Georgia epidemiology report, Vol. 21, no. 2 (Feb. 2005)

February 2005

volume 21 number 02

Escherichia coli 0157:H7 Infections in Georgia, 1993 - 2003

INTRODUCTION
Since it was recognized as a cause of diarrheal illness in 1982, and shortly thereafter as a cause of hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP), Shiga toxin-producing E. coli O157:H7 has emerged as an important public health concern in the United States, Canada and many other countries. E. coli O157 infections received relatively little attention from the public and the medical community in Georgia until 1998, when an outbreak of E. coli O157 infections associated with a water park in Atlanta caused 26 cultureproven cases in children, many hospitalizations, seven cases of hemolytic uremic syndrome, and one death1. We describe the characteristics of E. coli O157 infections in Georgia using summary data from 1993-2003 and detailed data from 2000-2001.

outbreak is included in Figure 1 because only one was culture-confirmed, while the others were diagnosed serologically. The 1998 outbreak1 occurred among children who swam in Pool A, an inadequately chlorinated pool at a large commercial water park. Twenty-six cases were cultureproven. The 2001 outbreak occurred in a prison for women. Thirty-five women became ill, but only 10 cases were confirmed by stool culture and included in the figure. The unusually high peak in July 2000 was caused by three unrelated outbreaks occurring in the same month.

METHODS
E. coli O157:H7 infections reported to the Georgia Division of Public Health (GDPH) since 1993 are available on-line at http:// www.ph.dhr.state.ga.us/epi/index.shtml. We used these data to describe the epidemiology of E. coli O157:H7 infection in Georgia during 1993-2001. Rate calculations used the Year 2000 United States Census population figures (http://www.ph.dhr.state.ga.us/programs/ ohip/birthdeath.shtml).

Since 2000, as part of the Georgia Emerging Infections Project (GA EIP) sponsored by the Centers for Disease Control and Prevention (CDC), medical epidemiologists from the Epidemiology Branch, GDPH have conducted enhanced follow-up of all reported cases of E. coli O157:H7 infections. This has included having the Georgia Public Health Laboratory (GPHL) perform "molecular fingerprinting" by pulsed field gel electrophoresis (PFGE) on all available isolates, and attempting to complete a five page questionnaire. We examined the data collected for the 2000-2001 cases.
RESULTS 1993-2003 cases During 1993-2003, 447 cases of E. coli O157:H7 infection were reported in Georgia. Not all of the variables listed (location, race, sex, age) are available for all of the cases, so each analysis is limited to the cases that have information on the variables under investigation.
The number of cases per year increased steadily during 1993 through 1997, peaked during 1998, and, except for the 1998 peak, has been stable at about 46 cases per year until 2003, when it dropped to 27 cases. The four outbreaks indicated on Figure 1 were particularly large. Investigation of the 1995 outbreak showed that it affected at least eight persons who were infected by eating hamburgers from three different outlets of a small fast food chain in northern Georgia and adjacent southeastern Tennessee. The 1996 outbreak was traced to swimming in a haphazardly chlorinated swimming pool in a trailer park2. Only one of the 18 persons known to have been infected in the trailer park pool

During 1993-2003 E. coli O157:H7 infections had marked seasonal changes. Cases reached a low point in February and March, peaked in June and July, and then gradually declined.
The 11-year incidence of reported E. coli O157:H7 infections was 7.4/ 100,000 in children <1 years of age, peaked in 1-4 year old children (20.5), fell steadily in the 5-14 year old (9.9), 15-25 year old (4.5), and 2549 year old (2.4) age groups, and then rose in persons 50+ years of age (3.6).
During 1993-2003, there were more cases of HUS in 1-4 year old children (31) than in all other age groups combined (21). Eighty-five percent of HUS cases but only 53% of E. coli O157:H7 infections occurred in children under 15 years of age.
Of the 337 cases with data on race, 285 (85%) were white (5.3/100,000 population during 11 years), 47 (14%) were black (2.0/100,000), and five (1%) were of other races. Thus, the eleven-year incidence in the white population was 2.7 (5.3/2.0) times greater than the incidence in the black population. The incidence of E. coli O157:H7 infections was higher in the white than in the black population in all age categories, and the black population had less predominance of cases in the early age groups (Figure 2).

