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Published Date: 2011-06-24 15:19:20
Subject: PRO/AH/EDR> E. coli O104 - EU (23): updates
Archive Number: 20110624.1940

E. COLI O104 - EUROPEAN UNION (23): UPDATES
*******************************************

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In this update:
[1] ECDC update
[2] Ischemic colitis/neurological symptoms without HUS
[3] Netherlands ex Germany, secondary transmission
[4] Probable USA ex Germany fatality

******
[1] ECDC update
Date: Thu 23 Jun 2011
Source: ECDC [edited]
http://www.ecdc.europa.eu/en/activities/sciadvice/Lists/ECDC%20Reviews/ECDC_DispForm.aspx?List=512ff74f%2D77d4%2D4ad8%2Db6d6%2Dbf0f23083f30&ID=1120&RootFolder=%2Fen%2Factivities%2Fsciadvice%2FLists%2FECDC%20Reviews

News since 22 Jun 2011, 11:00: in the EU/EEA, 862 HUS [hemolytic
uremic syndrome] cases, including 30 deaths, and 2930 non-HUS cases,
including 13 deaths, have been reported so far. Today, 22 Jun 2011,
Germany reports 8 additional HUS cases and 2 new HUS deaths. It also
reports 79 additional non-HUS STEC cases and 1 new non-HUS death.
Sweden reports 3 additional non-HUS STEC cases who visited Germany
mid-May. The latest known date of onset of diarrhea for cases is 16
Jun 2011.

Total cases: 3792 with 43 deaths -- 1.13 per cent case fatality
rate.

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[By noting the EU number of cumulative cases of HUS and non-HUS cases
and their total as well as deaths, the daily rise of the numbers can
be seen:

Date (2011): New HUS / New non-HUS / New Total / Overall Total
Deaths
Mon 6 Jun: 3 / 67 / 70 / 22
Tue 7 Jun: 13 / 83 / 96 / 23
Wed 8 Jun: 48 / 266 / 314 / 25
Thu 9 Jun: 35 / 121 / 156 / 27
Fri 10 Jun: 38 / 115 / 153 / 31
Sat 11 Jun: 14 / 177 / 191 / 35
Sun 12 Jun: 0 / 40 / 40 / 35
Mon 13 Jun: 8 / 34 / 42 / 36
Tue 14 Jun: 1 / 6 / 7 / 36
Wed 15 Jun: 3 / 17 / 20 / 37
Thu 16 Jun: 2 / 48 / 50 / 39
Fri 17 Jun: 14 / 92 / 106 / 39
Mon 20 Jun: 12 / 74 / 96 / 40
Tue 21 Jun: 4 / 89 / 93 / 40
Wed 22 Jun: 8 / 79 / 87 / 43

[A 44th death is now reported from Germany. With many less new cases
occurring (although the last case so far was only a week ago) and a
substantial number of patients still quite ill, the case fatality rate
will rise. A fatal case from the USA, most likely due to the epidemic
strain acquired in Germany is posted below.

The cases do not necessarily reflect date of onset of disease but
rather when the diagnosis was made and reported. The number of newly
reported cases per day clearly decreased from the corresponding day in
the previous week. - Mod.LL]

******
[2] Ischemic colitis/neurological symptoms without HUS
Date: Thu 23 Jun 2011
Source: Eurosurveillance edition 2011; 16(25) [edited]
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19895

Colonic ischaemia as a severe Shiga toxin/verotoxin producing _E.
coli_ O104:H4 complication in a patient without HUS, Germany, June
2011
---------------------------------------------------------
[authors: S Cordesmeyer, U Peitz, N Goedde, et al]

We report a Shiga toxin/verotoxin producing _Escherichia coli_
(STEC/VTEC) O104:H4 case without HUS, presenting with colonic ischemia
demanding surgery. This atypical clinical presentation of STEC O104:H4
infection might indicate new severe complications associated with this
uncommon strain, and highlights the importance of immediate
interdisciplinary assessment of STEC/VTEC patients.

