Euglenaformis parasitica

This parasite is invisible to the naked eye, can kill its host in 3 days, and it can be found lurking in the waters of rice fields. What I have just described may sound like a nightmare pathogen from a b-horror movie, but it is actually a microscopic flagellated protozoan that has given up a solar-powered life for one fuelled by the blood of its victims. The name of this microscopic monster is Euglenaformis parasitica, and it belongs to a group of otherwise innocuous single-celled critters called Euglenids.

Left: Scanning electron micrograph of Euglenaformis parasitica. Top Right: E. parasitica extracted from an ostracod host. Bottom Right: E. parasitica visible in the appendage of an infected ostracod.
Photos from Fig. 1 and Fig. 7 of the paper

Euglenids are single-celled flagellated organisms often found in freshwater. The most well-known and well-studied genus is Euglena, which is literally the textbook example of the group, appearing in many biology books as an example of a single-celled eukaryote organism. Many euglenids are photosynthetic, and historically they have been treated as sharing affinity with plants (due to their photosynthetic capabilities) or with animals (due to their active flagellum and being able to take in nutrient via heterotrophy), before getting shunted into a group called the "protist" which is just a jumble of different organisms that scientists couldn't classify into plants, animals, or fungi.

Euglena and its kin are mostly free-living, photosynthesizing when the sun's out, absorbing organic matter from the environment when it's dark. But the ancestor of E. parasitica was not content with this mostly peaceful lifestyle, and has evolved to live inside the body of animals. These euglenids were found parasitising ostracods (also known as seed shrimps) and flatworms in a rice field in Ibaraki, Japan.  Ostracods and flatworms belong to two entirely different phyla of animals, and most parasites that infect different phyla of host animals do so at different stages of their complex, multi-stage life cycles. But E. parasitica has just a simple life cycle, which makes it quite remarkable that it is able to adapt to the very different internal environments presented by ostracods and flatworms.

When E. parasitica is in an ostracod, it dwells in the body cavity, swimming in the hemolymph and bathing in its nutrients. Whereas in flatworms, since they don't have any body cavities to speak of, E. parasitica lives in the space between the spongy tissue that forms the bulk of a flatworm's body, burrowing between the cells of the parenchymal tissue. But whether it is in an ostracod or a flatworm, once E. parasitica establishes itself in the host's body, it starts absorbing the literal lifeblood of their host, using it to fuel its exponential growth as it divides and conquers from within. 

What started with just a single or a few E. parasitica soon turns into a swarm. This is particularly noticeable in flatworms - uninfected flatworms are semi-translucent, but infected flatworms darken in colour as their body becomes filled with brownish to blackish granules which are actually rapidly dividing E. parasitica. The same goes for ostracods as their blood becomes saturated with the parasite's progenies. After three days, the insides of the host are completely consumed by the swarm of E. parasitica, which proceeds to exit into the surrounding water, leaving behind an empty husk.  

There are still a lot of mysteries surrounding this flagellated organism, such as how it is able to make use of such radically different hosts as flatworms and seed shrimps, or how it enters the host's body in the first place. Does it somehow bore through the body wall, or perhaps it tricks the host into eating it, and then burrows through the digestive tract to other parts of the body? If so, it won't be the only parasite to use that trick. There are also questions about its evolutionary origin. Euglenaformis parasitica's close relatives are photosynthetic euglenids, so what made it abandon a solar-powered life in favour of living and reproducing in the bodies of small aquatic animals? Understanding that process would provide us with another clue as to how various different organisms ending up following the path of parasitism.

Reference:

Kato, K., Yahata, K., & Nakayama, T. (2023). Taxonomy of a New Parasitic Euglenid, Euglenaformis parasitica sp. nov.(Euglenales, Euglenaceae) in Ostracods and Rhabdocoels. Protist 174: 125967.

Aggregata sinensis

Apicomplexa is a diverse phylum of single-celled parasites. They are found in a wide range of different animals, and includes some well-known species which can infect humans such as the malaria-causing Plasmodium, the infamous and widespread Toxoplasma gondii, and the gut-busting Cryptosporidium. But it is not as if this group has any particular affinity for humanity - humans are just one species among many across the animal kingdom that are hosts for apicomplexan parasites. Most of the more well-studied apicomplexans are those that infect terrestrial animals, especially domesticated species, but far less is known about apicomplexan parasites that are found in the marine realm.

Top left: Aggregata sinensis oocysts in the membrane between the arms of an octopus. Top right: Oocysts in the branchial heart.
Bottom left: Sporocysts found within an oocyst. Bottom right: Sporozoite released from a sporocyst.
Photos from Fig. 1 and Fig. 2 of the paper. 

Aggregata is a genus of apicomplexan which specifically targets cephalopods - mainly octopuses. Octopus can become infected from eating crustaceans such as shrimps which harbours the asexual stage of the parasite. Once they get into the octopus gut, the parasite takes over the digestive tract, and undergo sexual reproduction in the cells of the gut lining. There are twenty different known species of Aggregata, and it seems that for octopuses, there is no escape from this genus of parasite - even deep sea species living around hydrothermal vents are targeted by their own specialised species of Aggregata parasite.

So there are no doubt many other species of Aggregata out there which are still undiscovered. The paper featured in this blog post describes a species of Aggregata called Aggregata sinensis which has been found in octopus from the eastern-central coastal waters of China and the northern tip of Taiwan. The parasite was found infecting two species of octopus - the webfoot octopus and the long arm octopus - both of which are commercially important species that are caught by the local fishermen. 

The parasite was rather common, and depending on the location, between 20-100% of the octopuses that the researchers examined were afflicted with A. sinensis. Because the way an octopus becomes infected is from eating parasitised prey, Aggregata infection initially starts in the digestive tract, but it doesn't stay there for long. In heavy infections, the parasite spills over into other parts of the body in a very visible way. As Aggregata proliferates in the octopus, it leaves tell-tale signs of their presence in the form of white cysts that speckle the octopus' body. Those white cysts are called oocysts, which are the results of the parasite's sexual reproduction. Aggregata can wreak a destructive toll on the octopus's health. As the parasite proliferates, they smother the gut lining and destroy the submucosa cells, which compromise the octopus' ability to absorb nutrients. 

As if that's not enough, those white oocysts are filled with microscopic spheres called sporocysts which need to depart from the octopus' body to continue the life cycle, and they do so in a destructive manner. The release of those Aggregata oocysts necessitates the rupture and shedding of the surrounding hosts cells, resulting in ulcers and atrophy of the gut lining and connective tissues. Once free in the surrounding waters, should the sporocysts find themselves in an unlucky crustacean, they unravel to reveal their payload of worms-shaped sporozoites. These squirm out and settle in the crustacean's gut where they undergo asexual reproduction, and start the life cycle anew.