The Georgia Epidemiology Report Via E-Mail
To better serve our readers, we would like to know if you would prefer to receive the GER by e-mail as a readable PDF file starting in 2004. If yes, please send your name and e-mail address to Gaepinfo@dhr.state.ga.us.

Seventy (72%) of the patients with information about ground beef consumption reported having eaten any ground beef in the seven days before onset of illness, and 53% recalled eating ground beef at home. The 2000 FoodNet survey3 found that 53% of well Georgians reported eating ground beef at home in the seven days before interview, so there was no difference. Twelve (15%) of Georgia cases with known data reported having eaten any undercooked or raw meat (beef or other), but there were no strictly comparable data from the FoodNet surveys. Although unpasteurized dairy products, venison, alfalfa sprouts, and unpasteurized juice have all been associated with E. coli O157:H7 infections in the past, no more than 2% of Georgians with E. coli O157:H7 infections recalled consuming these foods during the seven days before onset of illness.

The reported 11-year incidence of E. coli O157:H7 infection per 100,000 population during 1993-2003 was higher for the northern third (Health Districts: Athens, Atlanta, Dalton, Decatur, Forest Park, Gainesville, LaGrange, Lawrenceville, Marietta, and Rome) of Georgia (6.4) than in the southern two thirds (Health Districts: Albany, Augusta, Brunswick, Columbus, Dublin, Macon, Savannah, Valdosta, and Waycross) of the state (2.5). Although AfricanAmericans are a larger proportion of the total population in the southern part of the state, their lower incidence of E. coli O157:H7 infections does not explain the lower incidence in the southern twothirds of the state. The incidence of E. coli O157:H7 infections was higher in the north for both the white (3.1 times higher than in the south) and black (2.4 times higher than in the south) populations (Table 1).

Table 1. Incidence (cases/100,000 population) of E. coli

O157:H7 infections by race in the northern third and southern

two-thirds of Georgia, 1993-2003

Area North South Ratio (N/S)

White 6.73 2.16 3.1

Black 2.67 1.09 2.4

Ratio (W/B) 2.5 2.0

2000-2001 cases with detailed data The GDPH data for E. coli O157:H7 infections in 2000-2001 includes reports of 113 reported cases. We deleted 4 suspected cases, leaving 109 confirmed (86) or presumptive (23) cases for analysis.
Almost all of the cases (96% of those with known symptoms) had diarrhea, and a large majority (74%) had bloody diarrhea. Six (6%) of the 109 reported cases had HUS and two (2%) had TTP. All cases classified as HUS occurred in children under age seven (1, 1, 2, 2, 4 and 6 years of age). The two cases with TTP were in patients 23 and 81 years of age. Two of the 109 patients are known to have died; both were elderly women, 76 and 81 years of age. Forty-one (39%) of the 105 reported cases with data were hospitalized. For the 38 with data on duration of hospitalization, the median duration of hospitalization was 4 days. All had hospital stays <10 days except for two children with HUS who stayed for 20 and 33 days.
Matches were found for 34 (47%) of the 72 subjects who had PFGE patterns determined for their E. coli O157:H7 strains. These 34 included eight clusters of indistinguishable patterns in Georgia and one case whose pattern matched that of cases in other states. In these nine clusters, one was a large prison outbreak, two were associated with interstate outbreaks caused by ground beef, five were associated with person-to-person secondary spread, and two appeared to be common source outbreaks in which the common source was not detected. The single high peak in July, 2000, was shown by PFGE to be caused by three separate outbreaks.

