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Edited by David A. Warrell, Timothy M. Cox, John D. Firth

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Latest update

The November 2012 update sees updates to over 70 chapters, focusing on Neurology and Gastroenterology. This update also incorporates a selection of 29 Case Histories taken from related titles in the Oxford Case Histories series, linked to from related chapters. Each case includes several questions followed by detailed answers and discussion to enhance diagnostic and clinical understanding.

Neurology updates include substantial updates to key chapters and new material on a wide range of topics including spinal cord injury, autonomic nervous system disorders, and inherited neurodegenerative diseases. 

Gastroenterology updates
include extensive revisions of key chapters on liver failure and acute pancreatitis and new material on a wide range of matters, ranging from the common to the rare: including surgical treatments for colonic diverticular disease, antibody tests for immune disorders, and a revised treatment algorithm for small bowel bacterial overgrowth.

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Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Contents

Human African trypanosomiasis

Chapter:
Human African trypanosomiasis
Author(s):

August Stich

DOI:
10.1093/med/9780199204854.003.070810_update_001

Update:

Trypanosoma brucei rhodesiense—clinical differences between stage II patients in Uganda and Tanzania.

Updated on 31 May 2012. The previous version of this content can be found here.

Human African trypanosomiasis (HAT, sleeping sickness) is caused by two subspecies of the protozoan parasite Trypanosoma brucei: T. b. rhodesiense is prevalent in East Africa among many wild and domestic mammals; T. b. gambiense causes an anthroponosis in Central and West Africa. The disease is restricted to tropical Africa where it is transmitted by the bite of infected tsetse flies (Glossina spp.).

Although well under control in the mid 20th century, HAT has returned to Africa in epidemic proportions since the 1980s, causing a severe public health problem in countries such as the Democratic Republic of Congo, Angola, Sudan, and Uganda. A joint effort by national, international, and nongovernmental organizations, as well as the pharmaceutical industry, is required to reverse this trend.

Clinical features

HAT progresses through distinct clinical stages that invariably lead to death if left untreated. Progress is fast in rhodesiense HAT, often resembling the clinical picture of malaria or septicaemia, and slow—sometimes lasting years—in gambiense HAT.

Outside Africa, HAT is a rare diagnosis as an imported infection in travellers, but has to be considered in any patient with fever, chronic lymphadenopathy, or neurological changes returning from HAT endemic areas.

Diagnosis, staging, and treatment

Diagnosis—this is established by the detection of trypanosomes (usually by direct microscopy) in chancre aspirate, blood, lymph, or cerebrospinal fluid. Serology is useful for rapid screening under field conditions, but does not necessarily imply overt disease.

Staging—this is crucial for correct management: the cerebrospinal fluid must be examined in every patient found positive for trypanosomes in blood or lymph aspirate.

Treatment—HAT is curable, but many factors make this difficult: the disease is found in remote places, diagnosis is difficult, treatment is costly and complicated, and many drugs are not easily available. Aside from supportive care, specific treatment depends on the trypanosome subspecies and the stage of the disease, including (1) stage 1—pentamidine, and suramin; (2) stage 2—melarsoprol, eflornithine, and nifurtimox. There are no generally accepted recommendations on drug combinations, but—especially in late stages—treatment is difficult and dangerous to the patient; all of the drugs used are toxic and have many side effects, some potentially lethal.

Prevention

Control can be achieved by a combination of mass screening programmes, treatment of patients, and vector control, which together can lead to a complete break of the transmission cycle. There is no vaccine.

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