A recent study on the phylogeny of Apicomplexa suggests that Aggregata belongs to a group called the Marosporida - which occupies a key evolutionary position within Apicomplexa, separate from the rest of the phylum. Which means that understanding parasites like Aggregata may also help us understand the evolution of the Apicomplexa phylum as a whole, and how they became one of the most successful and ubiquitous group of parasites on the planet.

Reference:

Ren, J., & Zheng, X. (2022). Aggregata sinensis n. sp.(Apicomplexa: Aggregatidae), a new coccidian parasite from Amphioctopus fangsiao and Octopus minor (Mollusca: Octopodidae) in the Western Pacific Ocean. Parasitology Research 121: 373-381.

Acanthamoeba spp.

Today we're featuring a guest post by Sally O'Meara - a student from 4th year class of the Applied Freshwater and Marine Biology' degree programme at the Galway-Mayo Institute of Technology in Ireland. This class is being taught by lecturer Dr. Katie O’Dwyer and this post was written as an assignment about writing a blog post about a parasite, and has been selected to appear as a guest post for the blog. Some of you might remember Dr. O'Dwyer from previous guest post on ladybird STI and salp-riding crustaceans. I'll let Sally take it from here.

This blog post today is dedicated to all you visually impaired contact lens wearing folk out there! Before I begin, I just want to say that I truly hope all of you adhere to the instructions your optometrist gives you with regards to using contact lenses (washing hands before and after handing them, taking them out while showering/bathing). If not, I’m afraid you are running the risk of meeting my new acquaintance; Acanthamoeba spp., also known as the cornea guzzling free-living protozoa from hell!

Acanthamoeba in its two forms: (A) trophozoite, (B) impenetrable cyst
Image by Jacob Lorenzo-Morales, Naveed A. Khan, and Julia Walochnik, used under CC BY 2.0

Acanthamoeba spp. are microscopic organisms that can be found just about anywhere, from soil to water, to the air we breathe. They are the direct culprits of Acanthamoeba keratitis (AK) a relatively rare but sight-threatening disease which is actually caused by at least eight species of Acanthamoeba: A. castellanii, A. culbertsoni, A. polyphaga, A. hatchetti, A. rhysodes, A. lugdunesis, A. quina, and A. griffin. Ocular trauma and contaminated water are also associated with AK infections but it has been found that contact lens wearing accounts for > 80% of the cases. If found early the infection can be cured, but this gets progressively more difficult the longer it remains untreated. The difficulty lies with the life cycle of the Acanthamoeba species which consists of two stages: the trophozoite and the cyst.

The trophozoite is the vegetative form which feeds on organic matter and ranges in size from 10 to 25µm. When the going gets tough, the tough get going... tough being the trophozoite. When conditions become unfavourable, like under extreme heat or lack of nutrients, the trophozoite transforms itself into a double walled cyst which is almost invincible. The cyst remains unscathed by repeated cycles of freeze-thawing, and incredibly high doses of UV and even GAMMA RADIATION. Cue the Terminator and his infamous catchphrase…. “I’ll be back”.

Characteristics of AK include eye pain, redness, itchiness, and a general feeling of something being stuck in your eye. Sounds like most eye infections, right? One extra feature is the presence of a stromal ring-like infiltrate in the eye. Basically, an ulcer forms on the cornea of the infected eye as a result of the hungry Acanthamoeba. It has been discussed that contact lenses serve as vectors for transmitting Acanthamoeba trophozoites, and to make matters worse studies have shown that wearing lenses results in mild corneal trauma which alters the surface of your eye making it even more susceptible to infection!

Healthy human eye (left) vs infected eye with Acanthamoeba keratitis (right). Arrow indicating stromal ring-like infiltrate.
From Figure 1 of the paper

Scientists have tried to create vaccines to prevent AK by terminating the Acanthamoeba trophozoite or the cyst, but these have proved unsuccessful. However, it was discovered that using a vaccine composed of dead trophozoites stimulates the production of antibodies in the tears, and these block adhesion of the trophozoites to the ocular surface which in turn prevents the development of AK.

Now, before you all go destroying your contact lenses in a panic-stricken state let me inform you that over 30 million Americans wear contact lenses, yet remarkably the incidence of AK in contact lens wearers is less than 33 cases per million. Acanthamoeba species are found in virtually every environmental niche on our planet ranging from thermal springs to solid ice, yet why are AK cases so far and few between? Scientists believe the host’s immune system plays an important role in successful AK infections.

Serological analysis of IgG and tear IgA (both of which are antibodies found in blood) revealed that 50-100% of healthy individuals with no history of AK possessed antibodies against Acanthamoeba antigens. What’s more, the serum IgG and tear IgA levels were significantly lower in patients with AK compared to the cohort of normal individuals with no history of AK, suggesting a prominent role of the mucosal immune system in preventing AK.

In 1939, Winston Churchill referred to Russia as “… a riddle, wrapped in a mystery, inside an enigma” … one might classify Acanthamoeba and the infections it produces in the same way! Although scientists have a clearer understanding of Acanthamoeba keratitis and the parasite which causes it, there is still much to be learned about its cunning and conniving ways.

References:
Neelam S. and Niederkorn J.Y. (2017) Pathobiology and Immunobiology of Acanthamoeba Keratitis: Insights from Animal Models
. The Yale Journal of Biology and Medicine. 90:261-268.

This post was written by Sally O'Meara

Steinina ctenocephali

Cat fleas (Ctenocephalides felis) is a parasite that everyone would be familiar with one way or the other. It is found worldwide and is the bane of cats, cat owners and basically anyone who does not like getting their blood sucked by tiny insects. But cat fleas are themselves just another animal and are host to their own parasites, such as Steinina ctenocephali; a single-celled parasite that lives in the gut of cat fleas. In that sense I guess one can regard S. ctenocephali as a hyperparasite - a parasite that parasitise a parasite.

(A) Female cat flea infected with feeding stages of Steinina ctenocephali (indicated by white arrow heads), (B) Male cat flea infected with feeding stages of Steinina ctenocephali (indicated by white arrow heads), (C) Scanning electron micrograph (SEM) of the parasite's feeding stage, (D) SEM of oocysts infective stages in a flea's gut wall, (E) oocysts of the parasite as seen through a hematocytometer. [all photos from Fig. 1. of the paper)

Steinina ctenocephali belongs to a group of single-celled "protozoans" call gregarines. They are parasites of arthropod and other invertebrate animals, and despite being single-celled, they are comparatively large, with some species having cells that reach almost a millimetre in length. They also have some rather unusual shapes for a large single-celled organism, with some species shaped like worms and there's even a genus that looks kind of like a rubber chicken. Steinina ctenocephali is not nearly as oddly shaped those species - it is roughly pear-shaped, which is pretty generic for a gregarine. However, far more noteworthy is the way that this parasite has thoroughly integrated itself into the flea's life-cycle.

