Sleeping sickness

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Template:Infobox - onemocnění Sleeping sickness or african trypanosomiasis is a disease caused by flagella of the genus Trypanosoma. It can be caused by both T. gambiense (brucei) and T. rhodesiense, but the course of the disease then varies considerably. Template:Deatils

T. gambiense vs. T. rhodesiense[edit | edit source]

T. gambiense T. rhodesiense
Course: chronic (with CNS involvement) acute
Onset: slow quick
Death: > 4 years < 9 months
V: months or years days

Patogenesis[edit | edit source]

AfrTryp LifeCycle.png
  1. The tsetse fly stings → trypanosomes enter the lymph;
  2. They are carried by lymph into the nearest lymph node, which drains the relevant part of the body;;
  3. from there they enter the thoracic duct and into the bloodstream;
  4. they can cross the blood-brain barrier (HE) into the cerebrospinal fluid.

Clinical piscture[edit | edit source]

Two phases: 1. phase:

  • skin lesions (skin scab): local skin inflammation occurs at the site of the sting → skin edema develops → ulcerates the site over time → heals with a scar = disappears spontaneously.
  • Winterbottom symptome:
    • it is a swelling of the lymph nodes in the neck area;
    • it develops at an early stage when trypamosomes have not yet crossed the blood-brain barrier (so they are only in the blood and lymph);
    • typical fevers (in waves), headaches and joint pain, malaise , anemia, etc.

2. phase:

  • edema of a number of organs associated with CNS ingection;
  • at this stage, the trypanosomes have already crossed the HE barrier.

Periodic fevers[edit | edit source]

  • Trypanosomes have a mantle on the surface composed of many copies of a single glycoprotein (GP) = almost the entire trypanosome population in the body is therefore homogeneous;
  • furthermore, trypanosomes have at least 100 genes, in their genetic makeup that encode different glycoproteins = in certain circumstances, they may therefore "exchange" their glycoprotein mantle for another;
  • at the moment when the trypanosome in the organism multiplies sufficiently (5-7 days), the human organism starts to respond with IgM → production → trypanosomes are subsequently lysed by complement;
  • however, out of the whole lysed population having a mantle from one specific GP (eg GP A), there is about 1 % rypanosome with a different GP mantle (eg GP B) → the population with GP B starts to multiply again → the organism responds to them again by producing antibodies against GP B → however, there is still a certain percentage of trypanosomes that have GP C on their surface, and so it goes on and on;
  • whenever the majority of the parasite,population is lysed a fever occurs.

Diagnostics[edit | edit source]

  • Microscopy = direct proof:
    • we take material from ulcers, blood, cerebrospinal fluid;
    • must not be taken at a time of fever (trypanosomes are lysed).

Therapy[edit | edit source]

Untreated ends in death 1. phase: suramin; 2. phase: melarsoprol – an arsenic compound passing through the blood-brain barrier. It is a toxic but effective antiparasitic. It is currently hardly used (in 5–20% of fatal encephalopathies). It was colloquially referred to by doctors as "arsenic in antifreeze" (dissolved in propylene glycol) and among patients as "fire in the veins" (painful application).).[1][2]

Links[edit | edit source]

Related articles[edit | edit source]

References[edit | edit source]

Used literature[edit | edit source]

  • BEDNÁŘ, M, et al. Lékařská mikrobiologie. 1. edition. Marvil, s. r. o., 1996. ISBN 80-238-0297-6.
  • RNDr. Eva Nohýnková, Ph.D. [přenáška z parazitologie]