Few infomation of Trypanosoma evansi

1. TRYPANOSOMA EVANSI
Dr Ashish Tanwer
Teaching Associate
V. C.C, C.V.A.S
Bikaner

2. • Disease
 Surra in all hosts
 Tebersa in camels
 Murine in horses o 1st trypanosome shown to be pathogenic
for mammals and is a intercellular parasite in blood and
lymph.
• Host: Camel, Horses, Donkeys, Cattle, Buffalo, Sheep Goat,
Dog, Cat, elephant and other animals (tiger, fox, jackal, hyena,
orangutan and mongoose), rodents, rabbits and guinea pig.
• Vectors: Tabanids, Stomoxys, Haematopota, Hippobosca,
Ornithodorus tick.
• Location: Blood and lymph.

3. • Morphology
 T. evansi is monomorphic but polymorphism sporadically
 Slender, thin, indistinguishable from T. brucei and 15-34 μm
length.
 Has sub-terminal kinetoplast, well developed undulating
membrane and prominent free flagellum.
• Epidemiology
 Host susceptibility
 Increased incidence is in equines and dogs than cattle and
buffaloes.
 Buffaloes greater than cattle; Imported dogs greater than
native dogs; pups greater than adults.

4.  Transmission
 Mechanically biting flies- Tabanus, Stomoxys, Haematopota,
Chrysops, Hippobosca and Lyperosia; Ticks-Ornithodorus spp.
 Interrupted feeding of flies from one host to other as parasite do not
survive in the proboscis of the flies after 4-72 hours.
 Mechanically by non-blood sucking flies which transmit the diseases
by picking the infection from infected meat or open lesions or mucous
membrane of susceptible animals.
 Dogs get infection by ingestion of tissues from infected carcasses.
 During mass vaccination when sterilization procedures are
inadequate.
 Carrier status
 Several wild and domestic animals carry the latent infection, e.g.
cattle and buffaloes.

6.  Stress factors
Strain, malnutrition, vaccination against viral and microbial
infections and intercurrent diseases may reduce the vitality of
animals and increase the susceptibility to trypanosomes.
 Trypanotolerance
 Animal hosts are parasitaemic for prolonged periods of time,
but generally remain in good health.
 Half breeds resulting from Jersey bull and N’-Dama female
show good tolerance to trypanosomosis
 Incidence
In India, more common in areas where the environment for
breeding of insect vectors being the most suitable for
transmission.
Incidence coincides with rain, flood and inundations

7. PATHOGENESIS AND CLINICAL SIGNS
Pathogenesis
• Course of the disease depends on the factors like genetic
constitution of the host, previous exposure to disease and the
virulence of the infection, strain of the parasite and species of
the host.
• Mechanism responsible for anaemia-3 factors
 Haemolysis of RBCs by trypanosomes.
 Increased erythrophagocytosis mediated by antibody on
antigen with complement
 Haemodilution due to increased plasma production.
 Others- reduced erythropoiesis, intravascular coagulation
and death.

8. • Causes of death
 Progressive anaemia o Intravascular coagulation
 Hypoglycemia due to disturbed metabolism by malfunction
of adrenals, pancreas and thyroid and due to direct utilization
of glucose by the parasite.
• Biochemical changes
 Increase in globulin and decrease in albumin globulin ratio
by 14.4%.
 The infection is severe in dogs and horses than cattle and
buffaloes.

10. Clinical signs
• Equines
 Incubation Period: 4 to 9 days
 Severe in horses
 Donkeys are resistant
 Death within few days to few months depending on
the virulence of strain of the organism.
 Intermittent fever (44○C) and anaemia are main
symptoms.
 Transient local/ urticarial eruptions/ plaques on neck/
flanks; edema of legs and lower parts of the body.

11.  Hemorrhage at the junction of the skin and mucous
membrane at nostrils, eyes and anus and petechial
haemorrhage on mucous membrane of eye or vulva in
mares; pale and dirty yellowish mucous membrane
 Staggering gait, paraplegia, laboured breathing.
 Diarrhoea ,constipation, urine with albumin and blood and
dark yellowish; Increased thirst, signs of catarrh with yellow
tinged nasal discharge.
 Less common: Enlargement of lymph nodes, keratitis,
petechiae in vaginal mucus membrane.

