Infection with enterohemorrhagic Escherichia
coli (EHEC) has been spreading in Germany since the second week of May and
causing considerable concern among the population. At the time of writing, nine
deaths have been reported due to the subsequent development of hemolytic
uraemic syndrome (HUS), but the source of the outbreak is still unknown. As of
May 31, 2011, the Robert Koch Institut, Berlin, Germany, has confirmed a total
of 470 cases of HUS and stated that this epidemic has not yet reached its
climax [1].
A 72-year-old man presented with massive bloody diarrhea for 3 days.
On physical examination, he had a pulse rate of 102 beats per minute, the blood
pressure was 110/50 mm Hg, hemoglobin 15 g/dl (reference
values 13.5 – 17.5), and hematocrit 43.5 %
(40 – 53). Remaining laboratory parameters, including renal
function parameters, were unremarkable. We carried out emergency endoscopy to
rule out acute gastrointestinal bleeding. Sigmoidoscopy (Olympus, Tokyo, Japan)
revealed a markedly abnormal, ulcerative mucosa with diffuse reddening, edema,
and numerous petechiae ([Fig. 1 a]). In
addition, bowel obstruction was noted in the proximal sigmoid colon, due to
marked swelling of the ulcerated mucosa ([Fig. 1 b]).
Fig. 1 a Sigmoidoscopy showing
ulcerated mucosa with diffuse reddening, edema, and numerous petechiae.
b Bowel obstruction in the proximal sigmoid colon due to
marked swelling of the ulcerated mucosa.
The differential diagnosis included ischemic colitis, nonsteroidal
anti-inflammatory drug (NSAID)-colonopathy, and infectious colitis.
Histopathologic examination revealed patchy eosinophilic cytotoxic necrosis
with complete destruction of glandular structures and scattered infiltrates of
neutrophilic granulocytes ([Fig. 2]).
Fig. 2 Histologic section
showing patchy eosinophilic cytotoxic necrosis. There is complete destruction
of the glandular structures, with scattered infiltrates of neutrophilic
granulocytes. The inset shows early-stage lesions with fibrin thrombi within
the capillaries.
Early-stage lesions showed fibrin thrombi within the capillaries
([Fig. 2], inset image).
The discontinuous pattern of inflammation and necrosis, and presence of
microthrombi and granulocytic infiltration, ruled out ischemic colitis and
infection caused by common cytotoxic bacteria (i. e.,
Clostridium difficile) [2]
[3]. On day 4 of hospitalization EHEC was detected in stool
samples. However, owing to development of HUS, which signifies unfavorable
disease progression, the patient was admitted to the intensive care unit and
put on renal replacement therapy. At the time of going to press the
patient’s situation was still critical.
Our case demonstrates the clinical presentation and the endoscopic
and histological characteristics of EHEC infection. As EHEC is transmitted via
the oral-fecal route, increased precautions are warranted in the endoscopy
suite to reduce the risk of transmission during an epidemic. Physicians should
be aware of the currently increasing incidence of EHEC and should consider EHEC
infection in the differential diagnosis of patients admitted with bloody
diarrhea.
Endoscopy_UCTN_Code_CCL_1AD_2AZ
