Tag Archives: parasite

Wait, this isn’t sushi! It’s a blood-sucking sea parasite

Credit: Aquamarine Fukushima.

One of the most popular attractions at the Aquamarine Fukushima, a large aquarium in eastern Japan, is oddly enough a sea parasite that looks like a piece of salmon sushi with 14 legs.

The inch-long creature belongs to an order of armored-plated crustaceans known as isopods, which are plentiful both on land and sea. The spineless creature is related to crabs, shrimp, lobsters, and other actual seafood you might see on the menu of a sushi restaurant.

The sushi-shaped superstar at the Aquamarine Fukushima likely belongs to the Rocinela genus, home to more than 40 species. While most isopods feast on dead or decaying animals, Rocinela members tend to be parasites that piggyback on sea creatures and consume their tissue for food.

But while the vast majority of isopods look rather dull and brown in color, the cutest parasite in a Japanese aquarium sports a bright salmon-like color. The specimen was recovered from waters off the coast of Rausu in Japan’s northernmost island Hokkaido, at a depth of 800 to 1,200 meters. Its bright color may be owed to pigments and other substances consumed in the fish it hitched a ride on.

We may never know what animal the isopod was feeding on since the fishermen caught it in a gillnet. Whatever it fed on, though, it must have offered a plentiful bounty judging from the isopod’s protruding belly.

“Its belly is still swollen, which means it’s probably full from when it was still a parasite and feeding on another animal. When its belly gets flatter, that means it’s hungry,” Mai Hibino, a caretaker at the Aquamarine Fukushima, told VICE.

While the sushi-like creature on display at the aquarium has captured the hearts of thousands of visitors, isopods are no joke — they’re quite gruesome parasites. For instance, while scanning the head of a fish, Rice University biologist Kory Evans was startled to find an isopod inside. The parasite had eaten and replaced the tongue of the fish.

This parasite can eat the tongue of a fish and then take its place

Rice University biologist Kory Evans started his Monday like any other day, expecting it to be largely uneventful. He was wrong.

His day was about to change when he started scanning the head of a fish, which is not uncommon in his work. But what was uncommon what was inside the fish’s head. A crustacean had eaten and replaced the tongue of the fish.

Credit Kory Evans


The crustacean in case is an isopod, also known as tongue biter or tongue-eating louse, and it sucked the blood from the tongue of the fish, releasing an anticoagulant maintain the flow of blood even as there’s almost nothing left of the tongue. But that’s just the opening act — it gets much worse.

Then, the isopod takes the role of the tongue in the mouth of the fish.

The discovery was done by Evans, who works at the Department of BioSciences at Rice University in Houston, Texas, when digitizing the X-rays of the fish skeletons. He posted the images of the finding on Twitter, joking about the whole situation. “Mondays aren’t usually this eventful,” Evans joked in the tweet.

There are around 10,000 known species of isopods and a surprisingly large number of them have adapted to eat tongues: about 380 go after the tongues of specific fish. It’s not entirely surprising since isopods are one of the most morphologically diverse of all the crustacean groups, coming in many different shapes and sizes and ranging from micrometers to a half meter in length. About half of the known species of isopods live in the ocean.

Masquerading as a tongue

The specific type that Evans encountered enters the body of the fish through the gills, attaches to the tongue and starts to feed.It grabs the tongue with its seven pairs of legs and takes out the blood until the organ drops off.

But that’s just the start. Having already taken out the blood from the tongue, the parasite acts as a functional tongue for the fish, taking its place and feeding on its mucus. The link between the two can go on for years, with cases reported of fishes outliving their parasites, according to researcher Stefanie Kaiser. Not much is known about how these isopods reproduce, but the most common theory is something to behold. Researchers believe that juveniles that first attach to the gills of a fish become males. As they mature, they become females, likely mating on the gills of fish.

Speaking with Live Science, Evans said he made the discovery as part of his current research, which involves scanning a family of coral reef fishes called wrasses.

He aims at creating a 3D X-ray database of skeletal morphology of the fish group and then share it with researchers from around the world.

Credit Kory Evans

“I compare skull shapes of all these different fish to each other, that requires placing landmarks — digital markers — on different parts of the body,” Evans explained. He looked into the mouth cavity of one specific wrasse, a herring cale (Odax cyanomelas) from New Zealand, and found something strange.

“It looked like it had some kind of insect in its mouth. Then I thought, wait a minute; this fish is an herbivore, it eats seaweed. So I pulled up the original scan, and lo and behold, it was a tongue-eating louse,” he said, explaining that wrasses are actually a very strange fish with a second set of jaws on their throat.

It’s like being in the movie Alien, Evans said. Some wrasses known as parrotfish even have mouths so strong that they can bite through the coral. The slingjaw wrasse, for example, can launch its jaws forward up to 65% the length of its head in order to catch evasive pray.

A disease you might not have heard of is on track for elimination

Human African trypanosomiasis (HAT), also known as sleeping sickness, is a parasitic disease that attacks the central nervous system, causing severe neurological disorders and death if left untreated. It is transmitted by the bite of the ‘Glossina’ insect, commonly known as the tsetse fly.

The disease mostly affects poor populations in rural areas where agriculture, fishing, animal husbandry, or hunting are the main source of livelihood. Typically, HAT is not found in urban areas, although cases have been reported in suburban areas of big cities in 36 sub-Saharan African countries where the disease is endemic. Travelers also risk becoming infected if they go to regions where the insect is common.

HAT wreaked havoc in Africa at different times in the 20th century but over the past twenty years, huge efforts made by a broad coalition of stakeholders, curbed the last epidemic.

Human African trypanosomiasis takes two forms, depending on the parasite involved: Trypanosoma brucei gambiense, found in 24 countries in west and central Africa, accounts for 98% of reported cases of sleeping sickness and causes a chronic infection.

A person can be infected for months or even years without major signs or symptoms of the disease. When more evident symptoms emerge, the patient is often already in an advanced disease stage.

Trypanosoma brucei rhodesiense is found in 13 countries in eastern and southern Africa. This form represents under 2% of reported cases and causes an acute infection that invades the central nervous system.

A detailed analysis of data systematically collected by WHO in the years 2000-2018 in the HAT Atlas was published in PLoS NTDs showing the updated picture of the elimination trends in this disease. The analysis of global indicators and milestones of the WHO NTD roadmap has been updated to 2018 and recently published. The disease occurrence, the geographical distribution and the control activities show that:

  • 977 cases of HAT were reported in 2018, down from 2,164 in 2016.
  • The area at moderate or high risk of HAT has shrunk to less than 200,000 square kilometres. More than half of this area is in the Democratic Republic of the Congo. In the last 10 years, over 70% of reported cases occurred in the Democratic Republic of the Congo.
  • Health facilities providing diagnosis and treatment for HAT have increased since the last survey, meanwhile active screening is maintained at similar levels.

The number of cases, the main global indicator, is already well within the 2020 target (i.e. 2,000 cases). The areas at moderate or higher risk (i.e. > 1 case/10,000 people/year) are also nearing the 2020 target. The reliability of these data is backed by a reinforced coverage of the populations at risk by surveillance and control activities, providing strong evidence that global elimination of the disease is advancing.

