Sleeping sickness

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

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

Patogenesis

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

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

• 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

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

Therapy

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).).

Links

Related articles

• Chagas disease

Used literature

• 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]