Clinical presentation and initial evaluation
--------------------------------------------
A woman in her 80s presented to our emergency department on 1 Jun
2011 with increasing abdominal pain and a history of nausea, primarily
associated with dysuria that had been lasting for 5 days. On 29 May
2011, the day after the onset of those symptoms, non-bloody diarrhea
had followed. The initial physical examination showed a mildly
distended abdomen with diffuse pain and left upper quadrant tenderness
without rebound. Blood tests showed a massive elevation of white blood
cell count (29 300/microL; normal range: 4300-10 000/microL) as well
as an elevation of both C-reactive protein and lactate. Ultrasound and
computed tomography (CT) scans of the abdomen revealed distinctive
amounts of ascites and wall thickening of parts of the transverse and
descending colon, but did not show any disturbance of the main
arteries and veins. Considering pseudomembranous colitis as a
differential diagnosis, we decided to perform a colonoscopy.

The endoscopy showed a normal rectum and sigmoid colon,
macroscopically. The descending colon had a circularly swollen, partly
pale, partly bluish mucosa, with no evidence of bleeding after biopsy,
a combination of symptoms highly suspicious of ischemia (Figure 1 --
for all figures, see source URL - Mod.LL]).

Surgical intervention
---------------------
Following the confirmation of ischemia by endoscopy of the descending
colon on 1 Jun 2011, surgery was performed immediately. Non-occlusive
ischemia of the descending colon with gangrenous bowel wall was
detected during the operation, with patent macroperfusion of the
medial colic artery and inferior mesenteric artery arcade, as well as
the left colic artery up to the gangrenous bowel wall. Therefore, a
left hemicolectomy was performed, followed by thorough abdominal
irrigation.

Pathology
---------
Pathological examination of the removed part of the colon revealed
wall thickening up to 1 cm and extensive necrosis throughout the
entire intestinal wall with fibrinous-purulent exudation. The border
area showed vital mucosa with erosive and phlegmonous inflammation,
membranous-like fibrin exudation and crypt destruction, consistent
with an ischemic origin (Figures 2 and 3).

Postoperative course
--------------------
After the operation, which occurred late in the evening on 1 Jun
2011, the patient was admitted to the intensive care unit. The next
morning, as a precautionary measure, due to the ongoing Shiga
toxin/verotoxin-producing _E. coli_ (STEC/VTEC) O104:H4 outbreak in
Germany, the patient was placed in isolation and a stool sample was
sent for further evaluation. The 2nd day after surgery, 7 days after
the onset of the initial abdominal symptoms, neurological impairments
were observed in terms of decelerated reactions of the patient, lack
of orientation, and intermittent response when addressed. Clinical
examination was uneventful for abdominal, respiratory, and hemodynamic
findings. Laboratory studies were not suspicious for haemolytic uremic
syndrome (HUS). The patient was monitored closely and improved
neurologically during the next day. During the following 48 hours,
however, noticeable neurological deficiencies with disturbance of
vigilance, aphasia, and apraxia were observed, as well as myoclonia of
the extremities. Seizures did not occur. PCR analysis of the stool
samples confirmed Shiga toxin 2-producing _E. coli_ consistent with
the strain responsible for the current outbreak, O104:H4, on 6 Jun
2011. Monitoring the patient for an onset of HUS continued but has not
eventuated as of 21 Jun 2011.

Discussion
----------
The ongoing outbreak of infections with STEC/VTEC, also commonly
referred to as enterohemorrhagic _E. coli_ (EHEC), in Germany is one
of the largest worldwide (1). Besides causing non-bloody and bloody
diarrhea, the STEC/VTEC subtypes may also lead to HUS, a severe
complication that is characterized by thrombocytopenia,
microangiopathic haemolytic anaemia, and decreased renal function. So
far, _E. coli_ O157:H7 had been described as the predominant serotype
causing HUS in approximately 10 per cent of all cases to date (2,3),
whereas the strain responsible for the current outbreak, which has
been identified as _E. coli_ O104:H4, is an extremely rare strain,
hardly described during the last decade (4). With adults and
predominantly women being infected, the age and sex distribution in
the ongoing outbreak is unusual, but might be related to
gender-specific differences in dietary habits: vegetables, which are
generally more often consumed by women, are still suspected to have
been contaminated and at the source of this outbreak. In addition, an
unusually high number of patients have developed HUS: The latest data
account for 814 patients with HUS from a total of 3587 infected
patients in Germany (1). Neurological complications, which were seen,
on average, in about 25 percent of HUS patients in former outbreaks
(2), could also be more severe in this outbreak. Indeed, the exchange
among German clinicians, who set up a web-based platform to
communicate clinical information in the context of the current
outbreak, indicates higher numbers, but this has not been
systematically evaluated so far. Taken together, the various aspects
of the ongoing outbreak may suggest an increased virulent potential of
the identified strain.