There is no vaccine or drug for prophylaxis and preventive measures are aimed at minimizing contact with tsetse flies. Sleeping sickness is curable with medication but is fatal if left untreated. Surveillance networks, such as ProMED-mail and TropNetEurop should be maintained and expanded to ensure access to institutional databases. Due to the success of surveillance systems in Western countries, the possibility of introducing similar ‘alarm’ systems for HAT in Africa should be explored. Innovation in HAT control and surveillance is still needed but the 2030 goal of elimination as interruption of HAT transmission is on track.

New parasite species causing drug-resistant disease in Brazil

A new species of parasite causing symptoms like visceral and cutaneous leishmaniasis but resistant to currently available treatments have been identified by researchers from Universidade Federal de São Carlos, Universidade Federal de Sergipe, Universidade de São Paulo, US National Institutes of Health, and Fundação Oswaldo Cruz in patients treated at the University Hospital in Aracaju, state of Sergipe in Brazil. At least one person has died from complications associated with infection by the parasite.

Phylogenomic analysis showed that the recently discovered parasite does not belong to the genus Leishmania, which comprises over 20 species of parasites that are transmitted to humans by the bites of the infected female phlebotomine sandfly – a tiny insect vector. There are three main forms of leishmaniasis: cutaneous, visceral (VL) or kala-azar, and mucocutaneous. VL is the most severe form of the disease and can be fatal if misdiagnosed or untreated. Cases of VL in Brazil account for >90% of annual reported cases in Latin America.

“From the phylogenetic standpoint, the species analyzed in this study is closer to Crithidia fasciculata, a mosquito parasite that cannot infect humans or other mammals. We managed to infect mice with it, and for this reason we believe it’s a new protozoan, which we propose to call Cridia sergipensis,” said João Santana da Silva, a professor at the University of São Paulo’s Ribeirão Preto Medical School (FMRP-USP).

The first case was confirmed in a 64-year-old man, first treated in 2011 for classic symptoms of visceral leishmaniasis: fever, enlarged spleen and liver, and decreased production of all types of blood cells (pancytopenia).

The patient was given the standard treatment and improved but suffered a relapse a few months later. He was then administered liposomal amphotericin B, the best drug available for these cases, responded, but suffered another relapse some months later. Unfortunately, the patient died after the relapses and an operation to remove his spleen, as recommended in severe cases that do not respond to treatment. A biopsy of the skin lesions found cells full of parasites, which were isolated and cryopreserved for analysis.

The group initially thought the patient had been infected atypically by Leishmania infantum but molecular tests available to identify this pathogen were all inconclusive in the analyses performed on the parasites isolated from the patient. They then opted to do a whole-genome analysis of the parasites isolated from the patient in order to find out exactly what they were dealing with.

The bioinformatics analysis that revealed the phylogenetic similarity between the new species and C. fasciculata was conducted by José Marcos Ribeiro at the National Institute of Allergy & Infectious Diseases (NIAID) and Sandra Regina Costa Maruyama, a researcher in the Department of Genetics and Evolution at the Federal University of São Carlos. The team also performed a whole-genome analysis of parasites isolated from two other patients in Aracaju who were not responding to treatment, confirming that they too belonged to the new species.

According to Maruyama, initial results gathered from an analysis of fragments of the genome identified as key to the characterization of the species suggest that most of the protozoans present in the isolates match the profile of Cridia sergipensis.

Maruyama and co-investigators would like to know whether Cridia sergipensis alone can cause severe and potentially fatal disease or whether the cases observed resulted from co-infection. Another research priority is to discover how Cridia sergipensis emerged and how it is transmitted to humans. The team also plans to search for compounds (or existing drugs) that can kill the new parasite efficiently.


Climate change poised to expose millions to malaria, new study reports

Warmer climates will likely mean more malaria in more areas of the world, a new study suggests.


Image via Pixabay.

At lower temperatures, the malaria parasite (Plasmodium) develops faster in mosquitoes than previous research indicated, based on a study done by a team at Penn State and the University of Exeter. Their results suggest that even slight climate shifts could increase the malaria risk for hundreds of thousands to millions of people, both locals and travelers, in areas where the disease currently isn’t present.


“The rate of malaria transmission to humans is strongly determined by the time it takes for the parasites to develop in the mosquito,” said Matthew Thomas, professor and Huck scholar in ecological entomology, Penn State, and the paper’s corresponding author.

“The quicker the parasites develop, the greater the chance that the mosquito will survive long enough for the parasites to complete their development and be transmitted to humans.”

The team explains that previous work suggested that malaria parasites simply can’t develop fast enough in cool climates to be able to infect people — in essence, they took longer to mature than the host mosquito’s lifespan. However, that research was carried out almost a century ago using a Russian species of mosquito.

“Our results challenge this long-standing model in malaria biology,” says Thomas.

The team worked with Anopheles stephensi and Anopheles gambiae, the two most important malaria-carrying mosquitoes in the world. They kept malaria-infected mosquitoes of these species in the lab under a range of temperatures (16 to 20 degrees Celsius /  60 to 68 degrees Fahrenheit) to see how the parasite would develop. They also kept a control group of mosquitoes at 27 degrees Celsius / 80 degrees Fahrenheit, the temperature at which malaria transmission is known to be highest.

Daily temperatures were varied by 10 degrees Celsius — 5 degrees above and below the daily mean — to simulate natural conditions such as day-night shifts or other events.

Based on the traditional model, Plasmodium is estimated to take 56 days to fully develop at temperatures just above 18 degrees Celsius / 64 degrees Fahrenheit, which is considered the minimum threshold for its development. However, the current study shows that Plasmodium needs as few as 31 days to develop in Anopheles stephensi. At this lower end of its developmental range, variations in temperature also help promote faster development for the parasite. They fully developed in as few as 27 days at 18 degrees Celsius under realistic variable temperature conditions.

“Our work shows that even small increases in temperature could dramatically increase malaria infections in humans because the parasites develop much faster at these lower temperatures than has been previously estimated,” said Jessica Waite, senior scientist, Penn State.

“Parasite development rate further increases when temperatures fluctuate naturally, from cooler at night to warmer in the day.”

Waite says the findings suggest that millions of people living in the higher elevations of Africa and in South America could be exposed to malaria as climate change ever so slightly increases mean temperatures in these areas.

“As temperatures increase with climate change, infectious mosquitoes in areas surrounding mountains, for example, may be able to transmit the parasite higher up the mountains than they have in the past,” she said. “Our results suggest that small rises in temperature could lead to greater increases in transmission risk than previously thought.”

The paper “Exploring the lower thermal limits for development of the human malaria parasite, Plasmodium falciparum” has been published in the journal Biology Letters.

Adult Zatypota wasp. Credit: University of British Columbia.

Gruesome parasitic wasp turns social spiders into ‘zombies’

A newly discovered species of parasitic wasp has one of the most brutal and Machiavellian ways of securing resources. The wasp targets social spiders that live in colonies in the Ecuadorian Amazon, which it infects with larvae that hijack the arachnid’s brains. The spiders are no longer in control, virtually turning into zombies whose only purpose is to do the wasp’s bidding.

Adult Zatypota wasp. Credit: University of British Columbia.

