REVIEW

CURRENT
OPINION Approach to the patient with infectious colitis
Herbert L. DuPont

Purpose of review
To provide current recommendations for evaluation and treatment of patients with infectious colitis.
Infectious colitis is diagnosed in someone with diarrhea and one or more of the following: fever and/or
dysentery, stools containing inflammatory markers such as leukocytes, lactoferrin, or calprotectin, or
positive stool culture for an invasive or inflammatory bacterial enteropathogen including Shigella,
Salmonella, Campylobacter, Shiga toxin-producing Escherichia coli (STEC) or Clostridium difficile, or
colonic inflammation by endoscopy.
Recent findings
Standard stool culture should be performed in patients with infectious colitis. Epidemiologic findings
including prior international travel, shellfish-associated diarrhea, living in parasite-endemic regions may
suggest the need for specialized studies of etiology. When STEC is suspected as a pathogen because only
low grade or no fever is seen in a patient with acute dysentery, a competent laboratory should look for E.
coli O157:H7 and Shiga toxin directly in stool.
Summary
Once laboratory diagnosis is made, pathogen-specific antimicrobial therapy should be initiated for all
forms of infectious colitis other than STEC. For empiric treatment of febrile dysenteric diarrhea invasive
bacterial enteropathogens (Shigella, Salmonella, and Campylobacter) should be suspected and adults may
be treated empirically with 1000mg azithromycin in a single dose.
Keywords
bacterial diarrhea, Campylobacter, infectious colitis, Salmonella, Shiga toxin producing E. coli, Shigella

INTRODUCTION pathogens that present with clinical and patho-

Practitioners in the early 1900s differentiated
between a small bowel and a colonic process in
patients with acute diarrhea based on stool
frequency and approximate stool volume. They
diagnosed a colonic origin for an illness when the
stool number was large (>4 unformed stools/day)
and when the stool volume was small. They referred
to stools of colonic origin as fractional stools
because they were a fraction of the volume of
normal bowel movement. Most patients with infec-
tious colitis are suffering from enteric infection
caused by an inflammatory or invasive bacterial
pathogen. Most causative pathogens either invade
the colonic mucosa as is seen for strains of Shigella,
Salmonella, and Campylobacter or they attach to
the colonic mucosa and produce localized inflam-
mation as is seen for strains of Clostridium difficile,
enteroaggregative, or Shiga toxin-producing Escher-
ichia coli (STEC).
In this review we will focus on the bacterial
causes of infectious colitis and a few nonbacterial
logical evidence of colitis.
DEFINITION
Colitis is diagnosed when the patient has diarrhea
(passage of three or more unformed stools per day)
and has evidence of colonic inflammation based
on presence of one or more of the following:
positive fecal markers (numerous leukocytes,
positive lactoferrin, or calprotectin), passage of
many small volume stools containing gross blood
and mucus (dysentery), or colonoscopy or flexible
The University of Texas School of Public Health, St. Lukes Episcopal
Hospital, Baylor College of Medicine and Kelsey Research Foundation,
Houston, Texas, USA
Correspondence to Herbert L. DuPont, MD, MACP, 1200 Herman
Pressler, Suite 733, Houston, TX 77030, USA. Tel: +1 713 500
9366; fax: +1 713 500 9359; e-mail: Herbert.L.Dupont@uth.tmc.edu
Curr Opin Gastroenterol 2012, 28:3946
DOI:10.1097/MOG.0b013e32834d3208

