Search

Copyright of Avian Diseases is the property of American Association of Avian Pathologists, Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Wooden breast myopathy (WBM), or "woody breast" or "wooden breast" affects modern, rapidly growing, high breast-yield broiler chickens. Decreased meat quality due to undesirable organoleptic properties and condemnation of affected breast meat cause economic losses. The pathogenesis of WBM remains unknown. In this study, WBM lesion development was determined in three modern broiler strains and Athens Canadian Random Bred (ACRB) broilers, a 1950s unselected broiler chicken. Correlations between WBM severity and incubation temperature profile, sex, strain, body weight, and lymphocytic phlebitis were also determined. At 2, 4, 6, and 8 weeks of age, samples of breast muscle from 10 male and 10 female birds from each strain, incubated under optimal or low-early, high-late temperatures, were scored histologically for severity of WBM and lymphocytic phlebitis. WBM lesions, identified as early as 2 weeks, became progressively more severe with age and growth in the three commercial broiler strains. WBM severity was significantly correlated with lymphocytic phlebitis and body weight. Lymphocytic phlebitis and minimal WBM were present in the ACRB broilers at all samplings, but did not progress in severity over time. There were no significant differences in severity of WBM among the commercial broiler strains, between sexes, or between incubation temperature profiles. The positive correlation between WBM severity and lymphocytic phlebitis indicates vascular injury is likely an important factor in the pathogenesis. Mild muscle lesions in ACRB birds without overt clinical signs indicate subclinical muscle disease may have been present in broilers prior to the description of WBM. [ABSTRACT FROM AUTHOR]

Pathogenic strains of Enterococcus cecorum cause symmetrical paralysis in broilers due to infection of the free thoracic vertebra. The disease caused by pathogenic E. cecorum, known as enterococcal spondylitis or "kinky-back" continues to be responsible for significant losses to the broiler industry worldwide. In outbreaks of pathogenic E. cecorum, gut colonization and sepsis occur in the first three weeks-of-life. Since maternal antibodies are present during this period, we postulated that vaccination of breeders with a polyvalent killed vaccine would protect chicks from challenge. To test this hypothesis, representative isolates from seven genotype groups of pathogenic E. cecorum circulating in the US were chosen to produce adjuvanted killed vaccines (bacterins) and given to broiler-breeder hens. No single strain produced high titres of antibodies to all other strains; however, the combination of serologic reactivity of pathogenic isolates (designated SA3 and SA7) was sufficient to react with all genotypes. Vaccination of commercial broiler-breeder hens with a bacterin composed of SA3 and SA7 did not have any adverse effects. Vaccinated hens developed E. cecorum specific antibodies; however, no significant difference in survival was observed in infected embryos from hens in vaccine or adjuvant only groups. Chicks from vaccinated hens also failed to resist homologous or heterologous challenge during experimental infection. In a macrophage killing assay, pathogenic E. cecorum were found to evade opsinophagocytosis with elicited antibodies. These data suggest that pathogenic strains of E. cecorum possess virulence mechanisms that confound antibody-mediated opsinophagocytosis, complicating vaccine development for this pathogen of broilers. [ABSTRACT FROM AUTHOR]

Enterococcus cecorum (EC) is the dominant enteric commensal of adult chickens and contributes to the gut consortia of many avian and mammalian species. While EC infection is an uncommon zoonosis, like other enterococcal species it can cause life-threating nosocomial infection in people. In contrast to other enterococci which are considered opportunistic pathogens, emerging pathogenic strains of EC cause outbreaks of musculoskeletal disease in broiler chickens. Typical morbidity and mortality is comparable to other important infectious diseases of poultry. In molecular epidemiologic studies, pathogenic EC strains were found to be genetically clonal. These findings suggested acquisition of specific virulence determinants by pathogenic EC. To identify divergent genomic features and acquired virulence determinants in pathogenic EC; comparative genomic analysis was performed on genomes of 3 pathogenic and 3 commensal strains of EC. Pathogenic isolates had smaller genomes with a higher GC content, and they demonstrated large regions of synteny compared to commensal isolates. A molecular phylogenetic analysis demonstrated sequence divergence in pathogenic EC genomes. At a threshold of 98% identity, 414 predicted proteins were identified that were highly conserved in pathogenic EC but not in commensal EC. Among these, divergent CRISPR-cas defense loci were observed. In commensal EC, the type IIA arrangement typical for enterococci was present; however, pathogenic EC had a type IC locus, which is novel in enterococci but commonly observed in streptococci. Potential mediators of virulence identified in this analysis included a polysaccharide capsular locus similar to that recently described for E. faecium, an epa-like locus, and cell wall associated proteins which may bind host extracellular matrix. This analysis identified specific genomic regions, coding sequences, and predicted proteins which may be related to the divergent evolution and increased virulence of emerging pathogenic strains of EC. [ABSTRACT FROM AUTHOR]