Adult Zatypota wasp. Credit: University of British Columbia.

By far the greater number of wasps (over 100,000 species) are parasitoids which lay their eggs in or on the caterpillars of other insect species. This makes them excellent pest controls and farmers love them because they do little to no damage to crops. In fact, some farmers actually buy parasitic wasps to control insects in their fields.

However, some wasps have taken their freeloading role to a whole new level of gruesomeness. For instance, gall wasps (Bassettia pallida) drill tiny holes in oak trees to eat them from the inside-out. The wasps also use these tunnels, known as ‘crypts’, as shelter and as hatcheries. When the young gall wasps are ready, they will munch through the woody stems and emerge as adults. Another type of wasp, known as Euderus, caught on to this behavior and will lay eggs in these holes, even if they’re occupied by developing gall wasps. In fact, that’s the idea. Once they hatch, the Euderus wasps will chew their way to freedom, eating through the poor gall wasp and emerging through its head! The gall wasp can’t escape because the hole is only big enough to support a developing gall and  Euderus wasp, but not big enough to leave room for the gall wasp’s head to emerge.

The emerald jewel wasp’s strategy, on the other hand, involves “zombifying” cockroaches and injecting them with larvae. The infected cockroach starts grooming extensively, loses its survival instinct and normal responses, and becomes an unwilling host and breakfast for the wasp’s offspring. The offspring wasp will eat the cockroach’s organs in a way that makes the insect stay alive longer, increasing the odds of survival for the offspring. This behavior is rampant that cockroaches had to adapt by using “karate kicks” to protect themselves against the gruesome intruder.

Researchers at the University of British Columbia have recently discovered another zombifying wasp while surveying the rainforests of Ecuador. The wasp targets one of only about 25 species of social spiders known in the world. Anelosimus eximius spiders live together in large colonies, where they hunt together and share parental duties.

These spiders will rarely stray from their basket-shaped nests — unless they’ve come across the Zatypota wasp. Philippe Fernandez-Fournier, a former graduate student at the University of British Columbia and lead author of the new study, was puzzled by the strange behavior of some A. eximius spiders, which he saw wandering a couple feet away from the nest. The individuals would spin enclosed webs of dense silk and bits of foliage, known as “cocoon webs”. When some of these structures were collected and examined in the lab, much to everyone’s surprise, the researchers found that these were encasing a wasp.

“Wasps manipulating the behavior of spiders has been observed before, but not at a level as complex as this,” said Philippe Fernandez-Fournier, lead author of the study and former master’s student at UBC’s department of zoology. “Not only is this wasp targeting a social species of spider but it’s making it leave its colony, which it rarely does…These wasps are very elegant looking and graceful. But then they do the most brutal thing.”

Female wasps first lay an egg on the abdomen of the spider, whose larva hatches and then attaches itself to the host. The larva feeds on the spider’s blood-like haemolymph while it is slowly taking over the spider’s body. At some point, the zombified individual starts leaving the colony and spins a cocoon for the larva. After consuming whatever nutrients the spider has left, the larva enters the cocoon fashioned by its arachnid slave, emerging fully developed up to 11 days later.

“But this behavior modification is so hardcore,” Samantha Straus, co-author of the study published in Ecological Entomology and a PhD student at UBC, said in a statement. “The wasp completely hijacks the spider’s behavior and brain and makes it do something it would never do, like leave its nest and spinning a completely different structure. That’s very dangerous for these tiny spiders.”

The researchers believe that the wasps inject the spiders with hormones that make them believe they’re in a different life-stage or cause them to disperse from the colony.

“We think the wasps are targeting these social spiders because it provides a large, stable host colony and food source,” said Straus. “We also found that the larger the spider colony, the more likely it was that these wasps would target it.”

In the future, the researchers plan on returning to Ecuador where they want to further study the same spider colonies and parasitic wasps.

A male digger bee (Habropoda pallida) from the Mojave Desert covered with Meloe franciscanus triungulins (larvae). Credit: Leslie Saul-Gershenz.

Parasitic beetles trick sex-hungry bees by mimicking their pheromones

A male digger bee (Habropoda pallida) from the Mojave Desert covered with Meloe franciscanus triungulins (larvae). Credit: Leslie Saul-Gershenz.

A male digger bee (Habropoda pallida) from the Mojave Desert covered with Meloe franciscanus triungulins (larvae). Credit: Leslie Saul-Gershenz.

Sometimes, nature is simply ruthless. Meloe blister beetles might look like your ordinary flightless insects but don’t let their appearance deceive you — these are the ultimate freeloaders, and they will employ the slyest tricks to access resources. According to a recent study, these masters of deception adapt their arsenal of tricks to their bee hosts, which includes mimicking pheromones and cruising altitude.

The siren scent

Certain, more solitary, bee species rely on pheromones to find a mate, and the blister beetle couldn’t be more happy with that fact. The larvae of Meloe franciscanus, which hatch in the hundreds at a time, lure in male digger bees by generating chemical signals that mimic female sex pheromones. Once the males are in proximity, the larvae hitch a ride on the backs of the bees until they encounter a female. During copulation, the larvae switch and tag along with the female until they’ve infiltrated the nest. Here, they feed on the pollen, nectar, eggs, and bee larvae themselves, until they’re ready to emerge as adult beetles the following winter.

Saul-Gershenz, a graduate student in entomology at UC Davis, and colleagues studied the parasitic behavior in two related but geographically separate species of bees: Habropoda pallida from California’s Mojave Desert and H. miserabilis from the coastal dunes of Oregon.

The researchers found that the beetles produce pheromones made by females bees, some of which are not found in the scent given off by male bees. What’s interesting is that the pheromones produced by local beetles that parasitize Mojave bees did not attract male Oregon bees. Likewise, Mojave bees ignored the pheromones released by larvae which typically target Oregon bee males. 

“Male bees of both species were more attracted to local parasite larvae than larvae from the distant locale because the larvae tailored their pheromone-mimicking blends to the pheromones of their local hosts,” Saul-Gershenz said in a statement.

H. miserabilis infested with larvae. Credit: Leslie Saul-Gershenz.

That’s not all. The two different species of bees cruise at different heights when looking for a mate — about 35 cm above the ground in the desert and 10 cm above the beach. This behavior is hardwired into the bees as Oregon bees which were moved to the desert buzzed about the same altitude.

The beetles responded to this tendency as well, with larvae climbing to the appropriate height for each type of bee before releasing their pheromones.

It’s all a fascinating example of relatively rapid evolution via local adaptation of a parasite species to different hosts.

“The larvae cooperate with their siblings for a brief period; they mimic the pheromone of their hosts; they are locally adapted to different hosts both chemically and behaviorally; and their emergence times are plastic across their geographic range. It has been fantastic to unravel this species’ puzzle,” she said.

Business students are more likely to have a brain parasite infection spread by cat feces

Credit: Pixabay.

Students in the US who are infected with a weird brain parasite commonly spread by cats are more likely to major in business studies, according to a new study. The findings suggest that the infection may be promoting entrepreneurial tendencies by reducing fear and enhancing risk-taking behavior.

