E. coli O157:H7 Season is Nearly Upon Us
Will it be 2005 and 2006 or 2007 and 2008?
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.
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
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
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
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,
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
More outbreaks linked to swimming pools, recreational water, and
agriculture fairs during the summer
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.
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
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
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
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
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
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
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.