Trypanosomiasis: Haematolymphatic stage

The haematolymphatic stage lasts 6 to 12 months, but sometimes longer. It is characterised by intermittent, unpredictable bouts of fever separated by irregular intervals of days to a month or even more, headache and general malaise. The lymph nodes swell, especially those in the neck (Winterbottom sign). These glands are soft, mobile and not painful. They are present in fewer than half of the patients in the early stage, and in fewer than 25% in the late stage. Oedema sometimes occurs (face), as well as pruritus (itching) and transient red spots or a circinate rash (trypa­nides). This rash can be seen without difficulty on a white skin (reported in 50%) but is difficult to see on a dark skin, The liver and certainly the spleen can be clearly enlarged. There is moderate to severe anaemia. Neurological disorders (personality changes, increased sensitivity to pain, especialy deep hyperaesthesia ("Kerandel sign") can already be present in the first stage. This condition gradually evolves into increasing neurolo­gical collapse, characteristic of the menin­goencepha­lopa­thic stage.

The condition is characterised by a chronic course with flare-ups and quieter periods. These flare-ups are to be interpreted as destruction of the trypanosomes, followed by the development of a new population of parasites carrying a different surface antigen. Lysis of the parasites releases large quantities of antigen into the bloodstream. These form immune complexes with circulating antibodies which then precipitate, resulting in perivascular inflammatory symptoms (including vasodilation with increased vascular permeability and oedema). Successive generations of parasites each have a different glycoprotein on the outer membrane. It is to this outer membrane that the antibodies attach themselves. Whenever a new glycoprotein emerges, the immune system always has to start again from scratch, with the production of new antibodies. This explains the pronounced increase in the immune globulins (especially IgM) in blood and cerebrospinal fluid. The high IgM serum concentration thus results from chronic polyclonal B cell stimulation. Aspecific cross-reacting and auto-antibodies can also be produced, making the diagnosis more difficult. Meanwhile time goes on and the infection worsens.

Category: Medicine Notes