Triple La Sota re-vaccinations can protect laying chickens for 3 months against drop in egg production caused by velogenic viscerotropic Newcastle disease virus infection.

One hundred and ten Isa Brown layers were vaccinated with La Sota, once at point of lay at 18 weeks and three times at peak of lay which occurred at 27-29 weeks of age. Thereafter, they were weekly monitored for haemagglutination inhibition (HI) antibody decline. The first batch A of the layers were challenged with velogenic viscerotropic Newcastle disease (vvND) virus (vvNDV) on day 24 post-vaccination (PV), when the geometric mean titre (GMT) was 84.4, batch B were challenged on day 48 PV at GMT of 42.2, while batch C were challenged on day 97 PV at GMT of 21.1. The individual chicken HI antibody titres of the 10 layers in batch C at the day of challenge were: 7 layers had HI titres of 16, 2 layers had HI titres of 32 and 1 layer had HI titres of 64. Each challenge in the three batches produced no clinical signs including drop in egg production. But there was initial swelling of the spleen followed by atrophy with high antibody responses. The virus was recovered in all the cloacal swabs on days 3-9 post-challenge (PC) at low titres. On days 145 PV and 48, post-Batch C challenge the remaining hyperimmunized unchallenged layers demonstrated a drop in total % egg production (p < .05) and changes in egg quality. The HI GMT was 256. The virus was recovered in all the cloacal swabs on days 3-9 following appearance of clinical signs. There was no mortality in the experiment. Based on the above observations, it is concluded that triple La Sota re-vaccination can protect layers against a drop in egg production in areas where vvNDV infection is enzootic.

Pullets had higher bursal and thymic weight indices and more antibody response to La Sota vaccination than broiler chickens (Gallus gallus domesticus).

This study investigated the immune responses to La Sota vaccination, used in protection of chickens against Newcastle disease, in light weight type breeds of chickens (pullets) and heavy weight type breeds of chickens (broilers) used in commercial poultry production. Seven-week-old 50 White Marshall broilers (Br) and 50 Isa Brown pullets (Pu) were randomly divided into four groups: vaccinated broilers chickens; (VBr), unvaccinated broiler chickens (UBr), and vaccinated pullet chickens (VPu) and unvaccinated pullet chickens (UPu). Chickens in groups VBr and VPu were vaccinated with La Sota vaccine, whereas groups UBr and UPu were not vaccinated. On day 0 post vaccination (PV), six chickens from group Br and Pu, and on day 4 PV, three chickens from each four groups were sacrificed and the bursa weight index (BWI), thymus weight index (TWI) and the splenic weight index (SWI) were obtained. The chickens were observed for clinical signs and lesions. Serum samples were collected from the chickens in all the groups on days 0, 7, 14, 21, 28 PV and assayed for haemagglutination inhibition (HI) antibodies. The BWI, TWI and SWI were 0.37 ± 0.05, 0.35 ± 0.17, 0.65 ± 0.26 for pullets and 0.11 ± 0.04, 0.13 ± 0.02, 0.36 ± 0.17 for broilers on day 0 PV. On day 4 PV there was no significant difference (p < .05) between the indices of the vaccinated and unvaccinated chickens. The geometrical mean antibody titres (GMT) of the pullets were 2 to 3 times higher than those of the broilers on days 7 to 28 PV. Vaccination did not produce clinical signs or lesions. The above observations show that naturally pullets produce higher antibodies than broilers because of their higher BWI.

Evidence for subclinical H5N1 avian influenza infections among Nigerian poultry workers.

In recent years Nigeria has experienced sporadic incursions of highly pathogenic H5N1 avian influenza among poultry. In 2008, 316 poultry-exposed agricultural workers, and 54 age-group matched non-poultry exposed adults living in the Enugu or Ebonyi States of Nigeria were enrolled and then contacted monthly for 24 months to identify acute influenza-like-illnesses. Annual follow-up sera and questionnaire data were collected at 12 and 24 months. Participants reporting influenza-like illness completed additional questionnaires, and provided nasal and pharyngeal swabs and acute and convalescent sera. Swab and sera specimens were studied for evidence of influenza A virus infection. Sera were examined for elevated antibodies against 12 avian influenza viruses by microneutralization and 3 human viruses by hemagglutination inhibition. Four (3.2%) of the 124 acute influenza-like-illness investigations yielded molecular evidence of influenza, but virus could not be cultured. Serial serum samples from five poultry-exposed subjects had a ≥4-fold change in microneutralization titers against A/CK/Nigeria/07/1132123(H5N1), with three of those having titers ≥1:80 (maximum 1:1,280). Three of the five subjects (60%) reported a preceding influenza-like illness. Hemagglutination inhibition titers were ≥4-fold increases against one of the human viruses in 260 participants. While cross-reactivity from antibodies against other influenza viruses cannot be ruled out as a partial confounder, over the course of the 2-year follow-up, at least 3 of 316 (0.9%) poultry-exposed subjects had evidence for subclinical HPAI H5N1 infections. If these data represent true infections, it seems imperative to increase monitoring for avian influenza among Nigeria's poultry and poultry workers.

Antimicrobial resistance, integrons and plasmid replicon typing in multiresistant clinical Escherichia coli strains from Enugu State, Nigeria.

Eleven multiresistant Escherichia coli strains of animal and human origin were assayed for the presence of antimicrobial resistance genes, integrons and associated gene cassettes, as well as plasmid content. Ciprofloxacin-resistant strains were screened for amino acid changes in GyrA and ParC proteins. The E. coli strains were found to harbor a variety of genes including cmlA, aac (3)-II, aac (3)-IV, aadA, strA-strB, tet (A), tet (B), bla(TEM), sul1, sul2 and sul3. Four of the eight int I1-positive strains were also positive for qacE Δ1 -sul1 region and the following gene cassettes were detected: dfrA7, dfrA12 + orfF + aadA2 and bla(OXA1)+ aadA1. Five strains contained class 1 integrons lacking the qacE Δ1 -sul1 region and they showed a single type of gene cassette arrangement (estX + psp + aadA2 + cmlA + aadA1 + qacH + IS440 + sul3). The two int I2-positive strains carried the same type of gene cassette arrangement (dfrA1 + sat + aadA1). The seven ciprofloxacin-resistant E. coli strains exhibited a Ser-83-Leu substitution in GyrA protein and a Ser-80-Ile substitution in ParC protein; six of these strains presented an additional substitution in GyrA (Asp-87-Gly or Asp-87-Asn) and one strain in ParC (Glu-84-Gly). Eight different plasmid-replicon-types were detected among the 11 E. coli strains, IncF being the most frequent one detected, found in nine strains; other plasmid replicon types detected were IncX, IncI1, IncY, IncW, IncFIC, IncB/O, and IncK. Antimicrobial resistance in the E. coli strains studied was mediated by a variety of genes, some of them included in integrons, as well as by mutations gyr A and par C genes.