Eggs were cultured from four commercial chicken layer houses implicated in three human outbreaks of Salmonella enteritidis serotype enteritidis infection as part of the activities of the USDA-APHIS, VS, Salmonella enteritidis Task Force. Each house was part of a multiple in-line complex, ranging from three to seven houses. Houses were located on three separate farms, and each house contained between 50,000 and 80,000 chickens. S. enteritidis phage types 8, 13a, and 23 were isolated from samples taken from environmental and organ tissue samples, but only phage type 8 was cultured from eggs. Phage type 8 was isolated from humans in all three S. enteritidis outbreaks. Frequency estimates of contaminated eggs ranged from 0.03% to 0.90%.

An outbreak of H7N2 low-pathogenicity (LP) avian influenza (AI) occurred in a two-county area in Pennsylvania from December of 1996 through April of 1998. The outbreak resulted in infection of 2,623,116 commercial birds on 25 premises encompassing 47 flocks. Twenty-one (one premise with infection twice) of the twenty-five infected premises housed egg-laying chickens and one premise each had turkeys, layer pullets, quail, and a mixed backyard dealer flock. Despite dose proximity of infected flocks to commercial broiler flocks, no infected broilers were identified. Experimentally, when market age broilers were placed on an influenza-infected premise they seroconverted and developed oviduct lesions. The outbreak was believed to have originated from two separate introductions into commercial layer flocks from premises and by individuals dealing in sales of live fowl in the metropolitan New York and New Jersey live-bird markets. Source flocks for these markets are primarily in the northeast and mid-Atlantic areas, including Pennsylvania. Mixed fowl sold include ducks, geese, guinea hens, quail, chukar partridges, and a variety of chickens grown on perhaps hundreds of small farms. Infections with the H7N2 AI virus were associated with variable morbidity and temporary decreases in egg production ranging from 1.6% to 29.1% in commercial egg-laying chickens. Egg production losses averaged 4.0 weeks duration. Mortality ranged from 1.5 to 18.3 times normal (mean of 4.3 times normal). Duration of mortality ranged from 2 to 13 weeks (average of 3.9 weeks) in flocks not depopulated. Lesions observed were primarily oviducts filled with a mucous and white gelatinous exudates and atypical egg yolk peritonitis. Quarantine of premises and complete depopulation were the early measures employed in control of this outbreak. Epidemiological studies suggested that depopulation furthered the spread of influenza to nearby flocks. Thereafter, later control measures included quarantine, strict biosecurity, and controlled marketing of products.

A number of factors limit the usefulness of blood or metabolic profiles. These include sampling problems, low correlations with nutrient intake, inconsistent patterns in disease, and difficulties in interpretation. Despite these limitations, profiles properly used may serve as an adjunct to more conventional technology in alleviating some dairy herd problems. Their use appears justified when feed analysis, ration evaluation, disease testing, and checks on management do not alleviate herd problems. Considerable potential for misuse of profiles exists due to the complexities of interpretation.

An avian influenza (AI) outbreak occurred in meat-type chickens in central Pennsylvania from December 2001 to January 2002. Two broiler breeder flocks were initially infected almost simultaneously in early December. Avian influenza virus (AIV), H7N2 subtype, was isolated from the two premises in our laboratory. The H7N2 isolates were characterized as a low pathogenic strain at the National Veterinary Services Laboratories based on molecular sequencing of the virus hemagglutinin cleavage site and virus challenge studies in specific-pathogen-free leghorn chickens. However, clinical observations and pathologic findings indicated that this H7N2 virus appeared to be significantly pathogenic in meat-type chickens under field conditions. Follow-up investigation indicated that this H7N2 virus spread rapidly within each flock. Within 7 days of the recognized start of the outbreak, over 90% seroconversion was observed in the birds by the hemagglutination inhibition test. A diagnosis of AI was made within 24 hr of bird submission during this outbreak using a combination of virus detection by a same-day dot-enzyme-linked immunosorbent assay and virus isolation in embryonating chicken eggs. Follow-up investigation revealed that heavy virus shedding (90%-100% of birds shedding AIV) occurred between 4 and 7 days after disease onset, and a few birds (15%) continued to shed virus at 13 days post-disease onset, as detected by virus isolation on tracheal and cloacal swabs. AIV was not detected in or on eggs laid by the breeders during the testing phase of the outbreak. The two flocks were depopulated at 14 days after disease onset, and AIV was not detected on the two premises 23 days after depopulation.

No abstract