PPAARRAASSIITTIICC PPRROOTTIISSTTSS

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ZOOLOGY: SEM- VI, PAPER- DSE-3: PARASITOLOGY, UNIT 2: PARASITIC PROTISTS

P P A A R R A A S S I I T T I I C C P P R R O O T T I I S S T T S S

B B B Y Y Y

D D R R . . P P O O U U L L A A M M I I A A D D H H I I K K A A R R Y Y M M U U K K H H E E R R J J E E E E A A S S S S I I S S T T A A N N T T P P R R O O F F E E S S S S O O R R

D D E E P P A A R R T T M M E E N N T T O O F F Z Z O O O O L L O O G G Y Y

N N A A R R A A J J O O L L E E R R A A J J C C O O L L L L E E G G E E

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ZOOLOGY: SEM- VI, PAPER- DSE-3: PARASITOLOGY, UNIT 2: PARASITIC PROTISTS

Life Cycle of

Trypanosoma gambiense

Trypanosoma gambiense is digenetic; i.e., it completes

its life cycle in two hosts. The primary or definitive

host is man. The mammals, like pigs, buffaloes,

antelopes often act as reservoir hosts harbouring the

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parasite. The intermediate host is blood sucking insect called tsetse fly (Glossina palpalis).

Life cycle in man:

The metacyclic stage (infective form) of T. gambiense

is introduced into the body of man by the bite of the

tsetse fly, Glossina palpalis. The tsetse fly harbours

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the meta¬cyclic form in the lumen of its salivary glands.

When the vector sucks human’s blood, it intro¬duces the contained trypanosomes into his blood stream.

During sucking through the proboscis, the fly releases

metacyclic forms along with saliva. The saliva of

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tsetse fly contains an anticoagulant which prevents the clotting of blood.

Multiplication:

All stages of Trypanosoma in man are extracellular as

the parasites are found in blood plasma and not inside

blood corpuscles. Within the host’s blood the

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metacyclic forms (which are devoid of flagellum) become transformed into long, slender and flagellated forms.

They swim within the human blood by the beating of

their free flagella and the vibratile movements of the

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ZOOLOGY: SEM- VI, PAPER- DSE-3: PARASITOLOGY, UNIT 2: PARASITIC PROTISTS

undulating membrane. The adult forms of the parasite multiply by longitudinal binary fission.

The multiplication commences at the kinetoplast and is followed by the division of nucleus and cytoplasm.

Sometimes multiple fission has also been observed

but no syngamy occurs in the life cycle. It is to be

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ZOOLOGY: SEM- VI, PAPER- DSE-3: PARASITOLOGY, UNIT 2: PARASITIC PROTISTS

noted that multiplying trypanosomes gets energy by

anaerobic glycolysis.

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Mishra and Choudhury (1974) observed for the first time the presence of amastigotes and sphaeromastigote stages from arteriovenous shunts of laboratory animals after 5th day of infec¬tion.

These are active stages and show binary fis¬sion.

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Amastigotes are round to oval in shape with a large vesicular nucleus and kinetoplast; flagellum absent.

Sphaeromastigotes are round with a central nucleus.

Flagellum originates from kinetoplast wraps round

the cell body and leaves as a free flag¬ellum. These

forms are found in choroid plexus, cerebrum, heart,

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lung and some other arterio¬venous stumps of rats, cats and monkeys.

Metamorphosis:

When the glycolysis process is hampered and

trypanosomes stop multiplying. The long slender

parasites now shrink to short stumpy forms which are

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devoid of free flagellum. During transformation from long slender form to short stumpy form, the intermediate form along with a small free flagellum also appears.

The stumpy forms do not feed and ultimately die.

These stumpy forms remain latent till tsetse fly sucks

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them up along with the blood of the host. Unless this occurs within a reasonable time the stumpy forms degenerate and perish.

Relapse of infection:

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It is fact that some of the long and slender

trypanosomes do not under¬go metamorphosis but

change the antigens of blood to which the host has

produced antibodies so the slender forms of

trypanosomes survive and continue to multiply in

blood leading to future relapses of the infection.

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Life cycle in tsetse fly:

When this insect vector sucks the blood of an infected

person, it also takes short stumpy forms of

trypomastigote along with the sucked blood. Now

these stumpy forms continue development in the

midgut of insect vector.

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Development in the Midgut of Insect Fly:

Further change of trypomastigote occurs in the insect

vector’s midgut within peritrophic membrane and the

short stumpy forms of the parasites transform into

long slender forms. Now these long slender forms

appear which pass to posterior end of the extra-

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ZOOLOGY: SEM- VI, PAPER- DSE-3: PARASITOLOGY, UNIT 2: PARASITIC PROTISTS

peritrophic space (a space between the peritrophic membrane and epithelial cells), where they continue to multiply for some days.

By the 15th day they escape from the peritrophic

space and enter the lumen of the proventriculus (the

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periventricular form is the same as that of the midgut

form).

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ZOOLOGY: SEM- VI, PAPER- DSE-3: PARASITOLOGY, UNIT 2: PARASITIC PROTISTS

Development within the Salivary Gland of Insect Fly:

Later the long slender forms make their way into

salivary glands through the hypo- pharynx. Here they

multiply and change their morphology, first into

epimastigote and then into the metacyclic stage (short

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stumpy forms of trypomastigote) which are infective to man.

It has been reported that the time taken for the

complete evolution of the infective forms (metacyclic

stage) inside the vector insect is about 20 days. These

flies remain infective for the rest of their lives, a

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period extending upto 185 days. When the vector fly bites a healthy person, it transfers the metacyclic forms along with saliva into his blood where they initiate another infection.

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During a blood meal on the mammalian host, an

infected tsetse fly (genus Glossina) injects metacyclic

trypomastigotes into skin tissue. The parasites enter

the lymphatic system and pass into the bloodstream .

Inside the host, they transform into bloodstream

trypomastigotes, are carried to other sites throughout

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ZOOLOGY: SEM- VI, PAPER- DSE-3: PARASITOLOGY, UNIT 2: PARASITIC PROTISTS

the body, reach other body fluids (e.g., lymph, spinal

fluid), and continue the replication by binary fission .

The entire life cycle of African trypanosomes is

represented by extracellular stages. The tsetse fly

becomes infected with bloodstream trypomastigotes

when taking a blood meal on an infected mammalian

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host , . In the fly’s midgut, the parasites transform

into procyclic trypomastigotes, multiply by binary

fission , leave the midgut, and transform into

epimastigotes . The epimastigotes reach the fly’s

salivary glands and continue multiplication by binary

fission . The cycle in the fly takes approximately 3

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weeks. Rarely, T. b. gambiense may be acquired

congenitally if the mother is infected during

pregnancy.

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T T H H A A N N K K Y Y O O U U