Fleas are holometabolous insects that undergoes complete metamorphosis. This means much like butterflies and wasps they have larval stage that looks radically different to the adult form.
Newly hatched baby fleas look somewhat like bristly worms with chewing mouth parts and they are not at all equipped for blood-sucking. So what do baby fleas eat? Until they become fully-fledged jumping vampires, they mostly feed on organic detritus - some of that include poop from the adult fleas, which also contain undigested blood.

Steinina ctenocephali uses this cycle of poop-eating and blood-sucking to infect each subsequent generations of cat fleas and propagate in the flea population. In the adult flea, S. ctenocephali attaches to the gut wall as a feeding stage, eventually producing infective spores called oocysts which are released into the environment with the flea's faeces. Then, along come the flea larvae that gobble them up and inoculating themselves with S. ctenocephali. In the flea larva, the parasite take up residence inside the cells, eventually moving into the gut tract when the flea metamorphose into an adult and take its first blood meal.

Being infected with parasites usually carry some kind of cost for the host, in fact that is the very definition of parasitism. But the paper being featured in this post reveals another side to this gregarine-flea interaction. For their study, the researchers obtained flea eggs from a captive colony and raised them in microwells filled with a type of powder which is kind of like baby food for fleas. When the larval fleas hatch, they feed on this powder mixture until they metamorphose into blood-sucking adults. For the experiments, half of the fleas were raised on powder which had S. ctenocephali oocysts mixed in, while the other half were raised on a parasite-free diet.

The researchers did not find any differences in the survival of infected and uninfected fleas, but there was a difference in their growth rate. Parasites usually divert resources away from the host itself, and by doing so reduce the hosts' growth rate. But instead of what one might have expected, the researchers found that fleas raised on food dosed with S. ctenocephali actually grew faster than their uninfected counterparts. The infected fleas became mature adults a few days earlier than uninfected fleas. In fact, the more parasites they've been dosed with, the faster they grew. On average uninfected fleas took about 19 days to reach adulthood, whereas fleas that got a high dose of S. ctenocephali took only 16 days to become adults.

The researchers suggested that this faster development could be due to hormonal manipulation on the part of this (hyper)parasite. The sooner the infected fleas become adult, the sooner it can start pooping S. ctenocephali spores that can go on to infect even more fleas. Alternatively, it could be some kind of compensatory growth response by the fleas, and the cost of this accelerated growth may manifest later in life in other ways (such as reduced egg production or immune function)

Given that S. ctenocephali seems to give its host a competitive edge (at least when it comes to reaching reproductive maturity earlier) over their uninfected counterparts, is it really a parasite? One thing to keep in mind is that parasitism is just a another type of symbiosis. Terms like parasitism, commensalism, and mutualism are just categories that we have come up to place such interactions into some kind of context which are more convenient for our own understanding. But nature does not care about our categories and all symbiotic relationships exist along a gradient - in the natural world the line between friends or foes is fuzzy and may change at any time.

Reference:
Alarcón, M. E., Jara-f, A., Briones, R. C., Dubey, A. K., & Slamovits, C. H. (2017). Gregarine infection accelerates larval development of the cat flea Ctenocephalides felis (Bouché). Parasitology 144: 419-425.

Goussia ameliae

The fate of parasites are often inextricably linked to that of their hosts, and when there are changes in the host population, the effects cascade onto their parasites. The study featured today is focused on Goussia amelia - it is a newly described single-cell protozoan parasite which infects alewives and is known to cause erosion in the intestinal wall of their fish host.

Image modified from Figure 2 and 3 of the paper

Alewife is a species of herring native to the east coast of North America. They are anadromous fish that live in the coastal marine environments as adults, but enter freshwater streams to breed, much like salmon. Sometimes populations of alewives become trapped in lakes for one reason or the other during their migratory journey. These isolated fish eventually become adapted to the freshwater environment and evolved on divergent paths to their anadromous relatives. This is a relatively common occurrence which has happened multiple time in the last few thousand years, and it is also the origin for the population of alewives found in Lake Hopatcong. This lake was originally connected via a canal to the Delaware River and alewives from the coast of New Jersey used to migrate to Lake Hopatcong to spawn. But during the start of the 1900s the canal was blocked off, and the alewives that were in the lake at the time became isolated from their relatives on the New Jersey coast.

So how did this affect parasites like G. ameliae? A pair of scientists compared G. ameliae found in alewives from Lake Hopatcong to those found in the anadromous alewives from Maurice River and noted some key differences in the two forms. For example, G. ameliae from anadromous alewives have oocysts (the infective stage of the parasite) which are comparatively shorter and wider than those from landlocked hosts.

They also have different trends in their prevalence and distribution; adult anadromous alewives are more commonly and heavily infected with G. ameliae than young fish, possibly because adult fish become stressed while migrating upstream and dealing with changing salinity levels as they move from the marine environment to a freshwater one, making them more susceptible to parasitic infections. In contrast, G. amelia was very common in younger landlocked alewives, infecting over ninety percent of young fish, but it was only found in about a third of the adult fish, which may indicate that the landlocked alewives can acquire resistance to the parasite as they mature.

Given those differences, are the anadromous and landlocked G. amelia actually different species? The scientists compared the DNA of G. ameliae from the anadromous and landlocked hosts, focusing on the 18S RNA gene which can function like a barcode for distinguish different species of parasites. They found that despite the two form having slightly different morphology and ecology, it was not enough to make them separate species - their 18S RNA gene sequences were identical. But given their differences, much like their hosts, those separate populations might be in the process of diverging into two different species - it is just a matter of time.

Reference:
Lovy, J., & Friend, S. E. (2015). Intestinal coccidiosis of anadromous and landlocked alewives, Alosa pseudoharengus, caused by Goussia ameliae n. sp. and G. alosii n. sp.(Apicomplexa: Eimeriidae). International Journal for Parasitology: Parasites and Wildlife, 4: 159-170.

Ophryocystis elektroscirrha (revisited 2)

This is the fifth post in a series of blog posts written by students from my third year Evolutionary Parasitology unit (ZOOL329/529) class of 2015. This particular post was written by Kate Ives and it is about how a parasite messes with the migratory journey of monarch butterflies (you can read the previous post about hyena poop and tapeworms here).

