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By Kasra Hassani
What could possibly be interesting about a worm? What if it could enter your body through your mouth and somehow find its way to your foot? Or what if it could grow in your body from a microscopic size to potentially a couple of feet? These statements describe the Guinea Worm, a parasitic worm that was once widely endemic in Africa and parts of Asia, but that is now on the brink of extinction — while it used to infect 3.5 million people in the 1980s, the number of documented cases has dwindled to only 126.
While scientifically fascinating, the consequences of ingesting the Guinea Worm are medically devastating. The worm enters the body by drinking water contaminated with Guinea worm larvae. The larva survives exposure to stomach acids and digestive enzymes and somehow escapes the intestinal wall, finding its way to our limbs, usually our legs. Approximately one year after the initial infection, the worm rips open the skin and buds out, causing excruciating pain, forcing its host to do whatever he/she can for some relief, which usually involves dipping the foot in water. It usually takes days, even weeks, for the worm to completely exit the body and, as one could imagine, this is a very painful process. For those who have the fortitude to watch it, here is a video documenting this process. Upon first contact with water, the worm releases thousands of eggs, and it continues to release eggs while it is slowly exiting the body, spreading its offspring as much as it can.
Indeed through its evolution, the Guinea Worm has developed tricks to increase its chances of survival and of spreading its offspring. It lays hidden inside the body causing very little damage, subsisting in its host for a very long time — certainly not killing the host. When it is time to spread its offspring, it exits the body causing a lot of pain, leading the host to submerge his foot in water, providing the environment the worm needs to release its eggs and carry out the next phase of its life cycle.
The Guinea worm’s curious biology and ability to hide from its host’s immune system in plain site could provide important scientific knowledge. However, we don’t know much about the Guinea Worm, and chances are we never will. As cases of Guinea Worm disease dwindle mainly owing to Jimmy Carter’s eradication program, the Guinea Worm is becoming increasingly less relevant to Western clinicians and scientists. A quick search on PubMed (a database of publications on life sciences research) with the keyword “Dracunculus”, the worm’s scientific name yields about 1700 results, or scientific publications. That might sound like a lot, but compared to 230,000 that come up for “AIDS” and about 500,000 that come up for “Diabetes”, it’s negligible. Guinea Worm Disease is categorized by the World Health Organization as a “neglected tropical disease”, a term which has sparked some attention to the disease and other diseases of poverty. Rabies and Leprosy are some of the more familiar names on this list — once widespread diseases that now have a greatly reduced prevalence because of increased hygiene and sanitation.
There is no cure for Guinea Worm Disease and there is no vaccine. The only “treatment” available is to slowly wind the worm around a stick and manually remove it from the body, an agonizing process that has been practiced for centuries. This is not surprising because very little research has been done on Guinea Worm treatment.
Luckily, controlling and preventing Guinea Worm Disease is simple, at least in theory: (1) Don’t dip your infected foot in your household drinking water (2) Don’t drink water you suspect may not be clean. In practice however, it has not proven to be so simple. Over the past 30 years, The Carter Center, which is the leading organization in the effort to eradicate Guinea Worm Disease, has needed to engage in a number of diverse efforts to tackle this problem— from community-driven education for safe water consumption to negotiating for peace in civil-war-inflicted zones so that care can be given to those who need it. The 1995 Guinea Worm Cease-fire in Sudan is a famous example.
Another feature of the Guinea Worm that has facilitated eradication efforts is the fact that it has no known hosts other than humans. Therefore, if human infection is managed, you can control and potentially eradicate the disease. That is not the case for many other diseases. For example, Rabies can infect almost any mammal. Although a Rabies vaccine does exist, the fact that the Rabies virus can be freely transmitted in the wild without going through humans makes its eradication more difficult. But that’s a topic for another time.
So far in human history, only one disease has ever been eradicated — small pox. Could Guinea Worm Disease be next? Bill and Melinda Gates think so. They believe that through global efforts and distribution of free medication and vaccines, we could see the end of Guinea Worm Disease, River Blindness, Elephantitis, blinding Trachoma, Polio and even Malaria.
by Naomi Stewart
Leprosy seems to be a disease of the past — an antiquated issue and something not to worry about in our world of modern medicine. But it’s not completely gone, and there is a fascinating link in the United States that ties humans to leprosy through an unusual third-party vector. Leprosy is a bacterial disease, also called Hansen’s disease after Gerhard Hansen, a Norwegian doctor who isolated the bacteria Mycobacterium leprae as the cause of leprosy in 1873 —the first time a bacterium was identified as an agent of disease for humans. Leprosy had been noted historically as far back as 4,000 years ago, and the DNA of M. leprae has been found in funeral shrouds dating back 2000 years.
