African trypanosomiasis clinical features pathology and management
Infection with Trypanosoma gambiense causes an initialfebrile illness which progresses slowly to a chronic phasedominated by infection of the CNS, causing neuronaldeath and a variety of organic neurological syndromes.Neurological involvement occurs early in T. rhodesiense infections, within weeks of inoculation of parasites and,untreated, there is rapid deterioration and death. The twospecies cannot be distinguished on morphological grounds.Various species of tsetse fly, Glossina, are the vectors.
Distribution and incidence The specific names of these parasites suggest a WestAfrican (T. gambiense) or East African (T. rhodesiense)origin for the infections, but there is a considerable overlapof the distribution of the two species in Central Africa The total numbers of cases are far fewer thanmalaria, but rhodesiense infections have a considerable economic impact as valuable farming and grazing lands cannot be used because of the high risk of infection. Therehave been increases in both forms recently with importedcases seen in Europe.
Transmission and epidemiology Tsetse flies become infected by ingesting trypanosomes ina blood meal. Once infected, a fly remains infective for life.About 1 % of flies in an area are infected. Humans are thereservoir in gambiense infections, whereas a variety of wildmammals, including bush buck and hartebeest, are thereservoir of rhodesiense infection, and humans are an incidentalhost. Transmission of gambiense trypanosomiasisoccurs in wooded areas around rivers and streams that arewater sources for local populations. Blood transfusion andtransplacental transmission are also possible routes ofinfection.
Pathology and pathogenesis There is an early marked inflammatory response at the siteof inoculation and in the lymphoid tissues of the body,lymph glands, liver and spleen. Trypanosomes may be seenin tissue sections. Rhodesiense infections progress rapidlyto involve the heart and brain. Myocarditis and pericarditisare common. An obliterative endarteritis with vascularocclusion is found in the CNS, causing the degenerativechanges. The neuropathological features include thickeningof the meninges, which are infiltrated by lymphocytesand plasma cells. This infiltrate extends into brain substancein a perivascular distribution.The parasites continuously shed surface antigens whichevoke antibody responses in the host, but the antigenschange sequentially, a possible mechanism of evading hostimmune responses. Autoantibodies to brain and heart maycause tissue damage. Disseminated intravascular coagulationcan occur in rhodesiense infections.
Clinical features With both species, fever, chills and weakness are usualinitial symptoms, beginning about 10 days after the bite. Aninflamed lump is present at the bite site - the trypanosomal chancre and there is regional adenopathy. Onwhite skins it is possible to see transient irregular areas ofcircinate erythema in both types of disease. Posterior auricularand posterior cervical adenopathy develop after 1-2months of infection in gambiense infections. Unpleasantdysaesthesia follows squeezing of the calf muscles.Hepatosplenomegaly is often present in both infectionsearly on. Jaundice occurs in rhodesiense infections. Purpuricrashes on the extremities are occasionally seen insevere rhodesiense infections.Neurological involvement appears within weeks ofinfection in rhodesiense infections, but it may be months oryears later with T. gambiense. Indifference, lassitude, personalitychanges and altered behaviour are early features.Sleep rhythm is reversed. The basal ganglia, cerebellumand brainstem regions are most affected, producingtremor, incoordination, and problems with speech, balanceand walking. Parkinsonian features may be prominent. Epilepsy occurs. In the terminal stage the patient isscarcely reusable, unable to swallow or feed him/herself.Bronchopneumonia is a common cause of death.
Diagnosis Diagnosis depends on finding trypanosomes. Early in thecourse of infection with either species, parasites may befound in peripheral blood films. There are usually manymore parasites in rhodesiense than in gambiense infections.Repeated examinations must be made to detect the lowlevels of parasitaemia in gambiense infection. Gambienseparasites may be seen in bone marrow smears. Smallernumbers of parasites can be detected in smears of thebuffy coat. Material aspirated from a lymph node can besmeared on a slide and stained.CSF must also be examined. The cell count is determinedand the stained deposit examined for trypanosomes.An increased white cell count (>5/mm3) and/or anincreased CSF protein (>250mg/L) indicates CNS infectionin a patient with parasites in the blood or tissues.Serum immunoglobulin concentrations are increased, withIgM levels being very high. Increased CSF IgM indicatesnervous system involvement. Serological tests do not havediagnostic value for individual patients.
Management Suramin is used to kill parasites in blood and lymph nodes,and cures patients early in the disease. After an initial testdose of 100-200 mg given by slow intravenous infusionto ensure that the drug does not cause anaphylaxis orcardiovascular collapse, 1g doses are given by slowintravenous infusion on days 1, 3, 6,14 and 21.Pentamidine is the first-line drug for use in T. gambienseinfections, giving 3-4mg/kg of pentamidine base daily byslow intravenous infusion or intramuscularly until 7-10doses have been given. Sterile abscesses can occur at sitesof intramuscular infection. Pentamidine stimulates insulinrelease from the pancreas, with the consequent risk ofhypoglycaemia. Although pentamidine is used for earlydisease there is evidence that it crosses the blood-brainbarrier and has worthwhile actions in early neurologicaldisease in rhodesiense infections.Melarsoprol treatment regimens are complicated. Treatmentis given intravenously. There is a significant incidenceof arsenical encepholopathy with its use. For T. gambiensethe drug is given in doses of 3.6mg/kg, maximum 180mg,for 3 days, repeating the series after a week without drugin patients with 6-19 WBC/cu mm CSF, and giving a thirdseries for those with > 20 WBC/cu mm. For T. rhodesiensethe regimen builds the dose up slowly from 0.36mg/kg(day 1), 0.72 (day 2), 1.1 (day 3), 1.8 (days 10,11 and 12),2.2 (day 19), 2.9 (day 20), and 3.6 to a maximum of 180mg(days 21, 28, 29 and 30). The incidence of reactive arsenicalencephalopathy is reduced by giving prednisolone1 mg/kg before and throughout treatment. Eflornithine is effective in CNS disease due to T. gambiensewith none of the arsenical toxicity, and should replacemelarsoprol in this infection; initial treatment is with 400mg/kg/day in divided doses, 6-hourly for 14 days,followed by 300mg/kg/day in divided doses for 30 days.This amounts to a lot of drug!Examination of blood films, IgM levels, CSF and thepatient's condition is helpful in assessing the response totreatment. Improvement in the patient's condition and resolutionof the abnormalities indicate a good response.Relapse is indicated by a rise in the CSF protein or cellcount, and further treatment should be given.When patients are treated early, complete recovery is therule. In more advanced cases treatment arrests progressionof the disease.
Prevention and control Appropriate clothing in endemic areas is essential to minimizethe area exposed to biting. Tsetses can bite throughthin material. Pentamidine has been used as a prophylacticagent against gambiense infection in those heavilyexposed. Efforts to control vectors by destruction ofhabitats and trapping flies may be helpful.
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