Acute bloody diarrhea with right sided colitis

A SO-year-old woman prescnced with bloody diarrhea and radiological evidence of righ c sided col icis. Encerohemorrhagic Escherichia col, was isolated from the stool. The illness subsided spontaneously but was complicated by the development of hypoproteinemia and ascites. This disease presents a variable clinical picture but apparent 'ischemic colitis' in younger patients is especially suggestive of infection with £coli Ol 57:H7. Can J Gastroenterol 1988; 2(1):37-40

in the emergency department with abdominal pain and b loody diarrhea.
Six days earlier she had awoken with severe right lower quadrant abdominal cramps.Several hours later watery diarrhea developed with bowel movements every I co 2 h.Within 24 h the stools became grossly bloody.At this time she became nauseated and vomited several rimes.
Stool specimens for culture had been sent by her family doctor sho rtly after the illness bega n .These were reported as negative for pathogens.Three days prior to the o nset 0f symptoms, rwo family members had been acutely ill with watery diarrhea.Their illnesses resolved spontaneously.Stool cultures were not obtained.
There was no history of recent travel outside Canada.The patient had not had any animal contact, had not eaten any unusual foods and had not received antibiotics in several yea rs.
Her previous history was unremarkable.Specifically, there was no history of liver disease o r excessive alcohol intake.She was not receiving any medications.
On examination she appeared ill and was mildly dehydrated.Temperature was 36.8°C, pulse 115/ min and regular and blood pressure 170/ 100 mm Hg.Examination of the head and neck revealed no abnormalities.The chest was clear and heart sounds normal.Abdominal examination revealed no areas of tenderness, liver and spleen were not enlarged.Bowel sounds were normal but an cpigastric bruit was heard.There were no stigmata of liver disease and foot pulses were normal.µm o l/ L), scrum aspa rrate amino transferase (AST) was 17 iu/L (less than 38 iu/ L), alanine aminotransferase (ALT) was I 7 iu/L (less than 38 iu / L) and alkaline phosphatase was 74 iu/L (40 to I 20 iu/L).Scrum albumin was 27 g/ L (35 to SO g/L).Urinalysis showed a trace of protein a nd no red cells or casts.Repeat stool cul tures showed no growth of paLhoge ns.
Following admission the patient appeared to deteriorate.She had fr e-4ucnc h looc.lybowel movements and c.lcvclopec.l abdominal distension.Because of the possibil ity of ischemic colitis, a barium enema was performed (Figure l, left panel) anc.l this showeJ markec.lirregulari ty of the ascending a nd proximal transverse colon wi th thumb priming.This was co nsistent with the i.liagnosis of ischemic di sease.T he rest of the colo n a nd the terminal ileum were with in normal limits.
Six days after admission Escherichia co/10 157: H7 positive for Verotoxin was isolated from the patient's stool.
T he patient was created with in-Lravenous fluids and appropriate corrections were made to her electrolytes.T he di arrhea setcled spon taneously.On the l 0th <lay of her illness the wh ite cell count was normal.By the I 2th day her howel frequency d ecreased to two bloodless formed stools per day.At this point she was noted clin icall y to have ascites with a fluid thrill.At t h is time seru m albumin was 3 I g/L (no rmal 35 to 50 g/L) and urinalysis was negative fo r protein.Serum hilirubin was 5 µ mol/L, AST was 26 iu/ L and ALT was 36 iu / L. The prothrombin time was 13 s (12 to 15 s) anti partial thromboplastin time was 28 s (25 to 37 s).The ascites quickly resolved and because the patient was clinicall y well furt her investigations were not performed .
S he was c.lischargcd on che 16th day