Besides HUS, STEC/VTEC-associated bowel ischemia, as an additional
severe complication, is rarely described in the literature. Very few
reports of colonic necrosis and perforation due to Shiga toxin-induced
intestinal damage exist, and in all these reports, this type of
complication affected _E. coli_ O157:H7-infected individuals. This
complication was moreover mostly encountered in pediatric patients
with concomitant HUS (3). Only 1 case of ischemic colitis in a non-HUS
adult has been previously described (5).

Conclusion
----------
Besides leading to its major complication HUS, infection with
STEC/VTEC O104:H4 can also cause neurological complications and
atypically present as bowel ischemia, as shown in our patient. Since
ischemia-induced colonic wall thickening is difficult to differentiate
from pseudomembranous colitis in CT imaging, endoscopy is essential
and should be considered at an early diagnostic stage. Notably, our
patient has not shown any signs of HUS to date, but obviously, even
unexpected complications have to be considered as a differential
diagnosis in STEC/VTEC O104:H4 infected patients, calling for
interdisciplinary diagnostic investigations.

References
----------
1. Informationen zum EHEC/HUS Ausbruchsgeschehen. [Information on the
EHEC/HUS outbreak events]. Data from 20 Jun 2011, 3 pm. Berlin: Robert
Koch Institut; 21 Jun 2011, 11 am. German. Available from
http://www.rki.de/cln_116/nn_205760/DE/Home/Info-HUS.html.
2. Enterohemorrhagic _Escherichia coli_. Factsheet no 125. Revised
May 2005. WHO. Geneva. Available from
http://www.who.int/mediacentre/factsheets/fs125/en/.
3. Karch H, Tarr PI, Bielaszewska M: Enterohaemorrhagic _Escherichia
coli_ in human medicine. Int J Med Microbiol. 2005; 295(6-7): 405-18
[abstract available from
http://www.ncbi.nlm.nih.gov/pubmed/16238016].
4. Scheutz F, Moller Nielsen E, Frimodt-Moller J, et al.
Characteristics of the enteroaggregative Shiga
toxin/verotoxin-producing _Escherichia coli_ O104:H4 strain causing
the outbreak of hemolytic uremic syndrome in Germany, May to June
2011. Euro Surveill. 2011; 16(24): pii=19889. Available from
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19889.
5. Kravitz GR, Smith K, Wagstrom L. Colonic necrosis and perforation
secondary to _Escherichia coli_ O157:H7 gastroenteritis in an adult
patient without hemolytic uremic syndrome. Clin Infect Dis. 2002;
35(9): e103-5 [Abstract available from
http://www.ncbi.nlm.nih.gov/pubmed/12384855].

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[Several observations in this case report are quite interesting.
Since 13 of 2930 cases of non-HUS cases in this epidemic have died
(CFR=0.44 per cent), were these deaths related to ischemic colitis as
well? In addition, it is unusual to have prominent neurologic symptoms
in the absence of lab evidence of HUS. It will be interesting to
review the symptoms of the overall non-HUS cases in this epidemic to
see if other cases also demonstrated neurological symptomatology. -
Mod.LL]

******
[3] Netherlands ex Germany, secondary transmission
Date: Thu 23 Jun 2011
Source: Eurosurveillance edition 2011; 16(25) [edited]
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19897

Household transmission of haemolytic uraemic syndrome associated with
_Escherichia coli_ O104:H4 in the Netherlands, May 2011
------------------------------------------
[authors: EJ Kuijper, D Soonawala, C Vermont, JT van Dissel]