DISCUSSION During the decade after E. coli O157:H7 was found to be a human pathogen in 1982, only a few cases of human infection with the organism were detected and reported in Georgia, and the infection was not made officially reportable until January, 1996. The number of cases of E. coli O157:H7 infections reported in Georgia rose between 1993 and 1997 and peaked in 1998, probably because of improved case ascertainment and reporting after publicity about a large outbreak in attendees at a water park. The number of cases was then fairly stable until 2003, when it fell. The lack of an increase in the annual number of cases since 1998 may reflect a measure of success in controlling E. coli O157:H7 infections. The same trend--no increase in E. coli O157:H7 infections since 1998 and a drop in 2003--is also seen in the FoodNet data collected in nine U.S. sites in nine different states4. This flattening of the previously increasing incidence of E. coli O157:H7 infections in Georgia has occurred at the same time as greatly increased national attention to food safety, notably the U.S. Department of Agriculture's tightening of quality control in meat and poultry slaughter and processing plants beginning in 19974. Other national interventions have included better agricultural practices to decrease the contamination of fresh produce and regulation of fruit and vegetable juices4.
The reservoir for E. coli O157:H7 is cattle. The organism is in the cow's manure, and during the process of slaughtering the cow and preparing the meat E. coli O157:H7 is transferred from the manure to the meat. The proportion of cows infected is small, often less than 1%5. A steak comes from a single cow and has only an outside surface that can be contaminated, and even superficial cooking may be enough to kill any bacteria on that surface. In contrast, ground beef comes from many cows, and, while being ground into small pieces, can have bacteria spread throughout the meat. If the ground beef is not cooked thoroughly, the internalized bacteria can survive and infect the consumer. We had two outbreaks of E. coli O157:H7 infections during 2000-2001 that were linked to eating ground beef, but they accounted for just 5 of the 109 reported cases. While the majority of cases had eaten ground beef in the week before onset of illness, only 15% recalled having eaten undercooked or raw beef. Thus, we cannot directly link most of our cases with the presumed reservoir, cattle.
In all, only 34 (31%) of the reported cases in 2000-2001 were part of identified outbreaks, and our extensive PFGE testing gives us some assurance that there were few if any large undetected outbreaks with multiple cases in our series. However, many cases of E. coli O157:H7 infection are never diagnosed and reported, so each single (and apparently sporadic) case that is reported may be just the tip of a small iceberg of related cases occurring in the community at the same time, or one link in a chain of undiagnosed infections. The investigations of E. coli O157:H7 infections since their first recognition more than two decades ago have shown that E. coli O157:H7 organisms from cattle and from beef infect people directly and by cross-contamination of other food, and that the organisms excreted by these infected persons can then cause further infections in many ways, including contamination of food, drinking water, and recreational water, and by person-to-person fecal-oral transmission.
-2 -

Transmission of E. coli O157:H7 infections by exposure to recreational water has been documented in Georgia repeatedly in the past, with significant outbreaks in 19962 and 19981. E. coli O157:H7 bacteria are highly susceptible to small amounts of chlorine6. When the organism is introduced into a pool by a convalescent child's poorly cleansed perianal area, the organism may be able to infect other children for only a short period of time before it is inactivated even if the pool is poorly chlorinated. Thus, having one or two cases at a time caused by a pool exposure may be much more common than the outbreaks in which there are enough cases to draw attention to the pool.
The remarkably higher incidence of E. coli O157:H7 infections in 1-4 year old children than in other age groups has been seen repeatedly in the United States and is attributed largely to the very low infectious dose of E. coli O157:H7, which facilitates person-to-person spread7. Children in this age group either wear diapers or are recently toilet trained, and may be more likely than persons in other age groups to have fecal contamination of their hands. They are just learning about personal hygiene and to be careful about what they put in their mouths, they are in frequent intimate contact with their peers and their parents, and they often attend day care centers where diseases with person-to-person transmission spread easily. The relatively high incidence of E. coli O157:H7 infection and of HUS in children 1-4 years of age makes prevention of the infection in this age group a priority.
In 1993-2003 the incidence of E. coli O157:H7 infections was almost three fold lower in Georgia's African-American population than in the white population. It is not explained by differences in incidence in the northern and southern parts of the state, and the white population's much higher incidence among children is less marked in the AfricanAmerican population. Potential explanations that deserve further investigation include possible differences in foods eaten, food preparation customs, childcare and child rearing practices, and differences in completeness of case identification and reporting. Scattered data suggest that differences in consumption of rare or raw beef may be an important factor. A Behavioral Risk Factor Surveillance System (BRFSS) survey in eight states in 1995-1996 found that 22.3% of white subjects but only 6.5% of black subjects reported having eaten pink hamburgers during the previous 12 months8. Subsequently, a 2001 Georgia BRFSS survey of 18-44 year old women found that 32.3% of white women but only 3.0% of black women reported having eaten meat that was rare, raw, undercooked, or pink or red in the middle during the previous 12 months9.
The reason for the concentration of reported cases of E. coli O157:H7 infections in northern Georgia is unknown. The differences seen are too great to be explained solely by the larger proportion of African-Americans in the south, with their lower incidence of E. coli O157:H7 infection. Other factors may include food distribution patterns (e.g., ground beef from different sources), food preparation customs (e.g., how well meat is cooked and frequency of consumption of uncooked vegetables that can be cross-contaminated), childcare patterns (e.g., frequency of use of large day care centers), and differences in completeness of case identification and reporting.

