June 4, 2012
Taming Some of the Summertime Blues
By Carolyn Gutierrez
For The Record
Vol. 24 No. 11 P. 24
Taking proper precautions and leaning on research advances may offer a cure for the summertime blues caused by tick bites, poison ivy, and the sun’s powerful rays.
Whether it’s a pastoral picnic, a seaside jaunt, or just relaxing in your backyard, common nuisances such as ticks, poison ivy, and sunburn that turn tranquility into a trip to the emergency department can blight the lazy days of summer.
The good news is that experts are tracking weather patterns and studying the life cycles of ticks and their hosts to give the public a heads up on what to expect, and scientific research is bringing the medical community a few steps closer to finding cures or preventive treatments for some typical warm-weather ailments.
The Trouble With Ticks
Humans aren’t the only ones enjoying this year’s unusually balmy weather conditions. Mild spring temperatures have dramatically shortened the winter dormancy period for ticks, resulting in an extra month or two of tick activity that could create an alarming surge in Lyme disease transmission to people or pets this summer. Lyme disease is the most common tick-borne illness in the United States, causing chronic fatigue, joint pain, and neurological problems.
Tick season generally begins in early to mid-April. Once temperatures reach 45 degrees and above, ticks become active and begin questing (searching for a suitable mammal host). In early March, most of the nation experienced temperatures between 70 and 80 degrees, allowing ticks to set up shop ahead of schedule.
Paul Curtis, PhD, a professor of natural resources and an extension wildlife specialist at Cornell University who says ticks were active in central New York about three weeks to one month earlier than normal, suspects the insects may have been active as prematurely as February in certain parts of Long Island. But it’s not just New York that has seen increased activity; all the mid-Atlantic states are looking at a longer-than-usual tick season.
Other factors besides warm weather are at play. Curtis cites a report from the Cary Institute of Ecosystem Studies in Millbrook, New York, describing how the relationship between acorn crop abundance and the population of white-footed mice ultimately affects Lyme disease risk. When there is a boom in acorns, there is a corresponding increase in white-footed mice. In 2010, acorn production was at a record high, resulting in approximately a 10% to 20% increase in mouse abundance in 2011.
White-footed mice are the host of choice for black-legged ticks (also known as deer ticks) and are the principal reservoir for Borrelia burgdorferi, the bacterium that causes Lyme disease. Black-legged ticks go through three feeding cycles: larvae, nymphs, and adults.
Researchers at the Cary Institute found that great numbers of tick larvae fed on the booming mouse population in the summer of 2011, but this year the acorn crop has been sparse, and the number of white-footed mice has dwindled. This is significant because now there will be a tremendous number of ticks in their nymphal stage looking for hosts to feed on and since there are smaller numbers of mice, these spring-summer nymphs will be seeking out other warm-blooded hosts to compensate. According to the Cary Institute, the last time a heavy acorn crop was followed by a paltry harvest, the abundance of nymphal black-legged ticks reached a 20-year high. It is these warm-weather nymphal ticks the size of a poppy seed that pose the biggest health threat for Lyme disease.
Other than becoming a summer recluse, there are steps people can take to prevent ticks from ruining bucolic days under the sun. “If people know they’re going to be in areas where they’ve found ticks or have been exposed to ticks in the past, wear light-colored clothing so you can see the ticks,” Curtis says. “When I’m doing field work on Long Island in very tick-prone areas, I actually tape the top of my pant legs to the top of my boots so that ticks can’t get under my pant leg and crawl up that way.”
Checking yourself, family members, and pets after outdoor activities is a long-standing recommendation during tick season. Diligent use of commercial insect repellents that contain DEET can help although they should be used with care, as many insecticides can adversely affect the environment.
For tick prevention in pets, Curtis recommends flea and tick collars as well as consulting your veterinarian for advice.
