Trypanosoma brucei

Systematic position Trypanosoma – click here

Two species of Trypanosoma brucei are known to cause diseases in humans:

Note: Sub-species Trypanosoma brucei brucei does not cause infection in humans.

Habitat: Blood & Lymph

Habits:

• Obtain nourishment through osmotrophy from blood plasma.
• Pinocytosis occur in ‘reservoir’ at posterior end.
• Respiration & excretion occurs by diffusion through body surface.
• Osmoregulation absent.
• Reproduction through binary fission.

Infective Stage to human: Metacyclic form of the parasite.

Hosts: (Digenetic)

• Primary Host: Man
• Intermediate Host/ Vector: Tsetse fly
• Reservoir Host: Antelopes, Pigs, Buffaloes etc.

Morphology:

• Unicellular, microscopic, colorless.
• Spindle shaped body.
• At rest, body becomes curved, with one side concave & other convex.
• Pointed at both anterior, posterior ends.
• Anterior end:
  • Tapers gradually.
  • More pointed than posterior end.
  • Marked with free flagellum.
• Cytostome absent.
• Mouth absent.
• Polymorphism: (Based on adaptations of mitochondrion w.r.t. mode of respiration in relevant environment)
  • In Human blood, the parasite occurs in three forms-
    • Long Slender
    • Short Stumpy
    • Intermediate
  • In Tsetse fly, the parasite occurs in three forms-
    • Long Slender
    • Small Crithidial
    • Small Metacyclic
• Pellicle: Outermost, elastic, firm & protective body covering, supported by microtubules.
• Flagellum: (Uniflagellate)
  • Single, strong, locomotory flagellum.
  • Emerges from posterior end, from a small pocket called reservoir, arising from basal body.
  • Attached throughout the convex side of the body. But beyond pointed anterior end of the body, it becomes free.
  • 9 + 2 arrangement of microtubules present.
  • Uniplanar waves pass from tip to base not from base to tip, during movement.
• Undulating membrane: The pellicle attached to flagellum is drawn out into membranous fold known as undulating membrane. It is thin, lateral, fin like. Said to be adaptation for movement in blood.
• Cytoplasm:
  • Under electron microscope, it is not distinguished into ecto- & endo- plasm.
  • Contains Volutin granules (greenish in color) representing digestive enzymes & stored food (glycogen).
  • Contractile vacuoles absent.
  • Food vacuoles absent.
  • Nucleus: Single, large, round. Double nuclear membrane with pores. Chromosomes scattered in nucleoplasm. Centrally placed nucleolus present.
  • Mitochondrion: Single, elongated from one end of the body to the other. Cristae may or may not present, depending on form of parasite.
  • Basal Body/ Blepharoplast: Present below reservoir. Controls locomotory apparatus of the parasite & corresponds to centriole of higher animals.
  • Parabasal Body/ Kinetoplast: Rod shaped found near basal body. Mass of mitochondrial DNA. The mitochondrial tube dilates near & surrounds it.
  • Golgi body: Single Golgi body present between nucleus & reservoir.
  • Endoplasmic Reticulum: Abundant near nucleus & reservoir.
  • Ribosomes: Occurs on ER as well as in cytoplasm.

Life Cycle:

• Mammalian Stage (In man)
  • Infected Tsetse fly during blood meal on man, introduces metacyclic form through its saliva in the skin.
  • Through skin, they reach lymphatic system & further reaches bloodstream.
  • All stages/forms of the parasite are present in blood stream only i.e. are extracellular not entering RBCs.
  • Metacyclic form does not have free flagellum.
  • Soon, metacyclic form is transformed to long slender form, which swim freely in the blood with beating its free flagella & undulating membrane.
  • Long slender form actively multiply by binary fission (divide every 4-6 hours). Their mitochondria lack cristae & respiratory enzyme and seems to be inactive. Respire anaerobically.
  • During infection, when host starts producing antibodies, anaerobic respiration becomes impossible and then mitochondria becomes active & cristae develop, changing to aerobic respiration. The size of the parasite shrinks. Thus, long slender form via intermediate form changes to short stumpy form.
  • Short stumpy form lacks flagellum & does not feed.
  • If host develops sufficient antibodies the parasite dies. But during the course if tsetse fly feeds on the blood it gets infected.

Infection Relapse: Some long & slender form parasites does not transform but they show antigenic shift. That means with a new variant formed it is able to escape the antibody response by the host made actually for the preceding variant. This has made the vaccine development more difficult due to continuous changes in surface epitopes by the parasite.

• Tsetse Fly
  • During blood meal on an infected human, tsetse fly ingests short & stumpy form and it reaches midgut of the fly.
  • In the midgut, short stumpy form transforms into long slender form & multiply by longitudinal binary fission.
  • After several days, it reaches salivary glands via oesophagus & mouthparts.
  • Here, in the salivary glands, the long slender form transforms into crithidial form.
  • Crithidial form are small in size with reduced free flagellum & has kinetoplast shifted near the nucleus. Mitochondrion develops more cristae.
  • The form multiply being attached to the salivary gland wall & transforms into metacyclic form.
  • In the metacyclic form, kinetoplast moves back to posterior end & cristae of mitochondrion decrease significantly.
  • When the fly takes blood meal on human, it transfers the metacyclic form to the human blood, thus infecting that human.

Prophylaxis (Prevention)

• Use of insecticides against tsetse fly in its habitat esp. in bushes near rivers.
• Contact with tsetse fly should be avoided e.g. covering whole body properly, avoid going in areas where its population is abundant.

Treatment:

• Pentamidine is usually given at first stage of infection.
• After treatment, the patient is required to be monitored for next 24 months & in case of reccurrence of symptoms, blood should be examined.