In vitro efficacy of potentiated egg yolk powder against Campylobacter jejuni does not correlate with in vitro efficacy.

Campylobacter jejuni is a zoonotic agent responsible for the foodborne gastroenteritis campylobacteriosis. Control of C. jejuni load in the poultry primary production is recognized as an avenue to reduce human exposure to the pathogen. As for now, no commercially applicable control methods exist at the farm. Several studies tested egg yolk powders, potentiated or not against C. jejuni, as feed additives for chicken and suggested that the quantity and quality of the antibodies presence in the yolk are determinant factors for the full success of this approach. Unfortunately, data from these studies inconsistently showed a reduction of cecal C. jejuni carriage. Our first goal wwas to characterize (quantification by ELISA, agglutination test, bacterial antigen recognition profiles by Western blot, bactericidal effect by serum killing assays and C. jejuni mobility by soft agar migation) the antibodies extracted from egg yolk powders originating from different egg production protocols. Secondly, these powders were microencapsulated and recharacterized. Finally the protected powders were tested as a feed additive to destabilize C. jejuni colonization in an in vivo assay. Despite the in vitro results indicating the ability of the egg yolk powders to recognize Campylobacter and potentially alter its colonization of the chicken caecum, these results were not confirmed in the in vivo trial despite that specific caecal IgY directed toward Campylobacter were detected in the groups receiving the protected powders. More research is needed on Campylobacter in order to effectively control this pathogen at the farm.

Association between community socioeconomic factors, animal feeding operations, and campylobacteriosis incidence rates: Foodborne Diseases Active Surveillance Network (FoodNet), 2004-2010.

BACKGROUND: Campylobacter is a leading cause of foodborne illness in the United States. Campylobacter infections have been associated with individual risk factors, such as the consumption of poultry and raw milk. Recently, a Maryland-based study identified community socioeconomic and environmental factors that are also associated with campylobacteriosis rates. However, no previous studies have evaluated the association between community risk factors and campylobacteriosis rates across multiple U.S. states. METHODS: We obtained Campylobacter case data (2004-2010; n = 40,768) from the Foodborne Diseases Active Surveillance Network (FoodNet) and socioeconomic and environmental data from the 2010 Census of Population and Housing, the 2011 American Community Survey, and the 2007 U.S. Census of Agriculture. We linked data by zip code and derived incidence rate ratios using negative binomial regression models. RESULTS: Community socioeconomic and environmental factors were associated with both lower and higher campylobacteriosis rates. Zip codes with higher percentages of African Americans had lower rates of campylobacteriosis (incidence rate ratio [IRR]) = 0.972; 95 % confidence interval (CI) = 0.970,0.974). In Georgia, Maryland, and Tennessee, three leading broiler chicken producing states, zip codes with broiler operations had incidence rates that were 22 % (IRR = 1.22; 95 % CI = 1.03,1.43), 16 % (IRR = 1.16; 95 % CI = 0.99,1.37), and 35 % (IRR = 1.35; 95 % CI = 1.18,1.53) higher, respectively, than those of zip codes without broiler operations. In Minnesota and New York FoodNet counties, two top dairy producing areas, zip codes with dairy operations had significantly higher campylobacteriosis incidence rates (IRR = 1.37; 95 % CI = 1.22, 1.55; IRR = 1.19; 95 % CI = 1.04,1.36). CONCLUSIONS: Community socioeconomic and environmental factors are important to consider when evaluating the relationship between possible risk factors and Campylobacter infection.

An outbreak of food-borne enterotoxigenic Escherichia coli diarrhoea in England.

An outbreak of diarrhoea with abdominal pain occurred among members of the staff of a school and their guests after a social function at which a cold buffet was served. Sixty people attended the function and 43 subsequently completed questionnaires. Of these, 27 had diarrhoea. The median incubation period was 36 h and the range 12-66 h. Food history analysis showed an association between diarrhoea and eating curried turkey mayonnaise. Stool specimens from 13 of those who developed diarrhoea were examined: Escherichia coli 06.H16 (producing heat-stable and heat-labile enterotoxins) was found in nine specimens and E. coli 027.H20 (producing heat-stable enterotoxin) in 11 specimens. Eight patients had both strains and only one was negative for enterotoxigenic E. coli. Food samples were not available for examination. Enterotoxigenic E. coli should be considered as a possible cause in well-defined outbreaks of food-borne diarrhoea with abdominal pain.

Serotyping of Campylobacter jejuni from an outbreak of enteritis implicating chicken.

An outbreak of campylobacter enteritis involving 7 of 17 people over a period of 5 days followed a dinner at a restaurant. A chicken casserole dish was implicated with a food-specific attack rate of 58%. Campylobacter jejuni Penner serotype 18/21/29, resistant to metronidazole, was isolated from 3 of 4 symptomatic patients and from three raw fresh chicken samples closely associated with the implicated chicken. Numbers of C. jejuni in the chicken ranged from 5.3 X 10(1) to 7.5 X 10(2) colony forming units per square centimeter of surface area. This is the first outbreak of campylobacter enteritis reported in Australia in which C. jejuni has been isolated from both human and food sources and the isolates serologically confirmed as identical.

Foodborne outbreak of group G streptococcal pharyngitis.

An outbreak of pharyngitis associated with beta-hemolytic streptococci of Lancefield group G occurred among persons who had attended a convention that was held June 21-24, 1979, in a Florida hotel. Seventy-two (31 per cent) of 231 interviewed conventioneers were ill. Group G streptococci were isolated from the throats of 10 (63 per cent) of 16 persons with pharyngitis and 1 (2 per cent) of 41 persons without pharyngitis (p less than 10(-5)). Antistreptolysin O titers in convalescent-phase serum samples from persons with pharyngitis were significantly higher than those from age-matched controls. Fifty-seven (51 per cent) of 111 conventioneers who had attended a convention luncheon developed pharyngitis compared with 12 (10 per cent) of 117 persons who did not (p less than 10(-9)). All persons who had attended the luncheon and had become ill had eaten a chicken salad served at the luncheon. Their median incubation period was two days. The cook who had prepared this chicken salad developed pharyngitis after the luncheon and had a throat culture positive for group G streptococci. No instances of rheumatic fever were identified and secondary illness in household contracts was rare. This outbreak indicates that group G streptococci can cause outbreaks of pharyngitis similar to those caused by group A streptococci and suggests that penicillin therapy and prophylaxis may not be needed.