According to the Centers for Disease Control and Prevention, making simple landscaping changes at home may keep ticks at bay. Raking leaves and mowing the lawn frequently and creating barriers out of wood chips and gravel between your yard and patio and any wooded areas may discourage the creatures from getting too close to any warm-blooded hosts. Those who live in areas with heavy deer populations (adult ticks tend to be associated with high deer densities) should take special precautions when outdoors.
In addition to the black-legged tick, there are concerns in the environmental science community that the lone star tick, which used to be found mainly in southern states, is now thriving in more northern regions of the United States. It’s thought that the appearance of these ticks—which outnumber their black-legged counterparts by 10 to one on Long Island, according to Curtis—is another consequence of changing weather patterns.
“If you look at the 50-year trend data for temperatures, we’ve seen some of the mildest winters during the last decade of any kind during that 50-year period,” Curtis says. “And if the global warming predictions hold true, temperatures in central New York may well be similar to what they are in North Carolina right now in another 50 years, so I would expect this trend to continue.”
Leaves of Three, Let It Be
Other summer scourges that can threaten to put a damper on alfresco activities—poison ivy, poison oak, and poison sumac—all plants from the Anacardiaceae family, have long baffled scientists looking for a safe and effective preventive treatment. ElSohly Laboratories and University of Mississippi pharmaceutical researchers have recently developed a promising compound, currently known as HPT-721. It involves an intramuscular injection that could prevent contact dermatitis in those sensitive to the poisonous plants. The compound would act as a prophylactic treatment not only for those with an established sensitivity to poison ivy but also for those who have not yet been exposed, preventing sensitization after initial contact with the plants’ secretions.
Most people become sensitized to poison ivy only after their first exposure to the plant. During first contact, they generally do not experience any rash or other symptoms. Then, subsequent contact with the plant causes a reaction that can range from mild to severe contact dermatitis and include itching, a red rash, and bumps or blisters.
Poison ivy rash is caused by urushiol, an oily substance or resin within the plant that acts as a highly effective biological defense mechanism against predators. Urushiol contains compounds that bind to the skin proteins and trigger a reaction in the body’s immune system. Although a few fortunate people never seem to develop a rash after repeated exposure to poison ivy, for most the exposure can have insidious results, with the rash appearing anywhere from eight hours to five days after exposure. Contact dermatitis from poison ivy generally lasts one to three weeks. The smoke from burning poison ivy plants can be particularly potent and can actually cause severe respiratory reactions.
Urushiol is a difficult substance to remove from the skin and can penetrate in minutes. Quick rinsing with isopropyl alcohol may help because it removes skin oils as well as the poison ivy oil. If isopropyl alcohol isn’t available, wash the exposed area as soon as possible with water, but avoid using bar soap as it could actually spread the urushiol. Clothes, shoes, gardening implements, or anything else that may have had contact with poison ivy should also be wiped down with alcohol and water.
Scientists and homeopaths alike have experimented with an array of poison ivy therapies, most with negligible or inconclusive results. Preventive remedies that involved ingesting the plant’s extract worked only in extremely large doses, had limited efficacy, and oftentimes resulted in unpleasant side effects such as perianal dermatitis.
Various injected poison ivy compounds lost efficacy by binding to the plasma proteins—if they were absorbed at all. By binding to the plasma proteins, the compound loses its ability to induce the desensitization or tolerance because it never progresses to the “action” site to turn off the immune system’s response.
Despite these hurdles, pharmaceutical researchers at the University of Mississippi have been able to come up with a compound made from chemical derivatives of urushiol that works in a unique fashion.
“Our idea was to develop a compound that would be absorbed, would go into the bloodstream, but would be masked when it was absorbed,” says Mahmoud A. ElSohly, PhD, president and director of ElSohly Laboratories and a professor of pharmaceutics at the University of Mississippi’s School of Pharmacy. “The masked compound adheres to the blood cells: the cell membranes. Right there at the surface of the cell membrane, it breaks off and removes the mask. The mask comes off, and so the drug now is at the surface of the cells, and it binds to the cell membrane. And it’s the drug combined with the cell membrane that circulates and goes to the right place in the immune system and tells the immune system to turn off the response to this particular compound.”
