Presention On Trypanosoma Department of Zoology Sri Guru Granth Sahib World University
Presention On Trypanosoma Department of Zoology Sri Guru Granth Sahib World University
Presention On Trypanosoma Department of Zoology Sri Guru Granth Sahib World University
DEPARTMENT OF ZOOLOGY
SRI GURU GRANTH SAHIB WORLD
UNIVERSITY
SUBMITTED TO:
SUBMITTED BY :
Dr. Shatabdi Dutta Shrenika
singla
SCIENTIFIC NAME
• Kingdom – Protista
• Phylum – Protozoa
• Order – Kinetoplastida
• Family – Trypanosomatidae
• Genus – Trypanosoma
INTRODUCTION
• Commonly known as African sleeping sickness.
• Live in the blood or tissue of man or other animals.
• They pass their life cycle in two hosts that is vertebrate
and insects.
• While developing inside the insect host they pass through
various stages, Amastigote, Promastigote, Epimastigote,
Trypomastigote.
• Transmission is effected only by blood sucking insects.
• They are polymorphic in nature.
CLASSIFICATION
• Trypanosoma brucei – African sleeping sickness
• Trypanosoma cruzi – Chagas disease
• Trypanosoma rangeli – Found in blood of man in colombia
T.brucei
• Parasite causing African trypanosomiasis in man.
• African sleeping sickness is classified into two diseases
i.e. acute disease and chronic disease.
• Habitat – it localises in brain affecting the central nervous
system.
• Causes- blood transfusions are a rare causes of parasite
transmission .
• A bite from an infected tsetse fly causes African
trypanosomiasis.
LIFE CYCLE
• Trypanosomes are parasites with a two hosts life cycle :-
Tsetse fly and human stages.
• The life cycle starts when the trypanosomes are ingested
during a blood meal by the tsetse fly from a human
reservoir or an animal reservoir.
• The trypanosomes multiply over a period of 2-3 weeks in
the fly midgut ; then the trypanosomes migrate to the
salivary gland, where the develop into epimastigotes .
• The metacyclic trypomastigotes infect humans.
• Time taken for complete evolution in insect is 20 days.
• signs and symptoms – fever , headaches , joint pain ,
itching.
T.cruzi
• Known as Chagas disease .
• It is intracellular protozoan parasite Trypanosoma cruzi
which is transmitted by the insect vector Triatoma
infestans [reduviid bug]
• Reduviid bug live in mud filled walls of huts in rural areas.
• Transmission – T.cruzi parasite are mainly transmitted by
the infected faeces of blood sucking triatomine bugs .
• Normally they hide during the day and become active at
night when they feed human blood.
• They usually bite an exposed area of skin such as face
and the bug defecated close to the bite.
LIFE CYCLE
• The life cycle of T.cruzi :- the vector reduviid bug bites and
defecates on host . Parasites in the form of
trypomastigotes are able to enter the blood via mucous
membranes or a cut .
• During cell invasion the trypomastigotes transform into a
mastigotes and under go multiplication.
• Parasites are then released into the blood stream as
trypomastigote, where they either spread to other tissue
or are taken up by the vector to the life cycle.
• It occur immediately after infection may last up to a few
weeks or months and parasites may be found in the
circulating blood.
• They may cause fever.
T.Rangeli
• Transmission is occur when a healthy insect feed on an
infected mammal or when an infected bites a healthy
mammal.
• Found in peripheral blood of man in venezuela.
• Known pathogenic for man.
INFECTION AND SYMPTOMS
• Mother to child infection – the trypanosome can cross the
placenta and infect the fetus.
• Mechanical transmission through other blood sucking
insects is possible
• Transmission of the parasite through sexual contact has
been reported .
• Enlarger lymph nodes, joint pain.
• Changes of behaviour sensory disturbance.
• Treatment – depend on the form of the disease and the
stage of disease .
CONTD.
• Human American trypanosomiasis, or Chagas disease, is
a fatal disease of humans.
• The disease has two forms, a trypomastigote found in
human blood, and an amastigote found in tissues.
• The acute form usually goes unnoticed and may present
as a localized swelling at the site of entry.
• In the chronic stage, 10 to 20 years after infection, the
parasite invades the myofibrils of the heart causing
myocarditis.
• The gradual autoimmune destruction of heart myocardium
lead to cardiac enlargement and arrhythmias, and heart
failure.
TREATMENT : Nifurtimox and benznidazole for acute
disease. No effective drug for chronic disease.