Myxidium anatidum

The bile duct of a bird is probably the last place you'd expect to find a microscopic, parasitic relative of jellyfish, but that is exactly what the study featured in this post is all about. The parasite in question is a myxozoan, a type of single-celled parasites with complex life cycles which are found in a range of vertebrate animals. Evolutionary speaking, they're technically animals, but for whatever reason, over the course of their evolution, they had abandoned having bodies made of multiple cells to become the only known group of unicellular animals.

Left: Histology section show Myxidium anatidum spores in the bile duct, Centre: Myxidium anatidum myxospore under brightfield (top) and Nomarski Interference Contrast, Right: Photo of a bald eagle.
Photos from the paper (left), this paper (centre), and US Fish and Wildlife Service

There are over 2000 known species of myxozoan and most of them are usually found in fish, though there are also some species that infect amphibians and turtles. The myxozoan parasite being featured in this host was found in a rather unexpected host - a bald eagle, of all things. This eagle was found in Western Canada and was found in very poor condition prior to its death. The parasite's spores were found throughout the eagle's bile duct. While that may sound concerning, the parasite clearly played no role in the eagle's death. That's because based on the bird's condition when it was found and the toxicology findings, the eagle had died from lead poisoning. 

So why would a bald eagle be harbouring a type of parasite which is usually associated with fish and amphibians? While it is true that most myxozoan tend to be found in cold-blooded aquatic or semi-aquatic animals, some discoveries over the last decades have shown warm-blooded land-dwelling animals are not beyond the reach of these single-celled jellyfish cousins, and that includes the parasite found in the eagle's bile duct - Myxidium anatidum, a species that seems to specialise on our feathered friends

Myxidium anatidum was initially described back in 2008 from seven species of ducks (hence the "anatidum" species name) collected from across different parts of the United States. Much like with that bald eagle, the parasite resided in the bile duct and most of those infected ducks had died of other causes. This discovery overturned a lot of the previous assumptions about myxozoans and what they're capable of infecting, but since then there hasn't been any new findings about this peculiar parasite, which is still surrounded in mysteries. One such mysteries is the parasite's life cycle.

For other myxozoans, they have a complex life cycle which involves an asexual stage living in a vertebrate animal host, and the sexual stage living in either segmented worms or bryozoans (moss animals). But it is currently unknown how M. anatidum infects its feathery host, nor what invertebrate it infects for the sexual stage of its life cycle. 

When M. anatidum was initially discovered, researchers examined worms and fish from one of the ponds where an infected duck was collected, and while they did find some which were infected with myxozoans, none of them had M. anatidum. In nature, the prevalence of myxozoans in their worm hosts can be rather low, so it is possible that they had simply missed the infected worms, or the parasite was only present in worms during certain seasons, or perhaps the ducks have picked up the infection from elsewhere. Given what is known about myxozoan life cycles, since many ducks are dabblers, it is conceivable that they might have acquired the parasite through swallowing infected worms which had been hiding in the muck. 

But in that case, how did a bald eagle end up contracting this parasite? Bald eagles primarily eat fish, so it is possible that M. anatidum may have been using fish as a type of "paratenic host" - an animal that serves as an optional stopover that can potentially carry the parasite to its nominal host. It's kind of like going on a side quest which could help you complete the main goal. While the use of paratenic hosts is common among other parasites with complex life cycles, it has not been reported for myxozoans. But then again, myxozoans haven't been reported in bald eagles until now.

Since lead poisoning was what actually led to the infected eagle's death, there may be many other healthier bald eagles flying around with M. anatidum lurking in their bile duct. Between the eagles and the ducks, this humble parasite is clocking up some frequent flyer miles which its fish-infecting cousins could never hope to match. 

Reference:

Perdrizet, U. G., Lockerbie, B., & Bollinger, T. K. (2026). Myxidium anatidum in a Bald Eagle Haliaeetus leucocephalus from Western Canada. Journal of Wildlife Diseases 62: 257-259.

Myxobolus medusae

Myxozoans are a group of single-celled parasites which had evolved from jellyfish-like ancestors, thus making them a type of single-celled animal. There are about 2400 known species and they mostly infect fish, with a handful of them infecting other kinds of vertebrate animals including amphibians, turtles, ducks, and even shrews. The species being featured in this post, Myxobolus medusae, infects fish like most other myxozoans, but not just any fish, it's one with a notorious, but overblown, reputation - the red piranha (Pygocentrus nattereri). Despite its fearsome reputation, the red piranha are commonly caught and regarded as a regular food fish, so researchers in this study were able to obtain the piranha from local fishermen around Lake Sacaizal, and describe a previously undocumented species of myxozoan.

