Haematological and biochemical changes in human and animal trypanosomiasis. Part II

Abstract

Haematological and biochemical changes in human and animal trypanosomiasis Trypanosome infections are generally characterized by anaemia, leucopenia, thrombocytopenia, as well as biochemical aberrations such as hypoglycaemia, elevated BUN, hypoalbuminaemia;and hypogammaglobulinaemia primarily due to elevated IgM levels. Despite the variations in hosts (man, domestic and experimental animals) and trypanosomes (T. brucei, T. gambiense, T. rhodesiense, T. evansi, T. vivax, T. congolense), the severity of the haematological and biochemical changes associated with various host-parasite combinations is determined by the level of parasitaemia which develops during the early phase of infection. Three phases of trypanosome infections are recognizable including the “acute crisis” characterized by high parasitaemia and accelerated destruction of erythrocytes, development of thrombocytopenia and leucopenia, and of marked biochemical perturbations. A “chronic crisis” supervenes in surviving animals and is characterized by lower levels of parasitaemia but with persistence of the haematological changes, reversal of some biochemical changes such as hypoglycaemia and persistence of others such as the plasma protein changes. A third phase, “recovery”, occurs in animals that survive the two previous phases, and is characterized by abatement of parasitaemia or even sterilization, accompanied by gradual reversal of the abnormalities previously developed. Whether a host passes through these three phases depends on the severity of the lesions that develop during acute and chronic crisis, the existence of secondary infections, and the level of host’s nutrition. The haematological and biochemical abnormalities induced by trypanosomes arise from their direct and indirect effects via their products, on host cells such as RBC, WBC, platelets, and tissues such as liver, kidneys, bone marrow and lymphoid organs, resulting in cell destruction and organ malfunction, as well as from extractions from and additions to host chemistry associated with parasite metabolism.