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Dogs as sources and sentinels of parasites in humans and wildlife, northern Canada

A minimum of 11 genera of parasites, including 7 known or suspected to cause zoonoses, were detected in dogs in 2 northern Canadian communities. Dogs in remote settlements receive minimal veterinary care and may serve as sources and sentinels for parasites in persons and wildlife, and as parasite bridges between wildlife and humans. In the Northwest Territories, harvesting country foods is a key cultural activity and is important for sustenance; 75% of persons eat harvested meat and fish. Dogs fed fish and game can serve as indicators of parasites in these human food sources. Diet-associated zoonotic parasites detected in dogs included Diphyllobothrium spp., cestodes acquired by eating undercooked or inadequately frozen fish (found in humans throughout northern Canada); Alaria spp., trematodes acquired by eating frogs or paratenic hosts; and Toxoplasma gondii, tissue protozoans acquired by eating oocysts from felid feces or tissue cysts in intermediate hosts (a worldwide human pathogen). In aboriginal persons in northern Canada, seroconversion for T. gondii during pregnancy has been associated with diets that include caribou. High seroprevalence in dogs indicates that T. gondii is common in the study area; however, the source of exposure was not identified. Given potential consequences for infection of parasite-negative pregnant women, further research is warranted on the association of human toxoplasmosis with a diet of country foods in northern regions.
Toxocara spp. are nematodes that cause visceral and ocular migrans in humans, particularly children. Although Toxocara spp. are considered limited to more southern regions, their presence in puppies and adults in Fort Resolution suggests that completion of their life cycle at northern latitudes is possible. Continuing warming trends may lead to increased occurrence of this parasite in the north. Giardia sp. Assemblage A is a protozoan that causes gastrointestinal disease in humans. Isolation of this zoonotic strain was unexpected because dogs are typically infected with Assemblage D, and Assemblage A suggests transmission from humans to dogs. This finding highlights a need to further investigate the apparent emergence of Assemblage A in domestic and wild animals in remote northern regions and transmission patterns among dogs, wildlife, and humans (S.J. Kutz, unpub. data). Echinococcus spp. are cestodes that cause hydatid (E. granulosus) or alveolar cysts (E. multilocularis) in the lungs and livers of humans. Although a reduction in dog teams in northern Canada has resulted in decreased prevalence of E. granulosus spp., the distribution, epidemiology, and role of the more pathogenic E. multilocularis spp. are not well understood in this region. Uncinaria spp. and Toxascaris spp. are also occasionally reported as zoonoses; however, evidence for these findings remains equivocal.
Dogs can also be sources of disease in parasite-naïve wildlife populations. They were the source for devastating distemper outbreaks in lions in the Serengeti, and lice of presumed dog origin are causing serious disease in Alaskan wolf populations (K.B. Beckmen, pers. comm.). Neospora caninum detected in this study may be a new parasite in this ecosystem with potentially serious consequences for wildlife. The remaining parasites are presumed present in local wildlife and can have a negative effect on the health of dogs and wildlife. More detailed, quantitative investigation is required to evaluate the role of dogs as potential sources of new, or amplifiers of existing, pathogens for wildlife.
Our results highlight important health issues associated with the interface between dogs, wildlife, and humans in remote northern communities. Disease associated with parasites in this study is often subclinical but can have serious effects on health and productivity of humans, dogs, and wildlife (e.g., Giardia spp.). Although these parasites are relatively easy to control, there was no evidence that sporadic veterinary presence in Fort Chipewyan reduced parasitism. This finding emphasizes the need for a new approach to domestic animal healthcare in the north. Inaccessibility of communities, uncertain and changing roles of dogs, and current regulations in the veterinary profession restricting remote delivery of services hinder development of effective disease detection and preventative medicine programs. Innovative new methods for delivery of animal healthcare services are required. These methods should include long-term commitment to an integrated health approach, focusing on education, engagement, and development and support of local capacity for delivery of basic animal health services. Ongoing communication and partnerships between animal and human health professionals will enhance the effectiveness of such initiatives.

Emerging Infectious Diseases
January 8, 2008

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Lice threaten Canada’s salmon

Lice harboured by farmed fish are killing wild salmon on Canada’s west coast, new work has confirmed. The study shows serious declines in fish populations, which could lead to the total collapse of runs in those rivers in less than a decade. Salmon lice (Lepeophtheirus salmonis ) are natural parasites of fish in Canadian waters. They usually infect adult salmon, which can tolerate mild infestations well. The trouble begins when naturally infected wild pink salmon return to their home rivers to spawn, swimming past nets full of farmed Atlantic salmon on their way. Their lice shed larvae, which settle and thrive on the farmed fish. The wild juveniles then swim out to sea, passing by these shoals of infected farmed fish and dramatically increasing their chance of picking up a louse. The infection can have disastrous consequences on the young fish. Fisheries ecologist Martin Krkošek at the University of Alberta in Edmonton and his colleagues looked at estimates of the number of salmon returning to each of 71 rivers along the central coast of British Columbia from 1970 to 2006, and found that before the louse infestations began in 2001 the populations were stable.

Fish from seven of those rivers had to swim by at least one fish farm. Once the infestation took hold, those populations began to decline, even though they had been closed to commercial fishing. In 2002, most of the young pink salmon that had swum past farm pens on their seaward journey failed to return: fisheries managers expected 3.6 million fish, but counted only 147,000. Runs of pink salmon in the rest of British Columbia were healthy that year. In 2003, fisheries managers had emptied their farm nets before the smolts left their natal streams, to prevent lice transmission. This seemed to work. Fewer juveniles picked up lice and Krkošek calculated that deaths from lice fell to 1/3 the rate seen the year before. But the farm fish are back in their pens now; there are at present no plans to remove the fish again. At the current rate of decline, the runs in these rivers will drop to less than 1% of their natural levels in four generations, or eight years, the team reports in Science. “Right now, we’re already half way along that curve,” Krkošek says. “This is a cautionary tale,” says Ray Hilborn, a fisheries biologist at the University of Washington in Seattle. Although farming currently threatens “only a handful” of the salmon runs in this region, regulators should respond cautiously to the growing demand for fish farming, he says. “It raises the concern that you could have some other more contagious pathogen that could be incubated in the farms and then spread around from there.”

Nature
January 8, 2008

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Cat fleas’ journey into the vacuum is a ‘one-way trip’

Homeowners dogged by household fleas need look no farther than the broom closet to solve their problem. Scientists have determined that vacuuming kills fleas in all stages of their lives, with an average of 96 percent success in adult fleas and 100 percent destruction of younger fleas. In fact, the results were so surprisingly definitive that the lead scientist, an Ohio State University insect specialist, repeated the experiments several times to be sure the findings were correct. The studies were conducted on the cat flea, or Ctenocephalides felis, the most common type of flea plaguing companion animals and humans. The lead researcher also examined vacuum bags for toxicity and exposed fleas to churning air in separate tests to further explore potential causes of flea death. He and a colleague believed that the damaging effects of the brushes, fans and powerful air currents in vacuum cleaners combine to kill the fleas. The study used a single model of an upright vacuum, but researchers don’t think the vacuum design has much bearing on the results.

“No matter what vacuum a flea gets sucked into, it’s probably a one-way trip,” said Glen Needham, associate professor of entomology at Ohio State and a co-author of the study. Needham theorized that the vacuum brushes wear away the cuticle, a waxy outer later on fleas and most insects that allows the bugs to stay hydrated. Without the waxy protection, the adult fleas. larvae and pupae probably dry up and die, he said. “We didn’t do a post-mortem, so we don’t know for sure. But it appears that the physical abuse they took caused them to perish,” he said. Conventional wisdom has suggested for years that homeowners should vacuum carpeted areas to physically remove fleas, and some recommendations went so far as to say the contents of the bags should be emptied, burned or frozen. Lead study author W. Fred Hink, professor emeritus of entomology at Ohio State and a longtime researcher in nontoxic controls of fleas on dogs, sought to test the effects of vacuuming on all flea life stages and whether any extra disposal steps or additional chemical controls are necessary.

Fleas have multiple life stages. Adult fleas eat blood meals and mate while living on a host animal. Females lay eggs, which roll off of the animal and onto the floor, furniture or pet bedding. After hatching from the eggs two to 14 days later, the insects go through three larval stages, the last of which spins a cocoon to protect the pupa stage. New adults typically emerge within a week or two. The study involved groups of 100 adult fleas at a time, as well as groups of 50 pupae and 50 larvae, by vacuuming them up from a tightly woven kitchen-type of carpet. Six tests of vacuuming the adult fleas yielded an average of 96 percent of fleas killed; three tests of vacuumed pupae and one test of vacuumed larvae (in their third stage of development) resulted in 100 percent killed. In comparison, an average of only 5 percent of adult fleas died after being held in paper vacuum bags to test for toxicity, and an average of only 3 percent died when circulated in moving air. “I did not include eggs in the vacuum study, but I’m sure they would not have survived,” Hink said.

Flea survival in general is on the wane these days, Needham noted, because of numerous effective chemical treatments on the market that kill fleas on companion animals. “For awhile, fleas owned us. But now they’re on the run,” Needham said. “There are all kinds of ways to manage the problem, but how people feel about insecticides and how much money they want to spend factors into what they’re going to do for flea control. Vacuuming is a great strategy because it involves no chemicals and physically removes the problem.” He also said the effectiveness of some insecticides is likely to decrease as fleas inevitably develop resistance to the currently available compounds. Because of that, Needham is among researchers seeking other nontoxic ways to kill fleas and other household pests, including studying the use of ultraviolet light. “We’re hoping to find that exposure to UV light could knock the flea population down even further. It appears to be a pretty powerful technology for this purpose,” he said.