Photo by David R. Tribble

We have all experienced that sluggish lack of energy when we’re ill – it’s much easier to hit the couch and rest up for a few days than get out and run a marathon, right? Well for the Monarch Butterfly, the choice is not always that easy! In order to find the best breeding and feeding sites, and avoid freezing in cold temperatures, most Monarchs undertake long and energetically costly migratory journeys during autumn each year.

Monarchs are commonly parasitised by the protozoan Ophryocystis ktroscirrba. The spores of this parasite are ingested by the Monarch caterpillars and asexually reproduce within the host's intestinal tract. When ingested in high numbers, these parasites have been shown to have considerable detrimental effects on the fitness and migration ability of the Monarchs. A pair of researchers set out to explored how monarchs infected by parasites exhibited different patterns in their flight endurance, speed, deceleration ability, and loss of body mass over their relative migration distances.

They raised 100 Monarch caterpillars in captivity and infected them with parasitic O. ktroscirrba. When they metamorphosed into adult butterflies, they were placed on an automated flight mill apparatus which was used to calculate the above mentioned parameters. The flight trials found that parasitised monarchs flew 14% shorter distances, at 16% slower speeds, and lost almost twice as much body mass as unparasitised Monarchs undertaking the same journey.

Just like a viral infection may sap our energy, O. ktroscirrba has a similar resource-consuming effect on Monarchs. The parasites inhibit the host’s ability to absorb nutrients and utilise stored energy for powered flight. Along with parasite-induced damage to tissues, muscles and membranes, this makes powered flight a much more effort-demanding activity. The parasites live in clusters inside the host’s intestinal walls, leading to water loss and faster dehydration. This is thought to account for the greater loss in body mass with each kilometre flown, as compared to unparasitised monarchs. These  constraints contribute to overall reduced larval survival rates, smaller adult body size, shorter lifespans, and therefore the inability to migrate efficiently or survive long enough to migrate or reproduce. It becomes a sheer battle of survival – the host throwing every defence at the rapidly reproducing parasites living inside it.

Photo by Dwight Sipler

But if all this energy is used in defences, how much  left  for migration? Quite often, the story ends with the death of the Monarch - an alarming occurrence that has thrown the species into a threatened status in many parts of the world. However, in a different light, these long-migratory journeys can be seen as a mechanism for reducing parasite prevalence in the Monarchs. The eradication of human diseases provides a perfect analogy for the pathogen-monarch dynamics. Whether through the cycle of life and death, or advancements in vaccines and modern medicine, when a disease is reduced or eliminated from a human population, the remaining population experiences increases in fitness and survival. In the same way, if Monarch migrations are energetically costly, and diseased hosts experience lower successful migrations, with each death the prevalence of the pathogens also decreases, and the remaining Monarch population becomes more adapted to fight off infections.

This insight into host-pathogen interactions also gives rise to possible areas of further research. Throw the effects of climate change and human activities into the mix, and we have the potential to develop a deeper understanding of the mighty Monarch, and its risk of parasitism. But let us not forget the importance of continuing research into the Monarch itself – its physiology and its behaviour. After all, we cannot truly study a parasite without first understanding its host!

Reference:
Bradley, C. A. & Altizer, S. (2005). Parasites hinder monarch butterfly flight: implications for disease spread in migratory hosts. Ecology Letters 8, 290-300.

This post was written by Kate Ives

Ophryocystis elektroscirrha (revisited 1)

This is the third post in a series of blog posts written by students from my third year Evolutionary Parasitology unit (ZOOL329/529) class of 2015. This particular post was written by Aimee Diamond and it is on how the Monarch Butterfly can keep pesky parasite-induced blemishes at bay (you can read the previous post about a deadly parasite that causes rabbits to tilt their head like they are being animated by Shaft Studio here).

Photo by Derek Ramsey

The monarch butterfly, dubbed one of the most beautiful species of butterfly on the planet, has a beauty secret that helps reduce signs of pesky imperfections. BUT HOW, you may cry? You might see those ads for make-up and skincare products and they are always talking about visible pores, so how do you think butterflies feel about all these SPORES?

The imperfections I am talking about on these butterflies are caused by the protozoan parasites Ophryocystis elektroscirrha. These parasitic spores cover the surface of infected butterflies and get scattered onto the host plant - the milkweed - or onto the butterfly’s eggs. Once the eggs hatch, the caterpillar feeding off the contaminated milkweed plants end up ingesting these spores, which reside and mature in their gut.

The parasite then penetrate the intestinal wall and begin to clone multiple copies of themselves. They then undergo a sexual phase and form spores around the scales of the developing butterfly. And so, when the butterfly emerges from its cocoon, it is already infected.

Now, many studies have shown that virulence (how harmful a parasite is) is a parasite trait, and that its expression depends on the interactions between the genes of the host and the parasite. However, there is another factor that determine how virulent a parasite can be. It all comes down to host ecology; in this case, the species of milkweed that the monarch butterfly chooses for its host plant. There are over 100 species of milkweed, of which 27 are used by the monarch butterfly to lay their eggs for their little ones to feed on. What makes many species of milkweed relevant in determining O. elektroscirrha virulence is the fact that these plants contain toxic chemicals known as cardenolides which varies in quantity, depending on the milkweed species, but is used by the caterpillar in defense against predators, as well as parasites.

Photo by April M. King

In short, depending on which species of milkweed these butterflies land on, the amount of cardenolides that their caterpillar ingest can aid in defending them against those pesky parasite-induced imperfections.

A study was done to test how parasite virulence varies according to host ecology. For this, two milkweed species were used; Asclepias incarnata and Asclepias curassavica, and caterpillars were infected with cloned parasites and fed with either of the two milkweed species. These two species were chosen as they contain different amounts of cardenolides; A. curassavica has a much greater amount of these toxic chemicals than A. incarnata. If we put the pieces of the puzzle together, it can be assumed that the butterflies reared on A. incarnata will be more heavily infected with the parasite than those reared on A. curassavica.

And that was exactly the outcome of the study. The lower the chemical defense in the host plant species, the higher the parasite virulence in the caterpillar/butterfly. Host ecology, can sometimes drive parasite virulence more so than genetic traits and interactions between the host and parasite alone. The monarch butterfly can now have gorgeous spore-­free scales, as long as it chooses a milkweed species with greater chemical defense as their larval host plant.

The search for radiant, parasite-free exoskeleton is over. Maybe she’s born with it, maybe it’s cardenolides.

De Roode, J. C., Pedersen, A. B., Hunter, M. D., & Altizer, S. (2008). Host plant species affects virulence in monarch butterfly parasites. Journal of Animal Ecology, 77(1), 120-126.

