scholarly journals Clinicopathological and Microscopic Features of Trypanosoma brucei and Trypanosoma evansi Induced Infections in Sheep II

2021 ◽  
Vol 41 (2) ◽  
pp. 144-160
Author(s):  
Y.A. Wada ◽  
P.I. Rekwot ◽  
O.O. Okubanjo ◽  
B. Mohammed ◽  
S.J. Oniye

The present study elucidates further on clinical, gross, and microscopic pathologies induced by single or mixed infections with  Trypanosoma evansi and Trypanosoma brucei in sheep. Briefly, the experimental animals were divided into four groups of three  animals each. Animals in each group were either infected with T. brucei, T. evansi, mixed (T. brucei and T. evansi), or noninfected. Animals were observed for clinical, gross, and microscopic pathologies for 98 days (14 weeks). The clinical pathologies observed included loss of body condition, pale ocular mucus membrane, rough hair coat, scrotal oedema, scrotal degeneration, emaciation, and death. At necropsy, macroscopic or gross lesions included very pale and anaemic carcass composition, congested and pneumonic lungs with severe haemorrhages, serous atrophy of intestinal and body fats, lymphadenopathy, splenomegaly, and hepatomegaly. Microscopic lesions observed in the testes, spleen, liver, lungs, lymphoid, heart, and brain tissues of infected sheep were varied and included swollen kidney with renal tubular degeneration, the proliferation of lymphocytes at the germinal centers of the spleen, degeneration of the bronchioles, severe testicular degeneration with a reduction in the number of spermatogenic cell layers,  degenerated Leydig and Sertoli cells with loss of sperm reserves in the seminiferous lumen, congested liver with sinusoidal spaces and the proliferation of monocytes and lymphocytes. The results indicate that trypanosomosis due to experimental T. brucei, T. evansi, or mixed infections may be an important cause of various grades of tissue and organ pathologies in sheep in trypanosome-endemic areas. Keywords: Trypanosomosis; Clinico-pathological and microscopic features; Trypanosoma brucei; Trypanosoma evansi; Mixed  infections; Sheep

2021 ◽  
Vol 8 ◽  
Author(s):  
Keneth Iceland Kasozi ◽  
Gerald Zirintunda ◽  
Fred Ssempijja ◽  
Bridget Buyinza ◽  
Khalid J. Alzahrani ◽  
...  

While both human and animal trypanosomiasis continue to present as major human and animal public health constraints globally, detailed analyses of trypanosome wildlife reservoir hosts remain sparse. African animal trypanosomiasis (AAT) affects both livestock and wildlife carrying a significant risk of spillover and cross-transmission of species and strains between populations. Increased human activity together with pressure on land resources is increasing wildlife–livestock–human infections. Increasing proximity between human settlements and grazing lands to wildlife reserves and game parks only serves to exacerbate zoonotic risk. Communities living and maintaining livestock on the fringes of wildlife-rich ecosystems require to have in place methods of vector control for prevention of AAT transmission and for the treatment of their livestock. Major Trypanosoma spp. include Trypanosoma brucei rhodesiense, Trypanosoma brucei gambiense, and Trypanosoma cruzi, pathogenic for humans, and Trypanosoma vivax, Trypanosoma congolense, Trypanosoma evansi, Trypanosoma brucei brucei, Trypanosoma dionisii, Trypanosoma thomasbancrofti, Trypanosma elephantis, Trypanosoma vegrandis, Trypanosoma copemani, Trypanosoma irwini, Trypanosoma copemani, Trypanosoma gilletti, Trypanosoma theileri, Trypanosoma godfreyi, Trypansoma simiae, and Trypanosoma (Megatrypanum) pestanai. Wildlife hosts for the trypansomatidae include subfamilies of Bovinae, Suidae, Pantherinae, Equidae, Alcephinae, Cercopithecinae, Crocodilinae, Pteropodidae, Peramelidae, Sigmodontidae, and Meliphagidae. Wildlife species are generally considered tolerant to trypanosome infection following centuries of coexistence of vectors and wildlife hosts. Tolerance is influenced by age, sex, species, and physiological condition and parasite challenge. Cyclic transmission through Glossina species occurs for T. congolense, T. simiae, T. vivax, T. brucei, and T. b. rhodesiense, T. b. gambiense, and within Reduviid bugs for T. cruzi. T. evansi is mechanically transmitted, and T. vixax is also commonly transmitted by biting flies including tsetse. Wildlife animal species serve as long-term reservoirs of infection, but the delicate acquired balance between trypanotolerance and trypanosome challenge can be disrupted by an increase in challenge and/or the introduction of new more virulent species into the ecosystem. There is a need to protect wildlife, animal, and human populations from the infectious consequences of encroachment to preserve and protect these populations. In this review, we explore the ecology and epidemiology of Trypanosoma spp. in wildlife.


