Toxicity of chloroform extract of prunus africana stem bark in rats: gross and histological lesions.

Chloroform extract of Prunus africana (Hook f. (Rosaceae) did not cause clinical signs or pathology in rats at daily oral doses of up to 1,000 mg/kg for 8 weeks. The extract caused marked clinical signs, organ damage and a 50% mortality rate at a dose of 3.3 g/kg for 6 days. The main lesions observed at this dose were marked centrilobular hepatocellular degeneration and necrosis, diffuse nephrosis, myocardial degeneration, lymphocytic necrosis and neuronal degeneration. The morphological damage in these tissues caused a corresponding rise in blood biochemical parameters namely, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, creatine kinase and blood urea nitrogen. The target organs of toxicity of this extract are the liver, kidney and heart. Overt toxicity occurred only after the administration of multiple doses of 3.3 g/kg body weight. These findings confirm the suitability of this extract for therapeutic use, since the doses used in the therapy of prostate gland are much lower than those used in this study and would therefore not be expected to cause pathological changes.

Biochemical and haematological changes in rats administered an aqueous extract of Prunus africana stem-bark at various dosage levels.

An aqueous extract of Prunus africana (Hook. f.) Kalkm. (syn. Pygeum africanum) (Hook. f.) (Rosaceae) was administered daily at dosage rates of 10, 100 and 1,000 mg/kg body mass to randomized groups of Sprague Dawley rats. The extract caused a moderate rise in plasma alanine aminotransferase and creatine kinase mainly at rates of 1,000 mg/kg body mass, but it did not cause any significant variations in haematological parameters or in plasma levels of total proteins, albumin, aspartate aminotransferase, alkaline phosphatase and blood urea nitrogen at the dosage levels used. There were no overt clinical signs in any of the rats. It was concluded that the extract may contain components that are mildly toxic to the liver and heart of rats after repeated daily oral administrations of 1,000 mg/kg body mass.

Semen characteristics of goats with subacute, acute and chronic besnoitiosis.

A study on the semen obtained from breeding goats suffering from mild to severe chronic besnoitiosis revealed marked changes in semen volume, colour, density, concentration, mass and individual motility and percentage live. There were also many neutrophils and spermatozoa with primary and secondary defects, including missing tails and deformed heads and tails. The observed changes were considered to be severe enough to account for the infertility observed in the flock. Sections of testes obtained for histopathology were characterised by massive blockage of the pampiniform plexus, degeneration of the germinal epithelium, tubular necrosis with an inflammatory infiltrate and, in some cases, accumulation of haemosiderin-like material in the tunica vaginalis.

Prevalence of besnoitiosis in domestic ruminants in Kenya: a preliminary survey.

A preliminary survey on the prevalence of besnoitiosis in domestic ruminants in Kenya based on field and farm visits, clinical and post mortem examinations and histopathological examination of tissues and biopsies, showed that goats are the most affected, followed by cattle, while sheep were unaffected. Caprine besnoitiosis occurred in a continuous belt in 5 of the 8 provinces in Kenya stretching from the Coast, Eastern, North Eastern, Nairobi and the Rift Valley Provinces. Mandera, in the North Eastern Province, had the highest prevalence rate of 36%, followed by Kwale (35%), Isiolo (35%), Marsabit (33%), Wajir (28%), Nairobi (26%), Meru (24%), Garissa (21%), Taita Taveta (18%), Embu (17%), Kitui (9%), Machakos (7%), Laikipia (3%), Kajiado (2%) and Turkana and Elgeyo-Marakwet (1% each). In all flocks where the prevalence rates were over 6%, kids were observed to be affected. There were no significant differences (P < 0.05) between the prevalence rates in bucks and does (18% and 18.4, respectively), but kids were less (4%) affected. Bovine besnoitiosis was found only in the Tana River District, with an infection rate of 11%.

Experimental transmission of Besnoitia caprae in goats.

Experimental transmission of Besnoitia caprae from naturally chronically-infected goats to susceptible ones was achieved by intra-nasal instillation and intra-conjunctival inoculation of cystozoite-containing suspensions, subcutaneous implantation of fascia containing cysts and alternate needle pricking between the infected and non-infected goats. Typical chronic symptoms developed in the fascia-infected does. Cystozoite inoculation into the eyes and mouth did not result in infection. Kids born of dams with acute and chronic besnoitiosis did not contract the infection in utero, suggesting that intra-uterine transmission may not occur. In contrast to does with acute besnoitiosis, which occasionally aborted, the does with chronic besnoitiosis gave birth to healthy kids. Kids below the age of 4 months (pre-weaned period) born of both infected and non-infected does were susceptible to besnoitiosis but appeared to be more resistant than adult goats.

Comparative ultrastructural studies on Besnoitia besnoiti and Besnoitia caprae.

Comparative transmission electron microscopy on Besnoitia besnoiti and on a strain of Besnoitia derived from goats in Kenya revealed that the two organisms differ in their pellicle, micropore, microtubules, nucleus, wall-forming body 1 (W1), amount of lipids and amylopectin. Thus the caprine besnoitia is probably a different organism and the term Besnoitia caprae should continue to be used.