This post was written by Aimee Diamond

Trichomonas gypaetinii

What does the cause of pigeon canker, today's parasite, and the most common curable sexually transmitted infection in the world have in common? All of them are parasites from the genus Trichomonas. The species that causes pigeon canker is T. gallinae, a protozoan that lives in the upper gastrointestinal tract of pigeons, and it is currently posing a significant threat California's only native pigeon. While T. gallinae does not always cause disease, when the host is stressed, the parasite multiplies, causing lesions to develop in the throat and mouth of their host. The host eventually dies from starvation as the lesions makes it difficult for them to swallow anything. It is possible that a parasite like T. gallinae might have even brought down the occasional Tyrannosaurus rex over 65 million years ago - though the culprit is most likely to have been a different (but similar) species of parasite given how long ago that it all happened.

Photo composed from Fig. 5 & 6 of the paper

With T. rex being one of the most badass dinosaur of all time, it is appropriate that the species of Trichomonas that we are featuring today - T. gypaetinii - is found in some pretty badass living dinosaurs as well. This parasite was first isolated from a bearded vulture (Gypaetus barbatus) - which I am sure most would agree  is a very handsome and intimidating bird. When T. gypaetini was initially isolated, it was not fully described as a species, as there was insufficient material  to do so. However, this study reports on newer samples obtained from a wide epidemiological study of avian trichomonosis in Spain. The research team managed to obtain isolates of T. gypaetini from another two species of vultures - the Egyptian Vulture (Neophron percnopterus) and the Black Vulture (Aegypius monachus) - and now we have a formal description.

So what differentiates T. gypaetinii from canker-causing T. gallinae? There was nothing about their appearance which separates the two species, but when the research team did some genetic analysis on the parasite, they found that all the Trichomonas samples from vultures were perching on their own branch, far away from T. gallinae. When they search for previously published sequences of Trichomonas from vultures, they hit upon the previously undescribed isolate from the bearded vulture mentioned earlier.

So where does T. gypaetinii sit on the Trichomonas family tree? Genetically, T. gypaetinii is actually more similar to T. vaginalis - a sexually transmitted parasite that infects over 160 million people worldwide each year - most of the time without them being aware of it as most cases show no symptoms. Much like those cases of T. vaginalis infection, T. gypaetinii does not appear to cause any problems to their bird host either.

Furthermore, it seems that T. gypaetini is only found in carrion-feeding birds. Other birds of prey can get infected by T. galinae - the canker-causing species - through eating other birds, especially pigeons. But the vultures' comparatively specialised diet and digestion physiology (especially that of the bone-munching bearded vulture) means that  T. gypaetinii is the only Trichomonas that can successfully make vultures their hosts.

Reference:
Martínez-Díaz, R. A., Ponce-Gordo, F., Rodríguez-Arce, I., del Martínez-Herrero, M. C., González, F. G., Molina-López, R. Á., & Gómez-Muñoz, M. T. (2015). Trichomonas gypaetinii n. sp., a new trichomonad from the upper gastrointestinal tract of scavenging birds of prey. Parasitology Research 114: 101-112.

Sarcocystis cernae

This is the fifth post in a series of blog posts written by students from my third year Evolutionary Parasitology unit (ZOOL329/529) class of 2014. This particular post was written by Reece Dalais that he had titled "A fuzzy shuttle bus to a feathery airport" about what the parasite Sarcocystis does to its vole host (you can read the previous post about a midge that sucks blood from the belly of mosquitoes here).

Photo from here

Many protozoan parasites make use of one or more hosts before finally infecting the host species with suitable real estate for sexual reproduction (e.g. Sarcocystis dispersa and S. putorii). These ‘intermediate’ hosts act as temporary living quarters, in which the parasite accumulates resources, multiplies and then prepares for the trip to the next neighbourhood. In the Netherlands, the protozoan parasite Sarcocystis cernae, uses its intermediate host, the common vole (Microtus arvalis), to multiply itself and then as a vehicle to its honeymoon suite – the small intestine of the common kestrel (Falco tinnunculus). In the lining of the kestrel’s intestine, S. cernae lays its sporocysts, (which are equivalent to eggs) which leave the intestine with the stool of the bird.

Voles forage daily at regular intervals before scurrying back underground. During this time, they can accidentally consume kestrel faeces as they eat vegetation. Once inside the common vole, S. cernae develop in the rodent’s liver before entering its bloodstream and then declaring war on its muscles. In the vole’s musculature the parasite sits tight, and multiplies (asexually) to form large cysts – known as statocysts – which contain numerous bodies capable of sexual reproduction – or cystozoites. These cystozoites break free to reproduce (sexually) once the vole is torn apart and ingested by an adult kestrel or its young – which become the future protozoan distributors. In the mid to late 1980s, it was been discovered by a pair of scientists (Hoogenboom and Dijkstra) that infection with S. cernae makes the vole twice as likely to be taken in aerial attacks. The reason for this is still under question, and has oddly been ignored by researchers since 1987. Could it be due to some form of host manipulation whereby S. cernae forces a change in the behaviour in the vole? Or is it merely a helpful side effect caused by the protozoan running amuck inside the vole’s muscles?

Photo by Małgorzata Miłaszewska

The researchers collected vole samples by snap trapping and from nest boxes during the breeding season. Voles brought to the kestrel nestboxes for their young were taken and replaced them with lab mice of a similar weight – so feeding could continue as usual. Once these voles were dissected, the results revealed that 92% of infected voles had cysts present in the locomotory muscles (the biceps, triceps and quadriceps) – the muscles responsible for movement. Hence it is likely that infected voles were slower to escape the kestrels than their Sarcocystis-free pals. However, it was also proposed that once a vole becomes infected with S. cernae they may be forced to find food at dangerous times. Without infection, voles forage at the same time as other voles and, as a group, are more aware of predators. So if these inbuilt rhythms were to be interrupted by a parasite, the vole would become an easier target. This would be an example of host manipulation, as S. cernae, would be forcing the vole to change its foraging behaviour.

Although the effect of S. cernae on the common vole is not completely understood, it is without doubt that the cunning protozoan helps to drive its furry rodent host towards a feathery final destination.

Reference:
Hoogenboom, I., Dijkstra, C. (1987) Sarcocystis cernae: A parasite increasing the risk of predation of its intermediate host, Microtis arvalis. Oecologia 74: 86-92

This post was written by Reece Dalais

Plasmodium relictum (revisited)

This is the third post in a series of blog posts written by students from my third year Evolutionary Parasitology unit (ZOOL329/529) class of 2013. This particular post was written by David Rex Mitchell on a paper published just this year on how an avian malaria parasite might make its bird host more attractive to mosquitoes which are the parasite's vector (you can read a previous post about toxic birds and their lice here and a post about bees protecting themselves against fungal parasites by lining their hives with resin here).

