Vaccinations against diseases to prevent disease outbreaks are strategic to disease prevention, but vaccination failures may constitute a challenge in practice. This study was aimed at assessing the adoption and failure rates of vaccinations in 80 chicken farms in Jos, Nigeria. Data were obtained through a structured questionnaire validated by interviews and checking of farm and veterinary records. Vaccination score (0–1) from the vaccination checklist (5 for broilers and 12 for layers) and vaccination procedure score (0–1), based on scored adopted procedures, were calculated for each farm. Vaccine effectiveness was calculated for each vaccine using the odds ratio from the association of frequencies of disease outbreaks in vaccinated and unvaccinated flocks. Farmers used more of imported than local vaccines. Vaccination procedure and vaccination scores did not influence frequencies of disease outbreaks, but vaccination scores tended to non-robustly correlate (r = − 0.89, p > 0.05) with rates of disease outbreak. Vaccination rates were highest against Newcastle disease and infectious bursal disease, and their vaccinations also had the highest effectiveness. There was an association (p = 0.009) between composite vaccination rates and disease outbreaks with 2.1 odds of outbreaks in vaccinated than unvaccinated flocks. Vaccination failures occurred in the use of 11 out of 12 vaccines and the highest failure rate (47.9%) was in vaccination against coccidiosis. Therefore, vaccination failure is a critical factor in poultry vaccination practice within the locality. The adoption of poultry vaccinations needs to be strategised in the context of a national poultry vaccination policy in order to promote effective poultry disease prevention and control.
Summary This paper describes the investigation of a disease outbreak among 10 adult pigs in Nsukka, Anambra State, Nigeria. Prior
to the investigation one sow died of the disease. Trypanosomes were later detected in the blood of two of the nine pigs subsequently
investigated. All the pigs were then treated with deep intramuscular injection of 8 mg/kg diminazene aceturate (Berenil).
Thirty six days after treatment a boar and a sow relapsed with signs similar to the ones shown previously. Further examination
of their blood and faeces revealed nothing of parasitological significance. Following deteriorating condition and development
of nervous signs the boar was salvaged while the sow died of the infection. Brain impression smears taken from both animals
during postmortem examination revealed numerous trypanosome parasites identified by morphology and blood incubation infectivity
test (BIIT) asTrypanosoma brucei brucei. The clinical and economic significance of the outbreak are discussed.
Resumen Se describe un brote de tripanosomiasis porcina en cerdos en Nsukka, Estado de Anambra, Nigeria. Antes de la investigación,
una cerda murió de la enfermedad. Se detectaron tripanosomas en dos de los nueve cerdos investigados. Todos los cerdos fueron
tratados con inyecciones intramusculares de 8 mg/kg de aceturato de diminazene (Berenil). Treinta y seis días después del
tratamiento, un macho y una henbra desarrollaron una sintomatología similar a la vista previamente.
Exámenes subsecuentes de sangre y heces no revelaron nada de significancia parasitológica. Después del deterioro de las condiciones
físcias y metabólicas y el desarrollo de síntomas nerviosos, el macho se sacrificó mientras que la hembra murió. Las impresiones
de cerebro revelaron numerosos tripanosomas, los cuales fueron identificados por morfología y mediante la prueba de incubación
de infectividad, comoTrypanosoma brucei brucei. Se discute la importancia económica del brote.
Résumé Cet article décrit l'enquête menée sur un foyer pathologique concernant dix porcs adultes à Nsukka, Etat d'Anambra au Nigéria.
Prélablement à l'enquête proprement dite, une truie était morte de trypanosomose. Ultérieurement des trypanosomes furent trouvés
dans le sang de deux des neuf porcs traités par une injection intramusculaire profonde d'acéturate de diminazéne (Bérénil)
à la dose de 8 mg/kg.
Trente six jours après le traitement, un verrat et une truie firent une rechute avec des signes identiques à ceux déjà constatés.
Des examens ultérieurs du sang et des fèces ne revélèrent aucun parasite. A la suite d'une aggravation de leur état général
et de l'apparition de signes nerveux, le verrat guérit mais la truie succomba de l'infection naturelle. Les frottis par décalque
du cerveau prélevés sur les 2 animaux lors d'une autopsie, ont révélé de nombreux trypanosomes. Par leur morphologie et par
le test d'infectivité du sang, après incubation, ceux-ci furent identifiés comme étantTrypanosoma brucei brucei. La signification clinique et économique de ce foyer fait l'objet d'une discussion.