Our data show that PFGE is highly useful in attempting to understand the epidemiology of E. coli O157:H7 infections. It helped health authorities to identify outbreaks, and it also enabled them to rule out outbreaks when cases occurred at the same time but had different PFGE patterns, saving time that might have been needlessly devoted to futile attempts trying to find links between the cases. A new challenge is the availability and increasingly widespread use of a relatively inexpensive stool test for Shiga toxin that does not require a stool culture, providing a diagnosis for the clinician but no isolate for identification and PFGE. Identification is important because E. coli O157:H7 is not the only pathogenic E. coli that can produce Shiga toxin. We encourage laboratories to use the Shiga toxin test to screen stools, and then, for those few that are positive, send the original sample or broth to the Georgia Public Health Laboratory for culture for Shiga toxin-producing E. coli and to perform PFGE.
This article was written by Ronny Grana, M.D.*, Stepy Thomas, M.S.P.H., and Paul A. Blake, M.D., M.P.H.
*CDC epidemiology elective student from University of Bergen Faculty of Medicine, Bergen, Norway.
REFERENCES 1. Gilbert L, Blake P. Outbreak of Escherichia coli O157:H7 infections
associated with a water park. Georgia Epidemiology Report, Vol 14, No 7, July 1998, pp 1-2. 2. Friedman MS, Roels T, Koehler JE, Feldman L, Bibb WF, Blake PA. E. coli O157:H7 outbreak associated with an improperly-chlorinated swimming pool. Clin Infect Dis 1999;29:298-303. 3. Centers for Disease Control and Prevention. Foodborne Diseases Active Surveillance Network (FoodNet): Population Survey Atlas of Exposures: 2000. Atlanta: Centers for Disease Control and Prevention; 2000: 8-25. 4. CDC. Preliminary FoodNet Data on the Incidence of Infection with Pathogens Transmitted Commonly Through Food -- Selected Sites, United States, 2003;53:338-343. 5. Hancock DD, Besser TE, Rice DH, Herriott DE, Tarr PI. A longitudinal study of Escherichia coli O157 in fourteen cattle herds. Epidemiol Infect 1997;118:193-5. 6. Zhao T, Doyle MP, Zhao P, Blake P, Wu F-M. Chlorine inactivation of E. coli O157:H7 in water. J Food Protection 2001;64:1607-9. 7. Griffin PM, Tauxe RV. The epidemiology of infections caused by Escherichia coli O157:H7, other enterohemorrhagic E. coli, and the associated hemolytic uremic syndrome. Epidemiol Rev 1991;13:6098. 8. Yang S, Leff MG, McTague D, et al. Multistate surveillance for food-handling, preparation, and consumption behaviours associated with foodborne diseases: 1995 and 1996 BRFSS food-safety questions. In CDC Surveillance Summaries, September 11, 1998. MMWR 1998;47(No. SS-4):33-57. 9. Georgia BRFSS, July-December 2001, Women 18-44. Unpublished data, personal communication from Linda Martin, MS, MPH, Epidemiology Branch, Division of Public Health, Georgia Department of Human Resources, 2 Peachtree Road NW, Atlanta, GA 30303.

