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Babesiosis as an emerging zoonotic disease is caused by infection with hemoparasites of the protozoan genus Babesia which are the second most common blood-borne parasites of mammals after the trypanosomes [1]. Babesia, the first recognized arthropod-borne pathogen of vertebrates, was discovered originally by the Romanian bacteriologist Victor Babeș as a cause of febrile bovine hemoglobinuria or red water fever at the end of the 19^th century [2].

The first case of human babesiosis has been reported in 1957 near Zagreb, Croatia in a splenectomized young farmer and subsequently several Babesia species have been documented to involve in human infections in United States, Europe, China, Taiwan, Korea, Japan, India, Egypt, South Africa, Brazil and Mexico [3-10]. Up to now, over 100 species of Babesia have been recorded, infecting many mammalian and some avian species making this disease a global health threat [11].

It is well known that hemolytic anemia as a major clinical manifestation of this infection progression can lead to blood supply disruption, tissue hypoxia and eventually cell death [12]. Moreover, erythrocytes adherence to the microvasculature endothelium can also lead to excessive pro-inflammatory cytokine release and intensification of tissue hypoxia [13]. It is noteworthy to mention that blood reperfusion can also result in cell membrane damages and tissue devastation through reactive oxygen species over-generation and neutrophil infiltration [14,15]. Also, it should be borne in mind that activated neutrophils play critical roles in reactive oxygen species, proteases and elastases production resulting in endothelial cell dysfunctions and injuries as well as microvasculopathies [16]. Additionally, hemolysis and hemolytic anemia associated iron overload in tissues can augment oxidative damages, demolish essential macromolecules and exacerbate cytopathies [17].

On the other hand, it is well established that blood flow reduction is associated with testicular germ cell degeneration as well as spermatogenesis impairment [18]. It was also found that testicular ischemia induced oxidative stress triggers leukocyte activation causing increased microvascular permeability, edema and parenchymal cell death [19,20]. Further, hemolytic anemia-induced free iron concentration increase may also lead to testicular failure and male infertility [21].

In line with that, previous reports have shown that experimental babesiosis evoked hemolytic anemia causes remarkable histostructural disorganizations along with functional disorders in the rats’ liver and kidney [22]. Furthermore, it has been revealed that experimental Borrelia crocidurae inoculation leads to pre- and post-capillary blood vessels blockage in rats’ testicular tissue and causes testicular seminiferous tubules damages via disruption of normal testicular blood flow [23]. Accordingly, previous epidemiological reports have implied that higher rates of protozoan parasitic infections in infertile patients can highlight the non-negligible association of protozoan parasitic diseases and fertility disorders [24,25].

On the whole, it seems that Babesia infection as a male infertility risk factor can lead to spermatogenesis disturbances and orchiopathy (Figure 1) probably through testicular microcirculatory disruption and blood flow reduction along with oxidative stress, inflammatory reactions and germ cells apoptosis induction. Accordingly, comprehensive universal programs are urgently needed to promote general awareness about the hidden features of babesiosis and manage this emerging infectious zoonosis.

Figure 1: Possible mechanisms of babesiosis-induced testicular damage.