Further characterization of the agent causing coryza in turkeys

A total of 128 isolates of Alcaligenes faecalis, from the respiratory tract of turkeys and chickens, were identified and divided into two types designated type I and type II. Type I isolates were pathogenic in poults, hemagglutinated guinea pig red blood cells (RBCs), and did not grow on minimal essential medium (MEM) agar, and most did not grow in 6.5% NaCl broth. Type II isolates were nonpathogenic and nonhemagglutinating and grew on MEM agar, and most grew in 6.5% NaCl broth. Hemagglutination of guinea pig RBCs was a reliable characteristic for distinguishing type I from type II isolates, and it correlated with pathogenicity. In serological studies using 62 type I and 21 type II isolates, cross-reactions were observed when type I but not type II antigens were used to test antisera in the microagglutination test. Eleven bacterial isolates, different from type I and type II isolates, were urease-positive. Although frequently isolated from turkeys with coryza, these isolates were nonpathogenic and were always found in association with type I A. faecalis. Urease-positive isolates and type I and type II A. faecalis isolates were stable following 50 in vitro passages. Bordetella avium sp. nov. (the nomenclature suggested in Europe for A. faecalis) was pathogenic in poults. The colonial morphology, biochemical characteristics, and hemagglutinating activity of B. avium sp. nov. were the same as those of type I A. faecalis isolates. Based on the results of these studies, it was concluded that type I A. faecalis is the etiologic agent of turkey coryza.     

Preliminary Studies on Stocking Density and Production of Hamoor Epinephelus tauvina in PVC-Lined Raceways

The results of two stocking density trials on the nursery and grow-out stages of Epinephelus tauvina (Family: Serranidae), in PVC-lined raceways are presented.
At the nursery stage, fry of 17.1 g initial mean weight showed no significant differences in growth rate, survival rate and condition factor when stocked at densities of 200 and 400 fish/m³ over a period of 52 days. Fish grew to mean weights of 61.7 and 63.7 g, giving growth rates of 0.86 and 0.90 g/fish/day and final biomasses of 12.1 and 2S.2 kg/m³ for densities of 200 and 400 fish/m³, respectively. Survival rates were excellent for both treatments at 98percnt; or greater. Food conversion efficiency was slightly improved at the higher density.
At the grow-out stage, E. tauvina of mean weights ranging from 150-170 g cultured for a period of 215 days grew better at a density of 5 fish/m³ than at densities of 20 and 60 fish/m³ (final size: 770, 560 and 450 g with growth rates of 2.8, 1.8 and 1.4 g/fish/day, respectively). Survival rates were higher at the two lower densities. Overall, total biomass increased with stocking density (3.9, 11.1 and 23.4 kg/m³, for 5, 20 and 60 fish/m³, respectively). These results indicate that hamoor has potential to be successfully cultured in raceways.     

Structural proteins of classic and variant strains of infectious bursal disease viruses.

Structural polypeptides of six tissue-culture-origin (BGM-70 continuous cell line) infectious bursal disease viruses representing classic and variant strains of serotype 1 and one serotype 2 strain were analyzed and compared by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Additionally, two of the variant strains were propagated in vivo in bursa of Fabricius and compared with those grown in cell culture. Differences among the structural proteins of serotype 1 viruses were minor and probably of no value in differentiating these viruses. However, distinct differences were observed between serotype 1 and 2 viruses. The bursa-derived viruses were different from those propagated in cell culture in molecular weights and in proportions of the proteins. The bursa-derived strains had protein migration patterns similar to those described for tissue-culture-incomplete virus particles.     

Induction of functional defects in macrophages by a poult enteritis and mortality syndrome-associated turkey astrovirus.

