|(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)|
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.
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.
I wish I was a flea. But not tiny, human sized.ReplyDelete
I really like this parasite because it is a perfect example of the ultimate endosymbiosis. It reminds me of the bacteria that lives inside the protozoan that lives inside the termite gut; a Russian nesting doll concept of parasites, if you will… I also find it fascinating that being infected with the parasite gives the flea some sort of competitive edge (reaches maturity faster) even though this likely helps the parasite complete its life cycle faster. Could this be considered a mutualism then?ReplyDelete
Wow, very unique hyperparasite. It's really fascinating that it actually makes the cat fleas grow up faster. Really cool article!ReplyDelete
So cool that the parasite accelerates larval growth! I would not have thought a parasite would want their host to grow faster, what an interesting way to exploit their developmentReplyDelete