Science Daily
January 8, 2008

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Lyme disease’s unusual suspects

A new study challenges the widely held view that mice are the main animal reservoir for Lyme disease in the United States. The paper, published online this week in the Proceedings of the Royal Society B, shows that two shrew species are just as important and that chipmunks play a supporting role. Unless those species are taken into account, say researchers, efforts to control Lyme disease are doomed to fail. Lyme disease can cause anything from rash to arthritic and psychiatric diseases. Borrelia burgdorferi sensu stricto, the bacterium that causes Lyme disease in the United States, is transmitted to humans by blacklegged ticks. Researchers have assumed that the vast majority of ticks become infected when, as larvae, they take their first blood meal from a white-footed mouse. Indeed, lab studies have shown that as many as 90% of ticks feeding on an infected mouse pick up the bug, an “extremely high number,” says disease ecologist Dustin Brisson of the University of Pennsylvania.

But other species that transmit B. burgdorferi to ticks less efficiently might also spread the disease if they are more numerous or if they are bitten by a large number of ticks. And some studies had suggested this to be the case. For instance, a field trial published in 2004 showed that vaccinating mice against Lyme disease and then releasing them led to only a small decrease in the number of infected ticks. To get a fuller picture, Brisson and his colleagues pulled together data from their own studies in the Hudson Valley in New York state and from other papers. The team looked at an outer surface protein of B. burgdorferi found in ticks–which can give clues about the vertebrate host–as well as the probabilities that different host species transmit the microbe during a tick bite, the number of larvae feeding on the animals, and population densities. Then they calculated the importance of each of the host species.

White-footed mice account for only a quarter of the total number of infected ticks, the team found. Short-tailed shrews and masked shrews were responsible for another quarter each, and chipmunks for as much as 13%. That means that mice aren’t the “dominant” host at all, says Brisson, and vaccination strategies aimed at mice alone are unlikely to bring Lyme disease under control. Brisson speculates that mice have received a lot of attention in part because they’re conspicuous, easy to catch, and ideal lab subjects. “It’s a nice paper,” says Durland Fish of Yale University School of Medicine, a co-author of the 2004 vaccination study. However, he believes there are even more culprits. In particular, the team barely looked at birds, he notes, even though one study has shown that robins, which often live close to humans, are very good at transmitting B. burgdorferi to ticks in the lab. “The situation is probably even more complex than we think,” Fish says.

ScienceNow
December 11, 2007

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Parasites: Beat them or join them?

When a parasite, virus, or other pathogen attacks, animals typically fight back with their immune system. But a new study of rodents infected with malaria shows that animals have another option: They can evolve to live with their invaders. The findings, reported in the 2 November issue of Science, may help scientists understand the evolution and spread of infectious diseases, as well as allow them to create hardier livestock. Plants have two strategies for dealing with parasites: They can resist them–developing a hardy defense like tough leaves–or they can tolerate them–minimizing the damage the invaders cause by, say, increasing photosynthesis to boost energy stores. Most do a little of both. Lars Råberg, an ecologist at the University of Edinburgh in the U.K., wondered if animals make similar choices.

Råberg and his colleagues infected five strains of laboratory mice with a parasite that causes malaria. They then monitored changes in the animals’ health, as measured by anemia and weight loss, with relation to the amount of parasites in the blood. Like plants, the mice employed resistance and tolerance strategies. As parasites multiplied in the hosts, some mouse strains stayed healthier than others, indicating that they had developed a way to tolerate the parasites. Other strains were able to keep their parasite levels low, indicating that they were actively resisting the infection.

Resistance didn’t correlate with tolerance. Mice with stronger resistance to the parasite were less able to tolerate them, for example, losing more weight and becoming more anemic than more tolerant mice. This indicates that the genetics behind tolerance might be distinct from those driving resistance, says Råberg. He also notes that the findings may have important implications for the evolution of pathogens. If pathogens are tolerated rather than destroyed, they are not pushed to evolve and become even more deadly, he notes. At the same time, tolerance may not be ideal because if the body doesn’t destroy the pathogens, they are more likely to spread. These factors could influence animal breeding strategies, says plant evolutionary biologist Mark Rausher of Duke University in Durham, North Carolina. Breeding for tolerance in chickens and pigs, for example, may provide a better defense than breeding for resistance.

ScienceNow
November 12, 2007

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Consumption of raw fish raises potential health concerns for consumers

Two case studies from Japan presented at the 72nd Annual Meeting of the American College of Gastroenterology point to a potential health problem in the United States, as more Americans consume raw fish in the form of sushi and sashimi. Anisakiasis (round worm) is a human parasitic infection caused by the consumption of raw or undercooked seafood containing Anisakis larvae. Consumers should be aware that while larvae for the parasitic worm Anisakis cannot survive in a human host, the ingested larvae can produce severe intestinal problems warranting a visit to the emergency room. When ingested by humans, the larvae attach themselves to the tissues lining the stomach and intestines, resulting in sudden abdominal pain, nausea, vomiting, and diarrhea. Since the larvae cannot survive in humans and eventually die, intestinal anisakiasis usually resolves on its own.

Researchers in Japan examined two cases of intestinal anisakiasis presenting as an obstruction of the small intestine. In each case, both patients, ages 64 and 70, were rushed to the emergency room with sudden abdominal pain and vomiting after eating raw sardines as sashimi two days earlier. The diagnosis of anisakiasis in the stomach can easily be confirmed by endoscopy. However, small intestinal anisakiasis is difficult to diagnose. Both patients had abdominal X-rays showed air-fluid levels suggesting a small intestinal obstruction. Using a multidetector-row computed tomography (MDCT), doctors obtained high quality images of the small bowel, and found the intestinal blockage was caused by the presence of Anisakis larvae. Fluid replacement and resting immediately relieved the patients’ symptoms. Because the symptoms of anisakiasis can mimic other gastrointestinal diseases, it might potentially be misdiagnosed as appendicitis, acute abdomen (peritonitis) or stomach ulcers. According to Mashahiro Matshushita, MD of Haibara General Hospital, “Anisakiasis should be considered in the differential diagnosis of small intestinal obstruction.”

Science Daily
October 30, 2007

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Giardia genome unlocked

Giardia lamblia, one of the most common human parasites in the United States, causes more than 20,000 intestinal infections a year, often through contact with contaminated drinking or swimming water. In the September 28 issue of Science, an international team led by researchers at the MBL (Marine Biological Laboratory) describe the complete genome (genetic sequence) of Giardia, which could lead to the development of new drugs to combat this persistent infection, called giardiasis. “Even though there are treatments now available, a number of people get chronic giardiasis, which is difficult to eliminate. So there is interest in new treatments,” says Hilary Morrison, Ph.D., of the MBL’s Josephine Bay Paul Center for Comparative Molecular Biology and Evolution, the first author on the paper. The Giardia parasite lives in the human intestine in a swimming and feeding form called a trophozoite, which is eventually expelled through the stools. Outside the body, Giardia takes the form of a highly infectious cyst that can live for weeks in water, soil, food, or on other surfaces.

Giardiasis is most common among children, especially those who are exposed to diaper changing. Swimmers, hikers, campers and others who drink untreated water are also prone to the infection (hence the nickname “backpacker’s disease” or “beaver fever”), as are international travelers. Common symptoms include diarrhea, nausea, stomach cramps and gas, and usually persist two to six weeks. Because the parasite clings to intestinal cells that absorb fats and nutrients, giardiasis can lead to severe complications such as poor nutrient absorption and weight loss.Giardia spends one phase of its lifecycle in the environment and the other in the gut of an infected human or wild animal. To maintain this dual existence, the parasite has two radically different microscopic forms. In water, Giardia exists as a hardy, highly infectious cyst, which can survive for months, even in fresh water devoid of all nutrients. In the gut, Giardia exists in a swimming and feeding form known as a trophozoite.

The awakening of the dormant cyst happens quickly after someone swallows contaminated water or food. After the cysts encounter the warm acidic juices in the stomach, they change into trophozoites. Within about two hours, these trophozoites will be swimming in the intestines. Unlike many other parasites, trophozoites do not invade tissues or cells. Instead they simply attach to cells, drink in nutrients and multiply. The parasite evades the immune system and persists in the intestine by shifting the proteins it displays on its surfaces. Existing drugs can effectively treat people with Giardia infections, the disease known as giardiasis, but most infections resolve on their own. When trophozoites detach from the intestinal wall, they may swim and reattach to new intestinal cells, or they may pass down the digestive tract and into the bowels, transform back into cysts and be passed through the stools.

“Although not life threatening, Giardia is a rather fastidious parasite and quite important from an economical viewpoint worldwide and in the United States, where it constitutes a major cause of diarrheal disease in children in daycare centers,” says Mitchell Sogin, Ph.D., director of the Josephine Bay Paul Center and leader of the Giardia study. Analysis of the Giardia genome revealed several unusual proteins that are promising drug targets, Morrison says. “These proteins are different enough from human proteins that if you affect them with a drug, it’s not going to affect the human counterparts,” she says. “Drugs can be devised that will interfere with the parasite’s ability to replicate, or to move or bind in the small intestine, or to exist at all.”

The team also investigated the evolutionary history of this ancient parasite. Giardia is a single-celled eukaryote, meaning its cell has a nucleus, as do the cells of humans and most other multicellular organisms. But the Giardia genome is compact compared to other eukaryotes, with simplified machinery for several basic processes, such as DNA replication and RNA processing. If the Giardia genome had originally been complex and experienced gene loss over evolutionary time, Morrison says, one would expect to see parts of the machinery intact and parts missing. This, however, wasn’t the case. “It looks like the genome was just simpler to begin with,” she says. The authors hypothesize that Giardia diverged from other eukaryotes more than a billion years ago. “We embarked upon this genome project because of its importance to human health and suggestions from earlier molecular analyses that Giardia represents a very early-diverging lineage in the evolutionary history of eukaryotes,” Sogin says. “Giardia’s genome content and architecture support these theories about the parasite’s ancestral character.”