The disease is a chronic infection mostly found in the skin and nerves (also in eyes and respiratory tracts), resulting in many small nodules called ‘granuloma ’ which are the body’s natural defense mechanisms against the bacterial invaders. Diminished sensations and secondary infections cause the loss of extremities and limbs, all symptoms commonly associated with leprosy, though not caused by the disease itself. Despite low rates of contagiousness, the physical appearance of leprosy has created a long-lasting social stigma (think of the now-banned infamous leper colonies).
The incubation period is anywhere from five to 20 years, so it’s difficult for doctors to tell how many new cases actually occur each year. But with novel modern treatments, worldwide initiatives to halt the disease, and the fact that 95 percent of humans are now considered genetically immune, researchers estimate that infection rates have dropped from tens of million in the 1960s to just a few hundred thousand in 2012. New cases occur mostly in isolated, small pockets of India, China, Brazil, and a few countries in Africa, such as Mozambique, Tanzania, and Madagascar in tropical or semi-tropical areas stricken with poverty, where people have weakened immune systems, polluted waters, and are therefore more susceptible to transmittable diseases.
While understandably common in these conditions, leprosy also still lurks in North America: about 200 people in the US contract leprosy annually. Doctors noticed that while a majority (about two thirds) of these patients had lived or traveled abroad in areas with leprosy, the rest of the infected patients claimed that they had never traveled to somewhere with leprosy, and had no contact with anyone with leprosy. So how were they possibly contracting the disease? Suspicion fell on an odd, yet adorably armored agent of infection – the armadillo.
In addition to humans, the African chimpanzee, mangabey, red squirrel, and a few others, the armadillo* is part of a group of mammals vulnerable to the M. leprae. There were no known cases of leprosy in any creatures in the Americas prior to the arrival of European colonizers, so it is thought that settlers actually carried the disease across the ocean, somehow passing leprosy on to armadillos. It is likely that the cool body temperatures of armadillos are hospitable homes for M. leprae, who also like the cool extremities of the human body (noses, toes). Scientists knew that armadillos could carry the disease, as they were using them in the lab by the 1970s to study leprosy, and indeed, many of the outlying cases were occurring in Texas and Louisiana, where armadillos are commonly hunted, skinned, and eaten.
However, the connection between leprosy, humans, and armadillos remained a mere suspicion until 2011, when a landmark study was published in the New England Journal of Medicine. Lead author Richard W. Truman, who works for the US government, and collaborators in Switzerland had long wondered about this potential link. The researchers used whole-genome sequencing from a number of infected humans and armadillos, discovering a bacterial strain that was common to both, but unique when compared to strains found elsewhere. Thus, unlike the rest of the world where leprosy is still passed from human to human via respiratory droplets, Truman and his colleagues showed that armadillos are unwittingly giving humans back this special strain of leprosy, tossing it back and forth like a beach ball in a biological game that has lasted 400 to 500 years so far.
So, while only 20 percent of armadillos are suspected to be infected with leprosy, what can you do to avoid it? If you end up or live in the southern U.S. or Central America, avoid a meal with armadillo meat,, avoid piles of armadillo excrement, and generally stay away from their flesh and guts. Just admire them from afar — the way they jump and roll into a curled little ball is still cute from a distance. And in the meantime, as scientists can’t actually duplicate and grow M. leprae in a lab to study because they are difficult to culture, armadillos are now serving as excellent models to study leprosy and neuropathy for Truman and his peers. .
*Armadillos are colloquially called Hoover Hogs, dating back to the Great Depression in the USA. President Hoover was blamed for many of the economic issues that, out of desperation, forced people to consume animals previously considered pests, including the armadillo – thus, the Hoover Hog.
by Nicola Temple
Seafood is one of the most traded food commodities in the world. Squid caught off the coast of California are shipped to Asia to be cleaned and packaged, before being shipped back to the US for sale – a 19,000 km round trip. Shrimp have earned considerable air miles before ending up on our plates.
While globalization of the industry has provided a diverse selection of affordable seafood products to fish counters everywhere, it has created a complicated supply network that has made the industry more vulnerable to food fraud.
Numerous studies around the world have shown that the name on the label doesn’t always match the species being sold. Anywhere from 25 to over 90 percent of fish are mislabelled depending on the species, with commonly swapped species including red snapper, tuna, wild salmon and Atlantic cod.
