One of my big problems with the theory of evolution is this horrible misconception that it’s been ‘proven to be true’. Prove can mean several things, including 'to establish as true' and 'to put to trial or to test' – the first of these is incredibly hard to do scientifically; the second is also hard, but it’s also fun and rewarding. Scientists are very wary of claiming to have ‘proved’ anything to be definitely true, simply because history has shown us that as we advance through the ages we develop more techniques for analysis and finer tools for examination. What may be true in one century may not be true in the next. Indeed, what may be taught as true in high school is often discovered to be a vast simplification (if not an outright lie) at university. If you don’t believe me, go ask a graduate of any of the sciences how accurate the relevant high school text book was. Interestingly, the loudest voices of the complete and utter certainty of the theory of evolution rarely belong to people who are experts in the field. As a major in genetics and someone who has worked in the field of bacteriology (one of the better models for showing evolution through selective pressures), I know that there is a wealth of data that supports this theory. But, as someone who is very familiar with this work, I am also aware that there are some square pegs of data that don’t fit neatly into the round hole of evolution. My favourite of all of these examples is the humble yet devastatingly complex parasite.
Parasitology is a fascinating field. If you don’t mind being scared of food and water for the rest of your life, I advise you to pick up a book on the little guys. Rather than painting a broad love letter, I’m going to focus on one particular parasite that won’t be burrowing through your skin anytime soon: Euhaplorchis californiensis.
E. californiensis is a member of the family of trematode parasites, which live in several host systems (given the name, I bet you can guess where this system is based). E. californiensis starts off its life in the California horn snail, then steps up the food chain into the California killifish, and finally reaches the penthouse layer of hosts when it is taken up by the predatory birds that stalk the marshes these parasites call their home. Initially, they are tiny, baby trematodes in the marsh water, who stumble across the horn snails and burrow in through their flesh. From there, they exit the snails in search of either other snails to inhabit or something a little more challenging. Being small worms, they get eaten by many of the more complex organisms in the marsh ecosystem, including the Californian killifish. E. californiensis then migrate to the brain of the fish and secrete chemicals which change the behaviour of the fish, making it more likely to be eaten by the predatory bird, which allows the trematode to move into its third host environment.
There is no real understanding of why a parasite would develop a multiple-host system. The theory applied to all studies of multiple-host parasites is that they were initially prey to all of their later hosts. If an animal can turn a predator into an environment in which they can live, the likelihood of them being able to procreate and propagate their genes is much greater (the theory evolution centres on a trait being heritable; if it cannot be passed on to the next generation to give them an advantage then it is not a very useful trait).
For example, a key step in the lifecycle of E. californiensis is to be eaten by a fish. Any parasite that can survive or escape the digestive system suddenly has a much wider ecological niche in which to reside. It needs to survive stomach acid, be able to burrow through intestinal walls and further tissues, and to evade the host immune system. It makes sense that any parasite that can evade digestion in one organism can therefore similarly evade digestion in another organism which possesses a similar digestive system – no new skills would need to be developed.
E. californiensis had to find the right location in the California killifish host, and the right kind of chemical influence to exert in order to change the behaviour of the secondary intermediary host in order to increase the chance of it being caught and eaten by the third intermediary host, the predatory bird. Keep in mind that this involves sacrificing a stable host environment. E. californiensis can live in snails for approximately 20 years, in the fish host for two years (the fish needs to be eaten in that time, or the parasite is trapped in the host when it dies), and then only several weeks in its third host, the predatory bird.
The cercariae asexually reproduce within the horn snail, resulting in tens of thousands of genetically identical cercariae (with some room for random mutation of the genome) being released into the environment as they emerge from the snail’s rectum. The adult parasite is able to reproduce both sexually and asexually, and produces an unknown number of eggs in its third and final host (estimated to be in the millions of eggs) which are defecated into the marsh. There is no reproduction in the secondary host, the California killifish.
Let us recap the challenges that E. californiensis must overcome to reach its third and final host: being eaten by the California killifish, escaping the killifish digestive system, evading the killifish immune system, migrating through numerous killifish tissues, settling on the brain as the optimal tissue to take up residence in, developing the ability to secrete (or dictate host secretion) of certain chemicals that lead to attention-getting behaviours, survive the death of its secondary host, survive being eaten by the animal that will become the third host environment, escaping the third host digestive system, evading the third host immune system, finding an ideal organ or tissue in which to take up residence (in this case, the small intestine) and reproduce until the end of its days.
