Trypanosomiasis Jane Ngai

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TrypanosomiasisJane Ngai Simon Zappia
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Protista ? Kinetoplastida ? Trypanosoma
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• African Trypanosomiasis 400,000 affected
  causing 50,000 to 70,000 deaths/year.
• American Trypanosomiasis 11 million people
  affected causing 50,000 deaths/year.

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Trypomastigote Epimastigote Promastigote Amastigote
FORM
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• African Trypanosomiasis
• Sleeping Sickness
• ?Trypanosoma brucei brucei (cattle)
• ?Trypanosoma brucei gambiense
• ?Trypanosoma brucei rhodesiense
• American Trypanosomiasis
• Chagas Disease
• ? Trypanosoma cruzi

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AFRICAN TRYPANOSOMIASIS
Fly belt distribution
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Transmission

• Via vector bite from the tse tse fly
• Mother to child infection (perinatal death)
• Blood transfusion
• Sexual contact

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Lifecycle
Parasite reproduces asexually in the flys gut
(epimastigotes), migrates to the flys salivary
glands (metacyclic trypomastigote)
Fly injects metacyclic trypomastigotes when it
feeds on blood.
Fly ingests trypomastigotes when it feeds on
blood of infected individual.
Trypomastigotes reproduce asexually in the
bloodstream
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Pathogenesis (2 stages)

• Stage 1 Haemolymphatic stage (ACUTE)
• Most patients do not notice this stage of
  infection.
• Small papule from bite may develop exciting local
  inflammation.
• When trypomastigotes enter the haemo-lymphatic
  system to multiply,clinical symptoms include
• Fever, headache and joint pain
• Winterbottoms sign swelling of lymph nodes at
  the posterior neck region.

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• Stage 2 Meningoencephaltic stage (CHRONIC)
• Sleeping sickness stage because trypanosomes have
  crossed the blood-brain barrier
• Personality changes, headaches and withdrawal
  from the environment.
• Simple tasks become harder to accomplish as
  individual experience nocturnal insomnia and
  daytime lethargy, apathy and ultimately succumb
  to secondary infections such as pneumonia.

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Treatment

• Stage I
• Pentamidine 7-10 injections for T. b. gambiense
  infection. Side effects include Painful
  injections with risk of hypotension and shock,
  pancreatic, renal or hepatic dysfunction bone
  marrow suppression and polyneuropathy
• Suramin multiple doses on varying days for T.b.
  rhodesiense infection. Side effect include
  renal impairment, peripheral neuropathy and bone
  marrow suppression.

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Treatment

• Stage II
• Melarsoprol (arsenical compound) slow IV
  injection. Side effects include encephalopathy
• Eflornithine infusion for 2 weeks every 6
  hours. Drug is expensive and more effective
  against T. b. gambiense.

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Cyclical waves of infection
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Prevention

• Control in the reservoirs like livestock and
  wildebeest
• Remove scrub (where tse tse flies reproduce)
• DDT
• Education
• Public awareness

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• Only specific species of genus Glossina transmit
  the parasite resulting in a spotty distribution
  through the fly belt.

T. b. rhodesiense (Acute)
T. b. gambiense (Chronic)
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AMERICAN TRYPANOSOMIASIS
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Transmission

• Mediated via vector of genus Triatoma, Rhodnius
  and Panstrongylus also known as kissing bugs
• Ingestion of food contaminated with parasites
• Blood transfusion
• Fetal transmission (13 stillborn deaths/year in
  Brazil)

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Lifecycle
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Pathogenesis (Acute)

• Acute phase
• Starts 1 week after infection
• Fever, lymph node enlargement, unilateral
  swelling of the eyelids (Romanas sign), acute
  myocarditis, damaged muscle cells and edema.

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Pathogenesis (Chronic)

• Chronic Phases
• Starts 2 months after initial infection.
• Indeterminate form 60-70 of people with Chagas.
  Completely free of cardiac, gastrointestinal and
  neurological symptoms but 2-5 of patients
  convert to cardiac or digestive forms each year
  (reason not clear).

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Cardiac manifestation

• Cardiac form
• 30-40 of people with Chagas. Induces
  arrhythmia, cardiac failure, thromboembolism,
  atrioventricular fibrillation, ventricular
  hypertrophy

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Gastrointestinal manifestation

• Digestive form
• 10 of people. Megaoesophagus 3, megacolon and
  may be associated with cardiac form. Difficulty
  in swallowing, regurgitation, aspiration may
  cause pneumonia and death. Chronic constipation,
  fecal compacting causes perforation of the colon.

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Treatment

• Treatment exists for symptoms but there are no
  cures for the disease.
• All available pharmaceuticals are expensive and
  are of inefficient efficacy. No medications are
  given to patients with the chronic phase.

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Prevention

• Elimination of kissing bug environment with
  building structures that discourage the bugs
  habitation.
• Avoid pets in the home environment to limit
  attraction.
• Avoid building homes with palm roofs and cracks.
• Use of insecticides.
• Mechanical elimination of the vector (ie. squish
  it).
• Education.

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New developments

• Clinical manifestations of the cardiac and
  gastrointestinal forms are unknown.
• Heart problems may be linked to autoimmune
  responses triggered by parasites being engulfed
  in the macrophage and not completely destroyed.
• Others think heart problems may be linked to the
  parasites themselves.
• Inconclusive data.

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Questions

• Consider the nature of both diseases their
  vector, distribution and impact on local
  populations. Which disease, in your opinion,
  deserves more attention and funding? Why? How
  would you invest the money?