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Sleeping sickness in Uganda: a thin line between two fatal diseases

BMJ 2005; 331 doi: https://doi.org/10.1136/bmj.331.7527.1238 (Published 24 November 2005) Cite this as: BMJ 2005;331:1238
  1. Kim Picozzi,
  2. EricM Fèvre, epidemiologist1,
  3. Martin Odiit, medical officer, tropical diseases2,
  4. Mark Carrington, molecular and biochemical parasitologist3,
  5. Mark C Eisler, veterinary epidemiologist1,
  6. Ian Maudlin, epidemiologist1,
  7. Susan C Welburn (sue.welburn{at}ed.ac.uk), molecular biologist1
  1. 1Centre for Infectious Diseases, Royal (Dick) School of Veterinary Studies, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH25 9RG
  2. 2 Ministry of Health (Uganda), PO Box 7272, Kampala, Uganda
  3. 3 Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA
  1. Correspondence to: S C Welburn
  • Accepted 24 October 2005

Abstract

Objective To determine, through the use of molecular diagnostic tools, whether the two species of parasite that cause human African trypanosomiasis have become sympatric.

Design Blood sampling of all available patients between June 2001 and June 2005 in central Uganda and between July and September 2003 in northwest Uganda and analysis of subcounty sleeping sickness records in Uganda between 1985 and 2005.

Setting Sleeping sickness treatment centres in central and northwest Uganda and in south Sudan.

Participants Patients presenting at the treatment centres and diagnosed as having sleeping sickness.

Main outcome measure Classification of parasites from patients from each disease focus as either Trypanosoma brucei rhodesiense (acute form) or T b gambiense (chronic form).

Results Blood from 231 patients with sleeping sickness in central Uganda and from 91 patients with sleeping sickness in northwest Uganda and south Sudan were screened for T b rhodesiense (detection of SRA gene) and T b gambiense (detection of TgsGP gene). All samples from central Uganda were classified as T b rhodesiense, and all samples from northwest Uganda and south Sudan were identified as T b gambiense.

Conclusions The two focuses of human African trypanosomiasis remain discrete, but the area of Uganda affected by the acute form of human sleeping sickness has increased 2.5-fold since 1985, spreading to three new districts within the past five years through movement of infected livestock. Without preventive action targeted at the livestock reservoir of this zoonotic disease, it is likely that the two disease focuses will converge. This will have a major impact on diagnosis and treatment of this neglected disease. Real time monitoring is recommended, using molecular diagnostic tools (at a regional surveillance centre, for example) targeted at both livestock and human patients.

Footnotes

  • Contributors All authors contributed to the literature search, study design, interpretation of results, and writing the paper. SCW is the guarantor.

  • Funding This study was funded by the Animal Health Programme of the UK Department for International Development, the World Health Organization (EMF/SCW), and the Cunningham Trust (KP/SCW). The views expressed are those of the authors. The funding body had no inputs to the study design; the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the paper for publication.

  • Competing interests None declared.

  • Ethical approval Not needed.

  • Accepted 24 October 2005
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