DISCUSSION
A SO-year-old woman presented with bloody diarrh ea in the absence of feve r or systemic illness.The acute o nset of illness wich abdomi nal pain, watery diarrhea and later bloody d iarrhea was suggestive of an infectious etio logy.Two fami ly members h ad already been ill.SLool cul cures, however, s howed no growth of the common eneerie pathogens.Colo nic ischem ia was considered and the finding of an epigascric b ruit supported chis diagnosis.
Sigmoidoscopic examination showed edematous mucosa bur no specific abnormalities.Barium enema showed ch anges in che righ t colon compatible with ischemic d isease.
Until relatively recc nd y the diagnosis would nor h ave been elucidated fur-Lher.The isolation of cnreroh emorrhagic E coli from the repeat stool cultures and the recognition ch at chis orga nism may cause right sided colins e nab led t he correct diagnosis to be made.
The recognition o( E coli a, pathogenic b acrribucablc co Bray and Beavan ( l).In che 1940s, in England, th ey recognized chaL only a frat:tion of childhood d iarrheas were explicable on the basis of known pathogens.They postulated chaL E coli migh t, in some circumstances, be capable of producing diarrhea.Rabbit antiserum was prepared to E coli cultu red from the stool of a child with diarrhea.Using the antiserum they were able to demonst rate the prese nce of che sa1rn: organism in subseq ue nt outbreaks of diarrhea as compared Lo a control population without the illness.Thus they provided evidence of the pathogenicity of certain E coli st rains.
Since chat time there h as been an enormous increase in our knowledge of pathogenic E coli.The o rganism may be classified on the basis of the O (lipopolysacch aride), H (flagellar) and K (polysaccharide) antigens.Subsequent assignment to enceropath ogenic, en tertoxigenic, enteroinvasive, enrero ad herent o r cnterohemorrhag1<.groups is clinically of little benefit because pathoge nesis is not yet clear and because che organism does no t always produce disease appropriate to its classificatio n.The affected fa mily members in the present case likel y h ad enrero hemorrhagic E coli but yet had a CAN J GASTRt)cNTERL)L watery diarrhea without gross blood.
The ability of emerohemorr hagic E coli co produce watery Jiarrhca has been reported previously (2).
The O I 57:H7 strain of E coli was first recognized in lrish piglets in 1970 (3) as a cause of emeriris.Since then, ~poradic and clustered cases have been reported.Outbreaks have been described in homes for the ageJ (4) and in a day care centre (5).
The disease 1s Lharacccn:cJ by an incubation pcrioJ of cl1rcc to nine Jays with a median of four days (4).The organism may be ingested in LOntam1nated food.Hambu rger from a restaurant chain was responsible for an outbreak in the UnircJ States (6).lnfouiun via fecal o ral contamination and via fomites likely occun, (5).Typu.:ally the infection begins with nampy abdominal pain followed by watery diarrhea which may become grossly bloody.There may be nausea anJ vommng hut fever 1s uncommon.Some patients have symptoms suggestivc of an upper respiratory infection (6).
Laboratory evidence of tnflammanon may be absent.The erythrocyte sedimentation rate and wh ite cell count may be normal or only minimally elevated (6).
Sigmoidoscop1c examination may be normal or show abnormaliues ranging from edema co frank ulceranon (2).Colonoscopically the dbcasc may be most markeJ in the proximal colon and edema, inflammation and hcmor• rhage have been reported (2).Barium enema may be normal or show, as in chis case, changes suggestive of submucosal edema (2 ,6).
The disease appears to show a predilection for the right colon and may mimic ischemic disease.Lt seems likely in milder cases, or in cases where chc pat ient is seen some time afccr the onset of the illness, that no s1gnifiLanc lesion may be seen endoscopically or radiologically.The d isease appears to resolve without residual colonic scarring.
T he illness is usually self-limited 11•1th a mean duration of eight days (2) but in the elderly and very young it may be fatal.A mortality rate of 16% was reported for an outbreak in Lon-don, Ontario 1n 1985 (4).There is an association with hemolytic uremic syndrome a complication which carries a high mortality (2,5,7).
The organism may be found in the scools for up to 14 days (8) but is more likely ro he detected if stools are collected within t he fi rst six days of ill ness (9).
Treatment consists of fluid and elev trolytc replacement.Trimethoprimsulfamethoxazole or ampic1llin may be effective in shortening the Juration and severi ty of illness (10).There arc, however, no controlled tnals of anti• hiotic efficacy.In the retrospective data presented hy Remis and col• leagues (2) the mean duration L)f illness in patients receiving amibiotics was 7. 5 days as compared to 8. 5 days in untreated patients.Of particular impor• cancc would be a trial designed co show whee her antim1crob1al therapy rrevenced the development of disease and hemolytic uremiL syndrome in contacts.
The organism produces a toxrn 1denucal to chm of Shigelfo dvsenieriae type I ( 11 ).This toxin, designarcJ Verocoxin I, is cytotoxiL for HeLa and Vero cells (a cell line derived from monkey kidney cells).A second cytocoxin, Vcrocoxin 2, not neutralized by antibody to the Shiga toxin may also be found.Some strains produce fimbriae which may be an important factor in determining v1rulcnce ( 12).
Vcrotoxtn has been shown co cause platelet aggregation ( 13) anJ this may be important in the pathogenesis of the hemolytic uremic syndrome.E coli 0157:H? is not the only cmeric pathogen assoLiated with hemolyttL uremic syndrome.This associauon has also been reported for Salmonella , Shigella and Camp,lobaccer 1e11m1.ln the present case the disease followed a relatively benign course.There was no evidence of hemolys1s and renal E coli colitis fumnon remarncd normal.The disease subsided with suppon 1ve thcrap~.
The case presented here is unusual as asc1tes has not previously been reported as a complicanon of the illness.The ser um albumin was low possibly secondary to procein loss from the inflamed bowel.The low scrum onconc pressure due to hypoalbumincm1a no doubt contributed co chc asc1tes but docs not seem sufficcnt to explain it.There was no clrnical or laboratory l'Vi• dence of hepatic or pancreatic Jbcase and no evidence of periro111tis.
When seen in follow-up eight weeks after the onset of the illness thl' paticrn was well with a normal serum albumin and no evidence of ascites.Repeat hart• um enema showed resolution of the colonic abnormalicies.
E coli 0157:H?presents co the gas• troenrerologist in a variety of ways; as watery diarrhea, bloody diarrhl'a, colonic bleeding with no apparent cause or as apparent 1schcmit colitis.The reports of nght sided '1schcmic colius' m young adults (14) reporceJ 1n the liccraturc prior to recognition of this organism may be descriptions of cnterohcmorrhag1c E coli colitis.
Microbiological laboratories shou ld screen for this organism in all cases of bloody diarrhea when no ocher pathogen is found.Initial screening is based on the absent or slow fermentation of sorbitol by rhb strain o( E coli.Over 90% of ocher strains of E coli ferment sorbitol.If a nonfcrmeming strain is found it Lan be scrotyped to detcrm tnc i( 1r is cnterohcmorrhagic