Left: Myxobolus medusae cyst (indicated by arrowhead) in the eye of a piranha, Right: Illustration of M. medusa spore.
From Fig. 1 and 2 of the paper.

While myxozoan infections are often visible as white cysts in the host's tissue, the spores themselves are actually microscopic and come in various different shapes. Some myxozoans produce spores that have a pair of long wispy tails, but the spores of M. medusae are far more unique and extravagant, with multiple branching tendrils, like the medusa of Greek mythology, in unicellular form (hence its species name). But why have such an elaborate structure in the first place? The researchers suggested those appendages might help the spores disperse in water where they act like a web that catches the current and carry the spores far and wide.

But this parasite also has another connection to its medusa namesake, namely where M. medusae lives in its host. The medusa in Greek mythology can turn someone into stone with a stare from her eyes - and that's where M. medusae lives in the piranha. Myxozoans can occur in various different parts of the host's body, and the genus Myxobolus is an exemplar of that. With almost a thousand known species, they inhabit just about every part of a fish's anatomy including the gills, kidneys, liver, ovaries, muscles, and even the cartilages of the skull and spine, where they constricts and compress the fish's spinal cord and brainstem, resulting in symptoms called "whirling disease". In the case of M. medusae, they appear as a white cyst lodged in the eye's interior.

Myxobolus medusae is not the only parasite to inhabit fish eyes, they are also the favoured infection site for other species of Myxobolus, and a number of trematode flukes. But why the eye though? For the aforementioned fluke, hanging out in the eye would hinder a fish's ability to see, which makes it more vulnerable to birds - the next host in the flukes' life cycle. But it wouldn't do any good for M. medusae if its host gets eaten by a predator, because its spores need to make their way to worms, not the belly of a hungry bird.  However, the eyes are still considered prime real estate for any would-be parasites because along with the rest of the central nervous system, the eyes are "immune privilege sites" which are mostly off-limits to the immune system, thus they can act as potential parasite shelters.

This also applies to those eye flukes too, scientists have found that flukes which infect the fish's eyes are able to infect wider range of fish species than those infecting other parts of the host's body.

Since each species of fish have a slightly different immune system, for the body-dwelling flukes, they are more limited in their host choice because their tricks for overcoming one fish species' immune system might not work for another. But since eye flukes don't have to deal with the immune system, they are free to infect a wider range of fish. So M. medusae might also be hiding in the eye for the same reason.

So while beauty might be in the eye of the beholder, in this case, a medusa is found in the eyes of a piranha.

Reference:

de Sena, N. M., Eduard, J., Pereira, C. M. B., Neto, J. L. S., & Velasco, M. (2025). Myxobolus medusae n. sp., a new species of Myxozoa with dendritic appendages. Parasitology International 109:103106.

Henneguya aegea

Aquaculture is currently one of the world's fastest growing food-production industry, with about half of all the fish being eaten around the world coming from fish farms. There are about 580 species which are currently raised in aquaculture, and each species also comes with a set of ecological concerns, such as whether they are sustainable, or if they are being farmed outside of their natural ranges, whether they might escape and become invasive. And of course, there is always the looming concern of an introduced aquaculture species bringing along or picking up parasites

The red sea bream (Pagrus major) is a species of porgy that is being farmed in the Mediterranean region. It is native to Northwest Pacific, but was introduced to the Mediterranean as a supplemental aquaculture species. While the Mediterranean Sea has its own local species of porgies such as the gilthead seabream (Sparus aurata) and red porgy (Pagrus pagrus), which are both fine aquaculture species and highly-regarded food fishes, the skin of farmed red porgy darkens after capture, and consumers expect and prefer fish with bright red skin. And so the red sea bream was imported to supplement the Mediterranean aquaculture industry. But with new fish also comes new problems.

Top left: SEM micrograph of H. aegea spores from infected fish's heart, Bottom left: Close-up of the spores.