Photo of Culex pipiens
by Joaquim Alves Gaspar

One of the aspects of parasites that people tend to find a little more disturbing is the idea that they can control the minds of other animals. Although this may seem like the stuff of science fiction, this is indeed sometimes the case. For those parasites that live inside other animals, there are often several stages to their lives and each of these stages may require the use of a different type of animal. This presents a challenge in getting from one animal to the next and so if a parasite can influence the behaviour of one animal in some way, making it easier to reach the next, this is incredibly advantageous.

Many parasites have evolved abilities to do just this. For example, some blood-sucking insects infected with certain parasites are known to bite more frequently than when uninfected, helping to spread the disease to more animals. This is seen in malaria-infected mosquitoes, tsetse flies infected with sleeping sickness, and plague-infected fleas. But is it possible that a parasite can also influence a healthy, uninfected animal’s behaviour? The paper featured today attempts to address this question. Researchers used a species of avian malaria (Plasmodium relictum - a parasite that has been previously covered on the blog by this post here) and its natural mosquito carrier (Culex pipiens) to find out if malaria-infected animals are more attractive to mosquitoes than healthy, uninfected animals. This species of malaria is spread among birds via its mosquito carriers and thus the researchers chose canaries to carry out the experiment.

Photo of canaries by 3268zauber

Pairs of canaries, one infected with the parasite and one uninfected, were exposed to uninfected mosquitoes to see which bird they would prefer to feed on. The mosquitoes mostly fed on only one animal per sitting, so the blood inside their bellies could be removed and the DNA analysed to determine which bird it fed upon. The experiment was carried out on the day the birds were injected with the parasite, as well as 10 days and 24 days after injection, so as to monitor any changes as the parasites matured inside them.

From this experiment the researchers discovered that, not only did the mosquitoes clearly prefer to feast on the malaria-infected canaries, but also this behaviour became more prominent as the malaria parasites mature within the canary and become capable of crossing into a mosquito. The researchers suggest that the malaria parasite influences the mosquito’s decision to feed on the infected animal, assisting its transfer to said mosquito – the next stage in its life-cycle. The mechanism used to achieve this has not yet been determined but the researchers suggest that the parasite may alter the odours that are emitted from the host animal, enticing the mosquitoes to choose its infected animal over other uninfected animals. If these odours can be identified and reproduced, they may prove very useful in control of malaria in the future, for example in mosquito traps.

So is this an example of crazy sci-fi mind-controlling by parasites? Ok, so mosquitoes may not exactly be renowned for their calculated decision making skills. But the results of this experiment were still able to show us how the malaria parasite can influence a healthy mosquito’s decisions, offering further insight into the awesome manipulative powers of parasites.

Reference
Cornet S, Nicot A, Rivero A, & Gandon S (2013) Malaria infection increases bird attractiveness to uninfected mosquitoes. Ecology Letters 16: 323 – 329.

This post was written by David Rex Mitchell

Eimeria echidnae

We have previously featured a number of coccidian parasites on this blog from birds (here and here), alligators, and groundhogs. Today's coccidian parasite lives in a strange ant-eating, egg-laying mammal from Australia - the short-beaked echidna Tachyglossus aculeatus.

photo from Figure 1 of the paper

The parasite we are featuring today is found in the gut of the echidna where it resides alongside another species of Eimeria - E. tachyglossi. Both these coccidians are found exclusively in echidna guts (generally coccidians are highly host-specific), and both are known to cause mild to severe inflammation of the small intestine, and in some cases, associated with fatality in systemic infections where the parasites have spread to the echidna's other organs. However, the exact role they might play in disease is still unclear. The study we are featuring today was conducted to establish the baseline, background level of Eimeria infection found in healthy echidnas.

The researchers of this study collected fecal sample from echidnas from various zoos and wildlife parks, and examined them for oocysts (see accompanying photo) - the infective stage of coccidia that are shed by infected animals. They found that most echidna shed between a few thousand to tens of thousands of oocysts in each gram of feces. While that may sound a like lot, all the echidnas involved in the study were clinically healthy, and the oocyst numbers were comparable to those from wild marsupials. Furthermore, infection intensity did not change over the different seasons, though oocysts (the parasite's infective stage) were more commonly shed by animals that were housed in outdoor enclosures

Additionally, they also found that while wild and short-term captive echidna shed oocyst of both E. echidnae and E. tachyglossi, echidna that have been held in captivity for an extended period of time only shed E. echidnae, indicating that captive conditions are unfavourable for E. tachyglossi transmission . Because coccidian oocysts are commonly found in the soil, presumably the echidnas become infected while feeding on ants; as they poke their snout in the dirt and use their long sticky tongue to lick up ants, they also end up ingesting a lot of soil (see this video of a hungry echidna on the prowl)

Most newborn mammals become infected with coccidia within their first week or month of life. In contrast, juvenile echidnas that have not been weaned were found to be free of coccidia. Given that echidnas become infected with E. echidnae through exposure to oocysts while feeding on ants, and young echidnas do not start feeding on ants until they are weaned at 6 months old, this age-dependent diet shift most likely explains the absence of E. echidnae infection in juvenile echidnas.

Reference:
Debenham JJ, Johnson R, Vogelnest L, Phalen DN, Whittington R, Slapeta J. (2012) Year-long presence of Eimeria echidnae and absence of Eimeria tachyglossi in captive short-beaked echidnas (Tachyglossus aculeatus). Journal of Parasitology 98:543-549

Hematodinium sp.

Today's parasite, Hematodinium sp., infects blue crabs and causes a disease known as "bitter crab". While the name may sound just slightly nauseating for your palate, for the afflicted crabs, its symptom is down right horrific. The parasite causes the crab's hepatopancreas (equivalent of our liver and pancreas) to malfunction, it starts suffocating, and its muscles eventually dissolve within its exoskeleton. Crabs that are experimentally infected start dying about 2 weeks after initial exposure, and this deadly parasite may have even contributed to the recent decline of blue crabs in Chesapeake Bay.

Hematodinium and related species are dinoflagellates, and while most dinoflagellate are free-living, this species belongs to a group which have evolved to be parasites, with many different species infecting a wide variety of hosts. While several different stages of the parasite have been isolated from the blood of infected crabs, little is known about how they are transmitted between hosts, nor the inner life of those different stages in the hosts. Because many parasites live enclosed within the body of their hosts, it is almost impossible to directly observe how they live and grow the way you might be able to observe a fish or a bird. Ideally, if you can isolate a parasite out of its host, put in it a clear container which closely mimics the conditions found within its host, and still have it complete its life-cycle, then you can find out a lot more about how it lives.