Toxoplasma gondii is a parasite carried by cats and found in their feces, but which can also be acquired after consuming poorly cooked meat or contaminated water. A third of the world’s population is thought to be infected with the parasite.

Once it infects a human host, the parasite can cause toxoplasmosis, which is the leading cause of death attributed to foodborne illness in the United States. More than 60 million men, women, and children in the U.S. carry the Toxoplasma parasite, but very few display symptoms because the immune system usually keeps the infection from causing illness.

But even though they might not feel sick, Toxoplasma-carrying individuals may experience changes in their behavior induced by cysts in the brain formed by the parasite, which can remain for the rest of an individual’s life.

Lifecycle of T. gondii. Credit: Wikimedia Commons.

Lifecycle of T. gondii. Credit: Wikimedia Commons.

Jaroslav Flegr, a Czech evolutionary biologist, claims that the parasite is quietly tweaking the connections between our neurons, changing our response to frightening situations, our trust in others, how outgoing we are, and even our preference for certain scents.

A reduced response to fear seems to be a common occurrence. Studies conducted by Stanford’s Robert Sapolsky on rats infected with Toxoplasma showed that rodents actually turned their innate aversion to felines into attraction, luring them into the jaws of the predator. Basically, the parasite carried by the cat brainwashes the rat — and perhaps human owners too, some claim —  to become attracted to the feline.

An assessment of nearly 1,300 students from the US also found an association between exposure to the parasite and reduced fear response. The students who were exposed to the parasite were 1.7 more likely to be majoring in business studies. Particularly, they were more likely to focus on management and entrepreneurship than other business areas.

What’s more, the researchers found that individuals who attended business events were almost twice as likely to start their own business if they were infected by Toxoplasma gondii. Countries with a high prevalence of Toxoplasma infection showed more entrepreneurial activity, according to the results published in the Proceedings of the Royal Society B.

The parasite may be reducing a person’s fear of failure and promoting risk-taking behavior — the kind of fearless mindset that is generally required of entrepreneurs. Of course, that doesn’t mean that infected individuals are actually more successful entrepreneurs — most businesses actually fail within their first five years of activity and a poorer risk-evaluating ability induced by the parasite infection might actually be extremely detrimental to business activities.


Sick bees take care of themselves by eating better quality food

Sick bees will actively select for better food, study shows.


Image via Pixabay.

Being sick as an adult is quite a depressing experience. Not only do you feel horrible, but you have to call all sorts of people to let them know you won’t be coming in to work today, or that you’ll be paying them a visit at the clinic, respectively. You have to go get your own meds, make sure you’re staying hydrated — all in all, it’s a hassle, and often, we can’t really afford to take that sick leave. So we bear and power through it.

Bees, however, take good care of themselves when sick. A team led by Dr. Lori Lach, Senior Lecturer at JCU, reports that the black-and-yellow critters will actually select better food when sick, to get an extra energy boost.

For the study, the team worked with some healthy bees (as controls), others infected with the gut parasite Nosema ceranae, and compared their feeding habits. Nosema ceranae is one of the most widespread parasites of adult honey bees in the world, and its effects on the host bee’s physiology has been studied at length. However, this is “the first study we’re aware of to investigate effects on floral choice,” said Dr. Lach.

“The question then was — when the bees had the opportunity to select their own food, would they choose what was good for them?” said Jade Ferguson, the student who conducted the project for her Honours degree.

The team gave the bees artificial flowers to forage from, which housed either high-quality pollen (which was more nutritious and had a higher calorie count), low-quality pollen, or sugary water. Overall, the researchers report that healthy bees showed no preference for either type of pollen. However, twice as many infected bees picked the higher quality pollen over the lower quality one.

To their surprise, the team found that sick bees lived longer than healthy ones when they had access to the more nutritious pollen — even though it also increased the parasite count in their guts. This suggests that their preference for the higher-quality pollen stems from a bid to counteract the negative effects of the parasites.

It’s still unclear how the bees distinguish between pollens of different quality. However, the team believes that the bees’ preferences will affect what native and crop flowers the insects visit, as they can vary greatly in the quality of pollen offered. Since plants often compete for pollinators, the findings can be used to estimate which plants (both crops and wild) will be visited by a given colony. Parasite presence, the team reports, seems to be the only factor that influences which flowers are visited.


The paper “Honey Bee (Apis mellifera) Pollen Foraging Reflects Benefits Dependent on Individual Infection Status” has been published in the journal Microbial Ecology.


Scientists discover how Giardia causes one of the world’s most common gastric diseases


Credit: Pixabay.

If you’re not careful and ingest contaminated water or food, chances are pretty good you might end up getting giardiasis. You’ll immediately know you’re hit once severe, uncontrollable diarrhea sets in. Other symptoms include extreme fatigue, bloating, and stomach pain, which can last for weeks, even months if left untreated. Sometimes, however, there are no symptoms, making it a strange infection. Oddly enough, although scientists have been aware of the parasite for hundreds of years, it was never exactly clear how it infects its hosts. Now, British researchers have finally caught up with Giardia‘s tricks.

Tiny trojan horses

Researchers at the Norwich Medical School at the University of East Anglia (UEA) report that the waterborne parasite makes people ill by mimicking human cell functions to break open cells in the gut and feed inside. The clever micro-spies disguise themselves by releasing signaling proteins that look and behave just like genuine human cells. Once the cells are persuaded to open themselves up, a gruesome feeding frenzy ensues.

Kevin Tyler and colleagues analyzed several Giardia samples with a mass spectrometer which revealed the parasites’ protein composition. They identified 1,600 proteins, among them two families of proteins that are known to possess the necessary molecular machinery needed to cut through the protective mucus in the human gut. One such family is comprised of proteases, which are proteins specifically designed to help the human gut digest other proteins. When interacting with a cell, they’ll eat through the cell lining and cause damage.

Giardia parasites on the mucosal surface, as seen by a microscope. Credit: Pixnio.

Giardia parasites on the mucosal surface, as seen by a microscope. Credit: Pixnio.

The second family of proteins mimicked human proteins which biologists call tenascins. These proteins regulate cell adhesion and will break apart in certain cases, such as during wound healing. Tenascins can be likened to a sort of cellular glue that keeps everything together to form tissue. However, the Giardia tenascin-look-alikes instead prevent healing between the junctions that hold cells together. And in combination with proteases, Giardia’s version of tenascin can wreck havoc in the gut.

“Because the giardia have broken down the cell barriers and made all these nutrients available, other, opportunistic bacteria can move in to take advantage of these ‘ready meals’ which can make giardiasis even more severe for some,” Tyler said. 

Giardia infects about half a million people yearly, the vast majority of cases occurring in developing countries, particularly where sanitation is poor. If you like to travel, you might have been unfortunate enough to meet the parasite since it causes one of the most common gastric diseases caught by backpackers.

Although giardiasis can be pretty hardcore, severely upsetting the stomach, half of all cases are asymptomatic. Tyler says that the difference in symptoms can be put down to the specific balance of ‘good’ and ‘bad’ bacteria which reside in the human gut. Simply put, those with the upset stomachs have more of the ‘bad’ kind of bacteria —  the pro-inflammatory bacteria — that feed on the nutrients released by the Giardia. This also explains why giardiasis is treatable with probiotics.

