Describe the trypanosomes with their transmission, clinical features and diagnosis.

African Trypanosomiasis (sleeping Sickness)

• Caused by Trypanosoma brucei, transmitted by the TSETSE fly (Glossina), which bites by day and in which the parasite also multiplies
• The trypomastigote is a slender flagellate with an undulating membrane running the full length of the body and a kinetoplast — found extracellularly in blood, lymph and cerebrospinal fluid

• Stage 1 (haemolymphatic) — a chancre at the bite site, then intermittent fever, lymphadenopathy, headache and pruritus
• Stage 2 (meningoencephalitic) — invasion of the central nervous system with headache, personality change, reversal OF the sleep-wake cycle (daytime somnolence with nocturnal insomnia, which gives the disease its name), tremor, ataxia and finally coma and death
• Antigenic variation of the variant surface glycoprotein allows the parasite to evade antibody indefinitely, producing successive waves of parasitaemia and making vaccine development effectively impossible
• Diagnosis — thick and thin blood films, lymph node aspirate, and concentration methods; the CATT card agglutination test for screening in gambiense; and lumbar puncture to stage the disease, since the treatment differs entirely between stages
• Treatment — stage 1 uses pentamidine or suramin, which do not cross the blood-brain barrier; stage 2 requires drugs that DO cross — melarsoprol (an arsenical causing a fatal reactive encephalopathy in about 5%), eflornithine, and the newer oral fexinidazole, which treats both stages and has transformed management

American Trypanosomiasis (chagas Disease)

• Caused by Trypanosoma cruzi in Central and South America
• The vector is the reduviid or "kissing" bug (Triatoma), which bites at night around the face and then defaecates beside the bite. Transmission is by the faeces, not the bite — the parasite is rubbed into the wound or the conjunctiva when the sleeper scratches. This is stercorarian transmission, in contrast to the salivarian transmission of African trypanosomes
• It is intracellular in man, existing as an amastigote in cardiac and smooth muscle and in glial cells, with trypomastigotes in the blood — unlike the African species, which remain extracellular
• Acute phase — often in children; a chagoma at the inoculation site, or ROMAÑA sign (unilateral painless periorbital oedema) when the conjunctiva is the portal; fever, lymphadenopathy and occasionally acute myocarditis
• Indeterminate phase — asymptomatic, seropositive, lasting decades; most infected people remain here
• Chronic phase in 20 to 30% — cardiomyopathy with heart failure, arrhythmia, apical aneurysm and sudden death; and MEGA-syndromes (megaoesophagus and megacolon) from destruction of the autonomic myenteric plexus
• Also transmitted by transfusion, transplantation, orally in contaminated juice, and congenitally; blood donor screening is now routine in endemic countries and in migrant populations
• Diagnosis — blood film and concentration in the acute phase; serology (two different tests) in the chronic phase, when parasites are scanty; PCR; xenodiagnosis is historical
• Treatment — benznidazole or nifurtimox, which are effective in the acute and early chronic phases but of limited value once cardiomyopathy is established; management is then that of heart failure

Applied Aspects

• Neither disease is endemic in India, but both must be considered in travellers, migrants and returning workers, and Chagas disease can be transmitted by transfusion and transplantation from an infected donor anywhere
• Stage African trypanosomiasis before treating; the lumbar puncture is not optional, since the two stages require different and differently toxic drugs
• Antigenic variation prevents both immunity and vaccination in African trypanosomiasis — the same mechanism that operates in relapsing fever and in malaria, and a recurring theme in parasitology
• Chagas cardiomyopathy is irreversible, so the value of treatment lies in the acute and indeterminate phases — which argues for screening rather than waiting for symptoms
• Vector control is the mainstay in Chagas disease — improving housing, since the reduviid bug lives in cracks in mud walls and thatch, and spraying with residual insecticide
• Both are WHO-designated neglected tropical diseases, and both have seen genuine progress through donated drugs, active case-finding and vector control