Sleeping sickness

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.

T. gambiense vs. T. rhodesiense

 * {|class="wikitable"

|- ! !!style="background:#EE6AA7"|T. gambiense !!style="background:#EE2C2C"|T. rhodesiense |- ! Course: | style="background:#FFBBFF"|chronic (with CNS involvement) || style="background:#FFA07A" align="center"|acute |- ! Onset: | style="background:#FFBBFF" align="center"|slow || style="background:#FFA07A" align="center"|quick |- ! Death: | style="background:#FFBBFF" align="center"|> 4 years || style="background:#FFA07A" align="center"|< 9 months |- ! V: | style="background:#FFBBFF" align="center"|months or years || style="background:#FFA07A" align="center"|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: 2. 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.
 * 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).).

Related articles

 * Chagas disease

Used literature

 * RNDr. Eva Nohýnková, Ph.D. [přenáška z parazitologie]
 * RNDr. Eva Nohýnková, Ph.D. [přenáška z parazitologie]