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Missed #ABS2020 this year? No problem! You can still learn more about the link between malaria, bird migration and perfect timing!
This is part of my postdoc research with @Beth_macshack and Chris Guglielmo at @BirdsWesternU
Thread is long but the content is
@AnimBehSociety
This is part of my postdoc research with @Beth_macshack and Chris Guglielmo at @BirdsWesternU
Thread is long but the content is
@AnimBehSociety
Malaria is caused by Plasmodium parasites, which belong to a broader group of protozoans of the order Haemosporidia. There are several bird-only haemosporidian genera (e.g. Parahaemoproteus, Haemoproteus, Leucocytozoon), all of which are transmitted by invertebrate vectors.
I like to think that haemosporidians are like the chest busters in Alien, but instead of chests they are busting host cells. These parasites clone themselves within cells the host, which eventually burst releasing more clones.
Some of these clones may differentiate and become gamete precursors, namely gametocytes, which infect red blood cells. Gametocytes will then hang out in the peripheral blood circulation, ready to be picked by the next blood sucking vector.
Gametocytes are gorgeous little things! I think they look like jelly beans, so microscopy work usually gets me really hungry. 
Btw, haemosporidian sex happens in the midgut of blood sucking vector! The parasite offspring (aka sporozoites) then migrate to the salivary gland of the vector, where they'll be transmitted with the next blood meal.
Anyways, the fact that haemosporidian parasites can occur in tissues other than the blood makes prevalence data intrinsically underestimated. Hence, a negative PCR for a blood sample only tells us that the parasite DNA isn't in the blood.
When you add a migratory host to the equation, this system gets c-o-m-p-l-i-c-a-t-e-d. I demonstrated that migrants have low prevalence to no infections at all during winter, even when resident populations are LOADED. https://doi.org/10.1111/jbi.13760
I also presented evidence that gametocytes, those pesky transmission stages that infect the red blood cells, are rarely found in the blood smears of Plasmodium-infected birds wintering in the Bahamas –– we need more microscopy evidence on this! https://link.springer.com/article/10.1007/s00436-020-06646-y
There's also massive evidence that breeding bird populations in N America have high prevalence of infections. Makes sense through the parasite point of view: lots of vectors, lots of immuno naive individuals entering the host populations, and lots of stressed out parents! 10/
A hypothesis explaining this high infection prevalence during the breeding season is that infections relapse in spring and summer. This means that parasites will invest in producing stages that infect red blood cells, which maximizes the chances of transmission.
Problem is...it's hard to demonstrate relapse. You need longitudinal data on individual birds, which is often hard to get in the wild. The solution for that is to hold the birbs in captivity during winter and spring, and sample them multiple times.
I housed 21 yellow rumped warblers in captivity between November 2018 and May 2020. They had a buffet of a balanced diet and lots of mealworms. They were housed in vector free rooms with controlled temperature and programmed light schedule. 5 stars bird hotel, if you may.
I took a small blood sample of every bird in the fall, and another in the spring. In the fall, 14 birds were infected, whereas in the spring, 20 birds tested positive! In the figure, rows are individuals, red represents a positive PCR and gray a negative PCR.
Side note: I'm obsessed with false negatives, so I tested each bird using two nested protocols that amplify a fragment of the parasite's cyt b gene.
Thankfully, I had another batch of birbs, so I could test whether or not this infection relapse was linked to photoperiod cues. Changes in photoperiod trigger migratory restlessness in spring, so it could be the cue parasites use to relapse.
To test the effect of photo stimulation on infection relapse, I delayed the photo stimulation of another 29 birds. This group wintered (as in winter light schedule) for ~50 days longer than the first group. I took a small blood sample of the birds in the fall, winter and spring.
I was in awe when I visualized these data. Some infections relapsed before photo stimulation. Parahaemoproteus, Plasmodium and some Leucocytozoon parasites re-appeared in the blood while the birds were still under winter photoperiod.
I was lucky enough to be working with Jessica Deakin, a PhD candidate in Chris Guglielmo's lab. Jess had some birds with radio tags wintering with my study birds. From Jess's activity data, we know that birds weren't in migratory restlessness before photo stimulation.
There's a vast literature on circadian clocks of human malaria parasites; it's known that they're capable of rhythmicity independent from the host. However, as far as I know, this is the first evidence of a clock-like mechanism of relapse for Parahaemoproteus parasites.
These data also highlight the complex short-term temporal dynamics of haemosporidian parasite infections. Parasite prevalence in natural populations should be always seen as a snapshot of a highly dynamic process.
I also urge caution when interpreting prevalence data in migratory bird populations. It's often assumed that infections delay migration, so infected birds arrive later. These data suggest that parasites are more likely to be detected later on during migration.
I'm hoping to have the ms ready within the next month, so stay tuned. Currently working at a sloth pace, but it's happening everyone.