Eukaryotic organisms are so diverse that they include everything from amoebae to humans. But even within such a wide range, Giardia is unusual. In its trophozoite form, it has two nuclei instead of the more usual one. When it becomes a cyst, it multiplies its genetic material into four identical nuclei. But despite having these multiple copies of its nuclei, Giardia is really a genetic minimalist. It has fewer and simpler genetic components than most other eukaryotes. Why? According to one theory, Giardia is simple because it has lost complexity: evolutionary pressure favors parasites that shed genes coding for functions they can borrow from their infected hosts. An alternative theory holds that the parasite may have always been simple because it diverged from other eukaryotic organisms more than a billion years ago, long before the complex modern eukaryotes emerged.

Science Daily
October 16, 2007

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Ticks don’t come out in the wash

Before venturing into tick-infested territory, you used a topical repellent on exposed skin and outer clothing. When you returned, you did a body check and threw your clothes in the wash. But clean clothes may not be tick-free clothes. When he found a live lone star tick (Amblyomma americanum) on the agitator of his washing machine, Agricultural Research Service (ARS) entomologist John Carroll decided to find out how tough ticks are. So he bagged up nymphs from two species—the lone star tick and the deer tick, (Ixodes scapularis), the creature that transmits Lyme disease—and put them in the washing machine. Carroll used a combination of water temperature settings and detergent types to wash the ticks. The majority of lone star ticks survived all the water-detergent combinations with no obvious side effects. Most of the deer ticks lived through the cold and warm water settings as well. But when one type of detergent was used with a hot water setting, only 25 percent of the deer ticks survived. When it came time to dry, all the ticks of both species died after an hour of tumbling around at high heat. But when the dryer was set to “no heat,” about one-third of the deer ticks and more than half of the lone star ticks survived.

Carroll placed the ticks in mesh bags, which kept them from draining away during the rinse cycle and perhaps increased their odds for survival. However, ticks might also survive a sudsy interlude by sheltering in the folds and crevices of a typical load of laundry. Some tick species have been observed to survive hours of submersion in fresh water. Both adult ticks and nymphs can transmit disease. Carroll’s research reinforces recommendations by the U.S. Centers for Disease Control and Prevention to wash and dry clothes at high temperatures after spending time in areas known to harbor ticks.

Science Daily
October 16, 2007

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Defense mechanism found in infected ticks may protect against harmful parasite

A defense molecule isolated in ticks infected with the Babesia sp. parasite may protect animals and humans against infection. Researchers from the U.S. and abroad report their findings in the July 2007 issue of the journal Infection and Immunity. Babesiosis is a well-recognized disease worldwide and recently gained increased attention as an emerging zoonosis. Transmitted to animals and humans by ticks infected with the Babesia sp. parasite, symptoms may include fever, fatigue and hemolytic anemia. Antimicrobial peptides are defensive molecules found in the innate immune system of animals. Less toxic and more effective against multi-drug resistant bacteria, they are showing promise as a better choice for treatment of some bacterial and fungal infectious diseases.

In the study researchers identified a novel parasiticidal peptide named longicin from the tick species Haemaphysalis longicornis and tested its ability to inhibit infection. It showed a remarkable ability to inhibit the blood stage of equine Babesia equi by killing the parasites and resulted in reduction of parasitemia in animals with the zoonotic and murine Babesia microti. RNA analysis also demonstrated that longicin is capable of killing the canine strain, Babesia gibsoni. “Here we report a defensin peptide, longicin, from the tick H. longicornis that exerts a babesiacidal effect,” say the researchers. “Theoretically, longicin may serve as a model for the development of chemotherapeutic compounds against tick-borne disease organisms.”

Science Daily
September 4, 2007

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Lyme disease cases more than double since 1991

Reported cases of Lyme disease have more than doubled since 1991, when Lyme became a nationally notifiable disease, according to a report by the Centers for Disease Control and Prevention (CDC). The report also said 93 percent of reported cases were concentrated in 10 states. “This increase in cases is most likely the result of both a true increase in the frequency of the disease as well as better recognition and reporting due to enhanced detection of cases,” said Dr. Paul Mead, a medical epidemiologist with the CDC Division of Vector-Borne Infectious Diseases. Lyme disease is the most common of all the diseases in the United States transmitted by mosquitoes, ticks and fleas, with approximately 20,000 cases reported each year. It most commonly occurs in the Northeastern, Mid-Atlantic, and North-Central states. Connecticut, Delaware, Maryland, Massachusetts, Minnesota, New Jersey, New York, Pennsylvania, Rhode Island and Wisconsin had the most cases. The report says that during 2003-2005, a total of 64,382 Lyme disease cases were reported to CDC from 46 states and the District of Columbia.

Most illnesses occurred in June, July and August, when the infected ticks that carry the disease are most active. Lyme disease is caused by the spirochete Borrelia burgdorferi which is transmitted to humans by tick bite. From 2003-2005, the incidence of Lyme disease in the cases reported higher rates among two age groups-children aged 5 to 14 years (10 cases per 100,000 population per year) and adults aged 55 to 64 years (9.9 cases per 100,000 population per year). Early symptoms of infection include fever, headache, fatigue, and a characteristic skin rash called erythema migrans. Left untreated, infection can spread to joints, the heart, and the nervous system. People should watch for symptoms especially in these areas with intense Lyme disease transmission, and see a health care provider if these develop. Prompt diagnosis and treatment are important to prevent serious illness and long-term complications. “While this increase is of concern, these rates highlight the need to focus on prevention of this disease. People living in areas where Lyme disease is most frequently reported can take proactive steps to reduce their risk of infection,” Dr. Mead said.

Prevention steps include daily tick checks (self examination for ticks), use of repellent containing 20 percent or more DEET, selective use of insecticides that target ticks, and the avoidance of tick-infested areas. Removing ticks within 24 hours of attachment greatly reduces the likelihood of disease transmission. Tick populations around homes and in recreational areas can be reduced 50 to 90 percent through simple landscaping practices such as removing brush and leaf litter, and creating a buffer zone of wood chips or gravel between forest and lawn or recreational areas.

Science Daily
July 24, 2007

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New Leishmania genome sequences highlight gene targets for treatment development

A comparison of three parasite species that cause Leishmaniasis has identified a small number of genes, many new to biology, that will provide a framework to target the search for new treatments. Leishmaniasis is a devastating disease that affects about two million people each year and threatens one-fifth of the world’s population and new treatments are desperately needed. In their report in Nature Genetics the researchers compared the genomes of L. infantum and L. braziliensis, which cause life-threatening visceral and disfiguring mucocutaneous leishmaniasis, respectively, with the sequence they produced in 2005 for L. major, which causes a less severe, cutaneous form of the disease. Despite the major differences in disease type, only 200 out of more than 8000 genes present in each genome were found to be differentially distributed between the three species. This exceptionally small variation in gene content has given new insights into those processes that may determine disease severity in humans.

“Identifying factors that allow three closely related organisms to cause vastly different clinical outcomes is a major quest for researchers and in this study we have narrowed the search to a number that can be realistically studied,” commented Dr Matt Berriman, senior author on the paper, from the Wellcome Trust Sanger Institute. The researchers found only five genes in the L. major genome for which no trace could be found in the other two species. By contrast, in Plasmodium, which causes malaria, about 20% of genes differ between related species. “Clearly there must have been considerable evolutionary pressure over time to maintain the structure and sequence of the Leishmania genomes – the degree of similarity between these species was unexpected,” explained Professor Deborah Smith, collaborator on this project at the University of York. “Perhaps only a few parasite genes are important in determining which type of disease develops after infection and the host genome plays a major role in clinical outcome.” The results picked up another surprising finding: the team could assign a function to only one-third of the 200 genes restricted to one or two of the species.

“The genome sequences have given us a short-cut to a small number of largely novel genes,” explained Dr Chris Peacock, first author on the report. “Given their lack of similarity to human genes, they present a limited repertoire of potential targets for drug and vaccine development allowing researchers to optimise the use of limited resources.” Leishmaniasis is one of the neglected diseases that desperately need new research, as WHO/TDR notes: “Treatment of visceral leishmanisis by first-line drugs is long (4 weeks), given systemically, and expensive (US$120–150)”. The affordable drugs have been in use for more than half a century and drug resistance is rife, creating a desperate need for new treatments. Biological studies for the function of 50% of Leishmania genes are lacking, so this comparative genome study provides a route to find those that might be essential to each species.

One potential target is the CFAS gene that codes for cyclopropane fatty acid synthase, an enzyme that may be involved in producing components of the cell membrane. CFAS is present in the genomes of L. braziliensis and L. infantum, but is absent from the human genome. The parasite genes are thought to have been acquired from bacterial species that have very similar sequences. “CFAS is involved in virulence and persistence in Mycobacterium, causative agent of tuberculosis, so the identification of a CFAS gene in Leishmania raises the exciting possibility that some virulence factors are conserved between bacterial and eukaryotic intracellular pathogens,” said Jeremy Mottram, a collaborator on the project who is a Professor in the Wellcome Centre for Molecular Parasitology at the University of Glasgow. Some families of genes that determine the properties of the parasite cell surface have grown in number and some declined among the three species: ‘death’ of genes seems to be a major force for differences between the parasite genomes. Some genes, however, are evolving rapidly, leading the team to suspect they include key genes involved in interacting with the human host – where the battle between parasite and patient is fought and where rapid response is important to both.

Remarkably, L. braziliensis, the most ancient Leishmania species sequenced, contains genes that could provide a working pathway for RNAi, an emerging mechanism for gene regulation. The genome sequences show that components for this pathway are absent from the other two Leishmania species. This pathway might serve as an experimental tool in understanding the role of the many genes whose function is unknown, by using experimentally induced RNAi to ‘knock-down’ gene activity prior to host infection. “In addition to their function with respect to promoting diverse clinical outcomes,” commented David Sacks, PhD, Head of the Intracellular Parasite Biology Section at the National Institute of Allergy and Infectious Diseases, Bethesda, USA, “the remarkably limited number of species-specific genes should lead to the more rapid identification of sequences involved in specialized aspects of Leishmania biology, such as the development of L. braziliensis in the hindgut of its sandfly vector, and the restricted reservoir host range seen with L. infantum infections in dogs.”
Around 350 million people in 88 countries on four continents are at risk of Leishmaniasis and its incidence has risen sharply over the past ten years. It is transmitted by the bite of various species of sandfly: wild and domesticated animals – as well as humans – act as a reservoir for the disease.

