The presence of E. coli O157:H7 in hamburger was defined as an adulterant under the Federal Meat Inspection Act in 1994. However, recalls of E. coli O157:H7 contaminated meat and related illnesses continued over the next decade to grow, as did my law firm. Oddly too, and with near regularity, E. coli O157:H7 recalls and illnesses seemed to begin in the Spring and peak in late Summer and Fall from 1993 through 2002.
After 24 million pounds of contaminated beef were recalled in 34 separate incidents in 2002, recalls dropped off to just over a million pounds a year for the next three years, and then to just 181,900 pounds in 2006. The Centers of Disease Control and Prevention saw E. coli O157:H7 – related illnesses drop 48% between 2000 and 2006.
The reality is that from 1993 through 2002, children sickened with E. coli O157:H7 tainted hamburger made up the bulk of my law practice. However, as E. coli O157:H7 hamburger recalls fell from 2003 through the end of 2006, I wondered if the law firm would survive. Springs just simply were not the same.
But then came Spring 2007. E. coli O157:H7, which begins its life in the hindgut of a cow, mounted a surge on its home court. And, it came back with a vengeance. Since the Spring of 2007, forty-four million pounds of beef have been recalled in 25 incidents due to E. coli O157:H7. And, I am now back in the meat business, and look to Spring not just for the beginning of hay fever season.
Now, Spring 2009 is upon us. In preparing for it, I had some research done on the “seasonality” of E. coli O157:H7 in both humans and cattle and then say what was available in the literature as to the reasons behind it. Perhaps it does not fully explain what I experienced from 1993 though 2008, but it is a start. It is all about being prepared.
Seasonality in humans:
• A review of E. coli O157:H7 diarrhea in the US by Slutsker et al (1997) found that E. coli O157:H7 was isolated most frequently from patients during the summer months.
• Results from an epidemiological review of E. coli O157:H7 outbreaks in the US (1982-2002) showed that outbreaks involving ground beef peaked in summer months (Rangel et al, 2005)
• In a review of non-O157 STEC infections in the US from 1983-2002 revealed that these infections also were most frequent during the summer (Brooks et al, 2005)
• In Scotland, HUS and E. coli O157:H7 infections peaked in patients under 15 years of age in July/August, followed by a plateau from June to September (Douglas et al, 1997). Interestingly, the prevalence in Scottish beef cattle at slaughter was found to be highest during the winter, but the concentration of E. coli O157:H7 (number of bacteria shed in cattle feces) was highest during the warmer months (Ogden et al, 2004).
Seasonality in ruminants:
• Numerous studies in cattle indicate that fecal shedding of E. coli O157:H7 is typically low in the winter, increases in the spring, peaks during the summer and tapers off in the fall (Edrington et al, 2006; Hancock et al, 2001; Hussein et al, 2005, etc.)
• Barkocy-Gallagher et al (2003) found that the prevalence of E. coli O157:H7 in cattle feces peaked in the summer, and prevalence on hides (a known risk factor for beef contamination) was highest from spring through fall.
• A survey of ground beef samples in the US showed that they were 3x more likely to be contaminated with E. coli O157:H7 from June – September (Chapman, et al 2001)
• A survey in the UK found that the majority of retail meats that tested positive for E. coli O157:H7 were collected between May and September.
Hypotheses on why there are seasonal differences in prevalence in both humans and cattle
• Differences in handling and cooking food, or differences in consumption patterns during the summer, especially ground beef (outdoor BBQs, picnics, summer camps)
• Higher prevalence of E. coli O157:H7 in cattle feces and hides entering the slaughterhouse
• More outbreaks linked to swimming pools, recreational water, and agriculture fairs during the summer
• Speculation that temperature may affect shedding or survival in feces (warmer months promoting survival and/or growth of E. coli O157:H7).
• Studies by Edrington et al (2006 and 2008) suggested that day length and effects on hormones such as melatonin secretion from the gastrointestinal tracts may be the underlying mechanism for seasonality in cattle. The authors hypothesized that the seasonal variation is a result of physiological responses within the host animal to changing day-length. Hormones have been shown to play a role in the regulation of bacterial populations and host immunity.
1. Barkocy-Gallagher, G. A., T. M. Arthur, M. Rivera-Betancourt, X. Nou, S. D. Shackelford, T. L. Wheeler, and M. Koohmaraie. 2003. Seasonal prevalence of Shiga toxin-producing Escherichia coli, including O157:H7 and non-O157 serotypes, and Salmonella in commercial beef processing plants. J Food Prot 66:1978-86.
2. Besser, R. E., P. M. Griffin, and L. Slutsker. 1999. Escherichia coli O157:H7 gastroenteritis and the hemolytic uremic syndrome, an emerging infectious disease. Annu Rev Med 50:355-67.
3. Brooks, J. T., E. G. Sowers, J. G. Wells, K. D. Greene, P. M. Griffin, R. M. Hoekstra, and N. A. Strockbine. 2005. Non-O157 Shiga toxin-producing Escherichia coli infections in the United States, 1983-2002. J Infect Dis 192:1422-9.
