New STEC in Europe
E.coli O104:H4, Germany
- updates from Robert Koch Institute, Germany
- European CDC
- Centers for Disease Control
- European Food Safety Authority investigation implicates fenugreek seeds from Egypt
- fast track Lancet report on outbreak strain of STEC
49 deaths, 852 HUS cases, > 4000 infections, fewer new cases
- first take on the genetic origins of the new STEC in Europe
- interest in bean sprouts persists following latest food test results
- bean sprouts notconsumed by all victims of European STEC outbreak (details from Robert Koch Institute, translated courtesy CIDRAP). Further epidemiological survey analysis neededmap of HUS case distribution
- de novo assembly of genome sequence announced by Beijing Genomics Institute collaboration with University Medical Centre Hamburg-Eppendorf
- 27 deaths, 757 cases of HUS, 2142 infected, new cases diminishing. HUS peaked 21-MAY-11
- EU agriculture ministers consider 150m Euro compensation bill for European farmers, though damage to industry estimated at twice that sum
- Australian beef ruled out as cause of Japanese outbreak
- first round of STEC environmental tests negative from farm near Hamburg, Germany. Other results pending.
- reports that outbreak has been traced organic bean shoots from Germany
- update on the new STEC in Europe from the Centers for Disease Control
Reports of a European cluster of haemorrhagic uraemic syndrome (HUS) caused a stir in late May. European surveillance groups reported that this was caused by a verotoxin-bearing E.coli strain with the designation O 104:H4 that also had entero-aggregating and antibiotic resistance features. This combination of virulence and resistance is a genuinely new and potentially worrying development. Other notable differences with this infection are the predominance of adult female cases, subtle neurological complications and a longer than usual incubation period of 7-12 days. Australia is now on the lookout for cases closer to home, though none have been confirmed so far.
So far over 2000 cases, over 600 of which have had HUS and 22 deaths have been attributed to the infection in 11 countries, which was initially blamed on Spanish cucumbers and other vegetables including tomatoes and lettuce. More recent claims have been made that bean sprouts were the likely source. Further afield in Japan, Australian beef was blamed for similar infections following cooking in Korean barbecues though the MicroGnome has yet to learn of any convincing evidence.
Meanwhile, additional details come to light as a result of more discriminating laboratory tests, food investigations and heightened surveillance. The Centers for Disease Control reported infection in US citizens and the European CDC has started to regularly update the earlier data.
- The process of outbreak investigation is a complex one, requiring the assembly of different types of data from different sources gathered according to differing time lines. The preliminary stage gathers data from clinical cases and pathology laboratories, molecular biology tests, epidemiological surveillance and environmental health investigations. The overlap from these three main sources of data is critical to understanding the disease event. We refer to this as level 1 evidence, or congruence.
- When a similarly well-defined pattern of patient-microorganism-disease occurs at another time or location and not by simple extension of the original event, the evidence for causation strengthens to level 2, or consistency.
- Level 3 evidence concerns the decomposition of the patient-microorganism-disease process into is constituent parts at progressive levels of biological organisation i.e. molecular, cellular, tissue biology, organs & organ systems, whole patient, patient groups and the localisation of specific aspects of that process in order to establish a mechanistic understanding of disease outcomes. This level of evidence for causation is known as cumulative dissonance.
- The final level of evidence is curtailment. This concerns the use of specific interventions targeting one or more potential vulnerable stages in the progressive escalation of an infectious disease process, and highlights the aetiological significance of practical objectives to physicians and public health authorities.
The current data on the E.coli O104:H4 case cluster consists of strong but incomplete level 1 evidence, possible level 2 and 3, but a lack of level 4 evidence. That does not mean that curtailment of a potentially fatal food-borne infection has to wait until development of a full description of E.coli O104:H4’s actions at every level of biological organisation.
Clearly, identification of a specific contaminated food as the critical element in the genesis of this outbreak should lead to prompt introduction of control measures. Subsequent disappearance of the infection after these measures have been introduced establishes the food as a sufficient, but not as a necessary cause. Only when the evidence for causality has been strengthened by the missing items from levels 1, 2 and 3 will it be possible to fully understand the sequence of events that conspired to end in these sad consequences.
- Eurosurveillance report, Robert Koch Institute, Germany
- European E.coli O104:H7 surveillance
- World Health Organization IHR updates
- Centers for Disease Control & Prevention reports on E.coli O104:H7