Science Daily
July 10, 2007

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Toxoplasmosis infection trick revealed

Scientists have provided new insight into how the parasite which causes toxoplasmosis invades human cells. Toxoplasmosis is a parasitic disease, primarily carried by cats. It is transmitted to humans by eating undercooked meat or through contact with cat faeces. It is particularly dangerous for pregnant women, whose foetuses can be infected via the placenta, and those with a weakened immune system, such as people infected with HIV. In severe cases, toxoplasmosis can cause damage to the brain and eyes, and even death. Now researchers from London and Geneva have determined, for the first time, the atomic structure of a key protein which is released onto the surface of the parasite just before it invades host cells in the human body. They found that the protein known as TgMIC1 binds to certain sugars on the surface of the host cell, assisting the parasite to stick to, and then enter the human cell.

Using a novel carbohydrate microarray the team were able to identify the precise sugars to which the parasite protein binds. Following this the team used a combination of NMR spectroscopy and cellular studies to characterise the behaviour and interactions of the parasite protein and host cell sugars. This means that the team have a more detailed picture than ever before of exactly how the parasite recognises and attacks host cells in the body. Professor Steve Matthews from Imperial College London’s Division of Molecular Biosciences, one of the paper’s authors, explains the significance of the research, saying: “Understanding the fundamental, atomic-level detail of how diseases like toxoplasmosis pick out and invade host cells in the human body is vital if we want to fight these diseases effectively.

“Now that we understand that it’s a key interaction between a protein on the parasite’s surface and sugars on the human cell which lead to the cell’s invasion, there is potential to develop therapeutics that are targeted at disrupting this mechanism, therefore thwarting infection.” Toxoplasma gondii, the parasite that causes toxoplasmosis, is one of the world’s most common parasites. Around a quarter to half of the world’s population is thought to be infected, and around 1% of people in the UK catch toxoplasmosis each year. In the majority of cases, those affected don’t have any symptoms. But for those with weakened immune systems, and unborn babies, toxoplasmosis can cause very serious health problems.
Source: EMBO Journal

Science Daily
May 29, 2007

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Female ticks have market on gluttony

Sex makes you fat. If you’re a female tick, that is. The “truly gluttonous” female ixodid tick increases her weight an astounding 100 times her original size after she mates, so a University of Alberta researcher investigated what it is about copulation that triggers such a massive weight gain. In a new research paper published in the Journal of Insect Physiology, Dr. Reuben Kaufman, from the Department of Biological Sciences, suggests several differences between the ixodid tick and her blood-sucking counterparts that help explain the weight gain. Using mosquitoes, tsetse flies, bed bugs and kissing bugs as comparison, Kaufman found that no one compared to this female African tick when it came to weight gain following mating.

Kaufman suggests that the ixodid tick displays a significant difference in lifestyle from the other insects and that it is adaptive for the virgin to remain small before mating. First, this species of tick remain on the host for a number of days, rather than minutes. “In this family of ticks, mating takes place on the host,” says Kaufman. “Most other insects mate before or after their brief blood meal –the two acts are totally separate, but not with these ticks.” Female ticks require six to 10 days to engorge fully. First, she attaches herself to the skin. Then she feeds to 10 times her unfed weight and finally, after copulation she increases her weight a further tenfold. On the other hand, the virgin tick rarely exceeds the critical weight necessary for laying eggs. It will hang on to the host for weeks, waiting for a male to find her, says Kaufman. If the virgin gains too much weight and is groomed off the host, it won’t reattach itself to another host and continue feeding. “However, if she remains small she still has a chance to reattach itself to another host–hopefully infested with some feeding males– continuing feeding and potentially mate,” says Kaufman. “If a male eventually copulates with her, she will engorge normally and then be able to lay eggs. This is one reason why it might be adaptive for the virgin to remain small until mated.”

In terms of what causes the female to become so engorged, Kaufman says that when a tick does copulate, the male’s seminal fluid contains two engorgement factor proteins that together act as a signal to tell her to complete engorgement. Kaufman’s future research will look toward the potential to produce an anti-tick vaccine. Some experiments have already suggested that normal, mated ticks are unable to fully engorge when feeding on a host that has been immunized against the engorgement factor proteins. If these observations can be confirmed and extended, an effective anti-tick vaccine to protect livestock and pets could be on the horizon.

Science Daily
May 15, 2007

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Parasites may help put songbirds on this European sparrowhawk’s dinner plate

In natural selection’s dance of predator and prey, predators have long been thought to target the weak and sick. But this idea has seldom been tested because it’s not easy to know the health of the prey, and how this correlates with the possibility it will be killed by a predator. However, two researchers have now zeroed in on what may make certain songbirds more likely to end up in a raptor’s talons: parasites. Danish songbirds infected with either of two parasites were more likely to end up a meal. The study also sheds light on how predation may keep such parasites in check. To determine the health of the raptors’ prey, Jan Tottrup Nielsen, an ornithologist in Sindal, Denmark, spent 27 years collecting and identifying the remains of nearly 46,000 birds from some 3200 nests of European sparrowhawks and Eurasian goshawks in the forests of northern Denmark. The sparrowhawks targeted small songbirds from 64 species including tits, thrushes, finches, sparrows, and buntings. In contrast, the goshawks went after larger prey, such as gulls, pheasants, partridges, pigeons, and starlings, killing 76 different species.

To find out whether parasites played a role in the deaths of these birds, Nielsen’s colleague, Anders Pape Møller, an evolutionary biologist at the University of Pierre and Marie Curie in Paris, calculated how prevalent such parasites are in European birds overall by compiling several published and unpublished data sets. After taking into account such factors as the abundance and size of the prey, Møller’s analysis showed that the risk of predation for prey targeted by goshawks and sparrowhawks increased by a factor of 25 if the prey birds were infected with the protozoan blood parasite Leucocytozoon. Further, birds infected with the avian malaria parasite were 16 times more likely to find themselves in the talons of a sparrowhawk.

Besides bolstering the theory that weak and sick prey are more vulnerable to being eaten, the study indicates that predation may ultimately keep the malaria parasite in check, the authors note. The severity of a malaria infection correlates with the parasite’s replication rate: The higher the rate, the more virulent the infection. In essence, Møller and Nielsen argue in their study published in this month’s issue of Ecology, the sparrowhawks are helping to keep the malaria parasite relatively benign by killing songbirds with the most virulent form of the disease. The organism is spread via mosquito bites, and so once the host is dead, so is the parasite.

The team examined “an impressive sample size,” says Dennis Murray, a population ecologist at Trent University in Peterborough, Canada. But he cautions that the duo’s reliance on the databases of other researchers to calculate both the prevalence of parasites in prey species and the relative vulnerability to predation of prey species is correlative and risky. “Ideally, one would find a partially eaten prey, test it to see if it actually has malaria, and then compare prevalence of malaria in predator-killed prey to that found in live songbirds,” he notes. “That would make their case stronger.” Still, Murray acknowledges, Møller and Nielsen have shown for a great variety of birds that a heavy load of parasites is likely to put you in natural selection’s cross-hairs.

ScienceNow
May 15, 2007

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Parasite hijacks brains with surgical precision

A mere parasite controls the fate of rats and mice by hijacking the part of the brain that makes the rodents naturally fear cats, a new study shows. Rats and mice normally flee if they smell cat urine, but not if they’re infected by the protozoan parasite Toxoplasma gondii. The parasite can only complete its life cycle if its rodent host is eaten by a cat, so it “brainwashes” the creature into apparently liking the scent. Now Ajai Vyas and his colleagues at Stanford University in California, US, have revealed that the brainwashing is surgically precise. The parasites seem to reverse the rodent’s innate fear by interfering with the amygdala, the seat of conditioned responses in the brain. Vyas’s team looked at the distribution of the parasite in the brain of infected rats, and found it was almost twice as dense in the amygdala. The exquisite precision leaves intact all other neurological mechanisms for learning to avoid danger, so the rodents learn to survive all hazards except being eaten by cats – the only form of death beneficial to the parasite.

New Scientist
April 17, 2007

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Guidelines for heartworm infection in cats updated

The American Heartworm Society released the 2007 Guidelines for the Diagnosis, Prevention and Management of Heartworm Infection in Cats. The most notable update was the inclusion of information on the newly defined heartworm-associated respiratory disease. According to the AHS, some cats never develop clinical signs of heartworm infection, but even a small number of worms can be life-threatening. When signs are evident, they usually develop either in the first stage when the heartworms enter a blood vessel and are carried to the pulmonary arteries, or in the second stage when the adult heartworms die. The AHS reported that the signs associated with the first stage are often misdiagnosed as asthma or allergic bronchitis when, in fact, they are actually a result of HARD. The second stage often leads to fatal acute lung injury.

Another highlight of the updated guidelines is information on interpreting serology test results. According to the AHS, heartworm infection is harder to diagnose in cats than in dogs, and it is easy to overlook. Diagnostic tests have limitations, so test results negative for heartworms do not necessarily rule out an infection. Antigen tests, for example, detect only adult female or dying male worms. Immature or male-only worm infections are rarely detected. To help spread the word about the updated guidelines, the AHS will embark on a public awareness campaign called KNOW Heartworms in partnership with the American Association of Feline Practitioners and underwritten by a grant from Pfizer Animal Health. Information on the campaign is available at www.knowheartworms.org. Research for the guidelines is conducted by several sources, including pharmaceutical companies, private laboratories, private-practice veterinarians, and parasitologists at several universities. The AHS then compiles all the findings to create the guidelines, which are updated on an ongoing basis. To view the guidelines, log on to www.heartwormsociety.org.