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 Large intestine
KEY POINTS
 Most patients with infectious colitis have a bacterial
infection that can be diagnosed by laboratory study.
 The laboratory will identify some pathogens with an
order for stool culture (Shigella, Salmonella, and
Campylobacter), whereas others must be specifically
ordered [Shiga toxin-producing Escherichia coli (STEC),
Yersinia enterocolitica, noncholera Vibrio spp., and
many other less common etiologic agents included in
Table 1].
 Specific antibiotic therapy is indicated for essentially all
cases of infectious colitis (other than that caused by
STEC), which will require etiologic evaluation to
identify targeted therapy.
 A small list of less common causes of infectious colitis
should be considered depending upon travel history or
underlying medical condition, including Clostridium
difficile, Entamoeba histolytica, Schistosoma mansoni,
and cytomegalovirus.
sigmoidoscopy revealing mucosal inflammation.
Infectious colitis can be assumed when a micro-
organism linked with colonic mucosal inflam-
mation or its toxin is identified epidemiologically
(defined outbreak) or microbiologically by a diag-
nostic laboratory (see Table 1 for common causes of
&
infectious colitis) [1,2 ]. When colitis develops
within 14 days of diarrhea onset it is said to be
acute. If it occurs 30 or more days after development
of diarrhea it is said to be a chronic disorder.
EPIDEMIOLOGY
Most causes of infectious colitis are caused by
bacterial enteropathogens, which either invade
the gut lining or produce mucosal inflammation
&&
without invasion [3 ]. When infectious colitis
develops in a hospitalized patient or in any patient
taking antibiotic therapy, C. difficile infection (CDI)
should be suspected and sought. When acute
dysenteric diarrhea or colitis is diagnosed in an
international traveler one of the invasive bacterial
enteropathogens, Shigella, Campylobacter, and Sal-
monella, should be suspected. Other bacterial causes
of acute dysentery in travelers include enteroinva-
sive E. coli (EIEC), enteroaggregative E. coli (EAEC),
Aeromonas spp., noncholera Vibrio spp., and Yersinia.
When acute dysentery occurs in the USA the same
infectious agents should be considered as in travelers
although the frequency of identifying a pathogen is
lower than in international travelers. In outbreaks of
foodborne illness associated with dysenteric illness
and cases of hemolytic uremic syndrome, strains of
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STEC should be suspected. When dysenteric illness
lasts more than 30 days other diagnoses should be
considered including inflammatory bowel disease
(ulcerative colitis or Crohns disease) or, in endemic
areas, colonic infection by Entamoeba histolytica or
Schistosoma mansoni.
CAUSE
Table 1 provides a listing of infectious causes of
colitis along with recommended methods for
laboratory diagnosis. In Table 2 [4], recommended
antimicrobial therapy for pathogen-specific colitis is
provided. The various etiologic agents will be briefly
considered here.
Shigella, Campylobacter, Salmonella, and
Shiga toxin-producing Escherichia coli
Strains of Shigella, Campylobacter, or Salmonella
produce diarrhea after invasion of the mucosa
often associated with systemic signs and symptoms
including chills, fever, and toxicity. STEC is a non-
invasive but inflammatory pathogen that causes
community outbreaks, which often is not obvious
with an individual case of illness. Patients with
STEC diarrhea generally have low-grade fever or
no fever in contrast to higher temperature seen in
patients with infection caused by one of the invasive
bacteria. The spectrum of STEC infection varies and
includes: acute diarrhea, dysentery (more than 80%
of patients with STEC illness pass bloody stools),
hemorrhagic colitis, ischemic colitis-like picture in
the elderly, and hemolytic uremic syndrome (HUS),
especially in children less than 15 years of age and
in elderly adults.
Antimicrobial therapy is indicated for the
treatment of shigellosis and campylobacteriosis
(see Table 2). In-vitro susceptibility testing of
bacterial enteropathogens is needed because of
&
the emergence of quinolone [5,6 ] and azithromy-
&
cin resistance [7 ]. For nontyphoid Salmonella
diarrhea, the objective of therapy is to treat or
prevent the occurrence of bacteremic disease. Anti-
biotics are then given to a subset of patients in
which bacteremic disease is suspected. See Table 2
for patient groups in which sepsis should be
suspected in enteric infection caused by a strain
of nontyphoid Salmonella. Some antibiotics such
as trimethoprimsulfamethoxazole and fluoro-
quinolones may increase the induction of phage-
mediated production of Shiga toxin, possibly
facilitating the development of HUS, whereas other
drugs such as azithromycin [8] and rifaximin [9]
appear not to do this. Currently antibiotics are not
recommended for therapy of STEC infection but
Volume 28  Number 1  January 2012
 Table 1. Etiologic diagnosis of patients with infectious colitis suspected in patients with acute diarrhea and any of the following: fever, dysentery
(passage of grossly bloody stools, often with mucus), fecal markers of inflammation,a or colonic mucosal inflammation on endoscopy
Specialized stool examinations that must Specialized stool examinations that are available in
Etiologic agent Routine stool examination be requested research laboratories

Shigella Identified routinely with stool culture Not needed, employ standard stool culture Not needed
Campylobacter Identified routinely with stool culture Not needed, employ standard stool culture Not needed
Salmonella Identified routinely with stool culture Not needed, employ standard stool culture Not needed
STEC May or may not be part of normal Should be requested when patient is If positive, additional study will be needed at
stool culture exam passing grossly bloody stools looking a local or state health department laboratoryb
for Escherichia coli O157:H7 and Shiga
toxins directly in stool [1]
EAEC Not available Not available Performed only in research laboratories
EIEC Not available Not available Performed only in research laboratories using
PCR methods, or Sereny guinea pig eye test
Aeromonas Should be identified routinely with Advisable to request that the laboratory look Few research labs are working with this organism
stool culture for in dysenteric diarrhea
Vibrio (noncholera) spp. Not part of normal stool culture exam Should be requested when organism suspected Few research labs are working with this organism
(e.g., V. parahemolyticus) based on vehicle of transmission (shellfish,
seafood); laboratory will culture on
salt-containing media