The UEA researchers hope that their research might lead to better, more effective treatments. They also have a hunch that other parasites that seem to operate in a similar manner might be using the same molecular tricks.

Findings appeared in the journal GigaScience

2015 Nobel prize for Physiology or Medicine Awarded

This year’s Nobel Prize in Physiology or Medicine is split into three parts, being divided between William C. Campbell and Satoshi Ōmura — who jointly share a half “for their discoveries concerning a novel therapy against infections caused by roundworm parasites” — and Youyou Tu “for her discoveries concerning a novel therapy against Malaria.”

Image via wattsupwiththat


Alfred Nobel had an active interest in all areas of research, including medicine. In his will, he set for the Prize to be awarded each year for scientific excellence in five major fields of study: Physics, Chemistry, Physiology or Medicine, and Economic Sciences.

The Physiology and Medicine part of the Nobel prize is awardied by the Nobel Assembly at Karolinska Institutet in Stockholm, Sweden, for discovery of major importance in life science or medicine. Discoveries that have changed the scientific paradigm and are of great benefit for mankind are awarded the prize, whereas life time achievements or scientific leadership cannot be considered for the Nobel Prize.

A total of 327 scientists have been nominated for the 2015 Nobel Prize in Physiology or Medicine, among who 57 individuals were nominated for the first time. This year it was claimed by the guys studying the bugs, for research into the treatment of roundworm parasite infections and Malaria.

The winners of the Nobel Medicine prize 2015 (L-R) Irish-born William C Campbell, Satoshi Omura of Japan and China’s Youyou Tu. Photograph credits to: Jonathan Nackstrand

The winners of the Nobel Medicine prize 2015 (L-R) Irish-born William C Campbell, Satoshi Omura of Japan and China’s Youyou Tu.
Photograph credits to: Jonathan Nackstrand


William C. Campbell and Satoshi Ōmura discovered a new drug, Avermectin, the derivatives of which have radically lowered the incidence of River Blindness and Lymphatic Filariasis, as well as showing efficacy against an expanding number of other parasitic diseases. Youyou Tu discovered Artemisinin, a drug that has significantly reduced the mortality rates for patients suffering from Malaria.

Campbell’s and Ōmura’s Ivermectin is currently seeing use in all parts of the world that are plagued from parasitic diseases, invaluable for improving the wellbeing of millions of people with River Blindness and Lymphatic Filariasis, primarily in the poorest regions of the world. It’s so effective, in fact, that the diseases are on the verge of eradication, a major feat of medical history.

Artemisinin is used in all Malaria-ridden parts of the world, and with 200 million individuals who report infection with the disease each year, it’s seeing a lot of use. When used in combination therapy, it is estimated to reduce mortality from Malaria by more than 20% overall and by more than 30% in children. For Africa alone, this means that more than 100 000 lives are saved each year.

“The discoveries of Avermectin and Artemisinin have revolutionized therapy for patients suffering from devastating parasitic diseases. Campbell, Ōmura and Tu have transformed the treatment of parasitic diseases. The global impact of their discoveries and the resulting benefit to mankind are immeasurable,” Karolinska Institutet’s award decision reads.



Parasitic wasps turn spiders into zombies… again!

Wasps are a nasty bunch; you don’t want to mess with them no matter who you are. Not only can they sting you really bad and ruin your day, they can actually control your mind, force you weave a web for their offspring and then kill you – well, if you’re a spider at least.

A wasp larva perches on its hapless spider host. (Keizo Takasuka)

The Reclinervellus nielseni wasps deposit their eggs in spiders, which initially, is nothing but a nuisance to the spiders. However, after the eggs hatch, the larvae actually force the spiders to hatch a reinforced web to keep them safe as they transition into adulthood – after which, they kill their hosts.

Several parasites can control the minds of their hosts and lead them to demise. A certain fungus can control the mind of ants while jewel wasps can do the same thing to cockroaches. In fact, it seems like wasps are masters of mind control! New research out today in the Journal of Experimental Biology details the intricate process through which Reclinervellus nielseni does this.

In order to figure this out, Keizo Takasuka of Kobe University’s agriculture science graduate school looked at the Cyclosa argenteoalba spider’s web construction. He found that the spider weaves two different types of webs: an orb web, for hunting, and a resting web. The hunting webs are thicker and sticky in order to trap insects, while the resting ones are looser and with fluffy decorative elements. But he also observed that sometimes, infested spiders create a different kind of web, one that serves as a nest for their parasitic hosts – the wasps. After it’s done, for all its efforts, the spider just gets eaten.


A Cyclosa argenteoalba orb web. (Keizo Takasuka)

After they hatch from the eggs, they start feeding from the liquid inside the spider and compels it to follow instructions for a new type of web. The spiders actually destroy their orb webs to build a wasp cocoon; after this is done, the larva kill the spider and turn the web into an actual cocoon. It’s a cruel and painstaking process which you can watch below, if you have the heart for it.

The exact mechanism through which the parasite controls its host are, as with other parasitic cases, still a mystery. It is most likely some type of chemical, a hormone that encourages the spider to build a specific type of web. The next step for Takasuka is to understand this mechanism and see how the wasp evolved into such a complex breeding cycle.

In the meantime, we’re just thankful we’re not spiders.

Hookworm is an intestinal parasite most commonly found in tropical and sub-tropical climates of Africa, Asia and Latin America. Hookworm, one of three members of a family of parasites known as the soil-transmitted helminths (STHs), are half-inch long worms that attach themselves to the intestinal wall and feed on human blood. Image: Sabin Vaccine Institute

Fighting intestinal worm infections with its own genes

Parasitic hookworms infect half a billion people worldwide, causing severe health problems like gastrointestinal issues, cognitive impairment and stunted growth in children. As if the challenges weren’t big enough, the parasites are growing resistant to current drugs. Scientists are trying to tackle this by developing new treatments and vaccines based on the worm’s genome. A team of Caltech sequenced the genome of a hookworm species known as Ancylostoma ceylanicum and found the genes that code key proteins involved in infecting hosts. They hope blocking these proteins from being made might save millions from great sorrow and suffering.

Hookworm is an intestinal parasite most commonly found in tropical and sub-tropical climates of Africa, Asia and Latin America.  Hookworm, one of three members of a family of parasites known as the soil-transmitted helminths (STHs), are half-inch long worms that attach themselves to the intestinal wall and feed on human blood. Image: Sabin Vaccine Institute

Hookworm is an intestinal parasite most commonly found in tropical and sub-tropical climates of Africa, Asia and Latin America. Hookworm, one of three members of a family of parasites known as the soil-transmitted helminths (STHs), are half-inch long worms that attach themselves to the intestinal wall and feed on human blood. Image: Sabin Vaccine Institute

Most cases of infection happen in developing countries where access to safe drinking water is scarce. Because it’s very difficult to sanitize water sources for millions of people, the best thing we can do at the moment is fight the effects, not the causes. While Ancylostoma ceylanicum isn’t responsible for most infections in humans, the worm was appealing for research because it’s also found in rats. This way, researchers could follow the infection’s progress from start to finish.