Why fish are prone to alternate identities
As any seasoned traveller knows, there are challenges associated with entering a new country – different culture, different language, different rules. When fish move between countries, however, there is the added complication of market names.
Though intended to simplify things for those that break into a sweat at the sight of Latin, commonly used names can actually complicate seafood labelling. Atlantic cod, for example, has the species name Gadus morhua, but it has nearly 200 known common names around the world – 58 in the English language alone and 56 of them used in Canada. Basa can refer to both Pangasius bocourti and P. hypophthalmus in Canada, but only P. bocourti can be labelled as basa in the US.
To further complicate things, most fish and seafood products have had all recognizable traits removed during processing. It would be equivalent to showing up at Border Services with a passport picture of your earlobe – actually, an earlobe is probably more informative.
Finally, there are enormous economic incentives to change the identities of some species. Red snapper (Lutjanus campechanus) sold for an average of US$7.04 per kg in 2011, while Labrador redfish (Sebastes fasciatus) sold for about US $0.56 per kg that same year. The fillets of these two species are indistinguishable, but Dr Robert Hanner, Associate Professor at the University of Guelph and Associate Director for the Canadian Barcode of Life Network, was able to tell them apart using DNA barcoding.
DNA barcoding 101
To identify the fish species, Hanner sequenced a short segment of mitochondrial DNA that encodes a protein involved in the cell’s energy production, known as cytochrome c oxidase subunit I or COI for short. Mitochondrial DNA has an advantage over nuclear DNA in that it is more abundant as a cell may have hundreds of mitochondria, but only a single nucleus. It also has a higher mutation rate, which is more likely to produce DNA sequences that vary between species.
The COI sequence (or barcode) that is returned for the unknown fish sample is then compared with existing barcodes in a comprehensive database maintained by the University of Guelph. Having a database of expert-verified species from around the world with high-quality barcodes is a critical step in this process. This is why Dr. Hanner began the Fish Barcode of Life initiative in 2005 – a global effort to assemble a standardized barcode library of reference species from around the world. To date, over 10,700 fish species have been barcoded.
Europe, in the wake of the 2013 scandal in which horse meat was found in burgers and other ground beef products, is considering adopting the Guelph-based protocols across all member states to harmonize seafood testing. As of December 2014, Europe also adopted new tougher labelling laws that require fish products that are fresh, frozen, dried, or smoked (prepackaged or not) to have the species name on the label. This is not yet the case in Canada.
The implications of mislabelling
While food safety will likely always take precedence over testing for mislabelled products, there are significant implications of having misidentified species. If species are being misidentified at the point of catch, this can skew catch statistics that inform fisheries management. Mislabelling can also mislead consumers into thinking that a species is more readily available, and therefore more sustainable, than it truly is. It provides a market for illegal, unreported, and unregulated fishing. Finally, some substitutions can have health implications for consumers as the mislabelled species may contain allergens, contaminants (such as mercury), or toxins. In the best case scenario, consumers are victims of economic fraud, but in the worst case scenario consumer health is at risk.
If you eat fish, you can reduce your risk of fraud by reducing the number of steps between you and the fishermen by buying locally if you can. Some fishermen and processors are also voluntarily making their products traceable through systems such as ThisFish.
Nicola Temple is a Canadian science writer currently living in the UK. She’s writing a book on the science of detecting food fraud, which will be available in September 2015. Her friends and family have kindly asked her to stop sharing her research horror stories…admitting that sometimes ignorance is bliss.
This is from the folks at the Marine Biological Lab in Woods Hole, Massachusetts. I applied and was awarded two environmental hands-on lab fellowships, in 2007 and 2009. I highly recommend applying, it’s a fabulous experience, especially for science journalists who have not been part of environmental studies programs or have not done much biology, or field work, in general. As for the biomedical program, my colleagues who have taken part say it’s great too. The location is also special — MBL has a long history and a storied place in biological field research. One of my favourite “field trips” was across the street to see the rare books collection at the archives. Wow. And on one trip we spent a couple of nights in the field on Martha’s Vineyard. Magical. On the second fellowship I travelled to Alaska to the Toolik Field Station north of the Arctic Circle. Definitely the opportunity of a lifetime and I learned so much. The fellowship is a chance to indulge in your love of learning, science, and travel, and come back a better science journalist. These hands-on experiences gave me more confidence to head into the field with scientists I didn’t know already and write my first science book for grown ups, Salmon: A Scientific Memoir. — Jude Isabella
Get Your Hands On Research: Apply for an MBL Science Journalism Fellowship
Dive into hands-on research! The MBL Logan Science Journalism Program in Woods Hole, Mass., offers print, online, and broadcast journalists a chance to immerse themselves in hands-on biomedical or environmental research in one of the world’s most dynamic settings for scientific discovery. Room, board, lab fees, and U.S. travel/partial foreign travel are covered for accepted fellows.