The interaction of a poult enteritis and mortality syndrome (PEMS)-turkey astrovirus-Ohio State University (TAst-OSU) with the mononuclear phagocytic system cells, namely macrophages, was examined after in vitro and in vivo exposure. In vitro exposures were performed by incubating adherent turkey macrophages with various volumes of 10(6) 50% embryo infective dose (EID50)/ml TAst-OSU stock, whereas for in vivo challenge, poults were given a 200 microl inoculum of 10(6) EID50/ml TAst-OSU stock at 7 days of age. Results show that TAst-OSU in vitro exposure reduced macrophage viability relative to controls (P < 0.05) and decreased phagocytosis (P < 0.05) and intracytoplasmic killing of Escherichia coli (P < 0.05) after a 42-48-hr exposure. Poults challenged with TAst-OSU in vivo recruited almost 50% fewer Sephadex-elicited inflammatory cells in the abdominal cavity (P < 0.05) as compared with the sham controls. Similar to in vitro exposure, macrophages isolated from in vivo TAst-OSU-challenged poults exhibited reduced percentage of phagocytic macrophages (P < 0.05) as well as fewer intracytoplasmic E. coli per phagocytic macrophage (P < 0.05). TAst-OSU-challenged poults had a greater number of viable E. coli in their spleens (P < 0.05) after an intravenous E. coli challenge as compared with the non-TAst-OSU-challenged control poults. Macrophage-mediated cytokines and metabolites were also examined during this study. Both in vitro and in vivo TAst-OSU challenge resulted in reduced interleukin (IL)-1 and IL-6 activity. On the contrary, nitrite levels in macrophage culture supernatant fraction of TAst-OSU-challenged macrophages were significantly higher (P < or = 0.05). The findings of these studies indicated that TAst-OSU challenge induced defects in macrophage effector functions, implying that PEMS-turkey astrovirus can potentially impair the immune response of turkeys, thereby leading to enhanced susceptibility of turkeys to secondary, perhaps even fatal, bacterial infections.     

Immunogenicity and antigenicity of infectious bursal disease virus serotypes I and II in chickens

Chickens were inoculated with infectious bursal disease virus serotype I or serotype II to determine if their immune system can distinguish between the two serotypes. Chickens had neutralizing antibodies to only serotype I viruses following exposure to serotype I viruses, and chickens had antibodies to only serotype II viruses following exposure to serotype II viruses. No cross-reactions were observed between antisera prepared to each of these two serotypes using a cross-virus-neutralization assay. Signs of disease were detected only in birds exposed to a virulent serotype I isolate. Chicks exposed to the serotype II viruses were not protected from challenge with a virulent serotype I isolate. In one experiment, antibodies to a serotype II isolate, which were detected before challenge, did not protect chicks from challenge with a virulent serotype I isolate.     

Immunosuppression induced by infectious bursal disease virus.

Immunosuppression caused by infectious bursal disease virus (IBDV) is of major interest because of the widespread occurrence of the infection in commercial chickens. Infection with IBDV at an early age significantly compromises the humoral and local immune responses of chickens. The cellular immune response is also compromised by apparently to a lesser extent and for a short period. The immunosuppression seems to be a result of direct effect (lysis) of B cells or their precursors. Other mechanisms of immunosuppression have been suggested, notably the development of suppressor cells.     

Seroprevalence in Household Raised Pigs Indicate High Exposure to GII Noroviruses in Rural Nicaragua

Information about porcine norovirus (PoNoV), genetically similar to human NoV (HuNoV), is limited from rural areas where household‐raised pigs are heavily exposed to faecal material which could facilitate transmission. Histo‐blood group antigens (HBGAs) are known susceptibility factors to NoV in humans and in a germfree piglet model but their role in susceptibility in the porcine population remains unknown. This study reports: (i) the seroprevalence and antibody titres to human norovirus (NoV) VLPs in household raised pigs; (ii) the distribution of HBGAs in relation to NoV IgG antibody titres and further characterization by blocking of GII.4 VLP binding to pig gastric mucins (PGM). The majority of pigs were seropositive to all three VLPs tested (58–70%) with seropositivity and cross‐reactivity increasing significantly with age. However, pig sera could not block the binding of NoV GII.4 VLPs (Dijon) to PGM suggesting no previous infection with this genotype. The majority of the pigs were H‐positive (84%), a susceptibility factor for human infections. IgG antibody titres were however higher in H‐negative (GMT = 247) as compared with H‐positive (GMT = 57) pigs, but after age stratification, this difference in antibody titres was only observed in pigs ≤1 month of age. In conclusion, serological data show that the porcine population of Nicaragua is highly exposed to NoV infections, and the association to HBGAs warrants further investigation.