Mahatma Jyotiba Fule College of Veterinary And Animal Sciences, Jaipur (Raj)

Trypanosoma

Presented by :-Dr. Abhinav Meena

2020-2021Assistant Professor

Department of Veterinary ParasitologyCollege of Veterinary and Animal Sciences, Chomu , Jaipur

(Raj)

Brief Introduction:-

These are leaf-shaped haemoprotozoans found in the blood.

The seat of predilection is unlike that of Babesia or Theileria spp, which areintercellular and not intracellular.

The haemoprotozoans are global problems in humans as well as in animals.

In African countries the dreadful sleeping sickness is caused by T.rhodesiense and T. gambiense.

In the livestock industry the disease, trypanosomosis is a devastatingproblem and one of the major economic constraints.

History / Discovery:-

Trypanosome was first evident in the fish which was recorded by G. G.Valentin in the year, 1841.

T cruzi, a causative agent of chagas disease was first isolated by CarlosChagas in the year 1909.

Bruce in the year 1890 first discovered T brucei, a causative agent ofNagana.

Forde and Dutton first detected Trypanosoma gambiense in Gambia in 1902and Stephens and Fantham detected T rhodesiense in Rhodesia in the year1909.

Prevalence:-

This protozoa is cosmopolitan in distribution.

Salient morphology:-

1. The organisms are leaf-like.

2. One flagella is present which is attached to the body by a thin membranecalled undulating membrane.

3. One nucleus is present.

4. Posterior to the nucleus there is presence of a dot-like structure which iscalled as the blepharoplast. Posterior to the blepharoplast there ispresence of kinetoplast. The flagella originates from the basal granule orblepharoplast.

A glimpse of electron microscopic structure:-

1. A typical structure arises from the blepharoplast which is called asaxoneme.It is a neuromotor apparatus consisting of few fibrils which form the axialstructure of flagella.

2. The kinetoplast contains the genetic material (DNA).

Trypomastigote Epimastigote Promastigote Amastigote

Kinetoplast is present posterior to

nucleus.

Kinetoplast is present anterior to

nucleus.

Kinetoplast and axoneme is present at the anterior tip of

body.

Kinetoplast is present at right

angle to the nucleus.

Undulating membrane is well

developed.

Undulating membrane is

Short.

Undulating membrane is absent.

Undulating membrane is

absent.

Found in the arthropods and the

vertebrates.

Found in the arthropods and

vertebrates.

Found in arthropods. Found in the vertebrates

and arthropods.

Lifecycle:-

Developmental stages:-

• Trypomastigote.

• Epimastigote.

• Amastigote.

Description:-

Two types of development occur in the life cycle of Trypanosoma spp.

Anterior station development:-

At first broad organisms are formed which is followed by the formation ofslender form of organisms which are abundantly found in the space allied tothe peretropic membrane at the mid-gut region.

From this space the organisms migrate to the proventriculus and thenmigrate further to the salivary glands via the oesophagus, pharynx andhypopharynx.

In this area the epimastigote forms of the organisms are formed. Theepimastigotes again transform to trypomastigote (metacyclic forms).

Posterior station development:-

Posterior station development occurs in the posterior part of the gut of the insect. The life cycle of Trypanosoma cruzi is the best example of posterior station development. The first developmental stages occur in the cell of the insect's stomach. The trypanosomes after entry starts multiplication in the trypomastigotestage. From the stomach the organisms proceed to the rectal region of the gut. During this time of migration, the organisms transform into the epimastigote. These epimastigote stages further transform into the metacyclictrypanosomes.

Pathogenicity:-

Pathological features / lesions:-

Lesions in the mucocutaneous junction.

Anaemia.

Emaciation.

Spleenomegaly etc.

Description:-

1 . As the organisms are blood protozoa, haematological changes occursignificantly.

2. The organisms mechanically damage the R. B. C. resulting in significantamount of anaemia.

3. When this condition progresses in a chronic phase the anaemia leads toemaciation. The animals become highly emaciated in the later phase.

4. Spleen and lymph nodes are markedly enlarged. It is due to the stimulationof the immune system.

S. Urticarial plaques are formed which are common characteristic clinicopathological features found in trypanosomosis.

6. Frank haemorrhages occur at the junction of the mucus and cutaneousarea.

7. The plaques get ruptured and, later necrosed centrally.

Note: pathological features vary according to different species

Important diseases caused by Trypanosoma spp.

Name of Trypanosoma spp.

Name of Disease Vector

Trypanosoma evansi Surra Tabanu, Stomoxy, Lyperosia

Trypanosoma congolense Nagana Glossina spp.

Trypanosoma equiperdum Dourine The organisms are transmitted by coitus

Trypanosoma equinum Mal de caderus Tranmitted mechanically by biting flies.