Recently, a group of researchers from Virginia were able to successfully complete the life-cycle of Hematodinium - in vitro - which means they were able to grow it in a culture of chemical broth that sustained the parasite's every need, without any host animals involved. This was accomplished through a painstaking series of transfers, starting with isolating the parasite from infected crabs, then moving each stage into different culture mixes as it grew, all while keeping the conditions as sterile as possible. Out of the 10 isolates they attempted to grow, only 4 successfully completed their life-cycle in vitro. The researchers also found out that the parasite grows best in the dark, and indeed light exposure kills them within weeks, which makes sense given that it is pretty dark inside a crab (a variation on the Marx Brother joke).

Through this in vitro technique, they were able observe the different parasitic stages of Hematodinium directly, and view them as they would have been while floating in the blood and organs of a blue crab. They noted that when Hematodinium cells first enter the crab as "dinospores," they turn into a worm-shaped form called a "filamentous trophont" (see the accompanying photo which was from a figure in the paper). About a month after that, the cells begin transforming into clumps that are composed of multiple clones of the original infection stage. These clumps then grow into a stage called an "arachnoid trophont," which resembles a blob with numerous tendrils around its fringe (which would be embedded in the hepatopancreas of the crab). These clumps tend to merge and form larger blobs as they come into contact with each other. When those "arachnoid trophonts" fully develop, the cells in the middle of the blob start producing spores that eventually turn into the infective dinospores that escape from the crab to infect new hosts, starting the life-cycle anew.

Reference:
Li, C., Miller, T.L., Small, H.J. and Shields, J.D. (2011) In vitro culture and developmental cycle of the parasitic dinoflagellate Hematodinium sp. from the blue crab Callinectes sapidus. Parasitology 138:1924-1934.

Postscript: Three days after this post went up, I was contacted by Peter Coffey, who used to work on this species of parasite with a bit of additional information/correction: I just have one quick comment on the first sentence in your post. In blue crabs we don't see the same bitter flavor that we do in Alaskan Tanner and Snow Crabs, so we haven't been calling infections in blue crabs BCD.
Thanks Peter!

Parvilucifera sinerae

Phytoplankton are microscopic single-celled "plants" which float in the upper surfaces of the ocean, and their photosynthetic action is responsible for generating most of the oxygen in our atmosphere. While you might think that something so tiny would not be host to anything, there are in fact a myriad array of viruses, bacteria, and flagellate organisms that infect and exploit phytoplankton, and the parasite for today is one of them. Parvilucifera sinerae is a single-celled, flagellated organism which infects dinoflagellate algae such as Alexandrium minutum. The photo shows an infected A. minutum cell. While earlier in this post we extolled the virtue of phytoplankton, dinoflagellate algae are also known to be responsible for harmful algal bloom events such as "Red Tides", so there is a lot of interest in their ecology and the factors that can influence their likelihood of blooming.

For P. sinerae, infecting its host is not an easy task - not only does it have to find a swarm of its tiny host in the vast ocean, it also needs to make contact and accomplish what amounts to a cellular heist - the parasite needs to break through the protective shell of the alga in order to steal its valuable content. As you can imagine, during such an intense operation, being jostled around will probably throw you off your game. And indeed that is what a group of scientists in Spain have found. It appears that even a slight turbulence is enough to reduce the infection success of P. sinerae and that it performs best under calm, still conditions. These researchers suggested that turbulence would erode the zone of chemical emission around the dinoflagellate, making them more difficult to detect. Turbulence would also shorten the period of time which P. sinerae are in constant contact with the host cell - which is a necessary precondition for the parasite to perform its little cellular heist.

While both P. sinerae and its host are tiny, their interactions can have far-reaching ecological consequences, and as explained earlier they are among the most important organisms on the planet. In addition, parasitic killers, such as today's parasite, have been suggested as a possible biological control for harmful algal blooms, but it is like that the effectiveness of any such control would be at the mercy of environmental factors such as small-scale marine turbulence.

Image from figure of the paper.

Reference:
Llaveria, G., Garcés, E., Ross, O.N., Figueroa, R.I., Sampedro, N. and Berdalet, E. (2010) Small-scale turbulence can reduce parasite infectivity to dinoflagellates. Marine Ecology Progress Series 412: 45-56.

Isospora plectrophenaxia

Today's parasite is Isospora plectrophenaxia. A few weeks ago, you met a related species - Isospora lesouefi - the coccidian parasite found in the Regent Honeyeater which keeps a daily timetable, shedding most of its oocysts (the parasite's infective stage) in the afternoon. This is a well-described phenomenon among different species of Isospora - the parasite's shedding schedule appears to be calibrated by the light-dark cycle experienced by the bird host throughout the day. Indeed, experiments conducted on Isospora in house sparrow shows that if you disrupt the circadian rhythm of the host, you also mess up the parasite's shedding schedule.

Under natural condition, the usual light-dark cycle works just fine for most species of Isospora. But I. plectrophenaxia is found in the Snow Bunting (Plectrophenax nivalis) - a bird living in the High Arctic where there is perpetual sunlight during summer. So you'd think the shedding schedule of I. plectrophenaxia would be all messed up, right? Not so, researchers found that the parasite continues to stick to its regular regime of late afternoon shedding, just like all the other Isospora. At the moment researchers are unsure how I. plectrophenaxia is able to perform this feat. Perhaps this species is more sensitive to very low concentration of melatonin - the chemical secreted by the pineal organ which coordinates the bird's circadian rhythm, or perhaps it sets its timetable on different level of UV (ultraviolet) radiation exposure, which still varies throughout the Arctic summer day. Hopefully, ongoing research on this host-parasite system will shed further light on this little mystery, so watch this space!

Reference:
Dolnik O.V., Metzger B.J., Loonen M.J. (2011) Keeping the clock set under the midnight sun: diurnal periodicity and synchrony of avian Isospora parasites cycle in the High Arctic. Parasitology 138:1077-1081.

Isospora lesouefi

Isospora lesouefi is a coccidian parasite which infects the Regent Honeyeater (Xanthomyza phrygia), an endangered species of bird found in Australia. This parasite was found and described during a parasitological survey conducted on a group of honeyeaters at Taronga Zoo as a part of their captive breeding programme.

Before the birds can be released into the wild, their health needs to be assessed and a part of that procedure involves determining their parasite load. For animals that you want to keep alive, this usually involves counting the number of parasite eggs or spores found in their faeces. But here's the tricky bit - it turns out that I. lesouefi keeps to a daily timetable. The researchers in this study found that bird faeces collected in the afternoon contained about 200 times more oocysts (the parasite's infective stage) than those collected in the morning. Other species of Isospora also keep similar shedding schedules, and it is likely to be an adaptive trait which minimise the oocysts' exposure to desiccation and ultraviolet radiation.