The relevance of trypanosome-induced immunosuppression in relation to the efficacy of vaccine-induced immunity was studied in mice. Mice were immunised with crude Trichinella spiralis muscle larvae homogenate vaccine and infected with T. spiralis and/or Trypanosoma brucei. Vaccination significantly decreased adult worm burden (p<0. 05) and accelerated worm expulsion in mice infected with T. spiralis only. T. brucei superinfection resulted in monocytosis, suppressed eosinophilia, significant decrease in PCV (p<0.001), higher numbers of adult worms (p<0.001) and failure to expel all adult worms by Day 12 post infection (p.i.). Regardless, they produced anti-Trichinella IgG(1) responses similar to those of the vaccinated non-T. brucei-infected group. T. brucei also suppressed the proliferative responses of spleen cells to stimulation with Con A and T. spiralis antigen, and induced strong production of interferon-gamma (IFN-gamma) in culture supernatants of antigen stimulated spleen and mesenteric lymph node cells. Interleukin-5 (IL-5) production was suppressed by T. brucei in supernatants of Con A- and antigen-stimulated spleen cells. It was concluded that trypanosome infections and the associated immunosuppression are of great practical significance in trypanosome endemic areas, especially with regards to disease control programmes involving vaccine-induced herd immunity. 相似文献
The present study investigates the influence of α1‐adrenoreceptors in GnRH release in vitro and determines whether oestradiol modulates α1‐adrenoreceptor‐GnRH interaction. Within 10 min after ewe sacrifice, saggital midline hypothalamic slices were dissected, placed in oxygenated Minimum Essential Media‐α (MEM‐α) at 4°C and within 2 h were singly perifused at 37°C with oxygenated MEM‐α (pH 7.4; flow rate 0.15 ml/min), either with or without oestradiol (24 pg/ml). After 4‐h equilibration, 10‐min fractions were collected for 4 h interposed with a 10‐min exposure at 60 min to specific α1‐adrenoreceptor agonist (methoxamine) or antagonist (thymoxamine) at various doses (0.1–10 mm ). The α1‐adrenoreceptor agonist (10 mm ) increased (p < 0.05) GnRH release at 90 min both in presence and absence of oestradiol. However, in presence of oestradiol, α1‐adrenoreceptor agonist (10 mm )‐induced GnRH release remained elevated (p < 0.05) for at least 60 min. The bioactivity of the released GnRH was studied using a hypothalamus–pituitary sequential double‐chamber perifusion. Only after exposure of hypothalamic slices to α1‐adrenoreceptor agonist (10 mm ), did the hypothalamic eluate stimulate LH release from pituitary fragments (n = 9, 7.8 ± 12.3–36.2 ± 21.6 ng/ml) confirming that the α1‐adrenoreceptor agonist stimulated release of biologically active GnRH. In summary, GnRH release from the hypothalamus is under stimulatory noradrenergic control and this is potentiated in the presence of oestradiol. 相似文献
The present study examines the involvement of GABAA or B receptors in gonadotrophin‐releasing hormone (GnRH) release in vitro and determines whether oestradiol modulates γ‐aminobutyric acid (GABA)–GnRH interaction. Within 10 min after ewe killing, hypothalamic slices were dissected and placed in oxygenated Minimum Essential Media (MEM)‐α at 4°C; within 2 h, slices were singly perifused at 37°C with oxygenated MEM‐α (0.15 ml/min), with or without oestradiol (24 pg/ml). After 4 h equilibration, fractions were collected for 4 h interposed with a 10 min exposure to specific GABAA or B receptor ligands (0.1–10 mm ). The GABAA or B agonists (muscimol or baclofen) did not greatly influence GnRH release. However, GnRH increased (p < 0.05) after exposure to 10 mm GABAA or B antagonists (bicuculline or CGP52432, respectively). The GABAA antagonist stimulated greater sustained GnRH release (p < 0.05) in the absence of oestradiol than in its presence. The bioactivity of the released GnRH was studied using a hypothalamus‐pituitary sequential double‐chamber perifusion. Only after exposure of hypothalamic slices to the GABAA antagonist, did the hypothalamic eluate stimulate luteinizing hormone release from pituitary fragments (p < 0.05) confirming that the GABAA antagonist stimulated release of biologically active GnRH. In summary, GnRH release from the hypothalamus is predominantly under GABAA receptor inhibitory control and this is attenuated in the presence of oestradiol. 相似文献