Health

Sleeping sickness and its kin may have arrived via beehives

aRecent events She made it clear that new viral diseases in humans often start as spillovers from infections in other species. But viruses are not the only pathogens that do this. Leishmaniasis, sleeping sickness, and Chagas disease, three fatal diseases caused by single-celled organisms called trypanosomes, are also likely to be in this category as well. Not only are they spread by insects (sand flies, tsetse flies, and kissing bugs respectively), they are also presumed to have originated in insects (though not necessarily their current vectors)—because most known trypanosomes are insect parasites. This raises the question of how they jump the species barrier. A study just published in Proceedings of the Royal Society, by Evan Palmer-Young of the USDA, suggests that the answer may be “bees.”

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Dr. Palmer-Young’s starting point was the observation made a few years ago Crithidia mellificae, a type of trypanosome previously thought to be restricted to honeybees, was present in mammals. Marmosets (a type of New World monkey), koates (small carnivores related to raccoons), fruit bats, crab-eating foxes and ocelots are all now known to host them. So he wondered if there was something special about this particular type of trypanosome that allowed these jumps to happen in mammals — and whether their honeybee adaptation, if there was, might be that thing.

Two thoughts occurred to him. One is that although most insects are endothermic (meaning their body temperatures vary depending on their surroundings), bees, like mammals, often generate additional heat, and also benefit from the close proximity of their hives. This keeps their body temperatures at mammal-like levels in their mid-30s and up.

Dr. Palmer Young’s other thought was that honeybees’ guts are more acidic than those of most insects (this helps them digest nectar and pollen). In fact, they have a pH that matches that of the digestive system of mammals. So expect that mammalian heat, or acidity, or both, may create a barrier to mammalian trypanosome infection that parasites that have adapted to bees can easily overcome.

To test this idea, he and his colleagues considered C. melificae, as well as in the second trypanosome parasite of honey bees, Lotmaria. For comparison, they studied two strains of Crithidia fasciculata, Trypanosoma common in mosquitoes and closely related to C. melificae.

They cultured all four trypanosome species in flasks, and then exposed samples from each to a temperature range of 20–41 °C at a constant pH, or to a range of acidity from pH 2.1 (extremely acidic) to pH 11.3 ( very (alkaline) at a constant temperature. While doing so, they monitored the population growth rates of the parasites.

As postulated by Dr. Palmer Young, both honeybee parasites are tolerant of the types of temperatures common in hives. But they did not tolerate them as much. growth rate C. melificae, a well-established species in bees, peaked at 35.4 °C. that of Bassem, which was not reported in bees until 2014 and is believed to be a recent arrival, peaked at 33.4 °C. Both of my breeds C packageA, however, can only handle lower temperatures. Their growth rates peaked near 31°C. Acidity experiments similarly revealed that both bee parasites thrived at pH 5.2, which is the acidity level of the honeybee’s digestive system, while mosquito parasites needed an alkaline pH of more than 7.5 to grow well.

Finally, both the acidity of the honeybee and the temperature of the hive create a barrier for trypanosomes C. melificae You might pretty much beat it Bassem It’s just about acclimatization to it, which mosquito parasites cannot tolerate. How this happened is not clear. But what is clear from the repercussions of mammals C. melificae, is that it can lead to a parasite that is also able to grow in mammals.

Whether this is the path taken by the trypanosomes that cause leishmaniasis, Chagas disease and sleeping sickness remains to be seen—as does how their modern vectors fit into the picture. Dr. Palmer-Young’s findings, though, suggest that monitoring hives for diseases that can be transmitted to humans would be an endeavor worth pursuing.

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This article appeared in the Science and Technology section of the print edition under “Bad Sting”

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