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The literature on the diseases caused byTrypanosoma evansi is reviewed and the gaps in the available information are emphasized.Trypanosoma evansi, on the basis of combined similarities in morphology, biological behaviour, and to some degree based on geographical distribution, is a species closely related to and probably originating fromT.brucei. The distribution ofT. evansi is very wide in the Old and New World and it is transmitted by biting flies and vampire bats. It has a patchy distribution in any region and new foci of infection have a high incidence. Diagnosis is made on demonstration of trypanosomes, biochemical tests detecting increase in serum proteins, and on specific serological tests. The clinical signs vary with the acuteness of the syndrome, often being characterized by a chronic course with lack of pathognomonic signs. There is very little information on the pathology of the diseases in various species of animals, but the lesions apper to be similar to those caused byT. brucei and are associated with the distribution of trypanosomes in solid tissues. Immunological studies habe been limited primarily to serology in connection with diagnostic procedures. Laboratory models have been studied and the syndromes are similar to those produced byT.brucei. Chemotherapy is varied and to some degree dependent on the species of host. More information on the incidence and severity of diseases is required to identify priorities for further research.

In cattle infected experimentally with Trypanosoma brucei the trypanosomes localized extravascularly in the connective tissues and produced inflammatory reactions in the skin, subcutaneous tissue, heart, central nervous system, and eye. These observations indicate that, as in other domestic and laboratory animals, T. brucei is a parasite of connective tissues in cattle.

Twenty-five steers were infected with T. vivax (EATRO 1721), 25 steers with T. congolense (EATRO 1800) and 25 steers kept as controls. Serum levels of immunoglobulins (IgG1, IgG2, IgM), natural antibodies to erythrocytes of chicken and sheep, and complement-fixing antibodies to T. vivax were measured. A significant decrease of serum IgM and natural antibodies to chicken erythrocytes occurred in the T. vivax group at day 9, i.e. at the decline of the first parasitemic wave. This was followed by a transient moderate increase of IgM accompanied by a transient decrease of IgG2. The T. congolense group had moderate decreases (less than 30%) of the mean IgG1 levels and moderate increases (less than or equal to 50%) of the mean IgG2, levels. It was concluded that there was little evidence for polyclonal activation of lymphocytes and that the decreased IgG1 levels in the T. congolense group might have been a reflection of immunosuppression. The complement-fixation test proved to be a sensitive tool for monitoring the antibody response to T. vivax.

SummaryThe study of pathogenicity of haemoprotozoa and the pathogenesis of the diseases they cause requires quantitative descriptions. Statistical and mathematical methods are introduced to describe infectivity, parasitaemia, total body parasitosis and the severity of diseases.

Serum collected from cattle infected with Trypanosoma vivax or Trypanosoma congolense inhibited bovine granulocyte/macrophage colony formation in methyl cellulose cultures. Maximum inhibition was caused by serum collected two and three weeks post infection. The degree of inhibition appeared to be related to the degree of parasitemia. Inhibition of erythroid colony formation by serum collected from these animals was not observed.

Twenty-five Holstein-Friesian steers were experimentally infected with Trypanosoma congolense EATRO 1721. They were tested for their J blood group status. Twelve steers were found to belong to Ja blood group and thirteen steers were either Js or Jcs. The level of parasitemia did not significantly differ between these two groups of cattle. It was concluded that the level of parasitemia is not influenced by J blood group antigens.

Cattle infected with Trypanosoma congolense were intravenously immunized with Leptospira biflexa 15 days after trypanosomal infection. The primary immune response to L. biflexa was considerably reduced as compared to uninfected controls. The infected cattle mounted a secondary response when they were cured of trypanosomes by treatment with Berenil 25 days after infection and re-immunized 8 days later. The mean secondary response in these previously infected animals was lower tha, but not significantly different from that of the uninfected control animals. Serum collected 15, 20 and 25 days after infection was inhibitory to the migration of both autologous and isologous (control) peripheral blood leucocytes. The migration inhibitory activity was abolished by heating the serum at 56 degrees C for 30 minutes implying the involvement of a heat labile serum component(s). The same serum did not modify the mitogenic effect of PHA on autologous peripheral lymphocytes.

Infections with Trypanosoma congolense or T vivax did not significantly depress the neutralising antibody response of cattle to live rinderpest vaccine when vaccination was carried out eight or 25 days after infection.

Twenty five cattle were infected with T. vivax, 25 with T. congolense, and 25 served as controls. Pathogenic clinical signs of trypanosomal infection were not observed. Secondary bacterial infections were common. Fever, increased heart and respiratory rates, anorexia, and emaciation developed. Elevations in parasitemai and body temperature were positively correlated in the T. vivax group. Infected groups were affected non-uniformly, with some animals in each group remaining asymptomatic and tending to have lower parasitemias. The T. vivax parasitemia was cyclic and the organisms had a genaration time of 7.9 SD 2.5 hours. The first peak of parasitemia in both infections was closely associated with the development of pancytopenia, i.e. anemia, leukopenia, and thrombocytopenia. The bone marrow erythroid response in the T. congolense group was significantly greater thn that in either the T. vivax or control groups. Leukopenia was due to concomitant neutropenia and lymphopenia.

Serum levels of total protein, albumin, activity of hemolytic complement, and complement component C3 were decreased in cattle infected with either T. congolense or T. vivax. The hemolytic complement activity was reduced most, i.e. to 20% (T. congolense) or 5% (T. vivax) of control levels. The development of hypocomplementemia was closely associated with the first peak of parasitemia.

