Protozoa
A malaria-like parasite that lives inside the red cell — and in sickle cell disease the cell it moves into is already failing.
Not yet investigated
A malaria-like parasite that lives inside the red cell — and in sickle cell disease the cell it moves into is already failing.
This star is on the map because the show intends to take the question apart properly — the trials, how it is actually tested, whether the thing sold is the thing studied. That work is not done yet, and nothing here should be read as a conclusion. When the investigation is published it will appear on this page.
What we are reading
Gathered for the investigation and not yet written up. Each note says what the paper does and does not show.
The mechanism, measured. Using ektacytometry on AA, AS and SS red cells before and after Babesia infection, the damage lands on a spectrum: normal cells lose some deformability, sickle-trait cells more, and SS cells most of all — higher point-of-sickling values, loss of surface area, altered osmotic fragility, and hypervesiculation, shedding membrane as extracellular vesicles. That is a mechanistic explanation for why babesiosis in sickle cell disease produces hyperhaemolysis and extreme anaemia rather than the flu-like illness a healthy adult gets.
The counter-intuitive half, and the reason this topic is interesting rather than merely sad. Sickle cell TRAIT was selected because it protects against Plasmodium falciparum. So does it protect against Babesia, a close apicomplexan relative? Partly: in sickle-cell-ANAEMIA red cells the parasite does badly — defective merozoite infectivity, impaired egress, much lower parasitaemia. But sickle TRAIT cells support infection at rates comparable to normal red cells. So the trait that shields against malaria does not shield against its cousin, and the disease that limits the parasite is the same disease that cannot survive losing the cells.
The clinical trap, in two cases. Babesia microti and B. duncani are transmissible by TRANSFUSION — and people with sickle cell disease are among the most transfused patients in medicine. Post-transfusion haemolysis in a sickle cell patient looks exactly like a delayed haemolytic transfusion reaction, so the reflex is steroids or other immunosuppression, which is the wrong treatment and makes the parasite worse. The authors argue for universal blood screening in endemic areas. Note for the episode: the FDA did not require region-based Babesia screening of the US blood supply until 2019.
Connected on the map
Also in Protozoa
The letter
The full citation list for each investigation, the studies that didn't make the episode, and any corrections — sent the morning it publishes.
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