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Related Concept Videos

American Trypanosomiasis01:22

American Trypanosomiasis

Chagas disease, or American trypanosomiasis, is a vector-borne parasitic infection caused by Trypanosoma cruzi, a flagellated protozoan (kinetoplastid) of the family Trypanosomatidae. The disease is endemic in Latin America, although cases are increasingly reported worldwide due to human migration. Transmission most commonly occurs when feces of infected triatomine bugs contaminate bite wounds or mucosal surfaces; additional routes include congenital, transfusional, transplant-related, and oral...
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Leishmaniasis is a widespread parasitic disease caused by several Leishmania species. It affects millions of people each year and remains a major public health problem in endemic regions. First-line treatment relies on pentavalent antimonials, including meglumine antimoniate and sodium stibogluconate. Even so, how these drugs work has not been fully clear, especially their interaction with parasite-specific biochemical pathways. One key target is trypanothione reductase (TR), an enzyme that...

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Bioluminescence Imaging to Detect Late Stage Infection of African Trypanosomiasis
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Published on: May 18, 2016

THE BLOOD CHEMISTRY OF AN ACUTE TRYPANOSOME INFECTION.

R W Linton1

  • 1Department of Bacteriology, College of Physicians and Surgeons, Columbia University, New York.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary

Infection with Trypanosoma equiperdum significantly alters serum CO(2) capacity and increases blood lecithin. Liver glycogen depletes, while kidney function declines in later stages.

Area of Science:

  • Biochemistry
  • Veterinary Parasitology
  • Pathology

Background:

  • Trypanosoma equiperdum causes significant physiological disturbances.
  • Understanding metabolic changes during infection is crucial for treatment.

Purpose of the Study:

  • To investigate the biochemical and pathological changes in rats infected with Trypanosoma equiperdum.
  • To characterize the impact of infection on serum, blood, liver, and kidney parameters.

Main Methods:

  • Analysis of serum CO(2) capacity.
  • Quantification of non-protein nitrogen, uric acid, cholesterol, and lecithin in blood.
  • Assessment of liver glycogen levels.
  • Histopathological examination of kidneys.

Main Results:

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  • Serum CO(2) capacity decreased early in infection.
  • Blood lecithin markedly increased (20-50%).
  • Liver glycogen was reduced early and absent late in infection.
  • Non-protein nitrogen and uric acid increased in terminal stages.
  • Kidneys showed degenerative changes; cholesterol remained unchanged.

Conclusions:

  • Trypanosoma equiperdum infection induces profound metabolic alterations.
  • Lecithin increase and glycogen depletion are key biochemical markers.
  • Kidney pathology indicates severe systemic impact.