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Introduction
Babesiosis is a communicable infection caused by protozoa that belong to the phylum Apicomplexa and genus Babesia (Hunfeld, Hildebrant and Gray 1219). These parasites invade the red blood cells to cause disease and have the ability to infect a wide range of vertebrate hosts such as cattle, human beings, and birds. Babesiosis has high incidence rates in North America particularly in the United States through other cases have been reported in countries such as Egypt, Korea, and South Africa (Gray et al. 3). Human babesiosis is caused by Babesia microtia, which is “a rodent-borne piroplasm, and also occasionally by a newly recognized species, the so-called WA1 piroplasm” (Homer et al. 451). Babesia microti needs proficient vertebrate and nonvertebrate hosts to sustain its transmission cycle (Homer et al. 451). In this case, ixodid ticks are responsible for the dissemination of the parasites to the vertebrate host. Other species such as Babesia divergens, Babesia venatorum, and Babesia duncani are also known to affect humans (Gray et al. 4).
Human babesiosis may present slight flu-like signs or no symptoms at all in approximately a quarter of infected adults and half of the infected children making the disease go undiagnosed in many instances (Gray et al. 4). However, if the patient is splenectomized or is on immunosuppressive medication very severe symptoms such as hemoglobinuria (the presence of hemoglobin in the urine), relentless high fever, severe sweating, headache, and abdominal pain may occur. These symptoms greatly resemble those experienced in malaria. Babesiosis may also induce critical difficulties such as acute malfunction of the respiratory system, congestive heart breakdown, coma, and failure of the kidney.
This paper looks at the pathogenesis of Babesia microti, which is the most common Babesia species that cause human babesiosis. It pays attention to the life cycle of the parasite in the progression of the disease as well as the accompanying side effects.
Pathogenesis
The life cycle of Babesia microti in the human host begins with the transfer of sporozoites from the salivary gland of the tick into the host bloodstream during feeding. Blood transfusion with contaminated blood may also introduce sporozoites into the bloodstream of healthy individuals. The effectiveness of sporozoite transmission is directly proportional to the duration of contact between the tick and the host (Homer et al. 454). The sporozoites infect red blood cells (erythrocytes) where they multiply by binary fission. In the erythrocytes, the sporozoites develop into multinucleated schizonts, which undergo further differentiation to form merozoites. The merozoites grow off from the schizonts. They then lyse the red blood cells and continue infecting other red blood cells. The parasites exhibit a high rate of reproduction that causes immense harm to the host cells.
The key pathological occurrence of serious infection is hemolysis (the bursting of the red blood cells) as a consequence of erythrocyte infestation by sporozoites. This leads to hemolytic anemia and jaundice (Gray et al. 4), which can further lead to anoxia and toxic outcomes thereby causing loss of life and organ breakdown in the absence of medical intervention. The extent of anemia does not correlate with the parasitemia (magnitude of infection or number of parasites in the system) suggesting that other mechanisms play a significant role in the progression of the disease. It is thought that pro-inflammatory cytokines are produced in abundance leading to symptoms such as fever, renal deficiency, clotting difficulties, muscle pain, and low blood pressure.
There is an immense correlation between the pathogenesis of babesiosis and the normal host immune response to infections and parasite-generated alterations in the membrane of the red blood cells (Vannier and Krause 2401). According to Hunfeld et al., the changes in the surface of the membranes of the red blood cells promote their clearance in the spleen (1227). In the mild instances of babesiosis, “inflammatory cytokines (e.g., tumor necrosis factor α [TNF-α] and interleukin-6) and adhesion molecules (e.g., E-selectin, intracellular adhesion molecule 1 [ICAM-1], and vascular-cell adhesion molecule 1 [VCAM-1]) are up-regulated” (Vannier and Krause 2401). The overproduction of cytokines amplifies the magnitude of the immune response thereby leading to severe babesiosis and its related difficulties such as high fever and immense pain.
The sequestration of white blood cells and the parasite-infected red blood cells may result in the blockage of the microvasculature as well as a reduction in the oxygen content of the tissues. Proteins may also be transported to the exterior of the affected red blood cells. Such protein-coated red blood cells tend to stick to the inner surface (endothelium) of the blood vessels and in so doing slow down their elimination by the spleen. While trying to get rid of infected red blood cells, the body’s immune system may also eliminate uninfected erythrocytes. Such nonhemolytic machinery also worsens anemia in patients suffering from babesiosis.
In vitro experiments and studies on B. microti using animal models (mice and cattle) provide information on the pathogenesis of human babesiosis. It is shown from such studies that cellular immunity has an upper hand over humoral immunity in containing babesiosis (Hunfeld et al. 1227). This is evident in mice experiments where T helper cells play a significant role in keeping parasitemia under control. These findings are consistent with the inability of immunocompromised patients to control unrelenting parasitemia. In the same way, a reduction of natural killer cells and macrophages makes individuals more vulnerable to babesiosis infection. All these findings lead to the conclusion that the pathobiology of babesiosis is not a consequence of the parasite, but the host immune response.
Splenectomy, which is the surgical removal of the spleen, increases the risk of babesiosis. This is because the spleen performs a crucial function in host protection by eliminating infected red blood cells from the bloodstream. In addition, the spleen is a secondary lymphoid organ and participates in intensifying a protective immune rejoinder.
Conclusion
Babesiosis is a rare ailment that can occur in mild or severe forms. The mild form of babesiosis is asymptomatic and may resolve itself without any treatment. On the other hand, the severe form of babesiosis exhibits conspicuous symptoms such as fevers, chills, fatigue, and aches. The symptoms and pathogenesis of babesiosis closely resemble those of malaria infection. In addition, both parasites belong to the phylum Apicomplexa making it hard to distinguish between the two infections. The immune system plays a crucial role in controlling babesiosis thereby making immunocompromised individuals and the elderly highly predisposed to infections. It is also known that most symptoms experienced during the illness are consequences of the host immune response against the disease. Therefore, there is a need to establish efficient diagnostic tools to help in the distinction between babesiosis and malaria infections and ensure that patients get timely interventions to minimize the loss of lives from babesiosis.
Works Cited
Gray, Jeremy, Annetta Zintl, Anke Hildebrandt, Klaus-Peter Hunfeld, and Louis Weiss. “Zoonotic Babesiosis: Overview of the Disease and Novel Aspects of Pathogen Identity.” Ticks and Tick-Borne Diseases 1.1 (2010): 3–10. Print.
Homer, Mary J., Irma Aguilar-Delfin, Sam R. Telford, Peter J. Krause, and David H. Persing. “Babesiosis.” Clinical Microbiology Reviews 13.3 (2000): 451-469. Print.
Hunfeld, K.-P., A. Hildebrandt and J. S. Gray “Babesiosis: Recent Insights into an Ancient Disease.” International Journal for Parasitology 38.11 (2008): 1219–1237. Print.
Vannier, Edouard and Peter J. Krause. “Human Babesiosis.” The New England Journal of Medicine 366.25 (2012): 2397-2407. Print.
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