Shigatoxin-producing Escherichia coli
Bacteria of the species Escherichia (E.) coli are part of the normal intestinal flora in humans and animals. If they acquire the ability to produce a specific toxin, shiga toxin, they are called shiga toxin-producing E. coli (STEC) after this toxin. STEC are sensitive to heat but survive in frozen foods and in acidic environments. The terms verotoxin-forming E. coli (VTEC) and enterohemorrhagic E. coli (EHEC) are used as synonyms for STEC. These pathogenic types can also cause fatal diseases.
Transmission of the bacteria occurs mainly through the consumption of contaminated food, such as raw beef mince, Mettwurst, salami, raw milk, but also plant foods cultivated on fields fertilized with cattle manure and consumed raw, as well as industrially produced sprouts. Of importance are transmissions after contact with ruminants (petting zoos), if no appropriate cleaning of the hands (hand washing with soap) is carried out afterwards, as well as human-to-human chains of infection, which is to be observed especially in community facilities (kindergartens, old people's homes, etc.). It is assumed that 50-100 STEC germs are sufficient to cause the disease in healthy people.
The disease usually begins with watery diarrhea, which often becomes bloody after a few days and may be accompanied by severe nausea, vomiting and abdominal pain. The disease is predominantly self-limiting and lasts on average eight to ten days. In about 5-10% of cases, especially in young children, a characteristic secondary disease, the life-threatening hemolytic uremic syndrome (HUS), may develop days after the onset of diarrhea. The toxin binds to special receptors on the cell walls and damages blood capillaries; this can lead to kidney failure (lack of urine formation), anemia, reduced platelet count, skin hemorrhages and neurological changes.
Animals: calf diarrhea may occasionally be (co-)caused by STEC. STEC can also sporadically cause diarrhea in lambs, goats, dogs, and cats. In pigs, a subtype of STEC causes the so-called edema disease.
Treatment with antibiotics is generally considered contraindicated because the bacteria produce increased toxin when exposed to antibiotics, which can increase the complication rate. Therapy that rebalances the water and electrolyte balance is usually sufficient. In severe cases (e.g., HUS), intensive medical treatment is required, such as blood washing.
Since ruminants and wild ruminants are considered to be the reservoir of these bacteria, strict adherence to hygiene regulations, e.g. washing hands after animal contact, is of great importance. Persons who have contracted STEC infections must not be employed in the commercial production, handling or marketing of foodstuffs until a decision by the health authority indicates that they are no longer likely to spread the disease. This also applies mutatis mutandis to employees in kitchens of restaurants, canteens, hospitals, infant and children's homes and in communal catering areas.
In 2021, 384 laboratory-confirmed STEC cases were reported to the Epidemiologic Reporting System (EMS) (EMS, as of 03/01/2022). The incidence is thus 4.3/100,000 population. The increase in cases since 2016 is primarily due to the increased use of culture-independent detection methods in laboratories, which means that more patient samples are also being tested for STEC. The severe complication HUS occurred in 18 patients; this number of cases corresponds to the long-term average.
Foodborne disease outbreaks
In 2021, four foodborne illness outbreaks (LMbKA) caused by STEC were reported in Austria. Fourteen persons were affected, two of whom had to be treated in hospital. The sources of infection were named once each as beef and beef products, tap water or spring water, sweets and chocolate, and once unknown. This number of outbreaks is consistent with the long-term average; in the past 10 years, a total of 31 foodborne illness outbreaks due to STEC have been reported.
In 2021, approximately 1,100 food samples were tested for STEC, primarily meat and meat preparations (approximately 600 samples), ready-to-eat foods (approximately 80 samples), and milk and dairy products (approximately 220 samples). STEC were detected in 25 samples, including 10 times in fresh venison.
Meat: STEC were found in 13 of 150 raw meat samples (of different animal species, including game meat), with these pathogens detected mainly in meat samples from wild animals (10 of 61 samples). No STEC were found in any fresh beef sample (n = 51), but STEC were found in one minced meat sample.
Milk: STEC were detected in one sheep raw milk sample, all other milk products were STEC negative.
Four STEC strains could be isolated from baking mixes, prepared doughs and flour (n=129).
Based on their antigen structure, E. coli, and thus also STEC, can be classified into different serogroups (O-like surface antigens "without puff"). The most important STEC serogroup worldwide is O157. Other frequently isolated serogroups are O26, O91, O103, O111, and O145. More and more serogroups could be identified in association with human STEC diseases.
In addition, there are two types of shigatoxins, Stx1 and Stx2. The shiga toxin (stx) genes can be further subdivided into subtypes (stx1a to stx1c and stx2a to stx2i). Severe disease, especially bloody diarrhea and complications such as HUS, are mainly caused by stx2-positive STEC strains.
Diagnosis is made after clinical suspicion at the National Reference Center for Escherichia coli, including verotoxin-producing E. coli , by detection of a verotoxin gene or cultural culturing of the germs, by detection of verotoxin in stool, or (for HUS only) by detection of specific antibodies in blood:
- Detection of enteroinvasive E. coli (EIEC), enteropathogenic E . coli (EPEC), enterotoxic E. coli (ETEC), enteroaggregative E. coli (EAggEC), and STEC in human stool specimens.
- Isolation and cultural detection of STEC from human stool, food, and environmental samples using selective nutrient media, immunomagnetic separation, slide agglutination, and PCR
- Confirmation and typing of submitted isolates using biochemical and molecular biology methods
- Fine typing of STEC: typing of shigatoxin genes (PCR), subtyping of shigatoxin genes and typing of other virulence genes (whole genome sequencing)
- Identification of epidemiological correlations of different isolates using whole genome sequencing data
- Detection of specific antibodies in HUS in human serum
- Keeping a master collection of all human, veterinary, feed and food isolates
- Clarification of sources of infection and transmission routes in the context of outbreak investigations
- Consultation on questions of diagnostics, compulsory reporting, epidemiology, food safety, prevention and preventive measures.
STEC strains that express F18ab fimbriae as specific virulence factors in addition to Stx2e (shiga toxin 2e) appear as pathogens of edema disease (colienterotoxemia).
After weaning of piglets, excessive STEC multiplication in the small intestine may be favored by profound changes in the physiological conditions of the intestine. Stx2e leads to swelling in the tissues (edema) due to vascular damage, typically in the head area especially on the eyelids and on the bridge of the nose and also in the nervous tissue, which can also lead to central nervous phenomena (disturbance in the coordination of muscle movements, paralysis). Treatment of clinically ill animals is often no longer successful. Great importance is attached to metaphylaxis, in the course of which all animals of the affected group are treated non-specifically (e.g. feed deprivation, abundant water supply, possibly oral or parenteral chemotherapy). For prevention, herd-specific vaccines can be administered.
Last updated: 20.07.2022