TRYPANOSOMA CRUZI Flashcards

1
Q

What’s the disease caused by T. cruzi infection?

A
  • Chagas’s or South American trypanosomiasis.
  • It is a zoonotic disease
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2
Q

what’s the epidermiology of Chaga’s disease?

A
  • Endemic areas of 21 countries in South & central America.
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3
Q

What is the habit of T. cruzi parasites?

A
  • Amastigotes are intracellular parasites while trypomastigotes are found in the peripheral blood.
  • In the insect vector-reduviid bugs, amastigotes are found in midgut & metacyclic trypomastigotes are found in hindgut & feces.
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4
Q

Describe the morphology of T. cruzi parasites

A

❑Amastigote
* Amastigotes are oval(2–4 μm in diameter)with a nucleus, kinetoplast & absent flagellum
* It is the multiplication stage of the parasite.
* Found in muscles, nerve cells & reticulo-endothelial system.

❑Trypomastigote
* Do not multiply & found in the peripheral blood of man/ mammalian hosts.
* May appear as long slender flagellates (20 μm long) or short stumpy form (15 μm long) in blood.
* They assume different shapes in stained smears- e.g. letters U,S or C.
* This is the form taken up by the insect vector.

❑Epimastigote
* Are found in the insect vector- the reduviid bug and also in culture.
* Epimastigotes divide by binary fission in hindgut of the vector
* It has a kinetoplast adjacent to the nucleus & an undulating
membrane situated along its anterior half.

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5
Q

Hosts and Infective form of T. cruzi

A
  • Definitive host: Man
  • Intermediate host (vector): Reduviid bug or triatomine bug.
  • Reservoir host: Armadillo & domestic animals- cat, dog & pigs.
  • Infective form: The infective forms are metacyclic trypomastigotes found in feces of reduviid bugs.
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6
Q

Life Cycle of T. cruzi

A
  • The parasite occurs in 3 different but overlapping infection cycles.

=Sylvatic zoonosis in wild animals e.g. armadillos
=Peri-domestic cycle in domestic animals e.g. cat/dogs
=Domestic cycle in humans.

  • The reduviid bugs-Triatoma infestans, Rhodnius prolixus &
    Panstrongylus megistus are important vectors in human infection.
  • These are adapted to living in human habitations-cracked walls & roofs.
  • These are night-biting bugs which typically defecate while feeding.

❑Development in Man
* The metacyclic trypomastigotes => RES & spread to other tissues.
* Promastigote=> Epimastigote => Trypomastigotes
* No multiplication occurs in this stage except intracellularly in the
amastigote form.

❑Development in Reduviid Bugs
* Ingested Trypomastigotes=> Epimastigotes (in the midgut then migrate to the hindgut and multiply.)=>Metacyclic Trypomastigotes (infective form)
which are excreted in feces (stercorarian transmission).

  • Incubation period in the vector takes 8–10 days(extrinsic incubation period).
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7
Q

Mode of infection of T. cruzi infection

A
  • Infection in man & other reservoir hosts occur when mucus membranes or a sore on skin is contaminated by feces of the bug with metacyclic trypomastigotes.
  • Other modes of transmission are:
    -blood transfusion
    -organ transplantation
    -vertical transmission
    -rarely ingestion of contaminated
    food or drink.
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8
Q

Pathogenesis and clinical features (acute Chaga’s disease)

A
  • Average incubation period in man is 1–2 weeks.

❑Acute Chagas’ Disease
* Often in children under 2 years of age soon after infection.
* May last 1–4 months with the first sign appearing within a week post infection.

  • Chagoma is the typical subcutaneous lesion occurring at the site of infection.

=Inoculation of the parasite in conjunctiva causes unilateral, painless edema of periocular tissues in the eye called as Romana’s sign.
*This is the classical finding of the acute Chagas’ disease.

  • In some cases, patients may have generalized infection with fever, lymphadenopathy & hepatosplenomegaly.
  • The patient may die of acute myocarditis and meningoencephalitis.
  • Acute signs and symptoms usually resolve spontaneously within 4–8 weeks.
  • Thereafter patients ,enter the asymptomatic or indeterminate phase of chronic T. cruzi infection.
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9
Q

Pathogenesis and clinical features (chronic Chaga’s disease)

A
  • Usually seen years or even decades after the initial infection.
  • The chronic form is found in adults and older children.
  • In chronic phase, T. cruzi produces an inflammatory response, cell destruction, fibrosis of muscles and nerves that control muscle tone of hollow organs like heart, esophagus, colon etc.
  • Thus, it can lead to cardiac myopathy and mega-esophagus & megacolon (dilation of esophagus and colon).
    *Agaglionosis & fibrosis in myentericn plexus in case of megaesophagus
    *Severe chronic myositis in a case of megaesophagus
    *Mild chronic ganglionitis in esophagus without mega-arrow at ganglion cell
    *Myositis with granuloma in a case of megacolon-see giant cell & histiocyte
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10
Q

❑Congenital Infection of Chaga’s disease

A
  • Congenital transmission is possible in both acute & chronic phase of the disease causing myocardial and neurological damage in the fetus.
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11
Q

Laboratory Diagnosis of T. cruzi

A

❑ Microscopy
* Diagnosis of acute Chagas’= detection of parasites.
* Microscopic examination of fresh anticoagulated blood or the buffy coat is the simplest way to see motile organisms.
* In wet mount, trypomastigotes are faintly visible but their snake-like motion against RBC’s makes their presence apparent.
* Trypomastigotes can also be seen in thick and thin peripheral blood smear, stained with Giemsa stain.

❑Culture
* Novy, Neal, and Nicolle (NNN) medium or its modifications are used for growing T. cruzi.
* Epimastigotes and trypomastigotes are found in the culture.
* Culture is more sensitive than smear microscopy

❑ Animal Inoculation
* Done in Guinea pig or mice where blood, CSF or lymph node aspirate are inoculated.
* Trypomastigotes are looked for in the blood smears in a few days
after successful inoculation.

❑ Histopathology
* Biopsy examination of lymph nodes and skeletal muscles and aspirate from Chagoma may reveal amastigotes of T. cruzi.

❑Serology
* Antigens can be detected in
urine and sera in patients with chronic Chagas’ disease.
* ELISA has been developed for detection of antigens.
* Antibody detection done by the following the following tests – IHA ,CFT, ELISA, IIF, Direct agglutination test (DAT).
* Antibody tests are recommended for field use.
* Cross reaction occur syphilis & leishmaniasis hence false positives. Major drawback for antibody based tests.

❑ Intradermal Test
* The antigen ‘cruzin’ is prepared from T. cruzi culture is used for the test.
* A delayed hypersensitivity reaction is seen.
❑ Molecular Diagnosis
* PCR can be done but not commercially available.

❑ Other Tests
* Electrocardiography (ECG) and chest X-ray are useful for diagnosis and prognosis of cardiomyopathy seen in chronic Chagas’ disease.
* The combination of right bundle branch block (RBBB) and left anterior fascicular block is a typical feature of Chagas’ heart disease.
* Endoscopy helps in visualization of megaesophagus in Chagas’
disease.

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