Using state-of-the-art DNA sequencing techniques, Caltech researchers sequenced all 313 million nucleotides of the A. ceylanicum genome. Surprisingly, even though the worm’s genome is only 10% the size that of a human, it encodes far more genes – about 30,000 in total, compared to approximately 20,000-23,000 in the human genome. While this may look intimidating, those gene that count in fighting the hookworm are lesser in number.

The team led by  Paul Sternberg, the Thomas Hunt Morgan Professor of Biology at Caltech and a Howard Hughes Medical Institute investigator, investigated looked at the RNA involved in infections. RNA is the genetic material that is generated (or transcribed) from the DNA template of active genes and from which proteins are made. They found 900 genes that are turned on only when the worm infects its host—including 90 genes that belong to a never-before-characterized family of proteins called activation-associated secreted protein related genes, or ASPRs.

“If you go back and look at other parasitic worms, you notice that they have these ASPRs as well,” Sternberg says. “So basically we found this new family of proteins that are unique to parasitic worms, and they are related to this early infection process.” Since the worm secretes these ASPR proteins early in the infection, the researchers think that these proteins might block the host’s initial immune response—preventing the host’s blood from clotting and ensuring a free-flowing food source for the blood-sucking parasite.

Developing a drug that blocks these proteins from being generated could avoid infection. The problem is that you might need to block all 90 of them !

“It’s going to take a lot more careful study to understand the functions of these ASPRs so we can target the ones that are key regulatory molecules,” Sternberg said.

Such drugs could prove paramount in fighting hookworm infections, but if scientists know which proteins to target they can make something even better: an anti-A. ceylanicum vaccine. For example, if a person were injected with an ASPR protein vaccine before travelling to an infection-prone region, their immune system might be more prepared to successfully fend off an infection. Findings appeared in Nature Genetics.

“A parasitic infection is a balance between the parasites trying to suppress the immune system and the host trying to attack the parasite,” says Sternberg. “And we hope that by analyzing the genome, we can uncover clues that might help us alter that balance in favor of the host.”


High-salt diet could protect against microbes, but you still shouldn’t eat too much

Many people today are consuming more salt than they actually need – while this may make foods tastier, it also increases the risk of heart disease and stroke. But a new study found that dietary salt could actually have a dietary advantage, defending the body against invading microbes.

Image via Health only.

Salt is one of the simples minerals in the world, yet it has an extremely rich and controversial history. It used to be extremely valuable in ancient and medieval times, up to the point where only the elite could enjoy it in proper quantities in some areas of the world. Interestingly enough, only about 6% of the salt manufactured today in the world is used in food. Of the remainder, 12% is used in water conditioning processes, 8% goes for de-icing highways and 6% is used in agriculture. The rest (68%) is used for manufacturing and other industrial processes. Salt is really cheap pretty much virtually everywhere in the world but we’re dealing with a different problem – we’re eating too much of it.

The World Health Organization recommends that all adults should consume less than 2,000 mg of sodium (which is equivalent to 5 g of salt) per day with some advocating for less than 1,200 mg of sodium (3 g of salt) per day, but most people in the developed world go way above that limit, thus significantly increasing their risk of heart diseases. But a new study found that there might also be some advantages to eating a lot of salt; in mice, high salt intake boosts their immune response to parasitic skin infections, suggesting that this might also work in humans – promoting defense against microbial infections.

“Up to now, salt has been regarded as a detrimental dietary factor; it is clearly known to be detrimental for cardiovascular diseases, and recent studies have implicated a role in worsening autoimmune diseases,” says first study author Jonathan Jantsch, a microbiologist at Universitätsklinikum Regensburg and Universität Regensburg. “Our current study challenges this one-sided view and suggests that increasing salt accumulation at the site of infections might be an ancient strategy to ward off infections, long before antibiotics were invented.”

Common salt is a mineral composed primarily of sodium chloride (NaCl), so naturally it contains a lot of salt. When you eat it, the sodium tends to deposit in your skin, where it can cause significant damage to the body, although the exact mechanism is not properly understood.

“Despite the overwhelming evidence linking dietary salt to disease in humans, the potential evolutionary advantage of storing so much salt in the body has not been clear,” says senior study author Jens Titze, who studies the link between sodium metabolism and disease at Vanderbilt University School of Medicine.

So the team set out to investigate what this advantage may be – and learned that high salt intake (and absorption in the skin) could make people more effective at fighting certain skin parasites.

“We also think that local application of high-salt-containing wound dressings and the development of other salt-boosting antimicrobial therapies might bear therapeutic potential.”

Still, scientists warn that this isn’t a green light for eating as much salt as possible. The dietary advantage they reported is very niched and does not compensate for all the damage salt can do.

“Due to the overwhelming clinical studies demonstrating that high dietary salt is detrimental to hypertension and cardiovascular diseases, we feel that at present our data does not justify recommendations on high dietary salt in the general population,” Jantsch says. “Nevertheless, in situations where endogenous accumulation of salt to sites of infection is insufficient, supplementation of salt might be a therapeutic option. But this needs to be addressed in further studies.”

Journal Reference: Cell Metabolism.

Tapeworms Can Cooperate or Fight to Control Host

If two tape worms infect the same host, they can either cooperate to thrive, or battle it out for complete control. A new study has found that the parasites actively sabotage each other in a competition to seize control of the host.

A copepod. Image via Fairfax County Public Schools.


Tape worms are nasty creatures. They live in the digestive tracts of vertebrates as adults, and often in the bodies of other species of animals as juveniles. Basically all vertebrates may be parasitized by some tape worm; the cow tape worm can grow up to 20 m (65 ft), while the whale tape worm can reach a whopping 30 m (100 ft). They’ve been around for at least 270 million years ago (geologists found them in fossilized feces), and they’re likely going to be around for a long time – it’s only natural that in this time, they’ve developed ways to accentuate their control over the host.

Scientists have long known that parasites can influence host behaviour. In many cases, parasites go through different life cycles in different hosts, thus encouraging the current host to perform action which would transfer the parasite to future cost. But it’s also quite possible for two parasites to inhabit the same host at the same time. Nina Hafer and Manfred Milinski wanted to see what happens when this situation occurs.

The two study parasites at the Max Planck Institute for Evolutionary Biology in Ploen, Germany. For this study, they infected small crustaceans called copepods (Macrocyclops albidus) with multiple Schistocephalus solidus tapeworms. These live in copepods and then move to fish for their next life-cycle stage. The tape worms make the copepods more active and agitated, and thus more likely to be eaten by a fish – thus transferring the parasite to its next host.

Scientists found that when copepods are inhabited by two similarly aged parasites, they become even more active – the parasites are cooperating for the same purpose. However, when an older tapeworm was sharing a host with a younger one, the older animal always came on top.

‘The activity of the host does not reach an intermediate level as a result of the two competing parasites. This suggests that the older parasite is “sabotaging” the younger one’s activity, says Hafer, because “we don’t expect the non-infective parasite to stop what it’s doing,” says Hafer. The older parasite even won out when it was in competition with two younger individuals’, Nature writes.

While it’s easy to understand why they would do this, we don’t yet understand how they do it. As a matter of fact, we don’t understand at all how the parasite influences the host’s behavior. Frank Cézilly, who studies host–parasite interactions at the University of Bourgogne in Dijon, France hopes that this research could ultimately shed some light on that matter. It could be very important to understand how parasites influence their hosts, and sabotage is a relevant and interesting behavior.

