Babesia - Life Cycle, Pathogenesis, Pathology, Host Immunity

Life Cycle of Babesia

The life cycle of Babesia is completed in two different hosts- The definitive host (hard tick of genus Ixodes, Boophilus, Dermacentor) and the intermediate host (man, wild animals, domestic animals – cow, horse, sheep, goat, pig, dog).

• humans acquire infection by the bite of infected ticks acting as vectors

• sporozoites are inoculated in the skin from where they are carried into the circulation

• these sporozoites transform into trophozoites

• trophozoites penetrate and enter the erythrocytes

• after undergoing asexual multiplication (schizogenesis), these trophozoites form two, four, or more trophozoites

• these trophozoites are leased into the bloodstream after rupturing the enlarged parasitized erythrocytes

• these new trophozoites invade new erythrocytes

• the sexual cycle takes place in a tick vector

• while taking a blood meal from an infected mammal, the female ticks become infected with Babesia spp trophozoites

• after reaching the intestine, the protozoa multiply sexually and later migrate to the salivary glands

• Babesia undergo multiple fission in the salivary glands to form vermicules

• these vermicules are:

  club-shaped

  measures 11 μm to 15 μm depending on the species

  consists of a single nucleus and cytoplasm

  the cytoplasm has a Golgi complex, endoplasmic reticulum

  lacks mitochondria

  vacuole surrounded by a bilayer membrane- consists of the outer fine plasmalemma and inner thick membrane

• vermicules undergo secondary schizogony in the tick salivary gland to produce sporozoites

• during the next blood meal by the infected tick, these sporozoites are transferred to humans or any mammals

Pathogenesis of Babesia

As Babesia spp infects and eventually destroys the host RBCs, they significantly affect the hematological systems resulting in thrombocytic anemia, and hemoglobinuria.

Factors that contribute to the pathogenesis of babesiosis include:

• rupture of parasitized erythrocytes

• increased destruction of altered and parasitized RBC in the spleen results in hemolytic anemia

• intravascular hemolysis causes anorexia

• secondary inflammatory lesions in the kidney and liver

• accumulation of parasites in the small capillaries as well as intra-vascular hemolysis results in various host cellular and tissue damage

Pathology of Babesia

Pathology of Babesia includes:

• Babesia spp infection activates the complement system which in turn produces Tumor Necrosis Factor (TNF) and interleukin-1 (IL-1)

• also associated with decreased complement levels of C4, C3, and CH50 and increased circulating C1q-binding activity

• this complement activation contributes to manifestations such as fever, anorexia, arthralgia, and myalgia

• organs such as the liver, spleen, and kidney are congested and pigmented due to the deposition of haemosiderin inside their macrophages

• these organ capillaries also contain parasitized as well as non-parasitized erythrocytes

Host Immunity of Babesia

Babesia spp infection activates host immunity- both natural and specific acquired immunity.

Natural immunity

• natural immunity against Babesia spp depends upon numerous factors such as the presence of an intact spleen, age, concurrent infections, and genetic factors

• patients without a spleen are more susceptible to Babesia infections and the severity of infection is also increased in such cases

Specific acquired immunity

It depends on both cellular and humoral immunity.

Cellular immunity

• the primary immune response, T-cell-mediated cellular immunity, is associated with an increase in T-suppressor and/or T-cytotoxic lymphocytes as well as decreased responses to lymphocyte mitogens

• the secondary immune response, B-lymphocytes reactivity is characterized by a polyclonal hypergammaglobulinaemia

• Cellular immunity response checks parasitemia by suppressing and destroying the multiplication of intra-erythrocytic Babesia

Humoral immunity

• the specific circulating antibodies of humoral immunity prevent the entry of Babesia into the RBC

• phagocytosis of parasitized RBC by opsonins and cell-mediated immunity protects the host from infection