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Articles by A. Rolon
Total Records ( 2 ) for A. Rolon
  J.S. Bailey , A. Rolon , C.L. Hofacre , P.S. Holt , J. L. Wilson , D .E. Cosby , L. J. Richardson and N. A. Cox
  Resistance to Salmonella challenge of breeders under three vaccination programs and of their chicks with and without mucosal Competitive Exclusion (CE) (CHR Hansen) treatment was assessed. Vaccine treatments combined a live Aro-A Salmonella Typhimurium (ST) vaccine and an autogenous commercially prepared (Lohmann Animal Health) trivalent killed vaccine (serogroups B, C2 and D1). Treatments combined: 2 live and 2 killed doses or 3 live and 1 killed dose delivered at 1, 21, 77 and 126 d of age; or 2 killed doses delivered at 77 and 126 of age; and a non-vaccinated control (C). At 3, 6, 11, 17 and 22 wks of age, a portion of breeder pullets was removed and challenged per os with 107 cells of a 3-strain mixture of antibiotic-resistant salmonellae. Chicks from eggs laid at 29, 34 and 40 wks of age were randomly divided into two groups, one group received a CE treatment by oral gavage. Both groups were given 107 cells of a 2-strain mixture of antibiotic-resistant salmonellae and kept in isolation units for one and two wks. Ceca and Liver-Heart-Spleen (LHS) samples were cultured for each strain on BGS+antibiotic plates and colonies enumerated. Log10 data were analyzed under factorial designs. Breeder Salmonella counts showed significant reductions between (live) vaccinates and non-vaccinates at 3 (0.82 log) and 6 wks (0.85 log) challenges. By 11 wks, there were no differences in Salmonella levels between vaccinates and controls, indicating that 1-d and 3-wk live vaccine protection had diminished with time. All vaccination treatments reduced breeder cecal counts (1.15-1.30 log) by wk 22. Passive immunity from breeder vaccination treatments was not effective in diminishing chick cecal counts as shown by comparable susceptibility of chicks from vaccinated and control breeders, regardless of breeder age. Chick CE treatment consistently diminished cecal (1.41 log) and LHS (0.306 log) counts. These results show that live Aro-A ST vaccination decreases counts during the first 6 wks of age, as do all programs by 22 wks of age and that competitive exclusion is the most effective treatment in reducing hatchling Salmonella counts.
  J. S. Bailey , A. Rolon , C. L. Hofacre , P. S. Holt , J. L. Wilson , D. E. Cosby , L. J. Richardson and N. A. Cox
  Salmonella vaccination programs using killed bacterins in breeders and live auxotrophic-strain vaccines early in the life of their progeny have gained popularity in today`s poultry industry. In this study we evaluated the intestinal humoral immune response to a live auxotrophic vaccine used on hatchlings with and without maternal antibody and related this response to challenge with a blend of two antibiotic-resistant Salmonella marker strains. Forty wk-old ISA Brown® (Institute de Selection Animale, France) breeders from a Salmonella-free flock were vaccinated twice at a three wk interval with commercially-prepared autogenous trivalent bacterin, serogroups B, C and D1 (Lohmann Animal Health International, Gainesville, GA), or a serovar Enteritidis bacterin (Fort Dodge Animal Health Inc, Overland Park, KS). Half of the progeny from these treatments (hatched from eggs laid 3 wks after second bacterin dose) were given a live Salmonella serovar Typhimurium (LiveST) mutant vaccine (Fort Dodge Animal Health Inc, Overland Park, KS), by coarse spray on arrival in the brooding premises. On days 3, 13 and 34, intestinal immunoglobulins (Ig) A and G were sampled and measured on enzyme-linked immunosorbent assay plates coated with Salmonella serovars Enteritidis (SELPS) or Typhimurium (STLPS) Lipopolysaccharide. On the same days, a second group of birds was challenged with a blend of antibiotic-resistant serovars Enteritidis and Typhimurium strains. Cecal and composite liver-heart-spleen samples obtained 7 days post-challenge were cultured and colonies enumerated. Maternal IgG observed up to 13 days had no effect on subsequent LiveST-stimulated antibody production. No protective effect of maternal antibody was demonstrated, except when combined with LiveST given to the progeny. Killed vaccines delivered to the breeders combined with a live vaccine delivered to the progeny resulted in reduced invasiveness after challenge, as shown by a reduction in liver-heart-spleen Salmonella counts. One dose of LiveST enhanced intestinal IgG [Optical Densities (OD) >0.576] up to 34 days when measured on STLPS, but only to 13 days when measured on SELPS, with titers decreasing with age. Increased IgA was observed only at 13 days. Three and 13 but not 34 days bacterial counts were decreased by the live ST vaccine treatment, for both cecal (1.05 and 1.09 log10) and liver-heart-spleen (0.32 and 0.06 log10) samples, indicating that a second dose might be necessary for prolonged protection. The protective effect of the live vaccine, but not of maternal IgG, leads us to hypothesize that protection might be due to stimulation of cell-mediated intestinal immunity and/or a competitive exclusion effect of the LiveST vaccine. Reduction but not elimination of Salmonella colonization by vaccination highlights the importance of vaccines as complementary tools and not substitutes of integral biosecurity programs to control Salmonella in poultry.
 
 
 
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