Trypanosomiasis in the camel (Camelus Dromedarius)

Röttcher, D; Schillinger, D.; Zweigarth, E.

doi:10.20506/rst.6.2.301

Cited by 25 publications

(19 citation statements)

References 24 publications

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“…The low-level and often cryptic parasitaemia observed in this study is characteristic of chronic T. evansi infection and agrees with observations made in rabbits and goats and in goats, sheep and camels following experimental and natural infections, respectively (Luckins et al 1978;Boid et al 1981;Rottcher et al 1987;Ngeranwa et al 1991). Throughout the infection the temperature fluctuated, ranging from 39.5° C to 40.1° C in the animals that eventually underwent self-cure and from 39.8° C to 40.5° C in those that remained parasitaemic until treated.…”

Section: Discussionsupporting

confidence: 91%

Haematological changes in sheep experimentally infected with Trypanosoma evansi

Onah¹,

Luckins²

1996

Parasitology Research

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Sheep were infected with 2 x 10(6) Trypanosoma evansi TREU 2143 through the external jugular vein. The parasite kinetics as well as the effects on body temperature, packed cell volume (PCV), erythrocyte counts and total and differential white blood cell counts were monitored twice weekly for 3 months. The results showed that T. evansi produced a chronic form of the disease in sheep characterised by low-level and often cryptic parasitaemia, with self-cure occurring in two cases; mild anaemia as evidenced by decreases in PCV and erythrocyte counts; and significant (P < 0.02) leucocytosis by day 22 post infection (p.i.). The leucocytosis was a result of marked lymphocytosis whose significant rises (P < 0.02) parallelled the rises in total white blood cell (TWBC) counts. These changes were less obvious in the animals that underwent self-cure. We conclude that T. evansi produces pathological changes in the peripheral blood of sheep similar to those produced by its tsetse-transmitted counterparts. It would thus appear that the sheep/T. evansi model is suitable for long-term study of the immunopathology of pathogenic trypanosomes since the sheep is easily available, easy to handle and a natural host to all pathogenic trypanosomes.

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Section: Discussionsupporting

confidence: 91%

Haematological changes in sheep experimentally infected with Trypanosoma evansi

Onah¹,

Luckins²

1996

Parasitology Research

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“…These speculations have not yet had any genetic support and must therefore be considered as pure hypothesis for further genetic characterization. However, selection of predominant slender forms of parasites by blood-sucking insects has been suggested for a long time [69]. Clearly, since it was mathematically demonstrated that the efficacy of mechanical transmission is directly proportional to parasitaemia [70], biting insects favour the spread of the most prolific strains of parasites in each host species.…”

Section: Disease Synonyms and Parasite Taxonomymentioning

confidence: 99%

“…Goats are also most often of low susceptibility [69, 138]; thus in experimental infections with a camel isolate from the Canary Islands they showed mild symptoms with a few episodes of fever in early infection and arthritis in the next 6 months; although low, parasitaemia remained persistent [139]. In the Philippines, experimental infection led to the observation of fluctuating fever, progressive emaciation, anaemia, coughing, testicular enlargement, and diarrhoea but not in all animals [140].…”

Section: Clinical Signsmentioning

confidence: 99%

Trypanosoma evansiand Surra: A Review and Perspectives on Origin, History, Distribution, Taxonomy, Morphology, Hosts, and Pathogenic Effects

Desquesnes

Holzmüller

Lai

et al. 2013

BioMed Research International

348

327

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Trypanosoma evansi, the agent of “surra,” is a salivarian trypanosome, originating from Africa. It is thought to derive from Trypanosoma brucei by deletion of the maxicircle kinetoplastic DNA (genetic material required for cyclical development in tsetse flies). It is mostly mechanically transmitted by tabanids and stomoxes, initially to camels, in sub-Saharan area. The disease spread from North Africa towards the Middle East, Turkey, India, up to 53° North in Russia, across all South-East Asia, down to Indonesia and the Philippines, and it was also introduced by the conquistadores into Latin America. It can affect a very large range of domestic and wild hosts including camelids, equines, cattle, buffaloes, sheep, goats, pigs, dogs and other carnivores, deer, gazelles, and elephants. It found a new large range of wild and domestic hosts in Latin America, including reservoirs (capybaras) and biological vectors (vampire bats). Surra is a major disease in camels, equines, and dogs, in which it can often be fatal in the absence of treatment, and exhibits nonspecific clinical signs (anaemia, loss of weight, abortion, and death), which are variable from one host and one place to another; however, its immunosuppressive effects interfering with intercurrent diseases or vaccination campaigns might be its most significant and questionable aspect.

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“…The disease is caused by infection with hemoflagellated parasites belonging to the genus Trypanosoma. Trypanosoma evansi belongs to 48 Trypanozoon subgenus and is the most commonly reported cause of camel trypanosomosis called 49 surra (Röttcher et al, 1987). T. evansi is mechanically transmitted by blood sucking flies, such as A c c e p t e d M a n u s c r i p t 5 multistage stratified sampling methods was applied according to Toma et al (Toma et al, 1999).…”

Section: Introductionmentioning

confidence: 99%