Since early May 2011, one of the largest ever reported outbreaks of
hemolytic uremic syndrome (HUS) and bloody diarrhea caused by Shiga
toxin/verotoxin-producing _E. coli_ (STEC/VTEC), also referred to as
enterohemorrhagic _E. coli_ (EHEC) has affected Germany (1). The
outbreak strain was identified as an enteroaggregative Shiga
toxin-producing _E. coli_ O104: H4 (EAggEC) (2). Initial findings
suggested raw vegetables and salads as vehicle of infections and
recommendations were made to abstain from these products.
Epidemiological investigations implicated an organic sprout farm in
Lower Saxony near Hamburg as the potential source of the outbreak (3).
On 10 Jun 2011, German public health and food safety authorities
issued a joint statement recommending people to abstain from consuming
sprouts. A decrease in the number of new cases was seen after 6 Jun
2011 (4).

We describe here 2 cases of HUS and hemorrhagic colitis that occurred
in the Netherlands and were associated with the outbreak in Germany.

Case descriptions
-----------------
Patient A:
On 24 May 2011, a woman in her 30s was admitted to a hospital in the
Netherlands with bloody diarrhea and abdominal pain of 2 days. Common
bacterial gastroenteritis was considered and no antibiotic treatment
was initiated. 4 days after admission, blood examination revealed
severe HUS. The patient was transferred to the Leiden University
Medical Centre (LUMC) for hemodialysis which eventually proved not to
be necessary.

A tentative diagnosis of HUS due to Stx1-negative, Stx-2 positive,
extended spectrum beta-lactamase (ESBL)-producing _E. coli_ was
confirmed by culture on sorbitol MacConkey agar of a stool sample
collected 2 days after admission to the 1st hospital. Further
identification of _E. coli_ serotype O104 was performed at the Dutch
National Institute for Public Health and the Environment (RIVM). A
real-time PCR for Stx2 directly in stool sample was also positive (5).
Stool samples on admission to LUMC were already negative in culture
and real-time PCR. Since 30 May 2011, the patient has gradually been
recovering from HUS.

Patient A had travelled to Northern Germany for 2 days in May 2011,
accompanied by 6 relatives, among them her 10 month old child.

Patient B:
The 10 month old child of Patient A was examined first on 29 May
2011, a day after transfer of the mother to the LUMC. At the time, the
child had mild diarrhea free of blood, and blood examination did not
reveal any abnormality. A stool sample was collected and tested
positive for Stx2 in the real-time PCR. Culture revealed growth of
ESBL-positive _E. coli_ O104. On 30 May 2011, the child developed
fever and blood abnormalities compatible with HUS, and was admitted to
hospital. The next day, it developed neurological symptoms, that is,
seizures, and was transferred to a specialized child dialysis centre,
where experimental treatment with eculizumab was started. The patient
received prolonged mechanical ventilation and inotropic therapy. 3
weeks after transfer, the patient is still on dialysis and the
neurological outcome is unsure.

Family members
--------------
Of the other 5 relatives of Patients A and B who had also traveled to
Northern Germany, one developed mild diarrhea 16 days after their
return, but microbiological examinations were not performed since the
diarrhea resolved a day later and no HUS developed. The remaining
relatives did not develop any symptoms and were not investigated for
the presence of _E. coli_ O104.

Microbiological and public health implications
----------------------------------------------
HUS is a rare disease in the Netherlands, with approximately 20
patients per year (6). During the outbreak in Germany, 854 cases of
HUS and 2848 non-HUS STEC/VTEC cases have been reported as of 22 Jun
2011, of which 4.6 per cent and 2.2 per cent, respectively, were found
in other member states of the European Union (7). In the Netherlands,
4 HUS (including Patients A and B described here) and 5 non-HUS
laboratory-confirmed STEC/VTEC cases were detected. All acquired the
infection during a recent visit to Germany.

Microbiological examination of stool samples from Patient A gave
negative results in the real-time PCR and culture at the time of
transfer to another hospital when HUS had fully developed, 6 days
after disease onset, indicating the need to apply diagnostic tests
early in the disease. Similarly, Patient B had positive feces tests
and excreted the organism before hemorrhagic colitis and HUS
developed.

