MMI 426 - Lec 3 American Trypanosomes

differences between African vs American trypanosomiasis

• epidemiology

• different vectors

• pathogenesis

• clinical course

species that cause American trypanosomiasis

T. cruzi

another name for American trypanosomiasis

Chagas disease

epidemiology of Chagas disease

continental Latin American countries from southern US to north of Argentina and Chile

vector for Chagas disease

triatomine insects or kissing bugs

transmission of Chagas disease

• ingestion of contaminated food or drink

• Mother-Child

• Blood transfusion

• organ transplantation

• lab accidents

how do triatomine insects become vectors

becomes infected by sucking blood from humans or animals with trypomastiogotes

how do ingested parasites multiply inside triatomine insects

they multiply in the midgut as epimastigotes which transform in infective metacyclic trypomastigotes that are discharged with feces at the time of blood meal

how does transmission of Chagas disease to humans occur

when mucous membranes, conjunctive or breaks in the skin are contaminated with bug feces

what happens after the parasite enter human bodies

they enter the host's cells and multiply in the cytoplasm -> when multiplying amastigotes fill the host cell they can differentiate into trypomastigotes -> cell ruptures and the parasite can invade local tissue or spread thru blood to other sites

where are triatomine bugs found

in the wall or roof cracks of poorly constructed homes in rural areas

when are triatomine bugs most active

at night

unique property of triatomine bug saliva

their saliva has an anesthetic property into the skin

why are triatomine bugs also known as kissing bugs

b/c their bites are often found around the mouth

trypomastigote

• kinetoplast posterior to nucleus and the flagellum arising near it to run along a long undulating membrane the length of parasite

• not a human stage

• vector stage

epimastigote

• no undulating membrane

• not a human stage

• vector stage

promastigote

flagella and kinetoplast are at the anterior end far from nucleus

amastigote

• intracellular stage (found in cytoplasm), human stage

• no flagella or cilia

acute phase of T. cruzi infection

• lasts 8-12 weeks after transmission

• resolves following decreased parasitemia levels that are undetectable by microscopy and enters chronic phase

chronic phase of T. cruzi infection

• without antitrypanosomal therapy, this can last for the rest of the life of pts

• asymptomatic form during first 1-3 decades of the ___

chagoma

inflammatory lesion caused by T. cruzi at site of entry

Romana sign

inflammatory lesion caused by T. cruzi + painless edema when entry site is periocular tissue

acute chagas disease symptoms

fever/chills, anorexia, malaise, edema of the face and lower extremities, lymphadenopathy, and hepatosplenomegaly

can chagas disease affect CNS

sometimes-- leads to acute myocarditis with arrhymthmias

methods for diagnosing chagas disease

1. serology

2. wet prep of anticoag blood or buffy coat to demonstrate circulating parasites

3. tissue biopsies (amastigotes stained with Giemsa or H&E)

4. xenodiagnosis

5. PCR

diagnostic features of T. cruzi under microscope

Amastigotes: C-shape, large kinetoplast, no dividing forms

congenital Chagas

when mom has Chagas and spreads to newborn --> microscopic examination of cord blood or PCR *NO SEROLOGY TESTING

does antitrypanosomal therapy work on Chagas cardiac disease

no, therefore we try to provide supportive care for HF, arrhythmia, and thromboembolism

isolation protocol for pts with Chagas disease

vector transmitted disease so no need for iso, just focus on preventing it

infectious form of T. cruzi

metacyclic trypomastigotes

commonly infected organs in Chagas disease

heart and gut

morphological difference between American and African trypanosomes

trypomastigotes in American are bigger, and take on C-shape with dividing forms

diagnostic stage of T. cruzi

amastigotes