Right: Light microscope view of the mature spores (photos above from Fig. 2 and 3 of the paper)

The study being featured in this post was carried out at a red sea bream farm at Leros, a Greek island in the southern Aegean Sea. The researchers randomly picked out twenty healthy-looking fish from a farm, and while all the fish they examined looked healthy enough and showed no obvious signs of illness, they found that the hearts of ten fish were filled with some kind of white nodules.

When examined under a microscope, the white nodules resolved into masses of tadpole-shaped, microscopic single-celled organisms, and it was clear to the researchers that they are dealing with some kind of myxosporean parasite, specifically in the Henneguya genus - but it was one that has never been described before. They named it H. aegea after the Aegean Sea where this discovery was made.

Myxosporeans are a group of parasite that infects mostly fish (with a few species infecting amphibians). Despite being single-celled, these parasites actually belongs in the Animal Kingdom, and are in the same phylum of animals as jellyfishes. In fact, the polar filament, which is used by the parasite during the infection process andserves as a diagnostic characteristic for this group, was evolutionarily derived from the the stinging cells found in animals like jellyfish and anenomes, but it has been revamped over the course of the myxosporean's evolution for a different purpose.

For the sea breams that were infected with H. aegea, while the infected fish looked relatively healthy, their hearts showed signs of stress and muscular degeneration, and were filled with numerous white nodules which were composed of developing parasite spores. The mature spores were disseminated throughout the fish's body via the circulatory system, and their passage through the blood vessels results in lesions to the blood vessel walls. Some of the spores will eventually find their way out of the fish's body to proceed to the next stage of the life cycle, but many of them end up in the fish's kidney, where they triggered an immune reaction and get enveloped by white blood cells.

So how did the farmed porgies ended up with these parasites? Did they bring the parasite with them when they were introduced to the Mediterranean, or did they pick up H. aegea in their new range? The red sea bream that are being farmed in the Mediterranean Sea had arrived as eggs from Japan during the 1980s, and thus when they arrived, they would be free of the kind of parasites which usually infect fish - including myxosporeans. So this means H. aegea is a local parasite which took a liking to this new and exotic hosts.

The concerning thing here is that the existence of this parasite was only discovered when it started infecting an introduced aquaculture species. So what is the original host for this parasite? Given that these parasites are usually fairly narrow in their host preference, one of the many local Mediterranean species of porgies would most likely to be its original host.

But now that H. aegea has another host species that it can infect, how does it change the situation for its original host species? With the introduced sea bream effectively acting as incubators that amplify the amount of H. aegea spores in the environment, it means the native host fish would be exposed to a far higher parasite load that what it has been used to. This is known in ecological parasitology as "parasite spillback".

So introducing parasite-free fish to a region doesn't mean that they will stay that way for long. And it seems that even when you start a new life at a new place and have left all your old troubles behind, sometimes you might just pick up new ones, and end up causing more problems along the way.

Reference:
Katharios, P., et al. (2020). Native parasite affecting an introduced host in aquaculture: cardiac henneguyosis in the red seabream Pagrus major Temminck & Schlegel (Perciformes: Sparidae) caused by Henneguya aegea n. sp.(Myxosporea: Myxobolidae). Parasites & Vectors 13: 27.

Cystodiscus axonis

Myxozoans are a group of very unusual parasites. Despite their simplified structure, latest research has shown that their closest living relatives are actually jellyfish (which means they are technically animals). They are found in a variety of tissues and organs in their hosts which are usually fish, and in some cases, amphibians. Some causes diseases such as the salmon whirling disease, and in the case of certain fish-infected myxozoans, after the host dies, the parasite causes the flesh to melt - much to the frustration of fishermen. While the majority of known myxozoans infect fish, in the last decade, there has been increasing interest in studying myxozoans that infect amphibians, and the parasite featured today is one such species.

Photo of Cystodiscus axonis spore from this paper

Cystodiscus axonis is a myxozoan species which lives in either the brain or the gall bladder of their frog hosts. This parasite and its close relative C. australis is found in a range of native Australian frogs. This parasite was previously classified in another genus called Myxidium and its discovery (and reclassification) featured a number of twist and turns.

The parasite was first recorded in cane toads which have been introduced to Australia, so it was originally thought to be a parasite that the cane toads had brought with them into Australia and had since taken to infecting Australia's native amphibians. However, examinations of older frog specimens from museum collections, including those that were collected before the introduction of cane toads to Australia, revealed that the parasite had been in native Australian frog all along - the cane toad simply picked it up when they arrived and they turned out to be a really hospitable home for this parasite.

