October 29, 2013
One of the freakiest parts of getting bitten by a tick is the
insect arachnid’s incredible tenacity: If one successfully pierces your skin and you don’t pull it off, it can hang on for days at a time, all the while sucking your blood and swelling in size.
Despite plenty of research into ticks and the diseases they carry, though, scientists have never fully understood the mechanics by which
the insects they use their mouths to penetrate skin and attach themselves so thoroughly. To address that, a group of German researchers recently used specialized microscopes and high-speed video cameras to capture a castor bean tick burrowing into a mouse’s bare skin in real time.
Their work, published today in Proceedings of the Royal Society B, produced all sorts of new revelations about the structure and function of the tick’s mouthparts. Perhaps the most harrowing part of the research, though, is the microscopic video they captured, shown at an accelerated speed above.
The team of scientists, led by Dania Richter of Charité Medical School in Berlin, conducted the work by placing five ticks on the ears of lab mice and letting them have their fill of blood. Unbeknownst to the ticks, though, they’d been caught on camera—and by analyzing the footage, along with detailed scanning electron microscope images of the ticks’ mouth appendages, the researchers found that the insects’ bites are really a highly specialized two-step process.
To begin, after the tick has climbed aboard a host animal, a pair of sharp structures called chelicerae, which are located at the end of its feeding appendage, alternate in poking downward. As they gradually dig, their barbed ends prevent them from slipping out, and the tick slowly and shallowly lodges itself in the skin, as seen in the first few seconds of the video.
After about 30 or so of these small digging movements, the tick switches to phase two (shown just after the video above zooms in). At this point, the insect simultaneously flexes both of the telescoping chelicerae, causing them to lengthen, and pushes them apart in what the researchers call “a breaststroke-like motion,” forming a V-shape.
With the tips of the chelicerae anchored in the skin, flexing them outward causes them to penetrate even deeper. When this occurs, the tick’s hypostome—a razor-sharp, even-more-heavily-barbed spear—plunges into the host’s skin and attaches firmly.
The tick’s not done, however: It repeats this same breaststroke five or six times in a row, pushing the hypostome deeper and deeper until it’s fully implanted. With the hypostome firmly in place, the tick begins drawing blood—sucking the fluid up to its mouth through a grooved channel that lies in between the chelicerae and hypostome—and if left interrupted, will continue until it’s sated days later.
This new understanding of how ticks accomplish this feat, the researchers say, could help us someday figure out how to prevent transmission of the most feared risk of a tick bite: Lyme disease. Scientists know that the disease is caused by several different species of bacteria that adhere to the inner lining of the tick’s gut and typically make the jump into a human’s bloodstream only after a full day of feeding. Knowing how ticks are able to attach themselves so stubbornly could eventually allow us to determine a means of thwarting their advances, before the Lyme-bearing bacteria have a chance to cross the species barrier.
October 24, 2013
If you were stung by a bark scorpion, the most venomous scorpion in North America, you’d feel something like the intense, painful jolt of being electrocuted. Moments after the creature flips its tail and injects venom into your skin, the intense pain would be joined by a numbness or tingling in the body part that was stung, and you might experience a shortness of breath. The effect of this venom on some people—small children, the elderly or adults with compromised immune systems—can even trigger frothing at the mouth, seizure-like symptoms, paralysis and potentially death.
Based solely on its body size, the four-inch-long furry grasshopper mouse should die within minutes of being stung—thanks to the scorpion’s venom, which causes temporary paralysis, the muscles that allow the mouse to breathe should shut down, leading to asphyxiation—so you’d think the rodent would avoid the scorpions at all costs. But if you put a mouse and a scorpion in the same place, the rodent’s reaction is strikingly brazen.
If stung, the four-inch-long rodent might jump back for a moment in surprise. Then, after a brief pause, it’ll go in for the kill and devour the scorpion piece by piece:
This predatory behavior isn’t the result of remarkable toughness. As scientists recently discovered, the mouse has evolved a particularly useful adaptation: It’s immune to both the pain and paralytic effects that make the scorpion’s venom so toxic.
Although scientists long knew that the mouse, native to the deserts of the American Southwest, preys upon a range of non-toxic scorpions, “no one had ever really asked whether they attack and kill really toxic scorpions,” says Ashlee Rowe of Michigan State University, who led the new study published today in Science.
To investigate, Rowe visited the desert nearby Arizona’s Santa Rita Mountains and collected a number of mice and scorpions. Back at her lab, when she and colleagues put the two animals together in the same tank, they saw that the mice devoured the scorpions with gusto and were seemingly impervious to their toxic strings, showing no signs of inflammation or paralysis afterward. They even directly injected the venom into other mouse specimens to further confirm that it didn’t affect them physiologically.
