Search

Occurrence of mortality, wooden breast, and pulmonary disease in broiler chickens during the last 16 days of production in a teaching flock of 4000 commercial broilers was determined. A new syndrome was identified, in which broilers fell over for an unknown reason and were unable to right themselves (dorsal recumbency). Birds affected by dorsal recumbency were alert and responsive and showed no clinical signs except for occasional mild to moderate dyspnea. When turned over, they resumed normal behavior. Mortality (14 culls; 49 dead) during the last 16 days of production accounted for 1.6% of the flock and 36% of total mortality. Among these, 71% were heavy males, 70% had wooden breast, and 71% had pulmonary congestion and edema. Gross lesions of concurrent wooden breast and pulmonary disease occurred in 68% of the mortality, including 21 of 22 dead birds found on their backs. These findings indicate that wooden breast is associated with mortality prior to processing as a result of pulmonary disease in heavy male broilers. When birds with wooden breast fall onto their backs for unknown reason(s), they are unable to right themselves. If not found and turned over, they may not survive. Based on these findings, wooden breast is likely greater than just a problem with meat quality and should be considered an animal well-being issue.Reporte de caso- Presencia de “pechuga de madera” en pollos de engorde comerciales asociada con mortalidad, recumbencia dorsal y enfermedad pulmonar. Se determinó la presentación de mortalidad, “pechuga de madera” y enfermedad pulmonar en pollos de engorde durante los últimos 16 días de producción en una parvada de 4000 pollos de engorde comerciales. Se identificó un nuevo síndrome en el que los pollos se postraban por una razón desconocida y no podían enderezarse (recumbencia dorsal). Las aves afectadas por la recumbencia dorsal estaban alertas y respondían, y no mostraban signos clínicos, excepto casos de disnea ocasional de leve a moderada. Cuando las aves se colocaban en posición normal, retomaban su comportamiento normal. La mortalidad (14 aves eliminadas; 49 muertas) durante los últimos 16 días de producción representó el 1.6% de la parvada y 36% de la mortalidad total. Entre estos, el 71% eran machos pesados, 70% tenían “pechuga de madera” y 71% tenían congestión pulmonar y edema. Lesiones macroscópicas concurrentes de enfermedad pulmonar y de “pechuga de madera” ocurrieron en el 68% de la mortalidad, incluyendo 21 de las 22 aves muertas que fueron encontradas postradas sobre sus dorsos. Estos hallazgos indican que la “pechuga de madera” se asocia con la mortalidad antes del procesamiento como resultado de enfermedad pulmonar en pollos de engorde machos pesados. Cuando las aves con “pechuga de madera” se caen de espaldas por razones desconocidas, no pueden enderezarse. Si no se encuentran y se colocan en posición normal, pueden no sobrevivir. Según estos hallazgos, la “pechuga de madera” es probablemente más que solo un problema con la calidad de la carne y también debe considerarse un problema de bienestar animal.

Enterococcus cecorum was initially identified as a harmless commensal of the gastrointestinal tract of chickens. However, over the past 15 yr, pathogenic strains of E. cecorum have become a significant cause of morbidity and mortality in broiler breeders, and repeated outbreaks occur, but an environmental reservoir for pathogenic E. cecorum has yet to be identified. Genetic analyses of E. cecorum demonstrate that strains with increased pathogenicity are genetically related and share several putative virulence genes. Pathogenic E. cecorum carry increased antimicrobial resistance compared to commensal strains. These pathogenic strains can be recovered from retail meat and may serve as a reservoir for further spread of antimicrobial resistance among other Enterococcus spp. This review presents the current understanding of the pathogenesis of E. cecorum and briefly discusses antimicrobial resistance in E. cecorum due to the role of Enterococcus spp. in nosocomial infections in people.