4. Chapman, P. A., C. A. Siddons, A. T. Gerdan Malo, and M. A. Harkin. 1997. A 1-year study of Escherichia coli O157 in cattle, sheep, pigs and poultry. Epidemiol Infect 119:245-50.
5. Douglas, A. S., and A. Kurien. 1997. Seasonality and other epidemiological features of haemolytic uraemic syndrome and E. coli O157 isolates in Scotland. Scott Med J 42:166-71.
6. Dunn, J. R., J. E. Keen, and R. A. Thompson. 2004. Prevalence of Shiga-toxigenic Escherichia coli O157:H7 in adult dairy cattle. J Am Vet Med Assoc 224:1151-8.
7. Edrington, T. S., T. R. Callaway, S. E. Ives, M. J. Engler, M. L. Looper, R. C. Anderson, and D. J. Nisbet. 2006. Seasonal shedding of Escherichia coli O157:H7 in ruminants: a new hypothesis. Foodborne Pathog Dis 3:413-21.
8. Edrington T.S., T. R. Callaway, D. M. Hallford, L. Chen, R. C. Anderson, and D. J. Nisbet. 2008. Effects of exogenous melatonin and tryptophan on fecal shedding of E. coli O157:H7 in cattle. Microb Ecol. 55:553-60.
9. Fernandez, D., E. M. Rodriguez, G. H. Arroyo, N. L. Padola, and A. E. Parma. 2009. Seasonal variation of Shiga toxin-encoding genes (stx) and detection of E. coli O157 in dairy cattle from Argentina. J Appl Microbiol 106:1260-7.
10. Hancock, D., T. Besser, J. Lejeune, M. Davis, and D. Rice. 2001. The control of VTEC in the animal reservoir. Int J Food Microbiol 66:71-8.
11. Hancock, D. D., T. E. Besser, M. L. Kinsel, P. I. Tarr, D. H. Rice, and M. G. Paros. 1994. The prevalence of Escherichia coli O157.H7 in dairy and beef cattle in Washington State. Epidemiol Infect 113:199-207.
12. Hancock, D. D., T. E. Besser, D. H. Rice, D. E. Herriott, and P. I. Tarr. 1997. A longitudinal study of Escherichia coli O157 in fourteen cattle herds. Epidemiol Infect 118:193-5.
13. Hussein, H. S., and L. M. Bollinger. 2005. Prevalence of Shiga toxin-producing Escherichia coli in beef cattle. J Food Prot 68:2224-41.
14. Khaitsa, M. L., M. L. Bauer, G. P. Lardy, D. K. Doetkott, R. B. Kegode, and P. S. Gibbs. 2006. Fecal shedding of Escherichia coli O157:H7 in North Dakota feedlot cattle in the fall and spring. J Food Prot 69:1154-8.
15. LeJeune, J. T., T. E. Besser, D. H. Rice, J. L. Berg, R. P. Stilborn, and D. D. Hancock. 2004. Longitudinal study of fecal shedding of Escherichia coli O157:H7 in feedlot cattle: predominance and persistence of specific clonal types despite massive cattle population turnover. Appl Environ Microbiol 70:377-84.
16. MacDonald, K. L., M. J. O’Leary, M. L. Cohen, P. Norris, J. G. Wells, E. Noll, J. M. Kobayashi, and P. A. Blake. 1988. Escherichia coli O157:H7, an emerging gastrointestinal pathogen. Results of a one-year, prospective, population-based study. JAMA 259:3567-70.
17. Ogden, I. D., M. MacRae, and N. J. Strachan. 2004. Is the prevalence and shedding concentrations of E. coli O157 in beef cattle in Scotland seasonal? FEMS Microbiol Lett 233:297-300.
18. Ostroff, S. M., J. M. Kobayashi, and J. H. Lewis. 1989. Infections with Escherichia coli O157:H7 in Washington State. The first year of statewide disease surveillance. JAMA 262:355-9.
19. Pearl, D. L., M. Louie, L. Chui, K. Dore, K. M. Grimsrud, D. Leedell, S. W. Martin, P. Michel, L. W. Svenson, and S. A. McEwen. 2006. The use of outbreak information in the interpretation of clustering of reported cases of Escherichia coli O157 in space and time in Alberta, Canada, 2000-2002. Epidemiol Infect 134:699-711.
20. Rangel, J. M., P. H. Sparling, C. Crowe, P. M. Griffin, and D. L. Swerdlow. 2005. Epidemiology of Escherichia coli O157:H7 outbreaks, United States, 1982-2002. Emerg Infect Dis 11:603-9.
21. Rasmussen, M. A., and T. A. Casey. 2001. Environmental and food safety aspects of Escherichia coli O157:H7 infections in cattle. Crit Rev Microbiol 27:57-73.
22. Slutsker, L., A. A. Ries, K. D. Greene, J. G. Wells, L. Hutwagner, and P. M. Griffin. 1997. Escherichia coli O157:H7 diarrhea in the United States: clinical and epidemiologic features. Ann Intern Med 126:505-13.
23. Van Donkersgoed, J., T. Graham, and V. Gannon. 1999. The prevalence of verotoxins, Escherichia coli O157:H7, and Salmonella in the feces and rumen of cattle at processing. Can Vet J 40:332-8.