JAVMA
February 20, 2007

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Endangered primates harbour fewer parasites

Primates threatened with extinction harbour fewer parasites than their non-threatened counterparts, a new study shows. It could leave the most vulnerable more susceptible to infectious disease, the researchers say. Many primate species around the world are in danger of disappearing. Conservation efforts typically focus on habitat loss and poaching, but disease can also pose a danger, especially to populations already in trouble. In particular, outbreaks of Ebola virus are pushing Africa’s remaining gorillas and chimps to the brink of extinction. Ecologist Sonia Altizer at the University of Georgia in Athens, US, and colleagues wondered if there was a correlation between the diversity of parasites that a species hosts and its status on the Red List of threatened species published by the World Conservation Union.

The team surveyed the data from hundreds of studies with documented cases of primate infection with viruses, bacteria, protozoa, worms and insects. In total, the researchers recorded 386 species of parasites from 117 populations of primates. Threatened species hosted fewer species of parasites, probably because disease spreads less readily when animals are scarce, and their populations become geographically isolated, the researchers say. “People have debated whether endangered species experience higher or lower risk from infectious disease,” says Altizer. “This study suggests it might be lower.” But she warns that the overall lack of parasite species diversity in threatened primates could lower the animals’ natural resistance, because their immune system will not recognise new pathogens, making them more susceptible to diseases. She hopes her database will inspire field workers to gather more data on what diseases are out there and how they affect primate conservation. “We know depressingly little,” she says.

New Scientist
February 20, 2007

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A dose of worms, please

A prolonged bout of intestinal parasites seems to slow the decline of patients with multiple sclerosis, according to a study released today. The results suggest that immune-modulating molecules from parasites could be developed into drugs to ease autoimmune diseases, and that by conquering parasite infections, modern medicine may have inadvertently increased our vulnerability to these illnesses. Autoimmune diseases such as multiple sclerosis (MS) occur far more often in developed countries than in developing countries. And parasitic infections, which have been beaten down in the United States, are still common in South America and elsewhere in the developing world, says neuroimmunologist Jorge Correale of the Raúl Carrea Institute for Neurological Research in Buenos Aires, Argentina. What’s more, studies have shown that infecting mice with parasites eased symptoms of an MS-like syndrome.

To see if the parasite-autoimmune link held up in humans, Correale and his colleague Maurício Farez identified 12 MS patients with high levels of parasite-fighting white blood cells called eosinophils and then confirmed parasite infections by examining stool samples under the microscope. They tracked those patients and equal numbers of uninfected MS patients and healthy people for 4 and a half years. In MS, the immune system attacks the insulating myelin sheath of nerves, disrupting the transmission of messages. Infected patients as a group suffered just three instances of new or worsening symptoms, compared with 56 in the uninfected patients. As measured by a standard neurological test, the degree of disability increased in 11 of the 12 uninfected patients, but in only two of the 12 infected individuals.

Next, the team measured white blood cells and immune-signaling chemicals called cytokines from each patient to understand how the invaders changed the immune system. Parasite infections induced much higher levels of three types of immune cells called regulatory T cells, the researchers report in January 2007 issue of Annals of Neurology. They propose that while fighting the parasite infection, these three types of cells also happen to dial down a different arm of the immune system that attacks myelin to cause multiple sclerosis. By finding the immune-signaling molecules responsible, it may one day be possible to identify parasite molecules that deactivate the immune system arm that causes autoimmune attacks, Correale says. “It’s a provocative study, and it would be interesting to do this in a larger number of individuals,” says immunologist David Hafler of Harvard Medical School. If the results hold up, he says, it would underscore the emerging consensus that “an idle immune system is probably not good.”

ScienceNow
February 6, 2007

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Discovery may help predict when Toxoplasma can be deadly

Toxoplasma is arguably the most successful animal parasite on earth: It infects hundreds of species of warm-blooded animals, most notably half of humanity. Its unusual ability to overcome the numerous challenges of infecting and reproducing inside such a wide range of creatures has long intrigued scientists, and now researchers at the Stanford University School of Medicine have identified two of the proteins critical to its ability to thrive. The findings will be published in the Dec. 15 issue of Science by a team led by John Boothroyd, PhD, professor of microbiology and immunology. Working with mice, the researchers identified two genes that produce two proteins that Toxoplasma introduces into the cells of the host it infects. What’s more, the researchers showed for the first time that certain changes in either of the proteins – called kinases – ramped up 10,000-fold the damage that Toxoplasma inflicted on the lab mice. “This was a totally unknown phenomenon,” said Boothroyd.

Although the majority of people infected by Toxoplasma have no symptoms, it can cause severe infections in individuals with compromised immune systems. In addition, women infected for the first time while pregnant can pass the organism to their fetuses, potentially resulting in sight and hearing problems as well as learning disabilities. The new findings have implications for determining how to treat these and other infected people: More aggressive therapy may be warranted if a strain that contains the proteins that increase virulence is the cause of the infection. Humans can become infected by the parasite by accidentally consuming or inhaling the cysts from infected cat feces, by eating meat from an infected animal – especially pork, lamb or venison – or by drinking contaminated water. Cats are the primary carriers of Toxoplasma, though they rarely exhibit symptoms.

The significance of these newly discovered proteins is also highlighted in the same issue of Science by another paper with similar findings from a different group of researchers. Additional evidence of the proteins’ critical role will be offered by a paper slated to appear in an upcoming issue of Nature, in which Boothroyd and his colleagues describe the molecular underpinnings of the mechanism used by these parasites to hijack cellular processes in their hosts. “We think that the different versions of Toxoplasma strains evolved for optimal interaction with different hosts,” said Boothroyd, noting that the wrong pairing of parasite and host can have dire consequences. “If a given strain gets into the ‘wrong’ host, the result is a system out of kilter and extreme disease. It’s the bull in the china shop.”

The origins of the more virulent strains of Toxoplasma were first documented in a 2001 Science paper from Boothroyd’s group; the researchers found that the recombination of two relatively benign strains of Toxoplasma can result in a thousand-fold increase in their ability to cause serious disease. Over the last few years, the researchers have worked to track down exactly what happens to make some strains of Toxoplasma pack such an extra punch. By conducting a comprehensive scan of gene sequences of Toxoplasma strains, postdoctoral scholars Jeroen Saeij, PhD, and Jon Boyle, PhD, first authors of the paper in the Dec. 15 Science, searched for the gene or genes responsible for markedly increased virulence. To do such a survey, however, the researchers needed to produce an array of strains. Because Toxoplasma strains only recombine in cats, the researchers provided mice infected with different Toxoplasma strains for the cats to eat. The researchers then took the resulting recombinant strains from the cats and infected other mice with them. Based on how these mice fared, the researchers could pinpoint stretches of DNA that contain the genes underlying severe virulence. Based on the DNA sequences, they could determine the proteins involved.

From 140 candidate proteins identified in the initial screen, they focused on those with qualities logically involved in differing levels of virulence, such as high variability of the sequence and the ability to be secreted from the organism to enter the host. This led them to two particularly compelling proteins – ROP16 and ROP18. Both are protein kinases, molecules that are used in the transmission of cellular messages. “If a parasite needs to co-opt a host cell for its own purposes, there is no better way than to introduce a kinase that can completely alter the entire physiology of that host cell,” said Boothroyd. The findings may play a role in helping pregnant women who become infected for the first time with the parasite. If doctors can test whether the women have one of the more virulent strains, they can then better assess the risks to the fetuses. The group’s further exploration of the Toxoplasma virulence process may also have implications for immune-system modulating drugs that could specifically dampen the effects of toxoplasmosis.

Science Daily
January 9, 2007

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Study shows hot, dry air device eradicates head lice

University of Utah biologists invented a chemical-free, hairdryer-like device — the LouseBuster — and conducted a study showing it eradicates head lice infestations on children by exterminating the eggs or “nits” and killing enough lice to prevent them from reproducing. The study — published in the journal Pediatrics — “shows our invention has considerable promise for curing head lice,” says Dale Clayton, a University of Utah biology professor who led the research and co-invented the machine. It is particularly effective because it kills louse eggs, which chemical treatments have never done very well,” he says. “It also kills hatched lice well enough to eliminate entire infestations. It works in one 30-minute treatment. The chemical treatments require multiple applications one to two weeks apart. “The LouseBuster now is in early stages of commercial development by a University of Utah spinoff company, Larada Sciences, for which Clayton is chief scientific officer. Patents are pending on the LouseBuster technology, which Clayton hopes will be on the market within two years for use in schools and clinics.

“Each year, millions of children are infested with head lice, a condition known as pediculosis, which is responsible for tens of millions of lost school days,” the study’s authors write. “Head lice have evolved resistance to many of the currently used pediculicides [insecticide shampoos]. … Hot air is an effective, safe treatment and one to which lice are unlikely to evolve resistance.” The device blows warm air through a flexible hose, which has a rake-like hand piece on the end. It apparently kills lice and nits by drying them out, not by heating them. Clayton urges parents not to use hair dryers to try to kill head lice. “We don’t want kids getting burned by parents who think it’s the heat” that kills lice, he says. “This thing is actually cooler than a hair dryer, but requires twice as much air flow, and the special hand piece is critical because, unless you expose the roots of the hair, it doesn’t work. And it’s difficult to do that with a regular comb.” “The cool thing about the machine is, it works — unlike many other treatments that haven’t been rigorously tested,” Clayton says. “It came out of basic research, completely unplanned.” Clayton’s research focuses on birds and the lice that infest them. But when he moved to the University of Utah in 1996, he couldn’t keep lice alive on laboratory birds because Utah’s air was too dry. He had to humidify bird rooms to keep lice alive.