According to ElSohly, the new compound is stable, water soluble, has a long shelf life, and is designed for intramuscular injection.
During the testing process, researchers were able to induce tolerance to the poison plants by using HPT-721 in guinea pigs that had never been exposed to poison ivy. In addition, the scientists initially sensitized the guinea pigs and then reexposed them to poison ivy. The creatures reacted as humans would, with edema and rash. After giving the test subjects time to recover, researchers treated them with the compound and received promising results.
“Basically, we have proven through in vivo animal testing that the compound will actually induce tolerance in naïve guinea pigs and will induce desensitization in guinea pigs that have already been sensitized to poison ivy,” ElSohly explains.
ElSohly and his team have a few more hurdles to clear until the compound is available to eager gardeners and outdoorsmen. Pharmacokinetic studies and toxicology tests still need to be performed. Then the scientists need to file an investigational new drug application with the FDA. If approved, clinical trials may begin later this year.
Because safety and efficacy were shown in the preclinical animal models, the researchers are confident the compound will prove to be safe in humans. Until then, there are guinea pigs in Mississippi that are the envy of nature lovers everywhere.
The Case of the Missing Enzyme
Researchers at Ohio State University have been studying the intricate process of how enzymes heal ultraviolet (UV) light damage to the skin. Conducted over the past nine years, the studies may someday enable scientists to create sunscreen lotions and remedies that might actually heal UV damage to the skin that occurs with sunburn.
Led by Ohio State University physicist and chemist Dongping Zhong, PhD, the research team synthesized DNA and exposed it to UV light, mimicking the effects of sunburn. The team captured the motion of photolyases—minute enzyme molecules that heal damaged DNA—by using ultrafast pulses of laser light and taking laser “snapshots” of the enzyme’s actions in real time.
When a person is sunburned, UV light excites the atoms in the DNA molecule, which then spark chemical reactions resulting in accidental chemical bonds forming between the atoms. These errant chemical bonds can lead to molecular injuries known as dimers, which prevent proper DNA replication, resulting in genetic mutations that can eventually lead to skin cancer.
The enzyme repairs the DNA by harnessing the energy from photons to launch a single electron to break up the injured bonds, causing the bonds to reform and return to their original undamaged positions in the DNA molecule. According to Zhong, the enzyme acts as a mediator of sorts as it “borrows the sun energy, puts the electron in the DNA, repairs the DNA, and the electron comes back.” When the electron returns to the enzyme, the cycle is repeated until all the damage is repaired.
Putting together the laser snapshots of the enzyme at work, Zhong and his team were able to map an entire subatomic healing cycle that moves so quickly, it’s faster than the proverbial blink of an eye. “The whole process takes 100 picoseconds,” Zhong says. (A picosecond is one trillionth of a second.)
Fish, amphibians, birds, marsupials, insects, plant life, bacteria, viruses, and yeast all carry photolyase in their biological systems; humans do not. Somewhere in the evolutionary process, placental mammals lost the photolyase gene. Zhong’s research gives hope to future sun worshipers, as a synthetic form of photolyase could someday compensate for humankind’s innate lack of UV protection. Current sunscreen lotions safeguard skin by deflecting UV rays from the skin’s surface. Futuristic sunscreens may be fortified with protective photolyase, allowing sunbathers to while away the hours at the beach worry free. But more importantly, the enzyme research may help in designing therapies for skin cancer.
Zhong says a group of researchers in the Netherlands was able to generate transgenic mice with the photolyase gene. The researchers found that the UV threshold for skin damage to DNA increased 1,000-fold, Zhong says. This is promising news because it suggests that the cellular infrastructure for the enzyme may still exist in mammals. “Of course, the question is,” adds Zhong with a laugh, “do we really need an extra gene?”
— Carolyn Gutierrez is a freelance writer based in New York City.