We hypothesize that Patient B probably acquired HUS by secondary
transmission within the household, because the child developed illness
15 days after return form Northern Germany. The child had spent much
time with her mother during her stay at the 1st hospital, when the
mother developed diarrhea. Before admission of the child to LUMC, the
mother had not been advised to take any specific hygienic measures.
The child was not breastfed at the time. The age of the child makes it
unlikely that it had eaten a food product such as sprouts.

Recently, a group of investigators reported that the strain causing
the outbreak in Germany is in fact not a typical virulent Shiga
toxin-producing _E. coli_ strain, but instead is a more rare, hybrid
pathotype that harbors the phage encoded the Shiga toxin gene in an
EAggEC background (2). These findings are relevant for understanding
the epidemiology since EAggEC is a common pathogen causing diarrhea in
travelers and persistent diarrhea in infants and young children living
in countries with poor sanitation. In contrast to STEC/VTEC strains,
which that have an animal reservoir, mostly ruminants, EAggEC strains
probably have a human reservoir only.

Secondary transmission frequently occurs in outbreaks caused by
classical EHEC O157. A review of 90 confirmed outbreaks in the UK,
Ireland, Scandinavia, Canada, the USA, and Japan revealed that
approximately 20 per cent of all outbreak cases were the result of
secondary spread (8). Interestingly, the spread was significantly
influenced by age and modes of transmission. A lower median age of the
index patients was associated with a higher rate of secondary cases
and household contacts aged 1 to 4 years were most likely to become
infected. Immediate separation of a pediatric patient from its
siblings when there is a clinical suspicion of STEC/VTEC O157
infection has been suggested as an important measure in the prevention
of secondary cases (9). Isolation of all symptomatic primary patients
immediately after they receive a microbiological diagnosis of
STEC/VTEC O157 infection could potentially decrease the number of
secondary household cases by 50 per cent (9). In this family however,
the primary case patient was an adult. Since young children usually
have extensive close contacts with their parents; separation of young
children from a parent with a suspected STEC/VTEC or _E. coli_ O104
infection should be considered in order to prevent secondary
transmission to the child.

References
----------
1. Frank C, Faber MS, Askar M, et al. Large and ongoing outbreak of
haemolytic uraemic syndrome, Germany, May 2011. Euro Surveill. 2011;
16(21): pii=19878. Available from
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19878.
2. Scheutz F, Moller Nielsen E, Frimodt-Moller J, et al.
Characteristics of the enteroaggregative Shiga
toxin/verotoxin-producing _Escherichia coli_ O104:H4 strain causing
the outbreak of haemolytic uraemic syndrome in Germany, May to June
2011. Euro Surveill. 2011; 16(24): pii=19889. Available from
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19889.
3. Joint statement issued by the Federal Institute for Risk
Assessment (BfR), Federal Office of Consumer Protection and Food
safety (BVL), Robert Koch Institute (RKI). Press release. Berlin: BfR,
Braunschweig: BVL, Berlin: RKI; 10 Jun 2011. Available from
http://ecdc.europa.eu/en/press/news/Documents/1106_Joint_Press_Release_German_authorities_issue_a_joint_statement.pdf.
4. Informationen zum EHEC/HUS-Ausbruchsgeschehen [Information on the
EHEC/HUS outbreak events]. Data from 21 Jun 2011, 10 pm. Berlin:
Robert Koch Institut; 22 Jun 2011, 11 am. German. Available from
http://www.rki.de/cln_160/nn_205760/DE/Home/Info-HUS.html.
5. Schuurman T, Roovers A, van der Zwaluw WK, et al. Evaluation of
5'-nuclease and hybridization probe assays for the detection of shiga
toxin-producing _Escherichia coli_ in human stools. J Microbiol
Methods. 2007; 70(3): 406-15 [Abstract available from
http://www.ncbi.nlm.nih.gov/pubmed/17614150].
6. Havelaar AH, Van Duynhoven YT, Nauta MJ, et al. Disease burden in
The Netherlands due to infections with Shiga toxin-producing
_Escherichia coli_ O157. Epidemiol Infect. 2004; 132(3): 467-84
[Available from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2870126].
7. European Centre for Disease Prevention and Control (ECDC).
Outbreak of Shiga toxin-producing _E. coli_ in Germany (22 Jun 2011,
11:00). Stockholm: ECDC; 22 Jun 2011. Available from
http://www.ecdc.europa.eu/en/activities/sciadvice/Lists/ECDC%20Reviews/ECDC_DispForm.aspx?List=512ff74f-77d4-4ad8-b6d6-bf0f23083f30&ID=1119&RootFolder=%2Fen%2Factivities%2Fsciadvice%2FLists%2FECDC%20Reviews.
8. Snedeker KG, Shaw DJ, Locking ME, Prescott R. Primary and
secondary cases in _Escherichia coli_ O157 outbreaks: a statistical
analysis. BMC Infect Dis. 2009; 9: 144 [Available from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2741466].
9. Werber D, Mason BW, Evans MR, Salmon RL. Preventing household
transmission of Shiga toxin-producing _Escherichia coli_ O157
Infection: promptly separating siblings might be the key. Clin Infect
Dis. 2008; 46(8): 1189-96 [Available from
http://cid.oxfordjournals.org/content/46/8/1189.long].