Using 90 albino rats, a comparison was made between the response to experimental infections of Trypanosoma brucei and T congolense of approximately three weeks duration by observation of parasitaemia, packed cell volume values, post mortem spleen and lymph weights, and histology of thymus, spleen, lymph nodes and bone marrow. In T congolense infection, phagocytosis of trypanosomes in the spleen appeared to be the main response of the host's haemopoietic tissues to the parasites, which were observed only intravascularly. In T brucei infection immunological responses occurred in the spleen and lymph nodes in addition to trypanosome phagocytosis. Trypanosomes were seen intercellularly in thymus, mediastinal tissue and lymph node sinuses and parasitaemia reached considerably higher values than in T congolense infection. Erythrophagocytosis in the spleen was the only histological feature which could account for the reduction in packed cell volume which occurred near death in both infections, medullary haemopoiesis being increased. Changes in the thymus, incorporating plasma cell production and depletion of cortical small lymphocytes, occurred in both infections.

Dolan T. T. , Young A.S. , Losos G.J. , McMillan I. , Minder Ch.E. and Soulsby K. 1984. Dose dependent responses of Theileria parva stabilate. International Journal for Parasitology14: 89–95. A tick derived stabilate of Theileria parva (Maguga) was titrated in a large group of Boran (Bos indicus) cattle of the same age, sex and origin. The infectivity data was analysed using the independent action model. The cattle were identified as heterogeneous in their response to infection with 75% showing one ID50 (0.0014) and 25% showing another (0.01). The disease responses of the cattle given different dose levels were compared for a variety of parameters. The results obtained showed these parameters to be dose dependent including the time to onset of piroplasm parasitaemia. The stabilate is of large volume and can be used for controlled challenge in immunity studies and for comparison of susceptibility between cattle of different breeds and from different epidemiological backgrounds.

Sheep inoculated intravenously with Trypuiiosom bviicei had fever, irregular parasitaeniia, moderate anaemia, subcutaneous oedenia, dullness, anorexia, and nervous signs followed by death in 29-69 days. Emaciation, serous effusions into body cavities and generalised enlargement and oedenia of lymph nodes were seen at necropsy. Micro- scopically there was extensive localisation of trypanosonies in the extravascular body fluids, and in interstitial connective tissues, resulting in mononuclear inflammatory reactions in the heart, skeletal muscle, skin, brain, pituitary, eye, serosal surfaces, urinary bladder, epididyniis and testis, and in generalised lymphoid hyperplasia. These observa- tions in sheep are comparable to those made in other animals infected with trypanosornes of the brucei group. Trypanosoma brucei, T. congolense, and T. vivax cause the most econom- ically important forms of animal trypanosomiases in Africa. There is rela- tively little information on the pathogenesis and pathology of the diseases produced by these species in domestic animals (l 11. Infections and diseases causcd in sheep by T. brzxei occur naturally (2, 131, but there is little informa- tion on either the prevalence or the pathology. Sheep, however, have been used extensively in the past in investigations of the virulence of various human and animal isolates of trypaiiosonies in the brucei subgroup. Many of these isolates were associated with severe diseases characterized by ema- ciation, subcutaneous oedema, enlargement of lymph nodes, and corneal opacity (I, 3, 71. The present report is based on studies in sheep experimentally infected with T. brzrcei. This was part of a major investigation of the pathology of the diseases caused in ruminants by T. brucei, T. vivax, and T. congolense.

This paper describes a case of multiple myeloma in a 3-year-old mongrel bitch. The diagnosis was established by histopathological examination of post-mortem material. The tumour formed nodular masses on the fourth left rib and third and fourth lumbar vertebrae; it also involved the sternal lymph nodes, spleen, liver and kidneys. Demonstration of amyloid deposits in the kidney was inconclusive. Resume. Observation d'un cas de myelome multiple chez une chienne bâtarde de 3 ans. Le diagnostic a ete fait d'apres les donnees histopathologiques apres autopsie. La tumeur formait des masses nodulaires au niveau de la 4eme cote gauche et des vertebres L 3 et L 4; elle interessait aussi les ganglions lymphatiques parasternaux, la rate, le foier et les reins. La presence de depots amyloides dans le rein n'apportait aucun renseignement complementaire. Zusammenfassung. Diese Abhandlung beschreibt einen Fall von multiplem Myelom bei einer 3 Jahre alten Bastardhundin. Die Diagnose beruhte auf der histopathologischen Untersuchung von Autopsiematerial. Der Tumor bildete nodulare Massen an der vierten Rippe links und am dritten und vierten Lendenwirbel; er involvierte auch die sternalen Lymphknoten, Milz, Leber und Nieren. Der Nachweis von Amyloidablagerungen in der Niere war nicht uberzeugend.

In rats, rabbits, sheep, and goats experimentally infected with several strains of Trypanosoma brucei, the trypanosomes were observed to localise extravascularly in connective tissues. Focal inflammatory reactions were associated with the localisation of the parasites. Trypanosoma congolense in the same species of animals and T. vivax in sheep and goats, were not observed to localise outside blood vessels. On the basis of these observations it appears that the pathogenesis of the disease caused by T. brucei differs from that caused by T. congolense and T. vivax.

In a 4 year period, 77 zoo animals were brought to our diagnostic laboratory. Twenty-six of the 77 animals had diagnostic lesions. Of the diseases of primates, Herpes simplex encephalitis, pyrrolidine alkaloid poisoning and osteodystrophia fibrosa were prominent. Hydatidcsis, trypanosomiasis and myopathies were significant diseases in wild ruminants. Rabies was diagnosed in a lynx. The significance of these diseases to public health and epidemiology, is discussed.