“It could be sabotage, but it could be just that the younger parasite can’t overcome [pre-existing] manipulation by the older parasite,” he says.

New Hookwork Vaccine Passes Clinical Trials in Brazil

A permanent vaccine for hookworm has passed clinical trials. The hookworm is one of the most pervasive parasites, affecting over 600 million people worldwide. The virus is also known for affecting mostly poor populations.

The hookworm is a parasitic nematode (roundworm) that lives in the small intestine of its host, which may be a mammal such as a dog, cat, or (often times) a human. Affecting over half a billion people worldwide, it is the leading cause of maternal and child morbidity in the developing countries of the tropics and subtropics. In susceptible children hookworms cause intellectual, cognitive and growth retardation, intrauterine growth retardation, prematurity, and low birth weight among newborns born to infected mothers. The worm is especially prevalent in developing tropical countries; studies showed incredibly high figures of infection in areas in India (42.8% in Darjeeling), Brazil (62.8% in Minas Gerais), Vietnam (52% in the northern parts of the country) and even China (60% in the Xiulongkan Village).

For all the high infection rates, hookworms are also especially nasty. The parasites mainly live in the small intestine, feeding on blood leached from the intestine walls they hook into; they can also live in the lungs. But the problem is manageable with adequate medical treatment – getting rid of an infection takes between a few days and (at the very most) a couple of weeks. But sadly, in many parts of the world, people either can’t afford the treatment, or they simply aren’t aware of it (in many cases, they aren’t even aware they’re infected). This is why a lifetime vaccine would definitely come in hand.

“Developing lasting solutions for hookworm and other NTDs trapping people in poverty requires comprehensive collaboration, cutting-edge science and leadership among health and policy leaders in endemic countries,” Peter Hotez, president of Sabin, has said.

The vaccine itself, as most vaccines, is made with some ingredients from the culprit themselves – namely a protein from the hookworm. When your body is exposed to the protein, it starts to generate antibodies, without having to actually fight the infection. Should the body be infected at some later time, it will recognize the parasite and adequately fight it.

While the vaccine itself shows immense promise, it may still be a while before it actually starts hitting the shelves or before it is implemented in the nations’ vaccination policy system. Even though phase 1 trials were successfully completed, it may take until 2020 for the vaccine to get a license.

A Rogue gone Good: Mitochondria was initially an Energy Parasite

A new milestone study found that mitochondria – the energy factories in animal and plant cells – were initially very similar to parasitic bacteria some two billion years ago, and only later did they become energy sources. Very little is known about the origins of mitochondria, but by probing the genomes of bacteria closely related to the energy cell scientists at University of Virginia (UV) found early mitochondria were parasitic, and only became beneficial after switching the direction of their ATP (adenosine triphosphate) transport years down the road. The findings could help efforts seeking to treat human mitochondrial dysfunctions that cause diseases such as Alzheimer’s disease, Parkinson’s disease and diabetes.

A parasite at first

Image: knowingneurons.com

Mitochondria are often referred to as the powerhouses of the cells. They generate the energy that our cells need to do their jobs. For example, brain cells need a lot of energy to be able to communicate with each other and also to communicate with parts of the body that may be far away, to do this substances need to be transported along the cells, which needs lots of energy. Muscle fibres also need a lot of energy to help us to move, maintain our posture and lift objects. This energy is supplied by mitochondria in the form of ATP.

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The leading theory regarding their origin is that they were formed in an ancient symbiosis between a nucleated cell and an aerobic prokaryote.  The engulfed cell came to rely on the protective environment of the host cell, and, conversely, the host cell came to rely on the engulfed prokaryote for energy production. In time, descendants of the engulfed prokaryote developed into mitochondria which became essential to eukaryotic evolution since – or so the theory goes. UV scientists found, however, that mitochondria’s past isn’t that nice and dandy. Their findings suggest mitochondria was an energy parasite by leaching energy from the host cell. It is not known what turned mitochondria from an energy parasite into the host cells’ power source, but it is believed that ATP is related to the switch.

“We believe this study has the potential to change the way we think about the event that led to mitochondria,” Martin Wu, a biologist at the University of Virginia (UV) and the study’s lead author, said in a statement. “We are saying that the current theories – all claiming that the relationship between the bacteria and the host cell at the very beginning of the symbiosis was mutually beneficial – are likely wrong.”

Image: knowingneurons.com

That’s a bold statement, but will it hold up? Wu and colleagues sequenced the genomes of 18 bacterial species which are closely related to mitochondria. This way, the UV researchers were able to pinpoint human genes that were derived from mitochondria, which could help them gain insight into the genetic basis of human mitochondrial dysfunctions contributing to several diseases like Alzheimer’s or Parkinson’s.

“We reconstructed the gene content of mitochondrial ancestors, by sequencing DNAs of its close relatives, and we predict it to be a parasite that actually stole energy in the form of ATP from its host – completely opposite to the current role of mitochondria,” Wu said.

The findings were published in the journal PLOS ONE.



Vampire parasitic plants ‘sweet talk’ victims via DNA communication


Dodder plant straggling its victim. Photo : Wiki CC0

Every once in a while we get to write about some really crazy mechanisms in nature. One of these is used by a  parasitic plant called the  dodder, which essentially acts like a ‘vampire’ upon its unsuspecting prey. Namely, other plants some of whom are crops, so research into the dodder parasitic mechanism is of great important to food security. A new research found the dodder actually communicates using DNA with its host in order to lower its defenses. A true vampire to the end – it needs an invitation to step in.

A vampire plant

Due to the color and appearance, several other descriptive common names have been used for the plant, including devil’s hair, goldthread, love vine, strangle vine, and witch’s shoelaces. I'd add 'alien scum' to the growing list. Photo: Henderson State University

Due to the color and appearance, several other descriptive common names have been used for the plant, including devil’s hair, goldthread, love vine, strangle vine, and witch’s shoelaces. I’d add ‘alien scum’ to the growing list. Photo: Henderson State University

During summertime, long strands of yellow or orange string tend to form mats that seem to lie on top of other vegetation. The material most often is seen along rivers, creeks, and fields and looks like a wad of hay-string or fly-fishing line, or spaghetti. That’s not pasta, that’s the freaking dodder!

Some call the dodder  (Cuscuta sp.) a vampire plant, because it sucks nutrients from its hosts, but I think alien would describe it better. Seriously, do you know how the dodder infects its hosts? It probes it! Yes, it uses a specialized root called haustoria that penetrates and invades the tissue of the host plant. Water, minerals, and carbohydrates are obtained directly from the host, so the root portion of the dodder dies and the plant separates from the soil, now being entirely dependent on the host plant. Dodder can grow as much as 7.5 cm (3 inches) per day.

Researchers at Virginia Tech closely followed how the dodder interacted with two host plants, Arabidopsis and tomatoes. Previously, studies showed that while the dodder first probes the host with its horrific ‘fangs’, RNA is being exchanged between the dodder and host. The latest findings from Virginia Tech goes to complement this picture with more details. Specifically, the team found that considerable amounts of messenger RNA (mRNA) is being exchanged between the parasite and host. Essentially, the dodder is sweat talking the host into letting it invade it.

