Seroprevalence, hematological and biochemical alterations in Brucella-seropositive Muturu cattle in Nigeria.

This study evaluated the prevalence, hematological and some biochemical alterations in Brucella seropositive Muturu breed of cattle which may change the narratives of multi-disease tolerance of the breed. Sera from 33 Muturu cattle herds chosen by snow ball sampling were screened for Brucella antibodies with modified Rose Bengal test (RBT) supported with the cELISA. Eighteen (18) seropositive samples matched to18 sero-negatives, with regard to age and sex of the animals and chosen by simple random sampling, were analyzed for hematological and biochemical changes, following standard procedures. Individual seroprevalence of 38% and 10% were recorded with the RBT and cELISA respectively, while herd seroprevalence of 52% was recorded with the RBT and none with the cELISA. Seropositivity to brucellosis was significantly associated with farm origin (OR = 16.67; 95%CI = 1.56-153.85; p = 0.019). There was significantly lower packed cell volume (PCV) (p = 0.048) and absolute eosinophil count (p = 0.006), and significantly higher absolute lymphocyte count (p = 0.014) in the seropositive than the negative Muturu cattle. In addition, plasma fibrinogen (p < 0.001), serum albumin (p = 0.037), urea (p = 0.001) and cholesterol (p = 0.032) were significantly lower while serum globulin (p = 0.004), alanine aminotransferase (ALT) activity (p = 0.012) and bilirubin (p = 0.012) were significantly higher in the seropositive than sero-negative Muturu cattle. No significant variations were observed in the rest of the parameters assayed. These findings suggest that Muturu cattle are apparently susceptible to brucellosis and experience active organism-host interactions with resultant clinicopathological effects and therefore could be passive harbingers of Brucella for other animals as well as humans.

Effects of dietary supplementation of Vitamins E and C on oxidative stress induced by a Nigerian velogenic strain of the Newcastle disease virus (KUDU 113) in the brain and bursa of Fabricius of broiler chickens.

BACKGROUND AND AIM: Newcastle disease (ND) is widely recognized as an extremely harmful and contagious disease of birds. Therefore, the present study aims to evaluate the effect of oxidative stress induced by the virulent ND virus (NDV) (KUDU 113) on the plasma, brain, bursa of Fabricius, NDV antibody response, and hematology as well as the ameliorative effect of the individual or combined use of Vitamins E and C on the clinical signs of NDV-infected chickens. MATERIALS AND METHODS: In this study, a total of 150 broiler chickens were included and divided into five groups: Group 1, nonsupplemented and unchallenged chickens (UCC); Group 2, nonsupplemented and challenged chickens (ICC); Group 3, Vitamin C-supplemented + challenged chickens; Group 4, Vitamin E-supplemented + challenged chickens; and Group 5, Vitamins E and C-supplemented + challenged chickens. Groups 3, 4, and 5 were supplemented with Vitamins E and C (33 and 400 mg/kg/day, respectively). Virus challenge was done with 0.1 ml of KUDU 113 7 days after the start of vitamin inclusion in their diet. Concentrations of glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and catalase (CAT) were analyzed in the plasma, brain, and bursa on days 0, 3, and 7 post-infection (pi) using the biochemical method. The blood samples were randomly collected from five chickens in each group for antibody response and hematological analyses on day 0 previtamin treatment and at 0, 3, 7, 10, 14, and 21 days pi (dpi). RESULTS: A significant increase in the concentrations of MDA and NO in the NDV-challenged chickens was observed when compared with the UCCs. Moreover, a significant decrease in GSH concentration was observed in the NDV-challenged chickens when compared with the UCCs. The activities of CAT and SOD were reduced markedly in the NDV-challenged chickens. Increases in the mean antibody titers were observed in the NDV-challenged group when compared with the UCCs from days 3 to 21 pi. The mortality rates of groups 1, 2, 3, 4, and 5 were 0%, 30%, 3.3%, 3.3%, and 26.6%, respectively. CONCLUSION: The findings of this study suggest that KUDU 113 causes oxidative stress in the brain and bursa of Fabricius of chickens. Individual supplementation with Vitamin E or C was found to be more effective in ameliorating oxidative stress, improving the immune response, and reducing mortality in KUDU 113 infections than the combined supplementation of Vitamins C and E.

La Sota vaccination may not protect against virus shedding and the lesions of velogenic Newcastle disease in commercial turkeys.

