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Background Avian influenza (AI) viruses infect numerous avian species, and low pathogenicity (LP) AI viruses of the H7 subtype are typically reported to produce mild or subclinical infections in both wild aquatic birds and domestic poultry. However relatively little work has been done to compare LPAI viruses from different avian species for their ability to cause disease in domestic poultry under the same conditions. In this study twelve H7 LPAI virus isolates from North America were each evaluated for their comparative pathogenesis in chickens, ducks, and turkeys. Results All 12 isolates were able to infect all three species at a dose of 10 6 50% egg infectious doses based on seroconversion, although not all animals seroconverted with each isolate-species combination. The severity of disease varied among isolate and species combinations, but there was a consistent trend for clinical disease to be most severe in turkeys where all 12 isolates induced disease, and mortality was observed in turkeys exposed to 9 of the 12 viruses. Turkeys also shed virus by the oral and cloacal routes at significantly higher titers than either ducks or chickens at numerous time points. Only 3 isolates induced observable clinical disease in ducks and only 6 isolates induced disease in chickens, which was generally very mild and did not result in mortality. Full genome sequence was completed for all 12 isolates and some isolates did have features consistent with adaptation to poultry (e.g. NA stalk deletions), however none of these features correlated with disease severity. Conclusions The data suggests that turkeys may be more susceptible to clinical disease from the H7 LPAI viruses included in this study than either chickens or ducks. However the severity of disease and degree of virus shed was not clearly correlated with any isolate or group of isolates, but relied on specific species and isolate combinations.

A limited outbreak of nephropathogenic infectious bronchitis (NIB) occurred in three Delmarva (DMV) commercial broiler chicken flocks in 2011. Isolates of NIB virus (NIBV)—DMV/1639/11, DMV/3432/11, and DMV/3902/11—were characterized by sequence analysis of the N-terminal subunit (S1) of the spike (S) gene. Findings indicated that the isolates were identical to each other and to PA/9579A/10, a 2010 isolate from poultry in Pennsylvania. The 2010 and 2011 isolates appear to have originated from a 1997–2000 NIB outbreak in Pennsylvania. DMV/1639/11 and PA/9579A/10 were determined to be nephropathogenic in susceptible chickens, yielding virus reisolations from kidney and inducing characteristic interstitial nephritis microscopic lesions. In a controlled laboratory study, 40% of chickens vaccinated with a combination live vaccine containing infectious bronchitis virus (IBV) strains Massachusetts (Mass) + Connecticut (Conn) were positive on virus isolation attempts after challenge with DMV/1639/11, compared with only 13% of Mass + Arkansas (Ark) vaccinates. Both combination vaccines gave partial protection against the development of DMV/1639/11-induced renal lesions. Although numerically fewer chickens vaccinated with Mass + Conn had interstitial nephritis compared with those vaccinated with Mass + Ark, neither vaccine combination offered greater protection (P < 0.05) than observed in unvaccinated chickens challenged with DMV/1639/11. Mass + Ark vaccinations, applied under commercial conditions in the hatchery (spray) and on-farm (spray), did not protect the trachea or kidney from DMV/1639/11 challenge. Serologic testing of broiler flocks found <3% (2 of 69) tested to possess specific antibodies to DMV/1639/11, indicating the virus had not become established in the region. Caracterización del virus nefropatogénico de la bronquitis infecciosa DMV/1639/11 aislado de pollos de engorde en el área de Delmarva en el año 2011. Se presentó un brote limitado de bronquitis infecciosa nefropatogénica (NIB) en tres parvadas comerciales de pollos de engorde en el año 2011 en el área de Delmarva. Se caracterizaron los aislamientos de virus nefropatogénicos de bronquitis infecciosa DMV/1639/11, DMV/3432/11 y DMV/3902/11 se caracterizaron mediante el análisis de la secuencia del gene de la subunidad S1 de la espícula (S). Los resultados indicaron que los aislamientos eran idénticos entre sí y con el aislamiento PA/9579A/10, que es un aislamiento de aves comerciales en Pennsylvania del año 2010. Las cepas de los años 2010 y 2011 parecen haberse originado a partir de un brote de bronquitis infecciosa nefropatogénica que se presentó entre los años 1997 al 2000 en Pennsylvania. Se determinó que los aislamientos DMV/1639/11 y PA/9579A/10 eran nefropatogénicos en pollos susceptibles, que eran reaislados del riñón e inducían las lesiones de nefritis intersticial microscópica característica. En un estudio controlado de laboratorio, el 40% de los pollos vacunados con una vacuna viva que contenía la combinación cepas Massachussets (Mass) y Connecticut (Conn) fueron positivos a los intentos de aislamiento del virus después del desafío con el virus DMV/1639/11, en comparación con sólo el 13% de los pollos vacunados con la combinación Massachussets y Arkansas (Ark). Ambas combinaciones de vacunas confirieron una protección parcial contra el desarrollo de las lesiones renales inducidas por el virus DMV/1639/11. Aunque un número menor de los pollos vacunados con la combinación Massachussets y Connecticut mostraron nefritis intersticial en comparación con los pollos vacunados con Massachussets y Arkansas, ninguna combinación de vacunas ofreció una mayor protección (P < 0.05) que la observada en los pollos no vacunados y desafiados con el virus DMV/1639/11. Las vacunaciones con la combinación Massachussets y Arkansas, aplicadas en condiciones comerciales en la planta de incubación (aerosol) y en las explotaciones agrícolas (aerosol), no protegieron a la tráquea o a los riñones ante el desafío con el virus DMV/1639/11. Las pruebas serológicas demostraron que menos del 3% de las parvadas (2 de 69) poseían anticuerpos específicos contra el virus DMV/1639/11, lo que indica que el virus no se había establecido en la región.

