No abstract

The microbiological profile of an air-chilling poultry process was investigated from the farm through the processing plant. Within a 1-year period, nine broiler flocks from four different farm sources were studied. Numbers of total aerobes, coliforms, psychrotrophic organisms, E. coli Biotype I (generic E. coli), Salmonella spp., and Campylobacter spp. were determined for multiple sampling sites on the farm as well as in the processing plant. Farm samples were collected the day before the chickens were slaughtered at the plant. The same flock was sampled at the plant on the day of slaughter. Sites located before evisceration (BE), after evisceration (AE), and after chilling (AC) were sampled. Results indicated a positive correlation between contamination of ceca with Salmonella on the farm and the presence Salmonella in carcass samples from the plant for all three types of sampling sites. The in-plant trend for total aerobes, coliforms, and generic E. coli revealed a significant decrease from counts obtained before evisceration to those obtained for the (AC) final product when flock variations were taken into account. The average coliform counts were 3.91, 3.27, and 2.59 log10 CFU/ml of rinse for BE, AE, and AC samples, respectively. Generic E. coli counts were 3.74, 3.08, and 2.20 log10 CFU/ml of rinse for BE, AE, and AC samples, respectively. No reductions in numbers of Campylobacter or Salmonella were observed during processing, which suggests that practical intervention strategies for lowering pathogen levels are critical on a multilevel basis at the farm and in the plant.

The increasing incidence of fish-health problems, ranging from small external sores and lesions to large-scale fish kills in the Chesapeake Bay and other Mid-Atlantic estuaries, is of growing concern to natural resource managers and residents of the Chesapeake Bay watershed. Fish kills have been reported in North Carolina since the early 1990's. Reports of skin lesions on fish in the summer and fall of 1996 and 1997 in the Pocomoke River, Maryland and other tributaries of Chesapeake Bay stimulated a great deal of public and scientific interest. These skin lesions ranged from small pinpoint hemorrhages to abrasions to deep ulcers. In addition, there were two fish kills, involving primarily Atlantic menhaden, in the Pocomoke River during August 1997. The fish kills, as well as the variety of fish lesions, have been blamed on the presence of a toxic dinoflagellate, Pfiesteria piscicida, or Pfiesteria-like dinoflagellates. The occurrence of Pfiesteria has been attributed to nutrient enrichment, warm water temperatures, moderate to high salinity, and fish excretions (Burkholder and Glasgow, 1997). While Pfiesteria has been identified as a potential cause of fish kills in the Chesapeake Bay and other estuaries, there is growing evidence that other pathogens also are causing lesions in fish in the Bay. Skin lesions in fish can be caused by a variety of infectious and noninfectious insults. Lesions commonly are caused by opportunistic pathogens, which infect weakened or stressed hosts. These pathogens, which include bacteria, fungi, viruses, and parasites, may gain entry because of impaired immune or disease resistance factors, or because the natural defense mechanisms of the skin are impaired or breached. Several State and Federal agencies, including the U.S. Geological Survey (USGS), are currently working to understand the relation between Pfiesteria and other pathogens to fish and human health, and to natural and man-induced factors (such as nutrients