This article discusses a study conducted to establish selected blood chemistry and gas reference ranges for clinically healthy broiler breeder hens using CG8+ cartridges in an i-STAT handheld point-of-care clinical analyzer. The study involves samples from 165 hens, representing three broiler breeder strains reared by four integrators. The reference ranges and means determined for sodium, potassium, ionized calcium, glucose, hematocrit, hemoglobin, pH, carbon dioxide partial pressure, oxygen partial pressure, bicarbonate, total carbon dioxide, base excess and oxygen saturation are described. The values are useful for investigating breeder flock diseases of unknown etiology.

The article describes the case of a parvovirus-associated cerebellar hypoplasia and hydrocephalus in day old broiler chickens. Polymerase chain reaction (PCR) was used to detect parvovirus DNA in three of nine brains with oligonucleotide primers. Findings of the postmortem examination on the broiler chickens noted that a chicken parvovirus might cause a neurologic disease of young chickens characterized by cerebellar hypoplasia and hydrocephalus.

Two cases of orchitis and epididymo-orchitis in broiler breeders are described. The first case occurred in a 62-week-old rooster showing signs of breeding inactivity. Grossly, the left testis was abnormally shaped and had multiple yellow foci, prominent blood vessels, and a gelatinous mass on the surface. The right testis and other tissues appeared normal. A pure, heavy growth of Staphylococcus aureus was obtained on bacterial culture, and intralesional Gram-positive cocci were numerous on histopathology. The second case occurred in a 28-week-old rooster that was found dead. Both testes were abnormally shaped, swollen, firm, and had irregular, dark, depressed areas, prominent vessels, and multiple petechial haemorrhages. Epididymides were enlarged and nodular. Other lesions in this rooster included poor nutritional condition, distended cloaca, and urate scalding of the abdominal skin below the vent. Microscopically, there was extensive, severe heterophilic intratubular orchitis and epididymitis with intralesional Gram-negative bacteria. A heavy, pure growth of Escherichia coli was obtained from the testes and epididymides. In both cases, the findings suggested that the most probable route of infection was ascending via the ductus deferens. [ABSTRACT FROM AUTHOR]

The effects of time-limited feeding, genetic background, and egg storage on white striping (WS) and wooden breast (WB) in broilers were studied. Male chicks (240) from 2 genetic backgrounds and 2 egg storage periods were fed on either an ad libitum (AL) or time-limited (TL) program from 7 d of age. A rapid growth strain (Growth) and an enhanced yield strain (Yield) of broiler breeder males were mated to a single female line and eggs were stored for periods of either 1 to 7 d or 8 to 14 d. Body weight (BW), feed consumption, and feed conversion ratio (FCR) were determined weekly. Carcass data including WS and WB scores were collected at 42 d of age. Breast muscle scoring was conducted either visually or by hand palpation using a 1 to 4 point ordinal scale (normal to greatest severity). Data were analyzed using the Mixed procedure of SAS. The TL fed broilers presented less WS (1.64 vs. 2.87) and WB (2.14 vs. 2.89), lower BW (2.99 vs. 3.27 kg), and improved FCR (1.55 vs. 1.58 g: g), as well as reduced dressing percentage (79.5 vs. 80.1%), breast muscle yield (33.3 vs. 34.6%), and 24 h muscle pH (5.82 vs. 5.95) relative to AL broilers (P < 0.01). Yield broilers exhibited reduced BW (2.97 vs. 3.28 kg), lower WS (2.04 vs. 2.47), and greater WB (2.65 vs. 2.38) (P < 0.05) but similar dressing percentage (80.0 vs. 79.7%) and breast muscle yield (34.3 vs. 33.6%) when compared to Growth broilers. Longer egg storage generated lower BW (3.07 vs. 3.18 kg) and when fed AL, an increased WS score (2.58 vs. 3.15) compared to the shorter egg storage period (P < 0.05). It was concluded that WS and WB could be reduced by TL feeding and that genetic background and egg storage period may influence the expression of WS and WB. [ABSTRACT FROM AUTHOR]