Difference between revisions of "Trypanosomosis"
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==Control== | ==Control== | ||
| − | Separation of livestock and wild animals is effective but difficult. | + | '''Separation''' of livestock and wild animals is effective but difficult. |
| − | Use of trypanotolerant livestock breeds is the only option is some areas where economic restraints prevent constant treatment and control. | + | Use of '''trypanotolerant''' livestock breeds is the only option is some areas where economic restraints prevent constant treatment and control. |
| − | [[Glossinidae | Tsetse fly]] control by sprays, traps, dips and release of sterile male flies is effective but expensive and time consuming | + | '''[[Glossinidae | Tsetse fly]] control''' by sprays, traps, dips and release of sterile male flies is effective but expensive and time consuming. |
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| − | |||
| + | Prophylactic drug therapy is also effective but costly. | ||
==References== | ==References== | ||
Revision as of 12:10, 5 June 2011
Also Known As — Nagana—Typanosomiasis—Chagas' Disease—Sleeping sickness—Parrot Sickness
Introduction
Trypanosomosis is a disease caused by protozoan pathogens of the genus Trypanosoma. They are obligate parasites and can infect mammals, birds, reptiles, amphibians and fish.
Trypanosomes are divided into two categories depending upon their lifecycle: 'Stercorarian trypanosomes develop within an insect vector and are transmitted to mammals in the faeces of the vector.
Salivarian trypanosomes develop within tsetse flies and mammals are infected through their bites.
Trypanosomosis causes a wasting disease in cattle and sleeping sickness in humans.
T. cruzi is the most important species in veterinary medicine.
Trypanosomosis is notifiable to the World Organisation for Animal Health (OIE)
Signalment
Some breeds appear trypanotolerant and able to resist clinical disease and anaemia, such as African buffalo and N’dama and Keteku cattle.
Calves less than a year old are more resistant than adults, but lambs and kids appear more susceptible to T. congolense infections. Cattle 6-9yrs old appear most susceptible to trypanosomosis.
Causative Organisms
Salivarian Species
T. brucei affects all domestic mammals, including small and farm species, and humans. It also causes a specific skin disease in donkeys.
T. vivax infects ruminants, horses and camels causing significant disease.
T. equiperdum causes venereal equine disease dourine. It is the only trypanosome that does not immediately require an insect vector for transmission, being spread through coitus.
T. simiae causes fatal pyrexia in pigs while T. congolense is milder in the same species.
T. congolense can also affect dogs and cats causing acute fever, anaemia and neurological signs.
T. evansi also affects all domestic mammals.
Stercorarian Species
T. cruzi occurs in South America where it is transmitted by a triatomid (kissing) bug and infects armadillos, possums and humans. It is known as Chagas’ Disease. A similar acute disease is thought to be caused by T. cruzi in dogs in the USA.
T. melophagum and T. Theileri are non-pathogenic species present in the UK infecting cattle, buffalo and antelope. Stress and concurrent disease are thought to be contributors to the development of clinical disease from T. theileri.
Transmission
Trypanosomosis is spread by Tsetse flies and other insect vectors.
Horse flies and stable flies can also act as mechanical vectors for some trypanosoma species, but the parasites can not undergo lifecycle development within these hosts.
T. vivax and T. evansi are reported to achieve Transplacental transmission. [1]
Distribution
Worldwide
T. brucei, T. uniforme, T. congolense and T. simiae are found only in the tsetse fly belt of Africa due to the restricted spread of their vector.
Clinical Signs
Clinical disease varies widely with death occurring from 1 week to months after infection. T. vivax is known for its rapid mortality while T. brucei and T. congolense hosts often survive for prolonged periods. Infection of large numbers of insect vectors is common in these circumstances.
Significant losses may also be caused by increased susceptibility and prevalence of other concurrent diseases where trypanosomosis is present.
Multisystemic signs can be seen in any species so diagnosis from clinical examination is often impossible as no pathognomic signs are evident.
Ruminants
Enlarged lymph nodes and spleen.
Later in the disease course the lymph nodes and spleen shrink due to lymphoid exhaustion.
Haemolytic anaemia is a cardinal feature.
Chronic infection causes heart failure and associated signs and death.
Plasma cell hypertrophy and hypergammaglobulinaemia are evident on haematology and biochemistry.
Emaciation
Abortion, premature births and infertility are features, and orchitis in males reduces fertility.
Horses
Oedema of the limbs and genitalia.
Dourine – genital and abdominal oedema, paraphimosis, urticarial plaques known as “silver dollar spots” and neurological signs. Disease is usually mild and recurrent but can be fatal.
Donkeys
Dogs and Cats
Pyrexia, myocarditis, myositis, corneal opacity and neurological signs.
Diagnosis
Microscopic identification on trypanosome parasites in the host blood on a smear with Giemsa staining.
Where low levels of parasitaemia are present, filtration or haemolysis of a whole blood sample may be required and motile trypanosomes may be demonstrable in a haematocrit tube at the plasma: buffy coat interface.
On post-mortem examination, carcasses are often pale and oedematous due to anaemia and emaciation. Degenerative lesions can be found on the heart, liver, lymph nodes, testes, brain, conjunctiva, cornea, spleen, kidney and endocrine organs.
Many other seroimmunological techniques are also available variably in laboratories.
Treatment
A variety of drugs can be used to treat trypanosomosis including diminazene, homidium, isometadium, suramin and melarsomine.
Diminazene aceturate is most commonly used and is frequently curative. It however causes frequent local reactions in horses so should be given in multiple deep muscular sites and massaged well. The drug is also contraindicated in dogs and camels due to vascular damage. Diminazene also has a prophylactic effect for up to 3 months.
Resistance is increasing in Africa to trypanosomicidal drugs so multiple treatments may be required in some areas.
Control
Separation of livestock and wild animals is effective but difficult.
Use of trypanotolerant livestock breeds is the only option is some areas where economic restraints prevent constant treatment and control.
Tsetse fly control by sprays, traps, dips and release of sterile male flies is effective but expensive and time consuming.
Prophylactic drug therapy is also effective but costly.
References
- ↑ Ikede, B. O., Loso, G. J.(1972). Hereditary transmission of Trypanpsoma vivax. Brit Vet J, 128:i-ii
Animal Health & Production Compendium,Trypanosomiasis datasheet, accessed 05/06/2011 @ http://www.cabi.org/ahpc/
Merck Veterinary Manual, Tsetse-transmitted Trypanosomiasis accessed online 03/06/2011 @ http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/10413.htm [[Category:]]