Abstract
Babesia is an intraerythrocytic, obligate Apicomplexan parasite that has, in the last century, been implicated in human infections via zoonosis and is now widespread, especially in parts of the USA and Europe. It is naturally transmitted by the bite of a tick, but transfused blood from infected donors has also proven to be a major source of transmission. When infected, most humans are clinically asymptomatic, but the parasite can prove to be lethal when it infects immunocompromised individuals. Hemolysis and anemia are two common symptoms that accompany many infectious diseases, and this is particularly true of parasitic diseases that target red cells. Clinically, this becomes an acute problem for subjects who are prone to hemolysis and depend on frequent transfusions, like patients with sickle cell anemia or thalassemia. Little is known about Babesia’s pathogenesis in these hemoglobinopathies, and most parallels are drawn from its evolutionarily related Plasmodium parasite which shares the same environmental niche, the RBCs, in the human host. In vitro as well as in vivo Babesia-infected mouse sickle cell disease (SCD) models support the inhibition of intra-erythrocytic parasite proliferation, but mechanisms driving the protection of such hemoglobinopathies against infection are not fully studied. This review provides an overview of our current knowledge of Babesia infection and hemoglobinopathies, focusing on possible mechanisms behind this parasite resistance and the clinical repercussions faced by Babesia-infected human hosts harboring mutations in their globin gene.
Highlights
Human babesiosis is a zoonotic disease in which the natural acquisition of human cases is most often the result of an interaction with established zoonotic cycles [1,2]
In our previous report of B. microti infections in mice, we reported the increase in hemolysis in Babesia-infected mice, which was highly accentuated in mice harboring the sickle cell anemia (SCA) genotype, as observed by significantly reduced hematocrit and enhanced hemoglobinuria in these mice [13]
When Babesia sporozoites are first injected into the human host, they target the host red blood cell (RBC) immediately, unlike Plasmodium spp. which are required to undergo an exoerythrocytic phase in hepatic cells
Summary
Human babesiosis is a zoonotic disease in which the natural acquisition of human cases is most often the result of an interaction with established zoonotic cycles [1,2]. Babesia is an intra-erythrocytic parasite that causes malaria-like symptoms in infected people. Plasmodium, the causative agent of malaria, is the most studied Apicomplexan parasite and, like Babesia, resides within red blood cells. Epidemiological, and genome-wide association studies have identified multiple polymorphisms in the globin protein of hemoglobin within the red blood cell (RBC), commonly referred to as hemoglobinopathies, that attenuate or completely abrogate malaria pathogenesis. The evolutionary proximity of Plasmodium and Babesia [5], and the fact that they both infect RBCs, raises important clinical questions of Babesia infections in patients harboring hemoglobinopathies. We provide an overview of available clinical cases of the severity of Babesia infection in patients harboring these mutations and emphasize why it is essential to focus research in this area. We describe plausible mechanisms that could exert this protective effect and discuss ways we can use this double-edged sword to develop better therapeutics against blood-borne parasites
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