Carriage and Subtypes of Foodborne Pathogens Identified in Wild Birds Residing near Agricultural Lands in California: a Repeated Cross-Sectional Study.

Current California agricultural practices strive to comanage food safety and habitat conservation on farmland. However, the ecology of foodborne pathogens in wild bird populations, especially those avian species residing in proximity to fresh produce production fields, is not fully understood. In this repeated cross-sectional study, avifauna within agricultural lands in California were sampled over 1 year. Feces, oral swabs, and foot/feather swabs were cultured for zoonotic Salmonella spp., Escherichia coli O157:H7, and non-O157 Shiga toxin-producing E. coli (STEC) and characterized by serotyping and pulsed-field gel electrophoresis. Of 60 avian species sampled, 8 species (13.3%, bird groups of sparrows, icterids, geese, wrens, and kinglets) were positive for at least one of these foodborne pathogens. At the individual bird level, the detection of foodborne pathogens was infrequent in feces (n = 583; 0.5% Salmonella, 0.34% E. coli O157:H7, and 0.5% non-O157 STEC) and in feet/feathers (n = 401; 0.5% non-O157 STEC), and it was absent from oral swabs (n = 353). Several subtypes of public health importance were identified, including Salmonella enterica serotype Newport, E. coli O157:H7, and STEC serogroups O103 and O26. In late summer and autumn, the same STEC subtype was episodically found in several individuals of the same and different avian species, suggesting a common source of contamination in the environment. Sympatric free-range cattle shared subtypes of STEC O26 and O163 with wild geese. A limited rate of positive detection in wild birds provides insights into broad risk profile for contamination considerations but cannot preclude or predict risk on an individual farm.IMPORTANCE The shedding dynamics of foodborne pathogens by wild birds on farmland are not well characterized. This yearlong study sampled wild birds for foodborne pathogens within agricultural lands in northern California. There was a low prevalence of Salmonella spp., Escherichia coli O157:H7, and non-O157 Shiga-toxin producing E. coli (prevalence, 0.34% to 0.50%) identified in bird populations in this study. However, pathogens of public health importance (such as Salmonella Newport, E. coli O157:H7, and STEC O103 and O26) were identified in fecal samples, and two birds carried STEC on their feet or feathers. Identical pathogen strains were shared episodically among birds and between wild geese and free-range cattle. This result suggests a common source of contamination in the environment and potential transmission between species. These findings can be used to assess the risk posed by bird intrusions in produce fields and enhance policy decisions toward the comanagement of food safety and farmland habitat conservation.

Nucleophosmin protein expression level, but not threonine 198 phosphorylation, is essential in growth and proliferation.

Nucleophosmin (NPM), an oligomeric phosphoprotein and nucleolar target of the ARF tumor suppressor, contributes to several critical cellular processes. Previous studies have shown that the human NPM's phosphorylation by cyclin E-cyclin-dependent kinase 2 (cdk2) on threonine (Thr) 199 regulates its translocation from the centrosome during cell cycle progression. Given our previous finding that ARF directly binds NPM, impeding its transit to the cytoplasm and arresting cells before S-phase entry, we hypothesized that ARF might also inhibit NPM phosphorylation. However, ARF induction did not impair phosphorylation of the cdk2 target residue in murine NPM, Thr198. Furthermore, phosphorylation of Thr198 occurred throughout the cell cycle and was concomitant with increases in overall NPM expression. To investigate the cell's presumed requirement for NPM-Thr198 phosphorylation in promoting the processes of growth and proliferation, we examined the effects of a non-phosphorylatable NPM mutant, T198A, in a clean cell system in which endogenous NPM had been removed by RNA interference. Here, we show that the T198A mutant is fully capable of executing NPM's described roles in nucleocytoplasmic shuttling, ribosome export and cell cycle progression. Moreover, the proliferative defects observed with stable NPM knockdown were restored by mutant NPM-T198A expression. Thus, we demonstrate that the reduction in NPM protein expression blocks cellular growth and proliferation, whereas phosphorylation of NPM-Thr198 is not essential for NPM's capacity to drive cell cycle progression and proliferation.