The question remained, though, whether the mice were merely immune to the venom’s paralyzing effects, or were also unable to feel pain as a result of a sting. “I’d see the mice get stung, and they’d just groom a little bit and blow it off,” Rowe says. After she talked to people who’d been stung and heard how badly it hurt, she hypothesized that the mild reaction in the mice indicated that they were resistant to the pain itself.
Working with Yucheng Xiao and Theodore Cummins of Indiana University, she closely examined the physical structures that connect the sensory neurons (which convey external stimuli, such as pain) to the central nervous system (where pain is experienced). “There are big, long neurons that extend from the hands and feet all the way to the spinal cord, and they’re responsible for taking information from the environment and sending it to the brain,” she says.
Incredibly, the nerve cells associated with the interface between these two systems can continue functioning normally when they’ve been removed from the mice, if they’ve been properly preserved and cultured in a medium. As a result, her team was able to look at the mechanisms that control the flow of signals between the sensory neurons and the spinal cord—structures known as ion channels—and see if those present in grasshopper mice functioned differently than those in house mice when exposed to scorpion venom.
They found, in house mice, the venom caused a channel known as Nav1.7 to pass along a signal, causing the perception of pain. In grasshopper mice, though, something unexpected happened: The arrival of venom caused no change in the activity of Nav1.7, because proteins produced by a different ion channel, known as Nav1.8, bound to venom molecules and rendered them futile. In fact, this reaction produced an overall numbing effect on the entire mouse pain transmission system, leaving the animals temporary incapable of feeling all sorts of pain, including those unrelated to scorpion venom.
The researchers also looked at the underlying genetics, sequencing the genes that correspond to these alternatively-structured ion channels, which will allow them to investigate the specific evolutionary background of this remarkable adaptation. In theory, the incentives for the mouse species evolving an immunity to scorpion toxins seem obvious: The nocturnal rodent feeds on all sorts of scorpions, so unless it can visually distinguish between those that are benign and toxic, it will face severe consequences if it’s sensitive to the venom. “Death, after all, is a pretty strong selection pressure,” Rowe notes.
But on the other hand, pain serves a crucial evolutionary role, informing an organism when it’s in danger. Some other species have been know to evolve resistance to particular toxins (garter snakes, for instance, are resistant to the toxin produced by rough-skinned newts), but these examples all involve resistance to toxins that can kill, but don’t actually cause pain.
So the fact that grasshopper mice have evolved resistance to pain itself is novel—and likely a result of a very specific set of evolutionary circumstances. One important aspect is that bark scorpions are a significant proportion of the mouse diet, leading to frequent interactions between the two organisms. Additionally, says Rowe, “the mechanism is specific to the venom itself, so it doesn’t compromise the mouse’s overall pain pathways.” As a result, the mouse is still able to detect other sources of pain (just not right after it’s been bitten by by the scorpion), and thus will know when its faced with unrelated painful perils.
October 23, 2013
In recent years, scientists have found out all sorts of remarkable things about a group of creatures that are entirely invisible to the naked eye: the trillions of bacteria that colonize every surface of our bodies.
New science, though, is indicating that the relationship goes both ways. These microorganisms affect us, but our underlying genetics also control which species of bacteria are able to thrive in and on our bodies.
One of the most striking examples of this was published today in the journal PLOS ONE. In the study, a group of researchers from Ohio State University analyzed the species of bacteria that lived in the mouths—either in saliva, on tooth surfaces or under gums—of 192 volunteers.
By sequencing all of the bacterial DNA present in a sample swabbed from each person’s mouth, the researchers detected 398 different bacteria species in total. Each volunteer, on average, harbored 149 different species of oral bacteria.
But perhaps the most interesting finding was that there was a tremendous amount of diversity between individuals—only 8 species were present in every single participant’s mouth. “No two people were exactly alike. That’s truly a fingerprint,” Purnima Kumar, the study’s lead author, said in a press statement.
This bacterial diversity, though, wasn’t entirely random: It correlated with the ethnic group of the volunteer. In other words, people from each of the four different ethnic groups represented in the study (all participants self-identified as either Caucasian, African-American, Chinese or Latino) generally had similar species of bacteria, especially underneath the gums.
As a result, simply by counting which varieties of bacteria appeared in this area, the researchers developed a model that was able to guess a person’s ethnicity with an accuracy significantly better than chance—it got it right 62 percent of the time. Some groups were even easier to identify via the bacteria than others: It could correctly identify Latinos 67 percent of the time and African-Americans with 100 accuracy.