The aim of this project is to study the clinical signs and lesion of velogenic Newcastle disease (vND) in commercial turkeys, and also to find out if La Sota vaccination offered protection against these signs and lesions. The cockerels were included as positive controls. One hundred and twenty turkey poults and cockerels were divided into eight groups as follows: unvaccinated unchallenged turkeys (UUT), unvaccinated challenged turkeys (UCT), vaccinated unchallenged turkeys (VUT), vaccinated challenged turkeys (VCT), and along the same lines, the cockerel groups were UUC, UCC, VUC and vaccinated challenged cockerels (VCC). Vaccination was at 3 weeks of age while challenge was at 6 weeks of age. The unvaccinated turkeys and cockerels (UCT and UCC) showed different degrees of depression, diarrhoea and later paralysis at challenge. Total mortality was 100% in cockerels within 6 days, but 60% in turkeys. Similar but milder clinical signs were found in the VCC with a total mortality of 13.3%. The VCT showed mild drop in feed and water consumption, and no mortality. All the challenged groups had significant (p < 0.05) loss of weight when compared with their controls. Necropsy showed that while the UCC had severe proventricular haemorrhages, intestinal and caecal tonsil ulcers, the UCT had no digestive tract lesion. There was severe atrophy of the lymphoid organs in all the challenged groups. Histopathological sections of the bursa, spleen and thymus in all the challenged groups with special emphasis on the vaccinated and unvaccinated turkeys with mortalities of 0 and 60%, respectively, had very severe necrosis and depletion of the lymphoid tissue. Virus was isolated from the cloacal swabs. The haemagglutination inhibition antibodies were significantly higher (p < 0.05) in the challenged groups than the unchallenged. The above observations in the intestinal tracts of UCT are of diagnostic significance while the gross and microscopic lesions in the UCT and VCT show that La Sota vaccination may not protect turkeys against the destruction of the lymphoid organs by vND as earlier reported in chickens. This may lead to immunosuppression and production problems in areas where vND is enzootic.

Atrophy of the lymphoid organs and suppression of antibody response caused by velogenic Newcastle disease virus infection in chickens.

This project was undertaken to study the immunosuppressive capabilities of velogenic viscerotropic pathotype of Newcastle disease virus (VVNDV) infection in cockerels. Two hundred six-week-old cockerels were divided into four groups. Groups B/VUC and C/VC were vaccinated with LaSota in drinking water at 6 weeks of age. Groups C/VC and D/UC were challenged with VVNDV at 8 weeks of age. Three days post challenge (PC), the cockerels in group D/UC came down with clinical signs which included depression and greenish diarrhoea. Total mortality was 74.6 %. The C/VC cockerels showed no clinical signs. But both challenged groups showed significant weight loss, significant loss of total serum proteins, globulin and albumen (P < 0.05). These losses were more severe in the D/UC than in the C/VC. There was severe atrophy of the bursa, spleen and thymus in both groups. Histopathology showed severe necrosis and depletion of the lymphocytes in the three lymphoid organs. However, the lesions were more severe in the D/UC than in C/VC cockerels. On day 28, PC groups B/VUC, C/VIC and D/UIC were revaccinated with LaSota. The haemagglutination inhibition antibody response on days 35, 42 and 49 PC was very low in groups C/VIC and D/UIC when compared with B/VUC cockerels. These observations show that VVNDV infection both clinical and subclinical can cause immunosuppression and vaccine failure due to severe destruction of the lymphocytes in the lymphoid organs. This will be a serious problem for poultry production in those countries where the disease is enzootic.

Vitamin A dietary supplementation reduces the mortality of velogenic Newcastle disease significantly in cockerels.

This project was undertaken to find ways of reducing mortalities and economic losses due to velogenic Newcastle disease (VND) in areas where the disease is enzootic. Four groups of cockerels of 44 birds each were used for this experiment. The birds in groups 1 and 2 received no dietary vitamin A supplementation, whereas groups 3 and 4 received 300 iu and 600 iu of vitamin A per kilogram of commercial feed, respectively, from 1 week of age till the end of the experiment. At 6 weeks of age, the birds in groups 2, 3 and 4 were inoculated intraocularly with a VND virus (duck/Nigeria/Plateau/Kuru/113/1991). The birds in Group 1 were given phosphate-buffered saline intraocularly. Clinical signs appeared in Group 2 birds on day 3 PI and in groups 3 and 4 on day 5 PI. The clinical signs included a drop in feed and water consumption, depression, diarrhoea, torticollis and paralysis in all the infected groups. The average body weights of all groups were significantly different from one another on day 14 PI with Group 2 birds having the lowest body weight. Mortalities were highest in Group 2 birds (0%, 93.18%, 72.73% and 56.82% in groups 1, 2, 3 and 4 respectively). The antibody response in all the groups was significantly different from one another on days 14 and 21 PI. Group 2 birds had the lowest titres on those 2 days and showed more severe atrophy of the bursa, spleen, thymus and fibrin deposition in the spleen and thymus than the birds in groups 3 and 4. The above observations show that vitamin A dietary supplementation delayed the onset of clinical signs and significantly reduced body weight loss, atrophy of the bursa, spleen and thymus, and mortalities by 36%. It also significantly potentiated haemagglutination inhibition antibody response.