An avian influenza virus H6N1 outbreak in commercial layers: case report and reproduction of the disease.

An outbreak of low pathogenic avian influenza (LPAI) subtype H6N1 (intravenous pathogenicity index = 0.11) infection occurred in four productive brown layer flocks on three farms in the Netherlands within a period of two months. The farms were located at a maximum distance of 4.6 km from each other. The infections were associated with egg production drops up to 74%, pale eggshells and persisting high mortality up to 3.2% per week. Three flocks were slaughtered prematurely as they were not profitable anymore. Newcastle disease, infectious bronchitis, egg drop syndrome and Mycoplasma gallisepticum infections could very likely be excluded as cause of or contributor to the condition in the field. Also, the anticoccidial drug nicarbazin, which can cause egg production drops and eggshell decolouration, was not detected in eggs from affected flocks. Furthermore, post mortem examinations revealed no lesions indicative of bacterial infection. Moreover, bacteriological analysis of hens was negative. The condition was reproduced in commercial brown layers after intratracheal inoculation with virus isolates from affected flocks. It is concluded that the LPAI H6N1 virus is very likely the only cause of the disease. An overview of main manuscripts published since 1976 describing non-H5 and non-H7 avian influenza (AI) virus infections in chickens and their biological significance is included in the present study, in which once more is shown that not only high pathogenic AI virus subtypes H5 and H7 can be detrimental to flocks of productive layers, but also non-H5 and non-H7 LPAI viruses (H6N1 virus). RESEARCH HIGHLIGHTS LPAI H6N1 can be detrimental to productive layers Detrimental effects are severe egg drop and persistent high mortality LPAI H6N1 virus outbreak seems to be self-limiting.

Enterococcus cecorum infections in broiler breeders and their offspring: molecular epidemiology.

Increased mortality and problems with lameness were reported in Dutch broiler flocks from the year 2008 onwards. Therefore, a field inventory, including 10 affected broiler flocks, nine corresponding broiler breeder flocks and five hatcheries, was carried out. The onset of clinical signs (lameness and increased mortality) started at about 2 weeks of age. The flock mortality varied from 3.1 to 8.1% at slaughter. Post-mortem lesions of broiler flocks were characterized by the occurrence of pericarditis/hydropericardium, arthritis and femoral head necrosis. Enterococcus cecorum was isolated from approximately 30% of the lesions. In the broiler breeders, E. cecorum was not isolated from any of the lesions. However, it was isolated from 31 out of 65 (47%) cloacal swabs, from two out of 65 (3%) oviduct samples, from one out 65 (1.5%) bone marrow samples and from two out of 25 (8%) blood samples. E. cecorum was not isolated from the air samples or dead-in-shell originating from the hatcheries involved. In total, 78 isolates were subjected to further typing by means of tRNA intergenic spacer PCR and confirmed as E. cecorum. The genetic relatedness of these cocci was subsequently studied using pulsed-field gel electrophoresis. The banding patterns of approximately 68% of E. cecorum isolates originating from parent stock flocks were clonal to one or more isolates of the same or other parent flocks. In contrast, isolates originating from their diseased offspring showed much greater genetic variation. Therefore, the vertical transmission of E. cecorum could not be demonstrated.