The variation along ethnic lines, they believe, is a reflection of genetics, not environment. That’s because, if you assumed that the mouth microbiome is totally dependent on environmental factors, you’d expect that members of the same ethnic group would have different mixes of bacteria depending on whether they were first-generation immigrants to the U.S. or had family histories that stretched back generations in the country. Instead, people’s background—in terms of foods they ate and other lifestyle trends—didn’t seem to have any correlation with the bacterial communities in their mouths. But their ethnicity and thus their similar genetics matched their microbiome more often than chance.
Interestingly, the original goal of this research wasn’t to find new differences between people from different ethnic groups, but to examine the bacterial traits shared between people with good oral health (the researchers are mostly from OSU’s School of Dentistry). But when the researchers analyzed the data, they were struck by the ethnic similarities. Although they sampled bacteria from all regions of the mouth, those found under the gumline had the strongest correlation to ethnicity (and thereby genetics), likely because they’re the least disrupted by environmental factors such as diet or smoking.
The surprising ethnic finding could yield benefits for oral health. The fact that people of different ethnicities harbor different sorts of oral bacteria could lead to medical treatments that are tailored to a patient’s genetic background. If research eventually reveals that someone with certain oral bacteria species in high quantities is predisposed to certain ailments, for example, he or she could be proactively screened for these diseases.
October 22, 2013
If you traveled to the town of Kalgoorlie, in Western Australia, then headed about 25 miles north, you’d eventually reach a grove of large eucalyptus trees, some more than 30 feet tall, scattered across a dusty, arid landscape. Examining the dirt at your feet would reveal no trace of the gold deposits that lie roughly 100 feet underground, due to the thick layers of clay and rock that sit atop the precious metal.
But, scientists recently learned, if you peered closely enough at the eucalyptus trees—specifically, using X-rays to detect nanoparticles—you’d find that there’s gold in them thar leaves. As detailed in a study published today in Nature Communications, a group of researchers from Australia’s Commonwealth Scientific and Industrial Research Organisation has shown that plants can absorb gold particles deep underground and bring it upward through their tissues—a finding that could help mineral exploration companies mine for gold.
“In Australia, we’re faced with this problem of trying to explore through thick layers of sediments and weathered rock to reach valued minerals,” says Melvyn Lintern, an Earth scientist and lead author of the study. “At the same time, we’d previously heard from mining engineers that, in some places, they’d found eucalyptus roots going down to 30 meters [98 feet] or deeper in the mines.” With this observation in mind, and the knowledge that plants can absorb and transport minerals from the surrounding soil and bedrock all the way up to their leaves, Lintern and his colleagues were struck with an idea: Why not test eucalyptus leaves to see if they could indicate underground gold deposits?
To do so, they visited two Australian sites with known gold deposits deep underground (as revealed by exploratory drilling) that were covered by thick layers of rock and on top of which grew tall eucalyptus trees. When they tested leaves that grew on or had fallen from the large trees in both areas, they indeed found minute traces of gold—up to 80 parts per billion, compared with the 2 parts per billion they found in leaves that had grown 650 feet away from the underground deposit.
Other researchers had detected gold particles in plants and leaf litter before, but it was unclear whether they’d been transported all the way from underground deposits. “We were concerned that the gold might have been occurring as dust particles on the outside of these leaves, so it was important for us to locate the gold within the plant,” says Lintern.
His team did so by analyzing the leaves in even further detail (using a specialized X-ray microprobe located at the Australian Synchrotron research facility) and confirmed that the gold particles were located within the plant’s vascular tissue, indicating that they were moving naturally within the leaves. They also conduced greenhouse experiments and found that eucalyptus saplings, grown in soil laced with similar levels of gold, absorbed it and transported detectable levels into their leaves. These separate streams of evidence, they say, shows that the wild eucalyptus trees were indeed sucking up gold from deep underground.
“The eucalyptus acts like a hydraulic pump,” using its roots to suck ground water upward, crucial in an arid environment, Lintern says. “The plants, of course, are searching for water, not gold, but it just so happens that there’s gold dissolved in it.”
The fact that the gold has been found in the leaves, in fact, might be evidence that the eucalyptus is actively trying to get rid of it—after all, it’s a toxic heavy metal—by transporting it to its extremities. Additionally, the gold particles in the leaves were often found located near calcium oxalate crystals, theorized to be part of the removal pathway for toxic chemicals.