About the same time, his two children — Mimi and Roger, now 13 and 15, respectively — got head lice, “and we wondered if there was a way to kill head lice by drying them out,” Clayton says. “We started trying different methods of desiccation using hot air like conventional hair dryers, but those didn’t work well.” In the new study, the researchers tested six ways of applying hot air to children’s lice-infested scalps. The tests were conducted during 2001-2005 on 169 infested children who were solicited for the study by flyers distributed in dozens of Salt Lake Valley schools. The study was approved by the university’s Institutional Review Board, which reviews research involving human subjects. Parents and children signed consent forms. Children were excluded from the study if they had used other head lice treatments within the previous two weeks. Clayton dispatched his students in pairs to the homes of infested children to test the various methods. After completion of each treatment trial, each participant was paid $10 and given conventional treatments for lice.

Some 94 percent of the children were girls, who are more likely to have bad infestations because their hair is longer and they have more head-to-head contact on the playground, Clayton says. Before treatment, the researchers combed one side of each child’s head to remove all visible lice and nits, which were placed in an incubator. Then, the entire scalp was treated with one of the six methods being tested. After treatment, the other side of the scalp was combed for the same amount of time as the first side, with removed lice and nits also placed in an incubator. The researchers used a dissecting microscope to count the number of live and dead lice from each side of the scalp. They re-examined them up to 18 hours later to make sure all were dead. Nits were incubated for two weeks to see how many hatched.

“Effectiveness of the different treatment methods was assessed by comparing the percentage of dead lice and non-hatching eggs on the pre- and post-treatment sides of the scalp,” the researchers explain. The researchers measured the temperature and volume of hot air in each method and kept track of any discomfort. No household cleaning measures were taken because they are not considered essential; head lice cannot survive more than 24 hours off a host’s head. Each of the six treatment methods took 30 to 35 minutes and used air at about 140 degrees Fahrenheit. Here are the treatments, from least to most effective:

— Air hoses from two bonnet-style hair dryers fed air into one bonnet. This method killed only 10 percent of hatched lice but 89 percent of eggs.
— A handheld blow dryer was used to apply diffuse heating. Each child’s hair was divided into ten sections using hair clips, and the base of each section was heated three minutes while the dryer was moved to ensure even heating. This method killed only 21 percent of lice but 97 percent of eggs.
— A handheld blow dryer was used to apply directed heating. Hair clips were used to divide each child’s hair into 20 sections. The dryer was held still for 30 seconds to heat one side of each section, then held still another 30 seconds to heat the other side. This method killed 55 percent of lice and 98 percent of eggs.
— A hose was attached to a wall-mounted blow dryer like those in public restrooms. The dryer was put on a table, and the hose used to treat hair divided into 20 sections. The method’s larger air volume killed 62 percent of lice and 97 percent of eggs.
— With the hair divided into 14 to 20 sections, a LouseBuster without a hand piece was used to treat each section with diffuse heat for 60 seconds. Air speed was similar to the wall dryer. This technique killed 76 percent of lice and 94 percent of eggs.
— Aplastic hand piece with 10 coarse teeth (not like fine-toothed nit combs) was attached to the end of the LouseBuster hose and raked through hair while hot air blew the opposite direction. All areas of the scalp were raked and exposed to hot air for at least 30 seconds. The LouseBuster with the handpiece killed 80 percent of hatched lice — a larger proportion than any of the other five methods — and 98 percent of louse eggs.

The 80 percent kill rate was high enough to prevent remaining lice from breeding — possibly due to stress or sterilization — so “virtually all subjects were cured of head lice when examined one week following treatment with the LouseBuster,” the scientists write. Children and their parents reported none of the treatments had adverse effects. Kids reported less discomfort from the LouseBuster than from any other method. Clayton estimates it cost $500,000 to develop and test the LouseBuster, with funding from the Utah Centers of Excellence program, University of Utah, Primary Children’s Medical Center Foundation and the National Pediculosis Association.

Each year, 6 million to 12 million Americans are infested with head lice, making children miss 12 million to 24 million school days, the researchers say. “Although head lice do not produce an illness per se, they are physically and psychologically unpleasant for the child and an exasperating problem for parents and school authorities,” the scientists write. Treatments have been chemical shampoos, louse combs and home remedies. Annual U.S. sales of anti-louse shampoos exceed $160 million, yet the shampoos are not very effective at killing nits, requiring repeat treatment. Many parents dislike using insecticide shampoos on children, and lice rapidly are evolving resistance to chemicals. Louse combs are used to remove the eggs or nits, an effective procedure, but one that requires many hours over several days. “Most parents do not have the time or patience to comb out all the lice and eggs,” Clayton and colleagues write. Some parents resort to home remedies such as bug spray, mayonnaise or kerosene. “These remedies can harm the child and there is little hard evidence that they are effective,” the researchers say. Some of the scientists’ relatives got infested during the study. Clayton’s kids, Mimi and Roger, volunteered to be infested with lice and then were treated successfully. “They like to shock their friends by telling them they served as guinea pigs in their dad’s research,” Clayton says. “I’m waiting for the authorities to show up. They haven’t yet.”

Science Daily
November 21, 2006

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Bacterial protein shows promise in treating intestinal parasites

Scientists at the University of California, San Diego and Yale University have discovered that a natural protein produced by Bacillus thuringiensis, a bacterium sprayed on crops by organic farmers to reduce insect damage, is highly effective at treating hookworm infections in laboratory animals. Their discovery, detailed in this week’s early online edition of the Proceedings of the National Academy of Sciences, could pave the way for the development of more effective treatments for hookworm and other soil-transmitted nematode infections, which are a major global health problem in developing countries. Many of the nearly two billion people worldwide infected with these intestinal parasites are children, who are at particular risk for anemia, malnutrition and delayed growth.

The UCSD-Yale team found that a protein produced by the bacterium Bacillus thuringiensis, or Bt, given orally to laboratory hamsters infected with hookworms was as effective in eliminating the parasites, curing anemia and restoring weight gain in the hamsters as mebendazole, one of the drugs currently recommended to treat infections in humans. The scientists also discovered that this protein, called Cry5B, targets both developing, or larval, stages and adult parasites, as well as impairs the excretion of eggs by female worms. Hookworms cause anemia by attaching to the intestine and feeding on their host’s blood and nutrients, causing anemia and weight loss. The researchers said in their paper that because this naturally-produced protein is safe to humans and other vertebrates and can be produced inexpensively in large quantities, it has the potential to substantially improve this global health problem.

“Our ability to control parasitic nematode infections with chemotherapy on a global scale is dependent on the availability of medicines that are safe, effective, and inexpensive to manufacture,” said Michael Cappello, one of two principal authors of the study and a professor of pediatrics and epidemiology & public health at Yale School of Medicine. “We believe that Bt crystal proteins not only meet, but exceed these essential criteria.” The discovery is particularly relevant to global health, because of concerns about the potential emergence of resistance in human intestinal nematodes to currently available medicines. “There are only a few new agents under development for the treatment of hookworm and other intestinal parasite infections,” said Raffi Aroian, an associate professor of biology at UCSD and co-principal author of the study. ” Crystal toxins are safe to humans, mammals and other vertebrates. And it might be possible to improve the efficacy of current treatments by giving a drug like mebendazole and Cry5B simultaneously.”

Science Daily
October 10, 2006

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Deer-free areas may be haven for ticks, disease

Excluding deer could be a counterproductive strategy for controlling tick-borne infections, because the absence of deer from small areas may lead to an increase in ticks, rapidly turning the area into a potential disease hotspot, according to a team of U.S. and Italian researchers. “Deer are referred to as dilution hosts or dead-end hosts,” says Sarah Perkins, a postdoctoral researcher at Penn State’s Center for Infectious Disease Dynamics. “They get bitten by ticks but never get infected with tick-borne pathogens, such as the bacteria causing Lyme disease.”

However, deer are critical to adult female ticks in the last stages of their three-part lifecycle. Ticks use them for a final blood meal before dropping off to produce thousands of eggs, Perkins explains. Currently, health officials believe that removing deer from the equation could disrupt the tick lifecycle and leave fewer ticks to feed on rodents, which, unlike deer, can transfer a range of tick-borne pathogens. Ultimately the tick-borne disease will fade out. However, previous field studies show that removing deer sometimes leads to higher tick densities and sometimes lower, and the outcome seems dependent on the size of area from which deer are excluded. “Very few studies have looked at how removing the deer affects the intensity of tick bites on rodents, and how it relates to the size of the area from where the deer are excluded,” explains Perkins, whose findings are published in the current issue of the journal Ecology.

Researchers first collected data from published information on tick densities in deer excluded areas ranging in size from roughly 2.5 acres to 18 acres. Next, over a six-month period, they captured rodents from a 2.5-acre deer excluded area in the Italian Alps in a known hotspot for tick-borne encephalitis — a disease passed to humans through the bite of an infected tick. “From previous studies we found that tick densities decreased in (geographically) large areas and increased dramatically in smaller areas,” suggesting that there is a threshold area – from where deer are excluded – for tick populations to either increase or decrease, notes the Penn State researcher.

Statistical analyses of ticks on the captured rodents indicated that compared to the control areas, the deer-excluded areas hosted a significantly higher number of nymph and adult female ticks, as well as a high prevalence of tick-borne encephalitis. Because tick-borne encephalitis is transmitted only between ticks feeding on these rodents, the findings suggest how small deer-free areas could quickly turn into a disease hotspot. “This goes somewhat against conventional wisdom. When you remove deer, it does not always reduce the tick population,” says Perkins. “If you were to exclude deer from hundreds of acres, tick numbers will fall. But in an area less than 2.5 acres, you are more likely to increase tick density and probably create tick-borne hotspots.”

Researchers say the study demonstrates how the strategy of keeping deer away may work only for large areas but is likely to amplify tick populations in smaller areas. Fragmented patches of forest and small parks that are off-limits to deer could also turn into a disease reservoir, they caution. “We need to be cautious about keeping deer away from small areas, even people’s backyards, as it might only lead to more ticks that are infected with tick-borne pathogens,” says Perkins. She adds that forest areas deer consistently avoid also have the potential of turning into a haven for tick-borne disease.

