Haematological changes associated with Newcastle disease vaccination in chickens using gums from Cedrela odorata and Khaya senegalensis as delivery agents.

Our previous ex-vivo and in vivo investigations have established immunopotentiating property of Khaya senegalensis and Cedrela odorata gums; however the safety of the use of this gum combination in chicken has not been described. Hence this study evaluates the haematological profile of chickens vaccinated with Newcastle disease vaccine delivered through the oral and ocular routes using gums from Cedrela odorata and Khaya senegalensis as delivery agents. 252 one-day old chickens were grouped gum-vaccine oral (GVOR), vaccine oral (VOR), gum-vaccine ocular (GVOC), vaccine ocular (VOC), gum oral (GOR), gum ocular (GOC), no-gum-no-vaccine but challenged (NGNV/C), no-gum-no-vaccine unchallenged (NGNV/U). They were vaccinated on days 21 and 42 and challenged day 84. Blood samples were collected before first vaccination and at selected intervals afterwards. Analysis was done using one way ANOVA with P<0.05 considered significant. Packed cell volume, total white cell count, heterocyte-lymphocyte ratios and platelet count varied insignificantly (P>0.05) throughout the period of observation across groups with no observable derangements. Hence, the absence of derangement in haematological indices from this study suggests that the dilution rate recommended from the ex-vivo study is safe for administration of Newcastle disease vaccine in chickens irrespective of the routes of delivery.

Peripheral axonopathy in sciatic nerve of adult Wistar rats following exposure to vanadium.

Depletion of myelin and neurobehavioural deficits are indications that vanadium crosses the blood-brain barrier and such neurotoxic effects of vanadium on the brain of Wistar rats have been elucidated. The effect however on the peripheral nerves, is yet to be reported. Thus, this work was designed to evaluate the axonal and myelin integrity of sciatic nerves in Wistar rats following exposure to vanadium. Ten male Wistar rats were exposed to 3 mg/kg body weight of sodium metavanadate for 7 days, subjected to rearing and forelimb grip behavioural tests, and sciatic nerves processed for histology (haematoxylin and eosin, cresyl violet, and luxol fast blue). Dystrophic axons with vesiculated myelin, thinned myelin sheath, and demyelinated axons were observed in the vanadium exposed rats, suggestive of axonopathy, classified as fourth-degree nerve injury. Lower behavioural scores were recorded for vanadium-dosed rats; thus, corroborating histological pictures observed of the sciatic nerves. Authors posit that vanadium crossed the "blood-nerve" barrier and caused the observed axonal pathologies and myelin depletion in the sciatic nerves of these rodents with resultant motor deficits. The present paper discusses possible motor deficits and the likely public health importance in regions with crude oil pollution and gas flaring rich in vanadium products.