Given that C. axonis is not too discriminating when it comes to whether it infects native Australian frogs or introduced cane toads, there is potential for this parasite to infect other amphibians as well. And that's what the scientists behind today's featured study decided to find out. This time, they once again look to museum specimens, in this case from the Natural History Museum in London, and specifically they examined preserved specimens of caecilians for myxozoan parasites

Caecilians are very strange looking amphibians - they are legless, look kind of like giant earthworms, and they are very different to either toads and frogs. For this study, the scientists examined 148 caecilian specimens spanning across twelve species which are found in a variety kind of habitats, ranging from terrestrial, burrowing forms to aquatic species. Out of those, they found seven specimens which had myxozoan spores floating in their gall bladder. All the infected caecilians belong to one of two species - Typhlonectes natans and Typhlonectes compessicauda - and both of them are aquatic caecilians.

Based on the shape of those spores and sequences of their DNA, the parasite they found was almost identical to C. axonis from Australian frogs. So somehow, C. axonis has managed to successfully make a jump to caecilians too - but how? The native frogs of Australian and caecilians are separated not just by a vast ocean, but also 300 million years of divergent evolution - so how did these legless amphibian parasites end up with a parasite which is originally found in Australian frogs? A vital clue might be the fact that the infected specimens were originally captive animals.

Myxozoans use different host in their lifecycle - they usually alternate between a vertebrate and invertebrate host, so the infected caecilians might have become infected when they were fed invertebrates, such as tubifex worms, which were parasitised by C. axonis. Alternatively, they might have been housed or shared a water supply with other captive amphibians that were infected.

Given its ability to jump to a dissimilar host like caecilians, this explains why they were so receptive to cane toads when they were brought to Australian. Compared with the evolutionary gulf that separate frogs from caecilians, the native frogs of Australia and the introduced cane toads are practically kissing cousins. Given the presence of an Australian frog parasite in South American caecilians, just how widespread have C. axonis and similar parasite have become?

The lethal amphibian chytrid fungus Batrachochytrium is an amphibian pathogen which has now been spread all over the world due to the global trade in amphibians. So what other parasites might be lurking in the loads of frogs, salamanders, and caecilians which are currently being shipped all over the globe?

Reference:
Hartigan, A., Wilkinson, M., Gower, D. J., Streicher, J. W., Holzer, A. S., & Okamura, B. (2016). Myxozoan infections of caecilians demonstrate broad host specificity and indicate a link with human activity. International Journal for Parasitology 46: 375-381.

Kudoa islandica

Today's post features a newly described species of parasite, which is found in the muscles of some fish that are not exactly prized for their appearance. Regardless of how they look, these fish are commercially prized. But today's featured parasite has a queasy trick that ruins their host's value on the market - its tendency to liquefy fish fillet.

SEM photos of K. islandica spore (from the paper)

Kudoa islandica is a species of myxozoan parasite which infects a number of different marine fishes from the coasts of Iceland. The first of these are two species of wolffish - the Atlantic wolffish and the Spotted wolffish. Both have short bulldog-like faces and a formidable set of teeth to match. Wolffish is harvested for its flesh and it is commonly eaten in Iceland, but on top that, its skin can also be turned into a type of designer leather. The other host of K. islandica is the lumpfish, which is harvest for its flesh which are usually dried or smoked. Lumpfish eggs are also used as a caviar substitute.

Because of the many commercial uses for the wolffish, it was considered as a candidate for aquaculture and experimental farming of wolfish was initiated in the early 2000s. Samples of these farmed fish were also sent regularly to the Fish Disease Laboratory at the University of Iceland to examine them for any pathogens. It was during these routine examinations that K. islandica was discovered. While the parasite was not described at the time, its presence has been known informally for decades. Icelandic fishermen called soft-fleshed wolffish “hárasteinbítur”, which means “hairy wolffish” (the "hair" are the parasite's plasmodia stage).