This study illustrates the importance of taking multiple samples, as well as understanding the life history of the parasites when you want to obtain an accurate picture of parasite burden, and its actual impact on the health of an animal.

Reference:
Morin-Adeline, V., Vogelnest, L. Dhand, N.K., Shiels, M., Angus, W. and Šlapeta, J. (2011) Afternoon shedding of a new species of Isospora (Apicomplexa) in the endangered Regent Honeyeater (Xanthomyza phrygia). Parasitology 138: 713-724

Trypanosoma irwini

Today's parasite is about as Aussie as they come - Trypanosoma irwini - a blood parasite named in honour of the late Steve "Crocodile Hunter" Irwin. What's more, this parasite infects an iconic Australian host, none other than the Koala (Phascolarctos cinereus). While the vector host for T. irwini is currently unknown, it is likely that this parasite features a life-cycle broadly similar to other trypanosomes we have featured on this blog - that is alternating sexual and asexual stages in a vector host and a vertebrate host. Trypanosoma irwini is by no mean the only unique Trypanosoma found in Australian. Scientists have been describing many novel species of Trypanosoma from the marsupials of Australia, and no doubt there are many, many more waiting to be discovered.

In addition to T. irwini, the Koala is also infected by two other species of Trypanosoma. While on its own, T. irwini seems to be pretty benign, if it gets mixed up with the other Trypanosoma species or other infections such as chlamydia or the retrovirus which causes koala AIDS syndrome, it can lead to disease in its host. Like many other parasites, the pathogenecity of T. irwini is not so straightforward, and may only manifest itself under certain conditions.

Photo from McInnes et al. (2009)

References:

McInnes, L.M., Gillett, A., Ryan, U.M., Austen, J., Campbell, R.S.F., Hanger, J. and Reid, S.A. (2009) Tryapnosoma irwini n. sp. (Sarcomastigophora: Trypanosomatidae) from the koala (Phascolarctos cinereus). Parasitology 136: 875-885.

McInnes, L.M., Gillett, A.,Hanger, J., Reid, S.A. and Ryan, U.M. (2011) The potential impact of native Australian trypanosome infections on the health of koala (Phascolarctos cinereus). Parasitology 138: 873-883

December 26 - Plasmodium vivax

In Christian lore, three wise men, the magi, traveled from the East bearing gifts for the baby Jesus. These gifts were gold, myrrh and frankincense, a resin made from trees in the genus Boswellia. The reason for the gold seems obvious, myrrh was used as an incense, which had to have made the stable smell better, and frankincense was used for many things, several related to improving ones health, including ingesting the resin to combat arthritis and other ailments. Frankincense was also burned to ward off mosquitoes and thus the diseases that they carry. One of the most important mosquito-borne diseases at that point in time in that region was malaria, in this case caused by the parasite, Plasmodium vivax. Unlike it's cousin, Plasmodium falciparum, which kills many of the people it infects, P. vivax produces a milder form of the disease, though still with the classic symptoms of profound fever and chills. P. vivax has cycles every 48 hours and is sometimes thus known as "tertian malaria." (See the entry for Plasmodium malariae if that's confusing to you.) This species has a very widespread distribution and, in fact, used to cause early Americans as far north as Philadelphia and New York City to get sick every summer. Though it may kill fewer people, this parasite maintains stages in the liver of its host and can cause relapses of the disease for decades after the initial infection.

December 25 - Trypanosoma lewisi

On December 25, 1643, Captain William Mynors and his crew aboard the ship the Royal Mary, sailed past a small island in the Malaysian archipelago and dubbed it "Christmas Island." More than 300 kilometers away from the nearest other piece of dry land and uninhabitated by humans or their animals until the 1890's, many of the animals and plants found here were unique to this island. These species included two endemic species of rats, Rattus macleari and Rattus nativitatis. Despite the fact that the first settlers found them to be abundant, within a very short time, i.e. by 1908, the two species had gone extinct. Why? In the early 1900's, a tropical parasitologist had noticed several Rattus macleari individuals acting sickly and he speculated that they had been infected with trypanosomes. This was nothing but a hunch for almost exactly a century at which point molecular diagnostic techniques were brought into the picture. Scientists, including some of my colleagues at the American Museum of Natural History, took rats that had been collected from Christmas Island and deposited as specimens into natural history museums, extracted DNA from them and tested them for trypanosomes. Sure enough, many of the rats collected after humans arrived on the island showed evidence for infection with the parasite, Trypanosoma lewisi. The scientists also tested three rats collected prior to any settlements and none of those tested positive. Thus, it appears that fleas bearing T. lewisi hopped off the black rats (Rattus rattus) on the ship, bit the island's endemic rats and transmitted the parasite. The naïve hosts were likely killed by these parasites and went extinct.

You can read the whole paper here. Image is from this site.

December 18 - Haemoproteus turtur

On the second day of Christmas, my true love gave to me, two turtledoves (Streptopelia turtur)...and their blood parasite, Haemoproteus turtur? These parasites have a life cycle similar to the malaria parasites in the genus Plasmodium, but do not asexually divide in the host's blood cells, and only invade the erythrocytes as the transmission stages, the gametocytes (shown in photo). H. turtur has been shown to be vectored by the hippoboscid fly, Pseudolynchia canariensis. So, enjoy those turtledoves, true love - you're going to have 22 of them by the time the song is over - but if they get a little lethargic and don't want to "turrrr" (which is how they got their name - it doesn't have anything to do with turtles), it just might be a blood parasite to blame!

Photo by Vaidas Palinauskas.

December 15 - "Blastocystis hominis"

Single-celled organisms are difficult to classify. They don't have very much when it comes to morphology and so for a long time were just put into the large, amorphous group called "Protozoa" and treated as descending from a common ancestor. We now know that they are very divergent groups and today's parasite is a perfect example of the challenges of taxonomy. Blastocystis was originally thought to be closely related to yeasts, but then was moved to a large group called Sporozoa, which includes many well known parasites. DNA sequence data have shown, though that these parasites are part of another group known as the stramenopiles, which includes the diatoms, brown algae and Phytophthora infestans, the cause of Irish potato blight. Species of Blastocystis were classified based on the host that they had been found in, hence Blastocystis hominis. However, genetic studies showed that there is not a single species that infects humans, but rather nine or ten different subtypes, which have not yet been formally described (thus the quotation marks on the name.) Even more confusing than the taxonomy is the pathology. The protists live in the GI tract and are thought to produce typical types of GI-tract symptoms (do I have to list them?), but the symptoms reported are extremely varied and not everyone that tests positive for it shows symptoms.