Petromyzon marinus (revisited)

Today we're featuring a guest post by Darragh Casey - 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 Darragh take it from here.

What makes huge sharks jump skywards? Perhaps, the answer to this question is the ancient sea lamprey, Petromyzon marinus.

Image from Figure 1 of this paper

No one is quite sure about what makes the basking sharks of our oceans breach and leap like their predacious cousin, the great white shark. Many theorise this phenomenon is the shark’s action to rid itself of various menacing parasites from their bodies. It could be the case that the annoyingly adapted sea lamprey is proving one rowdy passenger too many, hence, pushing these sharks over the edge, or, in this case, the waterline.

Sea lampreys are one of the most noticeable and common ectoparasites observed on the second largest fish in the sea, the basking sharks. Interestingly, it’s not until the lampreys become adults that they begin to bother larger fish in the ocean, in fact, they don’t even enter the ocean until they’re adults.

Prior to becoming fully metamorphosed they will have spent the last 3 – 5 years of their lives burrowed in the sediment of rivers, filter feeding on organic matter in the water column, and then they transform to become parasitic wanderers. Once they find a suitable host they use their oval shaped sucking mouth and many small teeth to grasp on and feed on the tissues and blood of an unsuspecting donor.

When the victim is the basking shark, the lamprey show their unique abilities to full power. First off, they have to penetrate the hard dermal denticle armour of sharks, which is no mean feat! The next problem they face is the high urea levels in the tissues and the blood of basking sharks. To cope with this potentially toxic level of urea in their host’s blood, the lamprey has a fantastic capability to dispel the urea whilst feeding, using this ability for their survival as described by Wilkie and colleagues. The lamprey also use lamphredin, a chemical in their saliva with anti-clotting properties, to prevent wounds from healing while feeding.

A pair of sea lamprey feeding on a basking shark, from Fig. 1 of this paper

The resulting damage from sea lamprey, especially in great numbers, can be very negative on the basking shark. They deprive the sharks of some of their urea, which is vital for osmoregulation to keep constant pressure in their bodily fluids, and they leave the sharks with open wounds which can become infected, and who knows what could happen then? However, it is more likely, that the sharks, only experience minor lamprey-related health deficiencies.

After a few years, the lampreys will eventually jump ship from their aggravated marine host and return to riverine habitats to find a suitable ally to mate with, spawn, and die soon after. In doing so, they set the foundations for a new generation of lampreys to hassle the basking sharks of the oceans for many years to come.

Are the sea lamprey such a nuisance to these sharks that they decide to momentarily leave the water in an attempt to shake them off? It’s hard to know for certain but one thing is for sure, if blood draining parasitic fish were to latch on to me I would be trying to leave the ocean pretty fast too.

References:
Johnston, EM., Halsey, LG., Payne, NL., Kock, AA., Iosilevskii, G., Whelan, B. and Houghton, JDR. (2018). 'Latent power of basking sharks revealed by exceptional breaching events’. Biology Letters. 14: 20180537

Wilkie, M., Turnbull, S., Bird, J., Wang, Y., Claude, J. and Youson, J. (2004). ‘Lamprey parasitism of sharks and teleosts: high capacity urea excretion in an extant vertebrate relic’. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology. 138: 485-492.

This post was written by Darragh Casey.

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