An acute toxicity study of Heliotropium scottae Rendle in mice.

Twenty-four hour ip median lethal doses (LD50) of freeze-dried aqueous extracts of Heliotropium scottae Rendle leaves and stems in mice were determined and clinical signs noted. The LD50 of the leaf extract was 3.0 g/kg, while that of the stems was 3.5 g/kg. Clinical signs were excitement, prostration, rapid breathing, gasping for breath and death. The signs were the same for both the leaf and stem extracts. It was concluded that both the leaves and stems of H scottae have slight acute toxicity.

Preliminary findings from an experimental study of caprine besnoitiosis in Kenya.

Inoculation of cystozoites obtained from natural, chronic cases of caprine besnoitiosis produced clinical disease in goats but not in rabbits, mice, guinea pigs, hamsters, rats or cattle. Histological examination of tissue sections from the experimental animals showed Besnoitia cysts only in goats. This, together with field observations that cattle reared together with goats having besnoitiosis do not contract the disease, suggests that the Besnoitia species that infects goats in Kenya is host-specific and is not Besnoitia besnoiti. We suggest that the name Besnoitia caprae be adopted for the caprine pathogen.

Haemorrhagic pancarditis in cattle infected with Trypanosoma vivax.

Haemorrhagic pancarditis has been studied microscopically and ultrastructurally. Haemorrhages, oedema, mononuclear cell infiltration, degeneration, fragmentation, atrophy and lysis of myofibres, and extravascular localisation of the parasite were observed.

Arteriosclerosis and related lesions in rabbits.

Eleven female rabbits, mainly of the NZW breed, aged between 1 and 3.5 years, were examined post mortem. All had originated over the years 1982 to 1987 from the same rabbitry where they had been fed on pellets from the same manufacturer. Apart from one rabbit, all had a history of progressive loss of bodily condition and six of them had also been infertile. Grossly, most of them were emaciated and their arteries were hardened. In some, hepatopathy, nephropathy and pulmonary emphysema were evident. In one case, mummified foetuses were recovered from the abdominal cavity. Microscopically, degenerative changes and calcification were found in the walls of arteries, kidneys, lungs, hearts and ovaries.

Relapses in dogs experimentally infected with Trypanosoma brucei and treated with diminazene aceturate or isometamidium chloride.

Twenty dogs of mixed local East African breeds were used. Five of the dogs were uninfected controls and 15 were infected with T. brucei (ILRAD 273). Five of the infected dogs were untreated controls, five were treated with a high curative dose of diminazene aceturate, (7 mg kg-1 body weight (wt.), and five were given a subcurative dose of isometamidium chloride (1 mg kg-1 body wt.). The drugs, given at 8 days post infection (d.p.i..), led to apparent recovery. The antibody titres, however, remained high in both groups and at 42-49 d.p.i. there was at least one relapse in each treatment group. Parasite populations from relapsed animals were more resistant to the drugs than the original infecting populations. The implications of these findings are discussed.

Haematological and biochemical changes in cattle poisoned by Gnidia latifolia syn. Lasiosiphon latifolius (Thymelaeaceae).

Haematological and serum biochemical examinations were carried out on 12 high grade bull calves fed Gnidia latifolia (Meisn). This resulted in lymphocytopaenia, increased blood urea nitrogen and lactate dehydrogenase. There were no changes in the red blood cell counts, neutrophil counts, aspartate amino transferase, creatine phosphokinase and alkaline phosphatase. There was also no change in serum protein concentration. Post-mortem changes in the acutely intoxicated calves included petechial haemorrhages of the epicardium and submucosa of the rumen, abomasum and the intestines. The chronic cases showed a generalized emaciation with gelatinous atrophy of the body fat and accumulation of excess fluid in the body cavities. The lymph nodes and spleen showed lymphocytic degeneration with cellular depletion in the follicles. There were extensive liver fibroses in the chronic cases.

Acute toxicity of maytansine in F344 rats.

The toxicity of maytansine given by sc administration was studied in 5-week-old mald F344 rats. The LD50 (14-day) was 0.48 mg/kg. A dose response to drug administration was indicated by body weight changes and diarrhea. A single, acutely toxic dose of maytansine was shown to possess marked activity against dividing cells which was regarded as an important factor in the pathogenesis of acute lesions in tissues with a normal high rate of cell division. Histologically, mitotic figues were observed in many tissues from 6 to 24 hours after drug administration. Subsequently, necrotizing lesions led to atrophic changes in gastrointestinal tract mucosa, thymus, spleen, bone marrow, and testis. Maytansine also induced hemorrhagic lesions in parenchymatous organs and brain and perivascular monomuclear infiltration in the meninges, and chromatolysis and vacuolation of dorsal root ganglion cells, accompanied by clinical signs of ataxia. Ulcerative skin lesions were observed at the sc site of drug administration.