Pennsylvania State University
September 12, 2006

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Scientists prepare an innovative vaccine against leishmaniasis

Universitat Autonoma De Barcelona researchers working in collaboration with the INIA (National Institute of Agricultural and Food Research and Technology) and Germans Trias i Pujol Hospital in Badalona, near Barcelona, are developing the first vaccine against leishmaniasis produced using insect larvae. The new vaccine is based on introducing specific genes and proteins from the protozoan Leishmania infantum into the patient. Although it is currently in the preliminary phase, scientists believe it could be much more effective than conventional vaccines.

Leishmaniasis is one of the biggest global health problems. In our part of the world, it is produced by the protozoan Leishmania infantum, and dogs are the main reservoir. The disease is spread through the bites of the phlebotomy, an insect similar to the mosquito. Clinical manifestations go from light skin lesions to visceral complications and even death. The disease affects more than 12 million people in the world, and 250 million more are at risk. Current treatments are not satisfactory, and although an effective vaccine would be the best way to confront the disease, conventional vaccines have failed.

UAB researchers working in collaboration with the INIA and Germans Trias i Pujol Hospital are working on the development of an unconventional vaccine that could be more effective in treating the disease. In an effort to make the vaccine as specific as possible, the researchers are conducting epidemiological tests on dogs and humans to find out whether the degree of the illness and the differences between regions, species (dog or humans) and infected individual persons are related to the presence of different antibodies against the infectious agent, the protozoan Leishmania infantum.

To create the vaccine and the reagents used in the epidemiological studies, the scientists have isolated the protozoan gene and inserted it into a virus that affects insects (baculovirus) and have infected the larvae of a small worm (Trichoplusia ni) with them. These larvae act as bioreactors and produce large quantities – and at a much lower cost than with conventional reactors involving microorganisms – of the proteins that are codified by these genes and are responsible for the production of antibodies in those affected. Each person would be administered a DNA vaccine with the genes that codify for the proteins of the protozoan that generates most antibodies in the geographical region. Later, the person would be vaccinated again, but this time directly with the proteins associated with the genes (produced cheaply in insect larvae). The aim is to increase effectiveness. The vaccines could be used as prevention or therapeutically.

“Selectivity for each individual and the combination of the vaccination with DNA and protein will probably make this new vaccine much more effective than current ones. Furthermore, the method of producing them in insect larvae would considerably reduce the costs,” explains Jordi Alberola, the main researcher for the project.

Science Daily
August 1, 2006

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Researchers get to heart of leishmaniasis

A new study found that mice lacking a gene crucial to the normal functioning of their immune systems didn’t become ill when they were exposed to a pathogen that causes a horrendous infection in the liver and the spleen. The pathogen, called Leishmania donovani, infects certain internal organs. The parasite causes visceral leishmaniasis which, if left untreated, is almost always fatal. Cases in the United States are extremely rare, but the disease, which is transmitted through the bite of a sand fly, is common in tropical and subtropical countries such as Iraq, Iran and Afghanistan.

The finding may lend insight into creating new drugs to treat different diseases that affect the liver, said Abhay Satoskar, the study’s lead author and an assistant professor of microbiology at Ohio State University. The gene makes a protein called STAT1, and its production is triggered whenever the immune system senses a foreign bacterium, virus or other pathogen. STAT1 activation is a critical step in the immune system response, as this protein activates other key immune substances. So it didn’t make sense to the researchers that mice that couldn’t produce STAT1 would remain healthy. “It took us completely by surprise,” Satoskar said. “We knew from previous work that mice that lack the substances produced in response to STAT1 develop serious infections. We thought we’d see that in this study, too.” The study appears as a Cutting Edge paper in the July 1 issue of the Journal of Immunology website.

The researchers infected groups of mice with L. donovani. Mice in one group lacked the gene that makes STAT1. Mice in another group lacked the gene that makes an immune system protein called T-bet. In a normal immune response to infection, STAT1 triggers the production of T-bet. Together, these proteins are responsible for the production of interferon gamma, an important protein that helps launch a full-blown immune system attack against foreign pathogens. A group of mice with both STAT1 and T-bet genes intact served as a control.

About two weeks after infection, the researchers began measuring the number of L. donovani parasites in the animals’ livers. The pathogen went wild in the mice that lacked T-bet – the researchers found thousands upon thousands of the parasites in the livers of these animals. Yet there were next to no parasites in the mice without STAT1. “Two weeks after infection, the mice without STAT1 had 25-fold fewer parasites in their liver tissue than the normal mice, and about 100-fold fewer parasites than the mice without T-bet,” Satoskar said. “Visceral leishmaniasis never developed in the animals without STAT1 – the parasites weren’t able to establish an infection in the animals’ livers and spleens.”

The researchers also measured parasite levels in the livers two months after infection. Again, levels were quite high in the mice without T-bet, while normal mice and mice without STAT1 showed no sign of the disease. While the normal mice weren’t sick – they showed no physical signs of having leishmaniasis, such as inflammation of the liver and spleen – Satoskar said the parasite was still in their systems. “Once infected, the parasite never goes away completely,” Satoskar said. “It’s always hiding somewhere.”

Ironically, L. donovani thrives in the liver and spleen by infecting the very cells that the immune system uses to rid the parasite from the body. These cells are called macrophages – a kind of garbage collector for the immune system, as they clean out everything from red blood cells that have died to infectious pathogens. But enough L. donovani parasites can overtake a macrophage’s ability to clean up. “L. donovani infection failed to launch in mice without STAT1 because there weren’t enough macrophages in the liver for the parasite to infect, and these are the very immune cells that are essential for successful survival and replication of Leishmania parasites in the host,” Satoskar said.

The researchers aren’t suggesting that STAT1 activation should be stopped in order to prevent visceral leishmaniasis. However, they want to figure out how this protein’s absence keeps macrophages from flooding into the liver during the early stages of infection. If they can do that, it may be possible to create a drug to prevent L. donovani from infecting the liver and the spleen. Although there are medications available to treat the symptoms of visceral leishmaniasis, they can be toxic and sometimes expensive for the people who need them the most.

Science Daily
July 18, 2006

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Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm

The three main soil-transmitted helminth infections, ascariasis, trichuriasis, and hookworm, are common clinical disorders in man. The gastrointestinal tract of a child living in poverty in a less developed country is likely to be parasitised with at least one, and in many cases all three soil-transmitted helminths, with resultant impairments in physical, intellectual, and cognitive development. The benzimidazole anthelmintics, mebendazole and albendazole, are commonly used to remove these infections. The use of these drugs is not limited to treatment of symptomatic soil-transmitted helminth infections, but also for large-scale prevention of morbidity in children living in endemic areas. As a result of data showing improvements in child health and education after deworming, and the burden of disease attributed to soil-transmitted helminths, the worldwide community is awakening to the importance of these infections. Concerns about the sustainability of periodic deworming with benzimidazole anthelmintics and the emergence of resistance have prompted efforts to develop and test new control tools.

The Lancet
May 23, 2006

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Scientists step closer to new treatments for river blindness

Veterinary scientists in Liverpool have found that some African cattle have natural immunity to a parasite, similar to that which causes River Blindness in humans. These new findings, by scientists at the University’s Faculty of Veterinary Science and the Liverpool School of Tropical Medicine, indicate that it may be possible to vaccinate humans against River Blindness. The disease causes blindness in thousands of people in some of the poorest countries in the world, particularly in West and Central Africa.

River Blindness, or Onchocerciasis, is caused by a parasitic worm and leads to severe itching of the skin and lesions of the eye which can result in blindness. The parasite is spread by black flies which breed in rivers and deposit the larvae of the worm into the person they bite. The disease develops over a long period of time, particularly in young adults, eventually preventing them from working and farming and hence feeding themselves and rearing their families.

Professor Sandy Trees, at the University’s Faculty of Veterinary Science, said: “Onchocerciasis has been the target of major international efforts to control and ultimately eradicate it, but it still presents a huge burden to health in many impoverished countries. To see if a vaccine is feasible for the disease we looked at whether immunity exists naturally and whether it can be induced.” The team investigated immunity in cattle infected with a very closely related worm – Onchocerca ochengi – that causes lumps to appear on the animal’s skin but does not cause blindness or illness. Examining infected cattle in Cameroon, the team found that some cows naturally develop resistance to Onchocerca ochengi.

They also showed that cattle which were normally susceptible to infection could be successfully immunised using a vaccine composed of minute parasite larvae, weakened by a controlled dose of radiation in the laboratory. After two years of natural exposure to infected black flies, the number of worms in vaccinated cattle was far lower than in unvaccinated animals. Professor Trees added: “Although the immunisation method that we tested in cattle would not be suitable for human use, this research provides the first proof that immunisation against onchocerciasis is possible and hence it may be feasible to protect humans from the parasite using some form of vaccination.”

There is currently no safe drug available to cure the disease fully as treatments only kill the young Onchocerca volvulus worms and not the adults. Researchers are now looking to further understanding of how some cattle develop natural immunity when some do not, which will assist in targeting potential treatments for River Blindness. The research, funded by the Edna McConnell Clark Foundation, is published in Proceedings of the National Academy of Sciences.

Science Daily Health & Medicine
May 23, 2006

Original web page at Science Daily Health & Medicine

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Shift in feeding behavior of mosquitoes sheds light on West Nile virus outbreaks

Since its introduction to the United States in 1999, West Nile virus has become the major vector-borne disease in the U.S., with 770 reported deaths, 20,000 reported illnesses, and perhaps around a million people infected. The virus is transmitted by Culex mosquitoes (the “vector”) and cycles between birds that the mosquitoes feed on. Humans can also be infected with the virus when bitten by these mosquitoes. Scientists have struggled to explain these large outbreaks in the U.S., which stand in stark contrast to the sporadic European infections. In a new study published in the open access journal PLoS Biology, Drs. Marm Kilpatrick, Peter Daszak, and colleagues now present evidence that the major vector of West Nile virus in the USA, Culex pipiens mosquitoes, change their feeding behavior in the fall from their preferred host, American robins, to humans, resulting in large scale outbreaks of disease.

