AS RECENT EVENTS have made abundantly clear, new viral diseases in people often start as spillovers from infections affecting other species. But viruses are not the only pathogens to do so. Leishmaniasis, sleeping sickness and Chagas’ disease, three potentially lethal illnesses caused by single-celled creatures called trypanosomes, are probably in this category, too. Not only are they spread by insects (sand flies, tsetse flies and kissing bugs respectively), they presumably originated in insects, too (though not necessarily their current vectors)—for most known trypanosomes are insect parasites. That raises the question of how they leapt the species barrier. A study just published in the Proceedings of the Royal Society, by Evan Palmer-Young of America’s Department of Agriculture, suggests the answer may be “bees”.
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Dr Palmer-Young’s starting-point was the observation, made a few years ago, that Crithidia mellificae, a trypanosome once thought exclusive to honeybees, was turning up in mammals. Marmosets (a type of New World monkey), coatis (small carnivores related to raccoons), fruit bats, crab-eating foxes and ocelots are all now known to host it. He therefore wondered if there was something special about this particular trypanosome that allowed these leaps into mammals to happen—and whether, if there was, its adaptation to honeybees might be that something.
Two thoughts occurred to him. One was that, though most insects are ectothermic (meaning their body temperatures vary with their surroundings), bees, like mammals, often generate extra heat, and also benefit from the proximity, in their hives, of their neighbours. This keeps their body temperatures at mammal-like levels in the mid-to-upper thirties.
Dr Palmer-Young’s other thought was that honeybee guts are more acidic than those of most insects (this helps them to digest nectar and pollen). Indeed, they have pHs which match those of mammalian digestive tracts. He therefore speculated that mammalian heat, or acidity, or both, may create a barrier to trypanosome infection of mammals which parasites adapted to bees can easily overcome.
To test this idea, he and his colleagues looked at C. mellificae, and also at a second honeybee trypanosome parasite, Lotmaria passim. For comparison, they studied two strains of Crithidia fasciculata, a trypanosome common in mosquitoes that is closely related to C. mellificae.
They cultured all four types of trypanosome in flasks, and then exposed samples of each either to a range of temperatures from 20-41°C at constant acidity, or to a range of acidities from pH 2.1 (very acidic) to pH 11.3 (very alkaline) at constant temperature. While doing so they monitored the parasites’ population-growth rates.
As Dr Palmer-Young had theorised, both of the honeybee parasites tolerated the sorts of temperatures common in hives. But they did not tolerate them equally well. The growth rate of C. mellificae, a species well established in bees, peaked at 35.4°C. That of L. passim, which was not reported in bees until 2014 and is thought to be a recent arrival, peaked at 33.4°C. Both strains of C. fasciculata, however, could cope only with lower temperatures. Their growth rates peaked near 31°C. The acidity experiments similarly revealed that both bee parasites thrived at pH 5.2, the level of acidity in honeybee digestive tracts, whereas the mosquito parasites needed a more alkaline pH of around 7.5 to grow well.
All told, both honeybee gut-acidity and hive temperature create a barrier to trypanosomes that C. mellificae has largely overcome, that L. passim is just about coping with, and which the mosquito parasites cannot endure. How this happened is unclear. What is clear, though, from the mammalian spillovers of C. mellificae, is that it can lead to a parasite also able to thrive in mammals.
Whether that was a path once taken by the trypanosomes which cause leishmaniasis, Chagas’ and sleeping sickness remains to be seen—as does how their respective modern vectors fit into the picture. Dr Palmer-Young’s finding suggests, though, that monitoring hives for diseases which could spill over into humans would be an endeavour worth pursuing. ■
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This article appeared in the Science & technology section of the print edition under the headline “A nasty sting”