Since it was initially found in farmed fishes, the scientists at the Fish Disease Laboratory decided to see if this parasite was also found in wild marine fish of Icelandic waters. They caught some wild wolffish and lumpfish from Bay Faxaflói off the west coast of Iceland and found that the wolffish had relatively light to moderate level of infected by K. islandica. In contrast, some of the lumpfish were more heavily infected. In fact, some of them so were so loaded with the parasite that large proportion of their flesh had been replaced by K. islandica plasmodia. This parasite proliferates in the fish's flesh, taking over much of the muscle fibres they invade. However, it does not seem to cause the fish much ill effect, and the lumpfish seems surprisingly fine with their muscle tissues being replaced by parasites, with no signs of inflammation or fibrosis.

Photo of infected lumpfish fillet (from the paper)

It is after the host has died that this parasite begins to unleash its mayhem. Heavily infected fish exhibit "soft flesh syndrome" which seems to be caused an enzyme that is activate by changes in pH which accompanies fish death. This cause the flesh to literally liquefy. In the wild, this process would liberate the infective stages of the parasite into the environment where they can be ingested by the next host in the life cycle, which are small invertebrates such as marine worms. This process cannot be halted by freezing and the melting fish fillets becomes unmarketable.

One of K. islandica's host - the lumpfish - is currently being trialled as a potential cleaner fish that can be used to combat sea lice in salmon farms. Considering that parasites from the Kudoa genus are generally are not picky about what fish it hops into, there is potential for K. islandica to jump host from lumpfish to salmon (which is already infected with its own Kudoa parasite - K. thyrsites), making it key priority to work out the ecology and life-cycle of this flesh-melting parasite.

Reference:
Kristmundsson, Á., & Freeman, M. A. (2014). Negative effects of Kudoa islandica n. sp.(Myxosporea: Kudoidae) on aquaculture and wild fisheries in Iceland. International Journal for Parasitology: Parasites and Wildlife 3: 135-146.

Tetracapsuloides bryosalmonae

For many parasites, host castration is a very effective strategy. By specifically diverting energy from the host's reproductive functions, the parasite can horde as many resources as it can without compromising any organs or functions that are vital to everyday survival of the host. It is a strategy commonly used by digenean trematodes (parasitic flukes) and some parasitic crustaceans.

But, those parasites infect hosts that exist as discrete individuals (unitary organisms) - what about modular animals like corals and salps that live as colonies composed of many genetically identical individuals? Such organisms undergo alternating bouts of asexual and sexual reproduction throughout their life-cycle - so are there parasites that can castrate such hosts?

Today's parasite is Tetracapsuloides bryosalmonae - it is a myxozoan, parasites that were once thought to be protists, but are actually related to jellyfish and corals in the phylum Cnidaria. Throughout their evolution, they have simply been heavily modified for a parasitic way of life. Tetracapsuloides bryosalmonae has a very comprehensive scientific name in terms of describing its life-cycle - the species name encompass both of the parasite's hosts; bryozoans and salmon. In salmon, it causes a serious disease call Proliferative Kidney Disease (PKD), but less is known about its ecology in its bryozoan host

Bryozoans are also called "moss animals", and they are quite odd (even if rather common) little critters (you can read more about them on the Bogleech website here). They are colonial animals that live as a collective of individuals called "zooids", and are encased in a mineralized exoskeleton that can take on various shapes including fans, bushes, and flat sheets. Most of the time, the colony grows by budding genetically-identical zooids (clones), and colonise new habitats when fragments of the colony break off and settle elsewhere. But during lean times, the colony starts producing statoblasts, which are tough little capsules of cells that can be released into the environment to start the colony anew elsewhere, rather like seeds.

Most of the time, T. bryosalmonae exists as a quiet, secretive infection in the form of single-cells embedded in the body wall and proliferates as the colony grows. But this parasite can also switch into a more overt mode where it starts producing multicellular sacs of parasite cells, and because individual zooids are connected to each other in the colony via a common body cavity, during such flare-ups, the infection can spread throughout the colony. During the overt phase of the infection, T. bryosalmonae effectively castrates the bryozoan, and infected colonies cannot produce statoblasts.

However, on the flip side, because infected colonies aren't diverting resources towards producing statoblasts, they are better able to survive periods of starvation and suffer fewer overall zooid deaths comparing with uninfected colonies. In the natural setting, T. bryosalmonae usually enters its overt phase during late spring or autumn when the bryozoan colony undergoes its greatest period growth of asexual growth - which gives the parasite more opportunities to spread. As the parasite subsides back into its covert phase again, the bryozoan colony once again has an opportunity to produce statoblasts.

