Evaluation of the Bioactivity of Some Traditional Medicinal Plants Using the Brine Shrimp Lethality Test

The purpose of this experiment was to evaluate the bioactivity of extracts of Chrysanthemum cinerariaefolium Vis Albizia antihelmintica A. Brogn, Maerua edulis (Gilg) De Wolf, Maerua subcordata (Gilg & Bened) De Wolf and Myrsine Africana L. which are used traditionally as antihelmintic by using brine shrimp lethality test. Serial dilutions of 1000&#61549;g/ml, 100&#61549;g/ml and 10 mg/ml of the extracts were put in five test tubes. Ten (10) brine shrimp larvae were immersed into each of the test tubes and the number surviving after 24 hours counted and the percentage mortality and LC&#61493;&#61488; for each extract was determined. C. cinerariaefolium (pyrethrins) was active (LC&#61493;&#61488; < 1000 &#61549;g/ml) at LC50 of 1.3mg/ml while the methanol extract of A. antihelmintica bark was active with LC50 of 18&#61549;g/ml. The methanol extracts of Maerua edulis, Maerua subcordata and Myrsine Africana were not active (LC50 < 1000&#61549;g/ml). The result indicated that C. cinerariaefolium and A. antihelmintica extracts have bioactivity and is the basis for their use as antihelmintic by pastoral communities. Brine shrimp lethality test was found to be a simple and rapid test and is thus recommended for similar studies. The Kenya Veterinarian Vol. 26 2004: pp. 8-1

Occurrence of a Severe Acute Livestock Poisoning by Borehole Water in Marsabit District, Kenya A Case Study

This article reports on an outbreak of acute livestock poisoning by borehole water that occurred at Kargi in Marsabit District, Kenya in 2000. The borehole had been out of use for 3 years and after its rehabilitation, 7,000 animals died within a day after drinking the water. The most affected were shoats, cattle, camels and dogs with mortalities of up to 90%. Donkeys and humans were only mildly affected with no deaths reported. Clinical signs occurred within 1 hour after drinking the water. Initially, the animals displayed increased frequency of urination, followed by symptoms of respiratory insufficiency, comprising of dyspnea, cyanosis, rapid and weak pulse and general weakness. The signs progressed into methemoglobinuria, sever pain, trebling, convulsions, collapse, coma, and death within hours. Rapid decomposition, brown discoloration of mucous membranes, gastrointestinal tract corrosion and cooked appearance of visceral organs were observed at postmortem. Water samples that were collected from the borehole and neighboring wells contained arsenic (0.2 –66.8 ppm), selenium (1.1 –4.4 ppm) < lead (0.01-0.02 ppm) and nitrates (450-950 ppm) and other contaminants. The deaths were probably due to nitrate poisoning. The Kenya Veterinarian Vol. 28 2005: pp. 16-1

Pharmacokinetics of phenytoin following intravenous and intramuscular administration of fosphenytoin and phenytoin sodium in the rabbit

The purpose of this study was to evaluate and compare plasma phenytoin concentration versus time profiles following intravenous (i.v) and intramuscular (i.m) administration of fosphenytoin sodium with those obtained following administration of standard phenytoin sodium injection in the rabbit. Twenty-four adult New Zealand White rabbits (2.1 +/- 0.4 kg) were anaesthetized with sodium pentobarbitone (30 mg/kg) followed by i.v or i.m administration of a single 10 mg/kg phenytoin sodium or fosphenytoin sodium equivalents. Blood samples (1.5 ml) were obtained from a femoral artery cannula predose and at 1, 3, 5, 7, 10, 15, 20, 30, 45, 60, 90, 120, 180, 240 and 300 min after drug administration. Plasma was separated by centrifugation (1000 g; 5 min) and fosphenytoin, total and free plasma phenytoin concentrations were measured using high performance liquid chromatography (HPLC). Following i.v administration of fosphenytoin sodium plasma phenytoin concentrations were similar to those obtained following i.v administration of an equivalent dose of phenytoin sodium. Mean peak plasma phenytoin concentrations (C-max) was 158% higher (P = 0.0277) following i.m administration of fosphenytoin sodium compared to i.m administration of phenytoin sodium. The mean area under the plasma total and free phenytoin concentration-time curve from time zero to 120 min (AUC(0.120)) following i.m administration was also significantly higher (P = 0.0277) in fosphenytoin treated rabbits compared to the phenytoin group. However, there was no significant difference in AUC(0-180) between fosphenytoin and phenytoin-treated rabbits following i.v administration. There was also no significant difference in the mean times to achieve peak plasma phenytoin concentrations (T-max) between fosphenytoin and phenytoin-treated rabbits following i.m administration. Mean plasma albumin concentrations were comparable in both groups of animals. Fosphenytoin was rapidly converted to phenytoin both after i.v and i.m administration, with plasma fosphenytoin concentrations declining rapidly to undetectable levels within 10 min following administration via either route. These results confirm the rapid and complete hydrolysis of fosphenytoin to phenytoin in vivo, and the potential of the i.m route for administration of fosphenytoin delivering phenytoin in clinical settings where i.v administration may not be feasible