You have to admit, that’s a lot of work for a little trematode. Especially when you take into account that these are organisms that are acting on very basic stimuli-response instinct. They cannot learn, they cannot think their way out of a problem. Also, with no reproduction in the secondary host these little guys are essentially playing without a save point.
It is feasible that a trematode to not get killed in the process of being eaten – birds are not renowned for chewing their food thirty times before swallowing. The digestive system is quite a problem though – the acidity of the stomach and its mucus lining are both parts of the innate immune system, barriers that stop invading pathogens from entering the host body by sneaking in with the food. Before this moment the E. californiensis has never encountered the digestive environment. It has not been equipped with the genes for thicker skin or mucus secretion that could protect it from this hostile environment because no other E. californiensis has reached this point and stopped to have a few kids which could carry the genetic cheat codes for this level out into the wider ecosystem. If the trematode has a phenotype that enables it to survive in this hostile environment that is dramatically different from its norm, well, that’s one heck of a coincidence.
Then there is the immune system to evade – phagocytic cells trying to engulf the parasite, inflammation blocking its path, recruiting aggressive immune cells, and releasing chemicals that are detrimental to the parasite. It has to avoid both getting destroyed by the immune system, and also getting trapped in some tissue and encased in a sphere of scarred, dead cells. The immune system is elaborate, and aggressive, and adaptive. There are three main mechanisms for evading the host immune system: adapting more quickly than the host, hiding from the immune system by carrying receptors that fool the immune system into thinking that the parasite is host tissue, or distracting the immune system by throwing out red herrings.
Trematodes do all of these things – they constantly shed and regenerate their skin, changing the characteristics of the new tissues. By the time the host immune system has been primed to recognise the skin of the trematode the parasite is wearing a new skin but has left the old one lying around, and of course the host immune system has to take the time to clean that up. Some trematodes are able to mimic host tissues, but more common is their ability to mimic tissues of trematodes at different stages of their life cycle. For example, if an adult trematode is shedding receptors that are otherwise only found on a younger trematode, the immune system will be primed to remove any young punks who try to move in on the established trematode’s turf. This is bizarrely clever for an organism that has no cognitive abilities.
One worm would need to get through every single challenge listed above before it would be able to reproduce and pass the genes that gave it the ability to survive in two brand new host systems back into the gene pool. Once those genes have been acquired and passed on, everything is a piece of cake. All of the subsequent E. californiensis are just following the genetic road map. But all of that relies on there being one pioneer to get all the way though to the third host and then be able to release its parasitic embryos into the environment. Oh, and don’t forget that the eggs also need to work out their own escape plan, avoiding the digestive processes and immune system surveillance that is present in the small intestine.
This is an example of a life cycle in which the very mechanism of evolution – traits being heritable – is absent for the parts of the lifecycle in which the parasite is most challenged by its environments and most likely to be killed. If you were to justify this process of the first trematode working its way through its second host to luck, to the possibility that a tiny organism that had previously lived in marsh water and snails could be the product of enough mutations in its genome to have the genes, instincts, and chemical process it would require to travel through those hosts and then reproduce, taking into account that there has been no previous selective pressure that would give the ancestor-trematode (which was asexually reproducing inside a snail) any benefit at all in carrying around these superfluous genes nor pressures to maintain the function of these genes until such a time as that first trematode made the voyage through fish and bird... Look, the assumption that these genes for survival arose from nowhere is attributing drastic advances in behaviour and physical capabilities to some unknown mechanism. It is arguing that ‘God did it’ without the God part. And at least with the God-fallback there’s an explanation of how those genes came to be in an organism that had no prior need for them and no mechanism to evolve them gradually over numerous generations.
If a theory is not able to be applied sufficiently to all examples, then it’s pretty clear that the theory is lacking.
Bibliography
Fingerut, J. T. Et al. (2003) ‘Patterns and Processes of Larval Emergence in an Estuarine Parasite System’ in The Biological Bulletin, vol 205: 2, pp 110-120.
Little, J. W. (1970) ‘The excystment, growth and reproduction of Acanthoparyphiutn spinulosum Johnston, 1917 (Trematoda) in chicks fed various diets’ in Journal of Parasitology, vol 60: 1, pp 61-78.
Shaw, J. C. Et al (2010) ‘Ecology of the Brain Trematode Euhaplorchis Californiensis and its Host, the California Killifish (Fundulus Parvipinnis)’ in Journal of Parasitology, vol 96: 3, pp 482-490.