1985 ◽  
Vol 22 (6) ◽  
pp. 548-551 ◽  
Author(s):  
D. H. Embury ◽  
I. V. Jerrett

Mannosidosis was diagnosed in four stillborn Galloway calves and an autolyzed full-term fetus from experimental matings of carrier animals. Gross lesions were moderate internal hydrocephalus, and pallor and enlargement of the liver and kidneys and arthrogryposis. Histologic changes in the central nervous system of each calf were marked foamy vacuolation of the cytoplasm of neurones in the cerebral cortex, thalamus and brainstem, and vacuolation of the Purkinje cells of the cerebellum. Spheroids were common throughout the brain and there was also consistent severe foamy cytoplasmic vacuolation of renal tubular epithelial cells and hepatocytes. The activities of α-mannosidase, the lysosomal enzyme whose activity is deficient in mannosidosis, and activities of five other lysosomal enzymes were compared in brain, liver, and kidney tissues of three mannosidosis-affected calves and normal calf tissues. Tissues from the affected calves had a marked deficiency of α-mannosidase activity compared with the normal tissues; the greatest deficiency was in the liver (99%) and brain (98%). Activities of the other lysosomal enzymes were elevated in the affected tissues compared with normal. Mannosidosis is a lysosomal storage disease that results from a defect in glycoprotein metabolism and affects man,18 Angus and Angus-related breeds of cattle, such as Murray greys,12,21 and the cat.4 The congenital disease is caused by an inherited deficiency of the lysosomal enzyme α-mannosidase,14 and is inherited in an autosomal recessive manner. Mannosidosis was recently reported in a number of aborted and stillborn Australian Galloway calves3 from an experimental breeding trial. This is more detailed account of the histological and biochemical results obtained during the trial.


Author(s):  
J. Balis

Après avoir rappelé brièvement les connaissances actuelles sur le métabolisme glucidique de Trypanosoma evansi et Trypanosoma brucei, l'auteur expose les résultats obtenus par deux méthodes originales. L'une est utilisable uniquement pour Trypanosoma evansi, l'autre appelée "test de mobilité" est d'application plus générale. Elle permet une étude rapide du métabolisme des Trypanosomes. Trypanosoma evansi est capable d'utiliser les corps suivants: glycérine glucose, fructose, mannose, glucosamine. Le glycogène et le maltose sont métabolisés après hydrolyse par une maltase et une glycogénase sanguines. La production d'acide pyruvique est très importante. Trypanosoma brucei utilise les mêmes glucides mais également l'acide Alpha cétoglutarique, le pyruvate de sodium, la thréonine, l'acide glutamique et la proline. La mobilisation obtenue avec l'acide Alpha cétoglutarique est très nette et permet de différencier biochimiquement Trypanosoma evansi de Trypanosoma brucei


This species was only met with on one occasion during the work of the Commission in 1909. This was in the blood of an ox from the Mabira Rubber Estate (latitude 0° 30′ N., longitude 32° 55′ E.). The manager wrote that the animal came from the Bukedi District, about 100 miles to the north (latitude 1° 50′ N., longitude 32° 40′ E.). Not much is known of this district, as it has only recently come under administration, and therefore it is impossible to say whether the ox was infected in Bukedi or on the journey south. This is the species of trypanosome which was first discovered by Bruce, in 1894, in Zululand, to be the cause of Nagana, or tsetse-fly disease. During the work of the Sleeping Sickness Commission of the Royal Society in 1903, it was also met with in a herd of cattle from the same district of Bukedi, and then described as the “Jinja trypanosome.” It is impossible to name with any certainty the trypanosome seen in 1903, which affected the horses, camels, and dogs of the Abyssinian Boundary Commission. This was described as the “Abyssinian trypanosome.” Its morphology, as given in the coloured plate, shows it to be similar to Trypanosoma brucei , so that in all likelihood it was either this species or the closely related Trypanosoma evansi . As camels were infected, it was more probably the latter.


2006 ◽  
Vol 22 (2) ◽  
pp. 55-56 ◽  
Author(s):  
Feng-Jun Li ◽  
De-Hua Lai ◽  
Julius Lukeš ◽  
Xiao-Guang Chen ◽  
Zhao-Rong Lun

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