Trypanosoma brucei

Overview
  • Trpanosoma brucei is the trypanosomal species which causes African Sleeping Sickness. African Sleeping Sickness can manifest as two different syndromes which tend to occur in different geographic ranges. These two syndromes, termed East African and West African Sleeping Sickness, are caused by different T. brucei subspecies, T. brucei rhodesiense and T. brucei gambiense, respectively.
Transmission
  • Humans are inoculated with the T. brucei following blood meals by infected TseTse flies.
Pathogenesis
  • Following inoculation, T. brucei replicates at the site of inoculation causing a localized cutaneous lesion. Subsequently, the organism disseminates hematogenously throughout the body but especially the CNS.
Clinical Consequences
  • Overview
    • African Sleeping Sickness usually progresses through a series of distinct stages. The primary difference between East and West African forms of the disease is the speed of progression. The East African form, caused by T. brucei rhodesiense, progresses slowly and may have a course of months to years. The West African form, caused by T. brucei gambeinse, progresses quickly and may lead to death within weeks to months.
  • Localized Phase
    • T. brucei first proliferates at the site of inoculation, forming an indurated, ulcerative skin lesion termed a "Trypanosomal Chancre".
  • Hematogenous Phase
    • Following localized proliferation, the organisms disseminate hematogenously and deposits in a number of organs, especially the CNS. Hematogenous disease is characterized by fever and generalized lymphadenopathy. Notably, the T. brucei fever is intermittent, characterized by spikes of constitutional symptoms and fever, followed by afebrile intervals. This relapsing-remitting fever is due to antigenic variation on the part of the organism, allowing T. brucei to evade successful host humoral immunity by changing its surface antigens.
  • CNS Phase
    • Progressive neurological changes herald the end-point of the disease and precede coma followed by death. Daytime somnolence is commonly observed although insomnia is also frequent.
Treatment
  • Suramin, pentamidine, and eflornithine are used for early stages of disease. The highly toxic melarsoprol can be used when the disease has progressed to the neurological stage.