The onset of protection against Newcastle disease and the effect of maternal antibodies to Newcastle disease virus (NDV) and Marek's disease virus (MDV) on vaccine efficacy were determined following vaccination of chickens with a recombinant herpesvirus of turkeys (HVT) vaccine expressing the fusion (F) glycoprotein gene of NDV. Onset of protection following intra-abdominal administration of the recombinant HVT/F vaccine at 1 day of age and subsequent ocular challenge with the neurotropic velogenic Texas GB strain of NDV was determined to occur between days 14 and 21 post-vaccination (PV). Vaccination with the Hitchner B1 strain of NDV resulted in protection by day 6 PV, and vaccination with an inactivated NDV oil-emulsion vaccine induced protection by day 14 PV. One-day-old broiler-type chickens with maternal antibodies to both NDV and MDV and 1-day-old specific-pathogen-free (SPF) white leghorn chickens lacking maternal antibodies were vaccinated with the recombinant HVT/F vaccine or with control vaccines, challenged intra-abdominally with the very virulent RB1B strain of MDV on day 8 PV, and challenged with the Texas GB strain of NDV on day 29 PV. The HVT/F and NDV strain Hitchner B1 vaccines provided 73% and 80% protection, respectively, against NDV in broilers, whereas both vaccines resulted in 100% protection in SPF leghorns.

A limited outbreak of nephropathogenic infectious bronchitis (NIB) occurred in three Delmarva (DMV) commercial broiler chicken flocks in 2011. Isolates of NIB virus (NIBV)-DMV/1639/11, DMV/3432/11, and DMV/3902/11-were characterized by sequence analysis of the N-terminal subunit (S1) of the spike (S) gene. Findings indicated that the isolates were identical to each other and to PA/9579A/10, a 2010 isolate from poultry in Pennsylvania. The 2010 and 2011 isolates appear to have originated from a 1997-2000 NIB outbreak in Pennsylvania. DMV/1639/11 and PA/9579A/10 were determined to be nephropathogenic in susceptible chickens, yielding virus reisolations from kidney and inducing characteristic interstitial nephritis microscopic lesions. In a controlled laboratory study, 40% of chickens vaccinated with a combination live vaccine containing infectious bronchitis virus (IBV) strains Massachusetts (Mass) + Connecticut (Conn) were positive on virus isolation attempts after challenge with DMV/1639/11, compared with only 13% of Mass + Arkansas (Ark) vaccinates. Both combination vaccines gave partial protection against the development of DMV/1639/11-induced renal lesions. Although numerically fewer chickens vaccinated with Mass + Conn had interstitial nephritis compared with those vaccinated with Mass + Ark, neither vaccine combination offered greater protection (P < 0.05) than observed in unvaccinated chickens challenged with DMV/1639/11. Mass + Ark vaccinations, applied under commercial conditions in the hatchery (spray) and on-farm (spray), did not protect the trachea or kidney from DMV/1639/11 challenge. Serologic testing of broiler flocks found <3% (2 of 69) tested to possess specific antibodies to DMV/1639/11, indicating the virus had not become established in the region. Caracterizacion del virus nefropatogenico de la bronquitis infecciosa DMV/1639/11 aislado de pollos de engorde en el area de Delmarva en el ano 2011.

Apoptosis of smooth muscle cells is a common feature of vascular lesions but its pathophysiological significance is not known. We demonstrate that signals initiated by regulated Fas-associated death domain protein overexpression in rat vascular smooth muscle cells in the carotid artery induce expression of monocyte-chemoattractant protein-1 and interleukin-8, and cause massive immigration of macrophages in vivo . These chemokines, and a specific set of other pro-inflammatory genes, are also upregulated in human vascular smooth muscle cells during Fas-induced apoptosis, in part through a process that requires interleukin-1α activation. Induction of a pro-inflammatory program by apoptotic vascular smooth muscle cells may thus contribute to the pathogenesis of vascular disease.

Objectives. The effectiveness of case-managed residential care (CMRC) in reducing substance abuse, increasing employment, decreasing homelessness, and improving health was examined. Methods. A five-year prospective experiment included 358 homeless addicted male veterans 3, 6, and 9 months during their enrollment and at 12, 18, and 24 months after the completion of the experimental case-managed residential care program. The customary control condition was a 21-day hospital program with referral to community services. Results. The experimental group averaged 3.4 months in transitional residential care with ongoing and follow-up case management for a total of up to 1 year of treatment. The experimental group showed significant improvement compared with the control group on the Medical, Alcohol, Employment, and Housing measures during the 2-year period. An examination of the time trends indicated that these group differences tended to occur during the treatment year, however, and to diminish during the follow-up year. Conclusions. Within groups, significant improvements were observed with time from baseline to all posttests on the four major outcomes. We learned, however, that veterans had access to and used significant amounts of services even without the special case-managed residential care program. This partially may account for improvements in the control group and may have muted the differences between groups.

Mental illness and addiction are frequently comorbid. This volume is a major contribution to the literature and covers virtually every topic on a key clinical nexus, from long-established theories to the most modern research and development in the field.