The test monitors fragments of DNA released by the organ into the blood, when cells from the transplant tissue are naturally broken down. To validate this strategy, the researchers tried their test on stored blood plasma from organ transplant patients, some of whom had had confirmed rejection episodes. During a rejection event, the levels of circulating DNA from the donor organ go up, making up on average 3% of free DNA in the recipient’s blood rather than the typical 1%, the researchers report online today in the Proceedings of National Academy of Sciences.

Valantine hopes that this test can eliminate the need for regular biopsies as a means of rejection monitoring; patients often have one every month in the first year after a transplant. Instead, physicians would perform confirmation biopsies only if the DNA test results were positive. The new test can detect “very low levels of DNA to predict rejection,” Valantine says, making this approach more sensitive than the AlloMap test. If the test can alert doctors to rejection earlier, she notes, they can “tinker” with the levels of immunosuppressant drugs rather than go in with “a big-gun approach” that lowers the patient’s immune system so much that they are at risk of infection and cancer.

Bruce Rosengard, the surgical director of the cardiac transplantation program at Massachusetts General Hospital in Boston, is cautiously optimistic about the new test. “Organ rejection remains one of the primary obstacles to transplant success,” he says. “Anything that we can do to reduce the number of heart biopsies is a very positive development. … I think this approach will gain traction pretty quickly.”

Valantine hopes to have the new test available to doctors in a year’s time, adding that she sees no reason why it can’t be used to detect rejection of other transplanted organs.

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Nosing Out a Smell Gene

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The daily smells of the world—the freshness of spring flowers, the smokiness of charred morning toast, the invigorating aroma of a cup of coffee—are lost on those with anosmia, a complete inability to detect odors. Now, thanks to a trio of people who feel no pain, a new study has pinpointed the first set of mutations that are to blame for this condition. The finding could help scientists better understand the gradual loss of smell that happens with age.

The discovery was somewhat happenchance. It began when neurobiologist Frank Zufall of Saarland University in Homburg, Germany, was contacted by pain researcher John Wood of University College London and geneticist Geoffrey Woods of the University of Cambridge in the United Kingdom. Wood and Woods had been studying three people with an inability to feel pain. In 2006, they found that all had mutations in a gene that codes for a sodium channel called Nav1.7 that is involved in the firing of neurons. The researchers also noticed that the volunteers reported having no sense of smell. When the duo created mice with similar mutations, the pups were free of pain, but they also had difficulty smelling; they seemed unable to pick up the odor of their mother’s teats to suckle, for example.

To investigate how the lack of these channels causes anosmia, Zufall and his team studied the genetically engineered mice. They discovered that although neurons in the rodents’ noses respond to different odors, they were unable to transmit these signals to the olfactory bulb, the region at the front of the brain that processes smell.

The researchers also confirmed that the mice couldn’t smell. In a series of experiments, the rodents didn’t avoid the smell of predators, nor did they retrieve their pups when they were scattered around their cage, the researchers report online today in Nature. “This behavior supports that fact that the mice aren’t smelling,” says Lisa Stowers, a neurobiologist at The Scripps Research Institute in San Diego, California, who studies olfaction.

Zufall hopes to turn up more genes underlying anosmia by encouraging doctors to carry out a smell test in patients who present with neurological problems. Peter Mombaerts, an olfaction neuroscientist at the Max Planck Institute of Biophysics in Frankfurt, Germany, agrees that this would be a good approach. “It is a very cheap test,” he says, but he cautions that few doctors currently do it, even though smell can be an important indicator of neurological disease. For example, in Alzheimer’s patients, smell is often one of the first things to deteriorate.

The number of people that are anosmic from birth is likely quite small, says Mombaerts, but by better understanding how olfactory signals are disrupted in people born with this condition, researchers hope to gain insight into why many more develop it later in life.

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