Trypanosoma rhodesiense Acute form of African sleeping sickness

Glossina spp.

Trypanosoma gambiense Chronic form of African sleeping sickness

Glossina spp.

Nagana:-

This disease is caused by T congolense.

This disease occurs in the cattle.

Nagana is a Zulu word meaning to be 'in low or depressed spirit'.

Massive destruction of the RBC and depression 'of the haemopoitic systemresults in severe anaemia which may cause the death of animals.

The disease is transmitted by different species of Glossina.

Mal - de Caderas:-

This disease is caused by T. equinum which occurs in the equines.

Transmission is done by Tabanus sp.

The disease is characterized by recumbancy, eye lesions (conjunctivitis,keratitis etc) and pyrexia.

On the neck and the flank region there occurs cutaneous plaques.

African sleeping sickness:-

This disease occurs in human beings and are transmitted by differentGlossina spp.

The causative agents are T gambiense causing the chronic form of thedisease and T rhodesiense causing the acute form of the disease.

The organisms affect the nervous system.

Dourine:-

This disease is caused by T equiperdum occurring in the horse.

This is a venereal disease and transmitted sexually.

The disease is characterized by oedema in vagina and prepuce, urticarialplaques under the skin which are circular, sharply circumscribed.

These are called as the dollar spots.

The meaning of dourine is 'unclean'.

Surra:-

This disease is transmitted by the Tabanus and Stomoxys spp. and occur inthe equine, dog, camel and cattle.

The surra is a Hindi word meaning 'rotten'.

In horse, the disease is characterized by fever, anaemia, emaciation,urticarial plaques and ulcerative lesions in the mucocutaneous junction.

Surra occurs in different animals in different forms-

In Asia it occurs in chronic form in camel.In sudan it is called as Gufar.

Death occurs after few months. In dog, serious form of the disease occurswhich results in formation of oedema in larynx and other associated partswhich causes change of voice.

The changed voice is similar to rabies.

The cattle act as the reservoir hosts of T evansi but occasional outbreaksoccur due to introduction formation of new strain or post sequelae of FMDvaccination.

Chagas:-

This disease caused by T cruzi is characterized by oedema of face which isdue to blockage of lymphatics.

These lesions are called as chagoma.

Diagnosis of Trypanosoma:-

General-

1. Examination of blood smear by Leishmann's or Giemsa's stainingprocedure.

2. Stilbamidine test.

3. Mercuric chloride test.

Recent trends-

1. PCR (Polymerase chain reaction)- Primers of particular parasite is used toamplify the gene of target parasite in the presence of taq - polymeraseenzyme.

2. Random Amplified Polymorphic DNA (RAPD) – PCR.

3. RFLP (Restriction Fragment Length Polymorphism).

4. Xenodiagnosis is done for chagas disease.

Control:-

1. Chemotherapy - Inspite of having number of control regimen, chemotherapy is still the only resort for control of the disease.

2. Destruction of game animals - Game animals are killed in an attempt toreduce the population of the flies which feed on the games.

3. Breeding by the tolerant animals - Breeding policy can be developed by using the trypanotolerant animals (Bos Taurus). Other tolerant animalsare Lagone, Lagune and Bacosi etc.

4. Vaccination.

Earlier attempts-

b. Live vaccinec. Attenuated vaccined. Killed vaccine

Recent trends-

a. Recombinant vaccine - Specific immunodominant proteins are expressedin the E. coli or other organisms and that protein is utilized as vaccine.

b. Naked DNA vaccine - One unique enzyme is present in trypanosomeswhich is trans-sialidase (TS). Antibody response in mice was produced byinjecting DNA plasmid containing a gene encoding catalytic domain of TS.

Immunity to Trypanosoma spp.

1. Both cell mediated and humoral immunity occurs.

2. There is relation between the immunity and the genetic makeup ofanimals.

3. Solid immunity is never conferred as relapse strain of Trypanosomawhich occurs due to frequent change of antigenic character of surfaceantigen (glycocalyx, VSG). The surface antigen is changed due toreciprocal recombination of the genetic material. However, in T cruziinfection, there is good evidence of acquired jmmunity.

Treatment:-

General-

The important drugs used in the treatment of Trypanosomosisare as following:-

Diminazene aceturate (Berenil) - 3.5 mglkg (s/c).

Quinapyramine sulphate (Antrycide methylsulphate - 5 mglkg, s/c).

Recent trends-

Antisense therapy

Very recently, there have been extensive studies on the syntheticoligonucleotides to regulate the gene expression of some protozoanparasite.

In this technology, one enzyme, ribozyme is used to cleave any target RNAwhich is provided endogenously by transcription from a transient orintegrated gene.

Thank You