Please enable JavaScript.
Coggle requires JavaScript to display documents.
9.0 Kinetoplasta:Trypanosoma (T. cruzi) (Blood & Tissue…
9.0 Kinetoplasta:Trypanosoma (T. cruzi) (Blood & Tissue Flagellates)
Section Stercoraria:(Trypanosoma cruzi)
Etiological agent: Trypanosoma cruzi
Vector involve – Reduviid bug/ Kissing bug/ Assassin bug
Disease: Chagas’ Disease
Infects over 100 mammalian species:
Reservoir hosts: rodents, armadillos, dogs, cats
Transmitted by hemiptera from the family Reduviidae, such as Triatoma, Rhodnius and Panstrongylus (>30 species)
Endemic in Central and South America
Chagas disease remains a serious health and economic problem in Latin America, specially for the rural poor
Life Cycle
An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva.
Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodinius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes.
The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes.
Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites.
The ingested trypomastigotes transform into epimastigotes in the vector’s midgut.
The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut.
AMERICAN TRYPANOSOMIASIS
CHAGAS’ DISEASE
It was first described in 1909 by the Brazilian physician Carlos Chagas.
He was working in Lassance, a railroad-worker town at the end of the new railroad line across Brazil, where immigrant railroad workers were dying from what was thought to be malaria.
Chagas set up a lab and found that some symptoms were not from malaria and he found flagellated protozoa in the hindgut of the “barbeiro” which sucked blood from the workers at night. These protozoa were similar to the ones causing African sleeping sickness. Subsequent research proved the infection cycle of the trypanosome, later named T. cruzi (after Chagas' mentor), was directly related to poverty, such as what existed in Lassance.
Acute form:
7-10 days incubation period. Often in children: chagoma, Romaña sign, flu-like symptoms, myocarditis, encephalitis, lymphadenopathy, enlargement of liver and spleen.
Indeterminate form:
seropositivity but no symptoms or physical abnormalities, normal ECG. Aprox. 70-80% of infected individuals
Chronic form:
(months to decades after the first infection)
heart disease: 10-30% of cases sudden death, aneurism
intestinal form: megaesophagus, megacolon
PATHOGENESIS
The parasite enters the cells at the initial site of entry. Transforms into amastigote and duplicates. The cell ruptures and release more parasites. The combination of the parasitized cells plus the inflammatory reaction of the host is responsible for the initial pathology observed.
A. Trypomastigotes in a peripheral blood smear from a patient with acute Chagas disease. The arrow points to the kinetoplast. B: Nest of amastigotes within a cardiac myocite in a patient with chronic Chagas disease. The arrow points to the kinetoplast.
CHAGAS DISEASE – CHRONIC FORM
cardiac complications,
which can include an enlarged heart (cardiomyopathy), heart failure, altered heart rate or rhythm, and cardiac arrest (sudden death); and/or
intestinal complications
, which can include an enlarged esophagus (megaesophagus) or colon (megacolon) and can lead to difficulties with eating or with passing stool.
The average life-time risk of developing one or more of these complications is about 30%.
CHAGAS DISEASE – CONGENITAL (existing at birth) INFECTION
Approx 1-10% of pregnancies in women with chronic T. cruzi infection, the infant is born with congenital infection.
Most infected newborns are asymptomatic or have non-specific finding such as low birth weight, prematurity or low Apgar scores
Other signs: hepatosplenomegaly, anemia and thrombocytopenia ( ↓ platelet).
Serious manifestations: myocarditis, meningoencephalitis and respiratory distress.
Treatment
Does not respond to chemotherapy
Kills extracellular but not intracellular parasites.
Nifurtimox and Benzinidazole are somewhat effective in acute stage but have severe side effects.
Diagnosis:
Detection of parasites
detection in blood (rare), tissue, lymph, or CSF.
hemoculture
xenodiagnosis (parasite numbers are low)
Allow kissing bug to feed on patient
Look for epimastigotes in 10-30 days
Immunological (Immunodiagnostic)
indirect hemaglutination
immunofluorescence
ELISA
complement fixation
complement-mediated lysis
Molecular
PCR
Evidence of clinical disease