By cycling between a covert and overt phase, the parasite can persist without causing damage that can compromise the host's survival. Asexual colonial organisms can avoid permanent castration like that seen in snails infected with parasitic flukes. Theoretically, colonial modular animals can potentially live indefinitely due to their mode of reproduction. But another benefit associated with such a life-style could be an increased tolerance for infection - whereas discrete, unitary animal might be completely sterilised by host-castrating parasite, when infected with a parasite like T. bryosalmonae, modular animals can simply bide their time and reproduce when the parasite subsides between periods of overt infection.

Image from the Natural History Museum

Reference:

Hartikainen, H. and Okamura, B. (2012) Castrating parasites and colonial hosts. Parasitology 139:547-556

Sphaeromyxa cannolii

We've met other myxozoan parasites before, including the very well-known causative agent of whirling disease in salmonid fishes, Myxobolus cerebralis. Today, meet a newly described species of myxozoan that was found infecting seahorses collected from the Gulf of Mexico. Not only was this the first such species described from this seahorse, but this is also the first time that any pathology attributable to a species in this genus has been recorded. The abundance of the parasites in the liver was observed to obstruct the bile ducts of the fish, which caused noticeable accumulation of bile in the diseased hosts. The intermediate hosts are presumed to be some kind of annelid worm, but remain unknown for this species. And in case you were wondering, yes, the species name for this parasite comes from the fact that it looks like a cannoli.

Image from the paper.

Reference: Sears, B.F., P. Anderson, and E.C. Greiner. 2011. A new species of myxosporean (Sphaeromyxidae), a parasite of lined seahorses, Hippocampus erectus, from the Gulf of Mexico. Journal of Parasitology 97:713-716.

Myxidium sp.

When species of plants and animals are introduced to a new environment, this can often lead to some unexpected consequences. The parasite for today is Myxidium sp. - a myxosporean that lives in the liver and brain of native frogs in Australia. But in addition to the native amphibians, this parasite is also found in the invasive cane toad. The cane toad was introduced into Australia to control cane beetles, but has since become one of the most famous posterchildren of invasive species. While Myxidium was originally thought to have been a "present" brought to Australia by the cane toad, recent research indicates that it might actually be native to Australia.

The infamous cane toad does play a role in the story of Myxidium, but in a different manner to what was originally suspected. A collaborative group of researchers from Australia and the Czech Republic found that instead of bringing Myxidium to Australia, the toad has become embroiled in an ecological phenomenon known as "spillback". This is when a native parasite adopts a newly introduced host, this new species turns out to be a better host for the parasite than the native species it was originally infecting, and the parasite propogates more successfully in the new host species.

This can have dire consequences for the original host because the introduced species acts as an ampilifier for the parasite. As a result, the original host become exposed to more of the parasite than ever before. Because many parasites often have dose-dependent effects, this can mean a parasite, which would otherwise be tolerated, can become debilitating or even deadly to its original host.

Reference (and photo):
Hartigan A, Fiala I, Dyková I, Jirků M, Okimoto B, et al. (2011) A Suspected Parasite Spill-Back of Two Novel Myxidium spp. (Myxosporea) Causing Disease in Australian Endemic Frogs Found in the Invasive Cane Toad. PLoS ONE 6(4): e18871. doi:10.1371/journal.pone.0018871

June 15 - Myxobolus cerebralis

Fishermen are probably familiar with this parasite, which causes whirling disease in trout and salmon. These parasites, which belong to an enigmatic group known as Myxozoa, alternate between tubifex worms and the fish. The parasites in the worm release triactinomyxon spores into the water. These are not passive little cells just waiting to be eaten, though - oh no, these spores are a parasite-injecting machine. They can swim through the water to find a fish host, and then will discharge a coiled filament, which produces a hole in the fish skin and allows the parasite to enter. They will migrate through the fish, eventually coming to reside in the cartilage surrounding the brain. There they cause both skeletal and neurological damage, which frequently results in abnormal movement and behavior - the whirling for which the disease is named. When the fish dies either from predation or other causes, the parasites are released into the water to go find new worm hosts. The origin of this group has been controversial - though single-celled, some morphological and genetic data have placed these parasites as closely related to cnidaria (e.g. jellyfish), while others have suggested that they may actually be bilateria.