Trypanosoma brucei complex - Life Cycle, Pathogenesis, Pathology

Life Cycle of Trypanosoma brucei complex

The life cycle of Trypanosoma brucei complex takes place in vertebrate hosts (man, domestic animals, wild animals) and insect hosts such as the TseTse fly (Glossina palpalis, Glossina morsitans, Glossina pallidipes).

• the vertebrate host is infected by the bite of the tsetse fly during the blood meal

• the infective forms of Trypanosoma brucei (metacyclic trypomastigotes) are inoculated in the skin of the vertebrate host

• these metacyclic trypomastigotes immediately transform into dividing long and slender trypomastigotes

• the trypomastigotes actively divide between the host blood, lymphatic system, or tissues and eventually invade the heart, connective tissue, bone marrow

• in later stages, the central nervous system of the host is invaded by Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense

• at these sites, the parasites multiply as long, slender dividing forms which are abundant in the ascending phase of parasitemia

• high level of specific host IgM antibodies helps to curb the parasite infection resulting in remission of the African sleeping sickness

• during the remission phages of the disease, non-multiplying short, thick, and stumpy trypomastigotes are abundant which are infective to the tsetse fly

• when any of both genders of the tsetse fly take blood to mean from a vertebrate infected with Trypanosoma brucei complex, the vector also uptakes the non-multiplying short, thick, and stumpy trypomastigotes form

• In the mid-gut of the insect, these non-multiplying short, thick, and stumpy trypomastigotes transform into long, slender, procyclic trypomastigotes

• in a couple of week's time, the ecto-peritrophic space is completely filled with the Trypanosoma brucei parasites

• the procyclic trypomastigotes eventually migrate to the salivary gland where they transform into epimastigotes and then into metacyclic trypomastigotes

• the metacyclic trypomastigotes are infective to vertebrates (including humans) and the life cycle of the Trypanosoma brucei complex continues in the next blood meal

Pathogenesis of Trypanosoma brucei complex

• the pathogenesis of African sleeping sickness, caused by Trypanosoma brucei complex, is not entirely known

• The host tissue injury may be due to:

  auto-immune system

  release of lysosomal enzymes from degenerated phagocytes

  host inflammatory response

  production of antigen-antibody complexes which releases kinases

• anemia increased vascular permeability, and hypocomplementaemia are other forms of pathogenesis

Pathology of Trypanosoma brucei complex

• the pathology of Trypanosoma brucei complex infection includes trypanosomal chancre

• as the infection advances, parasites metastasize via blood to lymph nodes and produce systemic infection

• systemic African sleeping sickness without the involvement of the host Central Nervous System is called stage I disease

• stage I also involves infiltration of lymphocytes, plasma cells, and macrophages while the parasites are not usually demonstrated in the tissues

• once the parasites break the blood-brain barrier and invade the CNS, stage II Trypanosoma occurs

• stage II disease is associated with leptomeningitis which extends into the perivascular Virchow Robin spaces

• demyelinating panencephalitis in stage II is accompanied by an infiltrate of leucocytes that includes plasma cells with glycoprotein globules (flame cells or Mott cells)

• these conditions will eventually lead to progressive cachexia, wasting, and death

Trypanosomal chancre

• trypanosomal chancre is an acute inflammatory local response

• the incubation period is a week on average

• more common in Trypanosoma brucei rhodesiense

• the chancre is red, large, and rubbery and tissues are filled with parasites

• occurs due to intense inflammatory infiltration, vasodilation, and interstitial edema