American trypanosomiasis aetiology and management
American trypanosomiasis aetiology and management
AetiologyAmerican trypanosomiasis is an infection caused by T.cruzi, which exists in several forms during its lifecycle. Thetrypomastigote is found in the blood and has similarappearances to the African trypanosome. Amastigotes arefound within host cells. Human blood forms are ingested bythe vector species of reduvid bug, when it takes a bloodmeal. The bug defaecates infective faeces on the skin aftertaking a blood meal, and the metacyclic forms enter thehost through the bite or other skin abrasion, or through theconjunctiva if the faeces are carried to the eye on fingers.
Distribution and incidence American trypanosomiasis is most common in the countriesof South America among people living in poorly constructedhousing, as the bugs live in roof thatch andcracked mud walls. Many people are infected in SouthAmerica, with about 6000000 cases in Brazil, although notall those infected develop disease.
Transmission and epidemiology Contact with infected bugs (the most important source),transplacental infection and blood transfusion are theroutes of infection. Infection in bugs is maintainedfrom a reservoir of T. cruzi in dogs. Infection of childrenin the first decade of life is common. The bugs live inthe thatch and cracked mud walls of basic village housing.Hundreds if not thousands of bugs can be found whenthese houses are demolished. Chagas' disease is essentiallya disease of the rural poor.Pathology and pathogenesisTrypanosomes invade cells, including myocardial and gutsmooth muscle cells. Rupture of the cell releases trypomastigotesand evokes inflammatory responses in thesurrounding tissues. The trypomastigotes circulate, invadeother cells, and replicate as amastigotes. Phagocytic cellsin any tissue, as well as heart muscle, skeletal andsmooth muscle and CNS, are among the tissues involved.Pericarditis and cardiomegaly are often present. Ameningoencephalitis can occur in acute disease.The heart and the gut are the organs severely affectedin chronic Chagas' disease. The heart is enlarged, withapical ventricular aneurysm commonly present. Thrombusis often present in the atrial appendage and in the ventricles.There is diffuse myocardial cell necrosis, with fibrosisand involvement of the conducting system. Parasympatheticplexuses of the gut are destroyed, causing dilatationof the intestine, frequently the oesophagus or colon (themega-syndrome). Involvement of the conducting system ofthe heart is common and may be the only evidence ofdisease. Evidence of disease may come on at any time, evendecades after infection.The pathogenesis of the disease is complex. There areseveral different strains of T. cruzi, some of which causethe cardiac and mega-syndromes. Other strains cause lifelonginfection but no disease. Autoimmune mechanismsare probably involved in damaging tissues
.Clinical features Acute infection may be inapparent in young children, butin older children and adults there may be an acute febrileillness. The patient may find a lump in the skin markingthe site of the infected bite and initial parasite replication(the chagoma). Unilateral periorbital oedema indicates aconjunctival route of infection. Local adenopathy andhepatosplenomegaly are found.Cardiomegaly, heart failure, arrhythmia and conductiondefects indicate myocarditis in the acute illness. This maycause sudden death. Meningoencephalitis may occur. Thelocal signs at the bite site, hepatosplenomegaly and feversubside in 6 weeks.Chronic Chagas' disease presents with heart and gutdisease. Right- and left-sided cardiac failure are common.There may be signs suggesting pulmonary or systemicembolization from thrombus in the cardiac chambers. Conductionabnormalities are often present and may causeStokes-Adams attacks and sudden death.
Diagnosis Acute infections can be diagnosed by finding parasites inthe peripheral blood film. Trypanosomes may also be foundon microscopy and culture of CSF, even when evidence ofCNS involvement is lacking. Xenodiagnosis is also usedto make a specific parasitological diagnosis. Laboratoryrearedbugs, known to be free of infection, are fed on thepatient, up to 20 bugs being used. They are then kept in thelaboratory, dissected after 3 weeks and the hindgut examinedfor metacyclic forms. The polymerase chain reactionoffers a valuable technique for detecting low levels of infectiousagents and has been adapted for use in Chagas'disease. Serological tests are usually positive in both acuteand chronic cases by indirect imrmmofluorescence, indirecthaemagglutination and complement fixation techniques,and may be the only indication of infection.
Management Treatment is unsatisfactory. Two drugs are available, nifurtimoxand benznidazole. Both will clear the blood of parasitesin the acute phase, but prolonged follow-up suggeststhat neither gives a radical cure. There is now evidencefrom a prospective randomized controlled study that benznidazoletreatment, 8mg/kg body weight in divided dosesfor 3 weeks given to children with positive serology, willreduce the frequency of development of ECG changesduring follow-up and, with time, be followed by a declinein antibody litres. In adults with positive serology nonrandomizedstudies have shown a reduction in the frequencyof development of ECG changes during follow-upafter benznidazole therapy. However, the extent to whichthese findings indicate a definite benefit for treatment isstill uncertain. Control of arrhythmias and heart failure isall that can be done for cardiac disease in the chronicphase. Relief of obstruction at the oesophagogastric junctionby dilatation or surgery may help the patient withmegaoesophagus. A dilated segment of small or large intestinecan be excised.
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