12. • Cattle and Buffaloes
 Course varies from a symptomless carrier to per acute infection.
 Per acute - Death within in 2-3 hour; nervous form and death in
convulsion.
 Acute - Dull, sleepy, staggering gait, encircling movements, nervous
excitement, beating head against wall /manger, apparent blindness,
stamping of feet, bellowing, groaning, twitching of muscle, shivering
of body, coma and death within 6-12 hours.
 Sub acute/ Chronic -Parasitaemia is usually low and doesn’t coincide
with temperature and afebrile animal be positive for parasites, edema
of legs, diarrhea, intermittent fever, rapid pulse, dullness, sleepy,
bilateral lachrymation, progressive emaciation and death; abortion
reported in buffaloes.
 PM findings: Spleenomegaly, hepatomegaly, enlargement of
lymph nodes and kidney, petechial haemorrhage at the junction of
skin and mucous membrane

14. • Dogs
 Incubation period: 5 to 6 days; untreated dogs die within 12 months,
acute and fatal; more serious in pups and imported dogs.
 Fever, anorexia, edema of head and throat, corneal opacity or
blindness.
 Laryngeal edema resulting in change of voice simulating rabies.
 Muscular spasm of limb, staggering gait, excitement like biting
kennel bars simulating rabies.
• Cats: Chronic cases are reported; at times may be fatal.
•Sheep and Goats: Rare; intensity of symptoms are also moderate;
emaciation and anaemia may be present.
• Pigs: non-pathogenic and low parasitaemia.

15. DIAGNOSIS
• History of prevalence of T. evansi infection and biting flies
like tabanids.
• Clinical signs.
• Differential diagnosis
 Anthrax
 Snake bite
 Nervous ketosis,
 Organic and inorganic poisoning,
 Milk fever
 Hypovitaminosis,
 Milk fever,
 Brain tumor/ cyst

16. • Direct examination
 In acute cases-demonstration of organisms in blood smears
stained freshly with Giemsa stain.
 Chronic cases- examination of thick and thin blood smear at
the height of the temperature will be positive/ lymph node
puncture smears.
• Chemical tests
 To detect the changes in the chemical composition of the
blood produced by T. evansi, like alteration of proteins
 Non-specific and less reliable.
 Mercuric chloride test, Formal gel test, thymol turbidity
test are used for camels.
 Stilbamide test-diagnosis of latent infection in bovines in
India.

17. • Animal inoculation tests
 For detection of latent infection of bovines and more
reliable than microscopic examination. Albino mice/ rat are
most suitable for detecting sub patent infection; guinea pigs
and rabbits are less susceptible. Injection of 2 ml of blood
intraperitoneally into the mice causes organisms appear after
2-3 days in the mice.
• Immunodiagnostic tests
 IFAT, CFT, ELISA & IHA are most reliable tests.
 Allergic tests are doubtful- 1ml antigen is injected at the
side of the neck with a 2nd dose after 48 hours. Infected
cases show hot, edematous, painful swelling and healthy
cases show circumscribed, hard, nodular swelling.

18. TREATMENT
• Quinapyramines (Antryside) - Prophylactic (Triquin)- Drug of
choice.
 Antryside methyl sulphate solution
 3mg/kg as 10% aqueous solution, S/C; effective against
T. evansi, T. congolense, T. brucei, T. vivax.
 Antrycide chloride as antrycide prosalt
 In combination with antrycide methyl sulphate -3 parts of
A. M.S + 2 parts A. chloride
 A solution of 3.5 gm in 15 ml water is given @ 7.4
mg/kg; effective against T. evansi and T.brucei, for 3
months.

19. • Suramins (Sulphonated naphthalamines) - Curative (Naganaol,
Antrypol)
 Effective against T. evansi, T. brucei, T. equiperdum.
 Cattle: 0.5 g/ 45 kg followed by half dose after 2 weeks,
I/V.
 Horse: 4g/ 45 kg as single dose, I/ V. Dog: 3.5 ml-
10%solution followed by 2nd dose at 3-4 weeks interval,
I/V.
• Diamidines: Diminazene aceturate (Berenil) - Curative,@ 3.5 mg/
kg ;
 cattle - 10 mg /kg; S/C or deep I/M
 Very effective against T. congolense and less effective
against T. evansi, T. brucei , in bovines, ovines and caprines.
 Dog and camels react to dogs; resistance may occur to the
drug.

20. • Phenanthiridine compounds
 Homidium bromide and Homidium chloride- 1-2% sol @
1gm/kg b. wt, I/M against T. congolense and T.vivax but
not against T. evansi.
 Pyrithridium bromide - 4 % sol @ 2mg/ kg b. wt, S/C
or I/M against T.congolense and T.vivax.
 Isometamidium chloride - 0.5 mg / kg b. wt, against T.
simiae in pigs.

21. CONTROL
• Control is difficult and the factors responsible for the wide
spread existence are
 Latent cases of cattle and buffalo,
 Reservoir wild animals
 Drug resistant strains and
 Wide spread prevalence of vectors
• Control program consists of
 Treatment of affected animals
 Chemoprophylaxis
 Disposal of manures properly o Proper drainage

22.  Regular spraying of insecticides: Sprinkling of kerosene
oil over water in ponds, ditches, streams or insecticides to
kill adults and aquatic larvae.
 Removal of moist beddings, hay, dung from stable.
 Keeping animals clean by regular grooming.
 Segregation of sick animals from healthy during
outbreak in fly -proof shed.
 Identification of endemic areas by regular examination
of blood of animals for implementation of preventive
measures.

23. Thanks