These feeding shifts appear to be a “continent-wide phenomenon,” the researchers conclude, and may explain why West Nile virus outbreaks are so intense in the U.S. compared to Europe and Africa, where the virus originates. From May through September 2005, Dr. Kilpatrick, senior research scientist with the Consortium for Conservation Medicine, and his team collected mosquitoes and caught birds at six sites in Maryland and Washington, D.C. They determined the changes in mosquito populations throughout the West Nile virus transmission season, the abundance and diversity of bird species at these sites, and tested samples for West Nile virus. Dr. Kilpatrick says, “To find out which species mosquitoes favored as hosts, we collected thousands of Culex pipiens mosquitoes and selected those that had just fed and still had bloodmeals in them. We sequenced the DNA in the bloodmeal to identify the species of host they had fed on.”

Their findings showed that from May to June, the American robin, which represented just 4.5% bird population at their sites, accounted for more than half of Culex pipiens’ meals. As the summer wore on and robins left their breeding grounds, the probability that humans were fed on increased sevenfold. Because the overall number of birds increased during this time, Kilpatrick and his team concluded that mosquitoes changed to humans as a result of robin dispersal, rather than a lack of avian hosts. “This feeding shift happened, even though the total number of birds at our site increased as other species’ offspring joined the population,” said Kilpatrick.

With the data collected from the Washington, D.C., area, the researchers presented a model of the risks of infection of the West Nile virus in humans. The model predicted that the risk of human infection peaked in late July to mid-August, declined toward the end of August, and then rose slightly at the end of September. The actual human cases in the area that year, the authors point out, “showed a strikingly similar pattern.” This same pattern was seen in California and Colorado, with numbers of infected Culex tarsalis mosquitoes (the main vectors in the western USA) peaking in June and July, followed by a late-summer spike in human infections, suggesting a continent-wide phenomenon.

Dr. Peter Daszak, Executive Director of the Consortium for Conservation Medicine, comments: “This is a case study in how to understand emerging diseases. Our collaborative team includes ecologists, virologists, and entomologists, and uses state-of-the-art techniques, including DNA sequencing of mosquito blood meals, to piece together what drives a virus to cause outbreaks in people. At the CCM we study the ecology of diseases and develop predictive models that can help us prevent future outbreaks. We are now using this approach to help understand the emergence and spread of other viruses such as SARS, Nipah virus and avian influenza.”

Science Daily Health & Medicine
April 25, 2006

Original web page at Science Daily Health & Medicine

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A case of mistaken molecular identity

Researchers in Argentina have determined that night blindness is a new clinical symptom of Chagas disease. A team led by Howard Hughes Medical Institute (HHMI) international research scholar Mariano Jorge Levin and Cristina Paveto of the Institute for Genetic Engineering and Molecular Biology (INGEBI), National Research Council, National Council of Scientific Research and Technology in Buenos Aires, found that the immune system of individuals with the tropical disease can shut down a key reaction in the retina, causing night blindness. Triatomine bug, Trypanosoma cruzi vector, defecating on the wound after taking a blood meal. “This is a new observation, a new clinical symptom of Chagas disease,” said Levin, head of the Laboratory of the Molecular Biology of Chagas Disease at the University of Buenos Aires, Argentina. Levin and colleagues report their findings in the March 2006, issue of the FASEB Journal.

Chagas disease affects people living in regions of Latin America where insects carrying the parasite Trypanosoma cruzi thrive in crowded and substandard housing. At night, the insects emerge and bite, transferring the Chagas parasite into a new host. Their victims are often children. After an acute infection characterized by swollen eyelids, those infected usually feel better. But the parasite remains active inside them, in a chronic phase of infection, quietly invading cells and stimulating the immune system. As a result, people can develop heart and gastrointestinal problems months or years after being infected. Some 30,000 people die each year from Chagas disease, according to the World Health Organization, but the number of people who are carrying latent infections is unknown.

“We now know that Chagas patients may have trouble seeing at night,” said Levin. “And this gives us additional motivation to improve conditions for people living in areas where Chagas disease is common.” Silvia Matsumoto, a physician from the Dr. Teodoro Alvarez Hospital in Buenos Aires and first author of the paper, launched the investigation after noticing Chagas patients complaining about vision problems. “This was her idea, that the same antibodies that touch the heart cells might also block rhodopsin,” said Levin.

Matsumoto conducted thorough eye examinations of 45 Chagas disease patients with heart problems. She found that under bright conditions, the Chagas patients performed comparably to 50 healthy control individuals. But in the dark, 37 of 45 (82 percent) Chagas patients had trouble seeing with at least one eye, and 19 of 45 (42 percent) had trouble with both eyes. Matsumoto then approached Paveto, and both contacted Levin, whose laboratory was well-stocked with antibodies from Chagas patients and who had already developed the tests needed to study molecular mimicry. In previous research, Levin and colleagues showed that the immune systems of patients infected by T. cruzi generate antibodies that attack the parasite but also cause damage to heart cells. Levin suspected “molecular mimicry” as the cause of the misguided attack. Molecular mimicry occurs when a molecule that is part of an infectious agent resembles a molecule native to the body. Eventually, the immune system begins to mistake the native molecule for the invader. Levin’s investigations revealed that an intra-cellular T. cruzi protein resembles the beta1-adrenergic receptor on the surface of heart cells, a finding that helped explain why Chagas patients develop certain heart problems.

Now, it turns out, molecular mimicry can also upset the delicate machinery inside retinal cells. Levin and his team found that antibodies geared to attack T. cruzi also block rhodopsin, a molecule that converts light into electrical impulses sent to the brain. “Rhodopsin takes light and transforms it — that’s its function,” said Levin. To demonstrate molecular mimicry in the retina, Paveto extracted rhodopsin from cow’s eyes. Through a series of tests, the team showed that cow rhodopsin, which is similar to the human protein, reacts with antibodies produced by Chagas patients.

“We showed that the same antibodies that attack heart cells can also interfere with rhodopsin,” Levin said. “This is important, because it enlarges the concept of molecular mimicry in Chagas disease.” Rhodopsin and beta1-adrenergic receptors in heart cells belong to the same class of molecules, a subfamily of the G-protein-coupled receptors, he pointed out. Paveto, an independent researcher at INGEBI–an institute that is home to three HHMI international research scholars–conducted much of the painstaking work on the project by developing an original method to test rhodopsin function, said Levin.

Levin said that Chagas patients’ vision problems are caused exclusively by the antibodies that block rhodopsin, and not by inflammation. “In the hearts of Chagas patients, we see scarring because there is a complex reaction that causes inflammation,” he said. “But there are no such scars in the eyes of Chagas patients with reduced vision.” “No one knew about the night blindness, so we don’t know, for instance, if Chagas patients have more accidents at night,” Levin added. “That’s one of many ideas to explore now. The research also points out that we need new drugs or vaccines to stop the parasite, and at a social level, it stresses the need to improve living conditions of Chagas patients, particularly those living in rural areas.”

Science Daily
March 14, 2006

Original web page at Science Daily

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Candidate hookworm vaccine shows benefits in dogs

A paper published in this week’s PLoS Medicine shows that vaccination against a protein secreted by the dog hookworm can protect against blood loss and anaemia caused by the same hookworm in dogs. The researchers, led by Alex Loukas and Peter Hotez, showed that vaccination of dogs with recombinant Ac-APR-1, an enzyme that starts the digestion of hemoglobin in hookworms, induced an immune response and resulted in significantly reduced hookworm burdens and fecal egg counts in vaccinated dogs compared to control dogs after challenge with infective larvae of the hookworm Ancylostoma caninum. Most importantly, vaccinated dogs were protected against blood loss and most did not develop anemia, the major result of hookworm disease.

Hookworms are intestinal parasites of mammals, including humans, dogs, and cats; in humans these infections are a leading cause of intestinal blood loss and iron-deficiency anemia. Hookworm infections occur mostly in tropical and subtropical climates and are estimated to infect about 1 billion people worldwide– about one-fifth of the world’s population. People who have direct contact with soil that contains human feces in areas where hookworm is common are at high risk of infection; because children play in dirt, they are at the highest risk.

These results set the stage for the next stage of vaccine development in humans. Loukas and colleagues suggest that the ideal hookworm vaccine would be a mixture of two recombinant proteins, targeting both the infective larva and the blood-feeding adult stage (as targeted here) of the parasite. Such a vaccine would limit the amount of blood loss caused by feeding worms and maintain normal levels of hemoglobin.

Science Daily
November 8, 2005

Original web page at Science Daily

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“Whale lice” genes offer clues to whale evolution

Right whales always swim with passengers aboard: small benign parasites called cyamids. The creatures, which 19th-century whalers nicknamed “whale lice,” have coexisted with the whales for millennia. Now scientists at the University of Utah say they can use data about the evolution of these tiny crustaceans to reveal useful facts about the history of right whales. For example, the differences between certain genes in whale lice groups suggest that the right whale separated into three distinct species five to six million years ago.

“Cyamid populations on opposite sides of the Equator appear to have been fully (or almost fully) isolated for several million years,” the study authors write. “This finding strongly supports the view that the North Atlantic, North Pacific, and southern right whales also have been isolated for several million years and therefore should be considered distinct species.” The researchers report their findings in the October issue of the journal Molecular Ecology.

Whale lice don’t live freely in the water—they spend their entire lives on whales. The lice move from mother to calf and among whales in close contact with each other. The three types of right whale each carry three distinct species of cyamid that live in separate ecological niches on the whale’s body. Cyamus ovalis occupies the whale’s callosities, the distinctive patches of raised and roughened skin on the whale’s head. Another louse species, C. gracilis, lives in the pits and grooves between the callosities, while C. erraticus takes refuge in the smooth skin of the genital and mammary openings. The animals are small, measuring roughly one-fifth to three-fifths of an inch (one to two centimeters) long. About 7,500 of these hitchhikers live on a single whale, making their colonies large enough to be visible as white patches on a whale’s head and body.

National Geographic
October 25, 2005

Original web page at National Geographic