Phosphorylated histone 3 (PH3) and cleaved caspase 3 (CCASP3) were used to detect proliferating and apoptotic cells, respectively, in the jejunums of female sibling poults, with and without enteritis and depressed growth, from hatch to day 35. Poults that developed enteritis and depressed growth (SIB flock) were raised on a commercial farm in eastern North Carolina, whereas poults with normal growth and no enteritis (TAU flock) were raised in the Teaching Animal Unit at North Carolina State University College of Veterinary Medicine. Beginning on day 5 through day 35 and at processing, TAU poults were significantly heavier than SIB poults. Jejunal weights, relative jejunal weights, and jejunal densities were greater in SIB poults from day 10 through 35. Jejunal efficiency (body weight /jejunal length) was higher in TAU poults at day 5 and days 10 through 35. Mucosal thickness was greater in SIB poults between days 7 and 21 but greater in TAU poults at days 28 and 35. From day 7 to 35, villus-to-crypt ratios were higher for TAU poults and lower for SIB poults because hyperplastic crypts formed a greater percentage of the mucosa in SIB poults. By day 7, PH3- and CCASP3-positive cells were increased in SIB poults, showing that mucosal changes resulted from combined crypt epithelial hyperplasia and increased apoptosis of villous enterocytes. Findings in this study confirm that enteritis, in the absence of clinical signs, and depressed growth in turkey poults begins by day 7, can be identified microscopically, persists for at least 35 days, is associated with lower processing weights, and has a profound negative effect on turkey growth.

Pathogenic strains of Enterococcus cecorum cause outbreaks of arthritis and osteomyelitis in chickens worldwide. Enterococcal spondylitis (ES) is a specific manifestation of E. cecorum-associated disease of broilers and broiler breeders characterized by increased flock mortality, resulting from unresolved infection of the free thoracic vertebra by pathogenic E. cecorum. A study of 22 ES outbreaks in the southeast United States revealed that pathogenic E. cecorum strains isolated from spinal lesions were genetically clonal. Here, we compare the virulence of previously genotyped pathogenic strains (n = 8) isolated from spinal lesions and nonpathogenic strains (n = 9) isolated from ceca of unaffected birds in a chicken embryo lethality model. Strains were inoculated into the allantoic cavity of 12-day-old broiler and specific-pathogen-free (SPF) layer embryos; embryo survival was determined by candling eggs daily for 4 days. Significantly decreased survival occurred in both broiler and SPF embryos inoculated with pathogenic genotype strains compared with embryos inoculated with nonpathogenic genotype strains (broiler embryos, 23% vs. 60%; SPF embryos, 9% vs. 61%). Embryos infected with pathogenic strains were unable to control infection and consistently showed gross changes typical of sepsis, including hemorrhage and edema. After 48 hr, similar changes were not observed in embryos infected with nonpathogenic strains. This embryo lethality assay provides a useful tool for understanding the genetic basis of E. cecorum virulence.

Enterococcus cecorum was isolated from spondylitis lesions in broilers from two flocks in North Carolina that were experiencing increased mortality. Affected birds showed paresis and paralysis, clinical signs characteristic of enterococcal spondylitis (ES). Affected birds rested on their hocks and caudal abdomens with legs extended forward and were unable to stand or walk. Necropsy examination of affected birds revealed firm to hard inflammatory masses involving the vertebral bodies at the level of the free thoracic vertebra that bulged dorsally and compressed the spinal cord. When opened, lesions contained pale, tan to yellow caseonecrotic material. Microscopically, necrosis and fibrinoheterophilic spondylitis with intralesional gram-positive bacteria were seen. Heavy growth of E. cecorum recovered from vertebral lesions confirmed the diagnosis of ES. To investigate possible sources of the organism for one of the flocks bacterial cultures were made from the environment, water lines, mice trapped on the farm, cecal/cloacal swabs from one of the parent broiler breeder flocks, egg residue, hatching eggs, and the hatchery environment. Except for cecal/cloacal swabs from the breeders, E. cecorum was not isolated from any of these samples. When compared phenotypically and genotypically, cecal/cloacal isolates of E. cecorum from the breeders differed from isolates from spondylitis lesions in the broilers. The source of E. cecorum for the broiler flocks was not determined, but vertical transmission appears unlikely.