Lintern’s group plans to conduct further research into which plants are capable of transporting gold particles in this way and what environmental factors affect the rate of uptake. Mining companies in Canada, he mentions, have already toyed with the idea of using plants as mineral indicators, so this first scientific evidence for the process is likely to accelerate adoption of the method.
“Essentially, we’re tapping into a natural process,” Lintern says. In an age when most of the readily accessible gold near the planet’s surface has been mined, it makes sense to harness the natural mineral exploration plants are already engaging in when they drive their roots deep into the ground. Doing so might even reduce the number of exploratory mines we’re forced to drill—and consequently, lead to less environmental destruction of these plants’ habitats as a result of mining.
October 21, 2013
For decades, public health officials have puzzled over a surprising fact about HIV: Only about 10-20 percent of infants who are breastfed by infected mothers catch the virus. Tests show, though, that HIV is indeed present in breast milk, so these children are exposed to the virus multiple times daily for the first several months (or even years) of their lives.
Now, a group of scientists and doctors from Duke University has figured out why these babies don’t get infected. Human breast milk naturally contains a protein called Tenascin C that neutralizes HIV and, in most cases, prevents it from being passed from mother to child. Eventually, they say, the protein could potentially be valuable as an HIV-fighting tool for both infants and adults that are either HIV-positive or at risk of contracting the infection.
The research, published today in Proceedings of the National Academy of Sciences, was inspired by previous work by other researchers showing that, both in tissue cultures and live mice, breast milk from HIV-negative mothers was naturally endowed with HIV-fighting properties. Scientists suggested that a few different proteins in the milk could potentially be responsible, but no one knew which one.
As part of the study, the researchers divided breast milk into smaller fractions made up of specific proteins via a number of filters—separating the proteins by size, electrical charge and other characteristics—and tested which of these fractions, when added to a tissue culture, prevented the cells from being infected by HIV. Eventually, using mass spectrometry, they found that one particular protein was present in all the HIV-resistant fractions but in none of the others: Tenascin C.
“The protein works by binding to the HIV envelope, and one of the interesting things is that we were even able to narrow down exactly where on the envelope it binds,” says Sallie Permar, the study’s lead author. Her team found that the protein binds to a crucial region on the virus’ envelope that normally locks onto a receptor called CCR5 on the outside of human T cells,allowing it to fuse its membrane with the cell’s. With the region covered up by Tenascin C, HIV’s normal route of attack is blocked, and the virus’ effectiveness is greatly diminished.
Still, the researchers say that other natural elements in milk might play a role in fighting HIV as well. “It’s clearly not the whole story, because we do have samples that have low amounts of this protein but still have HIV-neutralizing activity,” Permar says. ”So it may be acting in concert with other antiviral and antimicrobial factors in the milk.”
Whatever those other factors are, though, the finding vindicates recent changes to UN guidelines that recommend even HIV-positive mothers in resource-poor countries should breastfeed, if they’re taking anti-retroviral drugs to combat their own infection. That’s because—as statistics bear out—the immense nutritional and immune system-boosting benefits of breast milk outweigh the relatively small chance of transmitting HIV through breastfeeding. Tenascin C, it seems, is a big part of why that transmission rate is surprisingly low, and sufficient access to anti-retroviral drugs can help drive it even lower—as low as 2 percent.
The next steps, Permar says, are determining which area of Tenascin C is active in binding to HIV and whether it can effectively prevent transmission in a live animal, as opposed to a tissue culture. If it works, it could potentially be incorporated into an HIV drug with broader applications. Possible uses include giving it in a concentrated form to infants who can’t breastfeed or even administering it to those who do to increase their level or resistance. It’s even conceivable that it could someday be adapted to reduce the risk of HIV transmission in adults as well.
One immediate advantage, says Permar, is that “it’s like to be inherently safe, because it’s already a component for breast milk. It’s something babies eat everyday.” Other potential treatments, on the other hand, must be screened for toxicity.
Tenascin C’s presence in breast milk, though, prompts a deeper question: Why would milk naturally include a protein that battles HIV, a virus that evolved extremely recently in our evolutionary history, sometime in the early 20th century?
“I don’t think it’s in breast milk to combat HIV specifically, but there have been other, related infections that have passed through breastfeeding,” Permar says. “Our work has shown that Tenascin C’s activity isn’t specific to HIV, so we think it’s more of a broad-spectrum anti-microbial protein.”
In other words, Tenascin C is effective at combating a large variety of infections (perhaps related to its role in adults, where it holds various types of tissue together, necessitating receptors that can bind to a wide array of different cells). The fact that it happens to bind at just the right spot on HIV’s outer envelope so that it combats the virus’ transmission, as Permar puts it, is “a gift from evolution.”