“The discovery of this novel form of inter-organism communication shows that this is happening a lot more than any one has previously realized,” Westwood said. “Now that we have found that they are sharing all this information, the next question is, ‘What exactly are they telling each other?'”

Researchers now believe that armed with this new found knowledge they may have stumbled across key information they would allow them to develop targeted pesticides. The dodder can ravage crops like itchweed and broomrape, so there’s a commercial interest.

“The beauty of this discovery is that this mRNA could be the Achilles hill for parasites,” Westwood said. “This is all really exciting because there are so many potential implications surrounding this new information.”

Findings were published on Aug. 15 in the journal Science.

A new cancer fighting vaccine could come from an unlikely place. Photo: petfinder.com

Mutated cat poop parasite treats cancer

A new cancer fighting vaccine could come from an unlikely place. Photo: petfinder.com

A new cancer fighting vaccine could come from an unlikely place. Photo: petfinder.com

Right now, I’m the happy caregiver of seven cats (five kittens. Yey!) which in most people’s books makes me socially challenged and insane. I do take special notice of my pets, and this means looking after them so they don’t get infected by parasites. Cats are typically clean animals, but when infested can spell trouble for family health – ZME cat owners, do be careful! Some cat parasites, however, can prove to be extremely useful if manipulated to our needs. For instance, researchers at the  Dartmouth-Hitchcock Medical Center have mutated a strain of parasite found in cat poop that they used to treat cancer in mice with extremely promising results.

Reversing a nasty parasite to work for us

The parasite in question, Toxoplasma gondii, thrives in the cats intestines and spreads to external environment through the back door. It  is extremely undesirable for a cat to harbor, since it causes illness and can infect both cat and human. A mutated version of T. gondii, called “cps”, has proven to have cancer fighting properties, however.

“We know biologically this parasite has figured out how to stimulate the exact immune responses you want to fight cancer,” explained David J. Bzik, a professor of Microbiology and Immunology at Dartmouth.

“The biology of this organism is inherently different from other microbe-based (treatments) that typically just tickle immune cells from the outside,” said senior research associate Barbara Fox. “By gaining preferential access to the inside of powerful innate immune cell types, our mutated strain of T. gondii reprograms the natural power of the immune system to clear tumor cells and cancer.”

A healthy immune system responds vigorously to T. gondii in a manner that parallels how the immune system attacks a tumor. In response to T. gondii, the body produces natural killer cells and cytotoxic T cells. These cell types wage war against cancer cells. Cancer can shut down the body’s defensive mechanisms, but introducing T. gondii into a tumor environment can jump-start the immune system.

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Lab tests demonstrated the cps is particularly adapted to treating  extremely aggressive cases of melanoma and ovarian cancer in mice. What’s more, the strain is non-replicating, thus safe, and can work its magic even in environments with weak immune systems, as is often the case for chemotherapy patients. Tests have revealed extremely promising survival rates.

“Aggressive cancers too often seem like fast-moving train wrecks,”  Bzik said. “Cps is the microscopic, but super-strong, hero that catches the wayward trains, halts their progression, and shrinks them until they disappear.”

What makes the bacteria particularly effective is the possibility to use it for specifically tailored treatments. Doctors can harvest cells from cancer patients, culture them along with the cps bacteria, then isolate an immunotherapeutic vaccine that generates an immune response specially customized for the patient, just like a Trojan horse.

The research is still in its incipient phase, and researchers are currently tweaking and exposing cps to more tests to get an idea which are its target molecules and mechanisms.

A parasite that might make you insane

While kitty litter might be seen with new eyes, it’s still important to be careful. The same parasite, T. gondii, has been found to drive cat owners literally crazy. T. gondii causes toxoplasmosis,  the leading cause of death attributed to foodborne illness in the United States. More than 60 million men, women, and children in the U.S. carry the Toxoplasma parasite, but very few have symptoms because the immune system usually keeps the parasite from causing illness. Jaroslav Flegr, a Czech evolutionary biologist, claims the parasite is quietly tweaking the connections between our neurons, changing our response to frightening situations, our trust in others, how outgoing we are, and even our preference for certain scents. When you add up all the different ways it can harm us, says Flegr, “Toxoplasma might even kill as many people as malaria, or at least a million people a year.”

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That’s some serious claims, which, as often is the case, had him ridiculed by the scientific community, but there are many voices that believe his research is well conducted and that he’s well on to something. One such voice is Stanford’s Robert Sapolsky, whose findings seem to lend credence to Flegr’s ideas. Sapolsky proved that T. gondii can turn a rat’s strong innate aversion to cats into an attraction, luring it into the jaws of the predator. Basically, it brainwashes the rat, and human owner maybe, to become attracted to the cat.

Parasitic vines may serve as lightning rods

The tropical rainforests of Central and South America aren’t threatened only by deforestation – they are also overrun by lianas, parasitic woody vines that clamber up trees and smother the forest canopy as they reach for sunlight. But the vines may actually help the trees in a way – scientists suspect they may in fact act as lightning rods.

Understanding how this works could prove to be instrumental in predicting how the rainforests will change in the coming years, especially given the predicted effects of climate change on both lightning and lianas. This is so important that in July, a group led by Steve Yanoviak, an ecologist at the University of Louisville in Kentucky, will head to Barro Colorado Island in Panama to begin a two-year study of lianas’ potentially protective role in the environment.

“Nobody has ever thought of lianas as anything but a structural parasite,” says Yanoviak. “But they might have this unforeseen secondary effect of protecting trees against strikes.”

Although in many areas of the world, lightning often sparks extremely dangerous forest fires, in the moist tropical forests of Panama, there is little risk of a forest fire. Instead, what lightning does is kill individual trees – something which seems to be not such a big deal. However, Yanoviak believes this could actually be quite important, especially in the context of climate change.

As the climate continues to warm more and more, droughts tend to become more and more pronounced, and the risk of lightning-triggered fires in tropical forests could increase; nobody has studied this yet.

Studies have shown that tropical forests are dealing with a massive liana invasion – by 2007, 75% of Barro Colorado Island’s trees were covered with lianas, up from 32% in 1968. Lianas are very opportunistic, taking advantage of any disturbance, taking over quickly when a fallen tree leaves a gap in the canopy and climbing higher and higher to reach the light.

Yanoviak’s initial studies have revealed that vines have lower resistance to electricity than tree branches, which means that they could serve as lightning rods, protecting the trees. Mark Cochrane, an ecologist at South Dakota State University in Brookings is excited by this idea:

“It’s an interesting hypothesis,” says Cochrane, who is not involved in the study. “But the only way the vines would shield the tree is if their conductivity was so much higher that almost all of the current flowed through the lianas.”

This seems to be indeed the key question, which even Yanoviak acknowledges. But, in his two year study period, he’ll have plenty of time to figure that out.

“At that scale they may not matter, but we don’t know that yet,” he says. “It could be that lightning is such a trivial agent of mortality that it doesn’t matter, but at least we’ll know.”

Nature doi:10.1038/nature.2014.15325