The program runs May 27-June 5, 2015 with opportunities available for extended fellowships in Woods Hole or Arctic Alaska. Deadline to apply is March 2.
For more information, visit mbl.edu/sjp or contact Diana Kenney:
By Meredith Hanel
Maybe you caught up on sleep over the holidays or you are only catching up now that all the parties are over. Busy schedules can make us wish we didn’t need sleep, but we do. We know there are health consequences if we don’t sleep enough or at the right times, but scientists still aren’t sure why animals, from fruit flies to humans, evolved to sleep in the first place. This past year researchers identified a possible primitive form of sleep in a type of zooplankton called the marine ragworm. At night, instead of sinking into a cozy bed, the larvae of marine ragworms sink into deeper water. Nighttime sinking is caused by pauses in the movement of the larvae’s cilia, microscopic paddles that otherwise propel them upward. There are parallels between the way melatonin and light/dark cycles control activity of ragworm cilia and how melatonin controls sleep in higher organisms.
When the sun goes down we feel less alert. This is due in part to the secretion of melatonin in our brains at night. If we don’t mess up our melatonin secretion by using our laptop late in the evening, we can easily fall asleep in our favourite position, and remain relatively motionless and not easily aroused. Meanwhile, inside our brains neurons are active with a characteristic sleep pattern. In vertebrates, including fish and mammals, melatonin regulates sleep and circadian rhythms.
Melatonin also serves a more ancient function. It scavenges free radicals, preventing these reactive molecules from causing too much cellular damage. This antioxidant job is performed by melatonin in nearly all life forms, from bacteria to humans, whether they sleep or not. At some point during animal evolution, melatonin was promoted to a managerial role in the control of sleep. What might have been the first animal to use melatonin for sleep regulation? What did sleep look like in those early days?
You guessed it – the marine ragworm.
The marine ragworm is considered a living fossil, found in the same environment as its ancestors millions of years ago. Darkness signals the ragworm larvae to sink through the night. As a result, they begin their morning deep under water and swim upward all day, only reaching the surface at dusk. In fact, the larvae of the marine ragworm join a massive vertical migration of many types of plankton on a day/night cycle, which is thought to keep these creatures away from harmful light-induced oxidative stress.
Researchers discovered a specific region in the brain of ragworm larvae that is responsible for sensing light, running an internal clock and producing melatonin at night. Applying melatonin during the day could induce the nighttime ciliary pauses and blocking melatonin during the night could induce the daytime ciliary beating pattern, something author Maria Antonietta Tosches says was like given them ‘jetlag’.
The researchers identified the specific nerve cells that control cilia motion and unexpectedly the application of melatonin increased neural activity. Interestingly the authors suggested that this distinct pattern of neural firing called rhythmic bursting, seen at night or after melatonin application, may be analogous to sleep specific mammalian neural activity that helps filter incoming sensory information, like noise-cancelling headphones, so we are not constantly being awakened.
Melatonin has been around for 3.6 billion years, starting out as a simple antioxidant molecule. It would have been a darkness indicator early on because light-dependent oxidation would have reduced its levels during the day. The evolution of melatonin receptors, present in all animals except sponges, would have harnessed this darkness indicator for circadian regulation of additional physiological processes and behaviours like sleep.
Melatonin harnessed in the control of vertical migration in water in plankton may represent a primitive example of melatonin controlling a sleep-like state.
Meredith Hanel earned her PhD in medical genetics and spent many years in the lab doing research in molecular and developmental biology related to medicine. Meredith works in science outreach with Scientists in School. She enjoys writing about science and loves to find out the biology behind just about anything in nature.
Melatonin Signaling Controls Circadian Swimming Behavior in Marine Zooplankton. Tosches, M.A. et al. (2014) Cell 159: 46-57. Get paper [http://www.cell.com/cell/abstract/S0092-8674(14)00992-1]
Deep, Dark Secrets of Melatonin in Animal Evolution. Schippers, K.J. and Nichols, S.A. (2014) Cell 159: 9-10. Get paper [http://www.cell.com/cell/abstract/S0092-8674(14)01115-5]
How plankton gets jetlagged: Evolutionary link between sleep and rhythmic swimming behaviour. (2014) Press Release – European Molecular Laboratory. September 25. (http://www.embl.de/aboutus/communication_outreach/media_relations/2014/140925_Heidelberg/)