E. coli 0104:H4 Infections Originating in Germany
E. coli strain (0104:H4) is similar to the 0157:H7 strain. In the spring of 2011, the E. coli 0104:H4 strain was identified in Germany and was documented in 15 European countries. In most people, exposure to the infection occurred in Germany, most likely when they ate contaminated food (salads). The strain has been identified as E. coli 0104:H4 (also termed STEC 0104:H4).
E. coli 0104:H4 seems to exhibit some of the worst overlap features in the diseases caused by ECC group members. For example, E. coli 0104:H4 is reported to contain about 93% of E. coli 0157:H7 genetics and produces the Shiga (Vero) toxin and many patients (about 30%) developed HUS. However, it also seems to have the ability like EAEC strains to attach to the gastrointestinal cells. The outbreak was one of the largest ever reported for E. coli (4,075 infected patients) and was the most lethal (50 deaths). In addition, most strains isolated were resistant to multiple antibiotics (aminoglycosides, macrolides, and Beta-lactams).
The source of the infection was considered contaminated bean sprouts and other seeds grown organically and then shipped to many German restaurants. One major difference in E. coli 0104:H4 from other E. coli that cause HUS (mainly E. coli 0157:H7) is that the organism causes HUS in adults, particularly young adult females. Usually, HUS caused by E. coli 0157:H7 is seen in children, the elderly, and the relatively not healthy adults. This strain caused 908 infections complicated by HUS.
The diagnosis, treatment, prognosis, prevention, and complications are very similar to those listed in this article for E. coli 0157:H7.
The most recent guidelines from the CDC are as follows:
The strain of E. coli O104:H4 causing the outbreak is resistant to many antibiotics, because it has many genes that code for that resistance. Since CDC doesn’t recommend that STEC infections be treated with antibiotics, the fact that this strain is antibiotic resistant is not likely affect the care that sick people receive. The presence of these genes simply means that the bacteria were likely, at some point in the past, to have been in environment with antibiotics in it. Other bacteria occur with this level of resistance. There is no reason to think that this strain has been modified intentionally to be antibiotic resistant.
Guidelines to ensure as complete as possible detection and characterization of STEC infections include the following:
- All stools submitted for testing from patients with acute community-acquired diarrhea should be cultured for STEC O157:H7. These stools should be simultaneously assayed for non-O157 STEC strains with a test that detects the Shiga toxins or the genes encoding these toxins.
- Clinical laboratories should report and send E. coli O157:H7 isolates and Shiga toxin-positive samples to state or local public health laboratories as soon as possible for additional characterization.
- Specimens or enrichment broths in which Shiga toxin or STEC are detected, but from which O157:H7 STEC isolates were not recovered, should be forwarded as soon as possible to a state or local public health laboratory so that non-O157:H7 STEC strains (including STEC 0104:H4) can be isolated.
- Often, by the time a patient presents with HUS, the causative STEC can no longer be easily isolated from a stool specimen. For any patient with HUS without a culture-confirmed STEC infection, stool can be sent to a public health laboratory or to the CDC through their public health laboratory for immunomagnetic separation (IMS) techniques that can increase the sensitivity of culture. In addition, with prior approval, serum can be sent through a state public health laboratory to the CDC for serological testing for antibodies to some STEC serogroups.
The benefits of adhering to the recommended testing strategy include early diagnosis, improved patient outcome, and detection of all STEC serotypes.
All patients with Shiga toxin-positive diarrheal illness or HUS should be reported to health departments.