Division of Public Health http://health.state.ga.us
Stuart T. Brown, M.D. Acting Director
State Health Officer

Epidemiology Branch http://health.state.ga.us/epi
Paul A. Blake, M.D., M.P.H. Director
State Epidemiologist
Mel Ralston Public Health Advisor

Georgia Epidemiology Report Editorial Board
Carol A. Hoban, M.S., M.P.H. Editor
Kathryn E. Arnold, M.D. Paul A. Blake, M.D., M.P.H. Susan Lance, D.V.M., Ph.D.
Stuart T. Brown, M.D. Angela Alexander - Mailing List Jimmy Clanton, Jr. - Graphic Designer

-3 -

Division of Public Health Two Peachtree St., N.W. Atlanta, GA 30303-3186 Phone: (404) 657-2588 Fax: (404) 657-7517

Georgia Department of Human Resources

Please send comments to: Gaepinfo@dhr.state.ga.us

The Georgia Epidemiology Report Epidemiology Branch Two Peachtree St., NW Atlanta, GA 30303-3186

PRESORTED STANDARD U.S. POSTAGE
PAID ATLANTA, GA PERMIT NO. 4528

February 2005

Volume 21 Number 02

Reported Cases of Selected Notifiable Diseases in Georgia Profile* for November 2004

Selected Notifiable Diseases
Campylobacteriosis Chlamydia trachomatis Cryptosporidiosis E. coli O157:H7 Giardiasis Gonorrhea Haemophilus influenzae (invasive) Hepatitis A (acute) Hepatitis B (acute) Legionellosis Lyme Disease Meningococcal Disease (invasive) Mumps Pertussis Rubella Salmonellosis Shigellosis Syphilis - Primary Syphilis - Secondary Syphilis - Early Latent Syphilis - Other** Syphilis - Congenital Tuberculosis

Total Reported for November 2004
2004 57
1809 11 3 57 851 9 8 54 3 0 1 0 5 0 146 53 2 7 4 14 0 37

Previous 3 Months Total

Ending November

2002

2003 2004

177

114

153

9014

8854

6724

34

34

62

6

5

7

244

241

194

4894

4366

3190

22

20

14

117

366

58

114

180

147

9

9

6

1

0

0

7

7

5

0

1

2

5

5

7

0

0

0

680

727

616

772

218

169

26

34

9

99

121

37

205

152

26

196

225

70

1

0

0

131

137

113

Previous 12 Months Total

Ending in November

2002

2003

2004

657

637

590

34552

35999

31698

129

118

200

45

30

25

898

866

817

18946

17812

14367

97

76

115

509

799

341

467

678

616

20

35

41

5

10

13

34

33

21

2

3

2

27

32

30

0

0

1

1967

2038

1977

1818

1325

666

110

127

100

328

452

353

746

735

314

778

870

545

14

11

4

603

529

542

* The cumulative numbers in the above table reflect the date the disease was first diagnosed rather than the date the report was received at the state office, and therefore are subject to change over time due to late reporting. The 3 month delay in the disease profile for a given month is designed to minimize any changes that may occur. This method of summarizing data is expected to provide a better overall measure of disease trends and patterns in Georgia.

** Other syphilis includes latent (unknown duration), late latent, late with symptomatic manifestations, and neurosyphilis.

AIDS Profile Update

Report Period
Latest 12 Months: 02/04-01/05 Five Years Ago: 02/00-01/01 Cumulative: 07/81-01/05

Total Cases Reported* <13yrs >=13yrs Total

7

1,565 1,572

8

1,140 1,148

223

28,000 28,223

Percent Female
26.8
27.7
19.1

Risk Group Distribution (%) MSM IDU MSM&IDU HS Blood Unknown

31.9

6.3

2.2

12.5

1.6

45.6

31.6

11.8

2.6

18.6

2.3

32.2

45.7

16.2

5.0

14.3

1.9

17.0

Race Distribution (%) White Black Other

20.9 76.7

2.4

19.1 76.8

4.1

32.1 65.3

2.6

MSM - Men having sex with men

IDU - Injection drug users

HS - Heterosexual

* Case totals are accumulated by date of report to the Epidemiology Section

- 4 -