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[The exact mode of this presumed secondary transmission from mother
to infant is not clear. It may have occurred prior to the mother
becoming ill during food preparation for the infant or could have
occurred in the 1st hospital from patient (mother) to visitor
(infant).

Eculizumab, a humanized, monoclonal antibody against a complement
component was used in the infant. We await information regarding the
results of this open trials as well as the German experience with
antimicrobials such as imipenem and rifaximin that in vitro do not
appear to increase toxin production. - Mod.LL]

******
[4] Probable USA ex Germany fatality
Date: Thu 23 Jun 2011
Source: CBC (Canadian Broadcasting Corporation) News, Associated
Press (AP) report [edited]
http://www.cbc.ca/news/world/story/2011/06/23/germany-e-coli.html

The death of an Arizona resident who recently traveled to Germany may
be linked to the food poisoning outbreak in Europe, health officials
say. The Centers for Disease Control and Prevention on Thu 23 Jun
2011, said the death is under investigation. The Arizona resident had
a severe _E. coli_ complication that can lead to kidney failure. If
confirmed, it would be the 1st USA death tied to the outbreak [and 1st
death outside Europe. - Mod.LL].

So far, there have been 5 confirmed cases in the USA connected to the
outbreak. Those cases are in Michigan, Massachusetts, Wisconsin, and
North Carolina.

On Wed 22 Jun 2011, scientists said a mix of 2 dangerous _E. coli_
strains caused the recent deadly food poisoning outbreak, according to
a further study of the bacteria's DNA. Scientists said the _E. coli_
outbreak strain combined one that makes a toxin and another that
sticks to the gut in a way that potentially speeds up the body's
absorption of the toxin. They described it as "unprecedented" in its
lethality.

"The 2 strains are in themselves quite nasty," said Hugh Pennington,
an emeritus professor of microbiology at the University of Aberdeen,
who wrote an accompanying commentary on the research. "It may be that
more of the bugs are sticking to the intestines, and that may result
in more toxin being produced," he said. Experts had earlier suggested,
based on an early DNA sequence of the bacteria, that the new strain
was particularly aggressive because it reproduced quickly and released
more toxin than similar bacteria.

In the new study, researchers at the University of Muenster and the
Robert Koch Institute analyzed samples from 80 patients sent to a
national laboratory between 23 May 2011 and 2 Jun 2011. The analysis
was paid for by the German government and Network Zoonoses. It was
published Thu 23 Jun 2011, in the journal, Lancet Infectious
Diseases.

In separate research published Wednesday [22 Jun 2011] in the New
England Journal of Medicine, German doctors released an early
description of the outbreak, including the cases of 59 people
hospitalized with the illness at the Hamburg University Medical
Center. They found about 20 per cent of patients developed the kidney
failure complication linked to _E. coli_.

Unlike in previous _E. coli_ crises, few children were affected. "The
pathogen seems to have a special affinity for adults," said Dr Gerard
Krause, a director at the Robert Koch Institute, and one of the
paper's authors. He said it could be that even if children picked up
the bacteria, they didn't fall sick.

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[We await the likely confirmation of the Arizona case being the
epidemic German strain. The Lancet Infectious Diseases and New England
Journal of Medicine reports will be further discussed in a later post.
- Mod.LL]

See Also