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Yersinia enterocolitica
Enterotoxigenic Bacteroides
fragilis
Clostridium difficile
Entamoeba histolytica
Schistosoma mansoni colitis
Cytomegalovirus
Should be identified routinely with
stool culture if present in stools
in high concentration
Not available
Stool test for C. difficile toxin (EIA,
PCR or cytotoxin by tissue culture)
or microbiologic culture
Identified routinely when parasite
test ordered by direct microscopy
or by commercial EIA tests
Stool examination for characteristic eggs
Not available
Should be requested when suspected based on Few research labs are working with this organism
epidemiology and the stool can be processed
by incubating the culture at 25 and 288C
The toxin is detected by PCR and the organism The importance of this organism has not been
is isolated by microbiologic culture methods established
Many diagnostic laboratories are moving to Not needed
sensitive PCR methods
Not needed Research laboratories can differentiate between
pathogenic and nonpathogenic Entamoeba
EIA available Endoscopic evaluation may be required to
&
establish diagnosis [2 ].
Mucosal biopsy material can be examined Not needed
histologically and/or the virus can be
cultured

EAEC, enteroaggreagative Escherichia coli; EIA, enzyme immunoassay; EIEC, enteroinvasive Escherichia coli; PCR, polymerase chain reaction; STEC, Shiga toxin-producing Escherichia coli; TCBS, thiosulfate citrate bile
sucrose agar.
a

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Fecal leukocytes or positive test for lactoferrin or calprotectin.
b
If the stool is negative for O157 but Shiga toxin positive, isolated Escherichia coli strains will have to be tested for serotype and confirmed to be toxigenic and organism will need to be serotyped and submitted to a
local health laboratory for analysis for pulsed field gel electrophoresis (PFGE) to determine whether it is part of an epidemic.
Approach to the patient with infectious colitis DuPont

41

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 42
Table 2. Antimicrobial therapy of infectious colitis in adults
Etiologic agent Recommended treatment
Shigella spp. Ciprofloxacin 750 mg (or other fluoroquinolone) once a day for
3 days; or azithromycin 500 mg once a day for 3 days
Campylobacter jejuni Azithromycin 500 mg once a day for 3 days; or erythromycin
500 mg four times a day for 35 days
Salmonella (nontyphoid) For milder illness, none; for possible bacteremic disease,
levofloxacin 500 mg (or other fluoroquinolone) once a day
www.co-gastroenterology.com
for 7 (if immunocompetent) or 14 days (if immunocompromised)
Shiga toxin producing E. coli (STEC) None
Enteroaggregative E. coli Rifaximin 200 mg three times a day for 3 days
Enteroinvasive E. coli Treat as for Shigella
Aeromonas spp. Treat as for Shigella
Travelers diarrhea complicated with Treat as for Shigella
fever or dysentery (uncertain agent)
Vibrio spp. (noncholera) Treat as for Shigella
Yersinia enterocolitica Treat as for Shigella
Clostridium difficile Metronidazole 500 mg three times a day for milder cases or oral
vancomycin 125 mg four times a day for more severe illness;
either drug is given for 1014 days
Entamoeba histolytica Metronidazole 750 mg three times a day for 510 days and
a luminal amebicide: paromomycin 500 mg three times a day
for 10 days, iodoquinol 650 mg three times a day for 20 days,
or diloxanide furoate 500 mg three times a day for 10 days
S. mansoni colitis Praziquantil 40 mg/kg body weight in a single dose
Cytomegalovirus Ganciclovir 5 mg/kg intravenously for 14 days
STEC, Shiga toxin-producing Escherichia coli.
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Large intestine
Comments
Secondary spread is common in families because of the low inoculum
size required to cause infection; fluoroquinolone resistance is being
reported.
Fluoroquinolone resistance is widespread. Azithromycin resistance
is being seen.
Bacteremic disease is considered if: febrile or toxic, at extremes of
age (3 months or 65 years of age), patient has sickle cell anemia,
cancer or AIDS, or is on steroids or is undergoing hemodialysis or
has inflammatory bowel disease.
Antibiotics or antimotility agents may encourage production of Shiga
toxin and increase risk of HUS.
Fluoroquinolones or azithromycin are equally effective.
This is an unusual cause of foodborne outbreaks.
This infection is most common in tropical and semitropical areas.
As bacterial agents cause most cases of travelers diarrhea, empiric
antimicrobial therapy is given.
Causes watery diarrhea and dysentery usually associated with shellfish
and seafood consumption.
Causes acute watery diarrhea, fever, and dysentery and
an appendicitis-like picture.
Recurrences are common and may require prolonged treatment with
oral vancomycin or other approach [4]. Fidaxomicin was recently
licensed for therapy in the USA.
It is necessary to treat the infectious trophoite phase with metronidazole
to improve symptoms and the cyst phase of the parasite to prevent
disease recurrence.
Cure rates in field studies have been approximately 85%.
Diarrhea may persist after treatment suggesting longer-term treatment
will be necessary.

more study with azithromycin and rifaximin treat-
ment is needed.
Enteric pathogens have been suspected to play a
role in the early pathogenesis of inflammatory
bowel disease (IBD) in a small subset of patients.
Careful studies of the relationship of Salmonella
or Campylobacter infection with the subsequent
development of IBD in a large study failed to find
& of nosocomial diarrhea. It is particularly likely
an association [10 ]. Also bacterial pathogens of the
colon appear not to predispose to gastrointestinal
& and develop severe diarrhea (six or more unformed
cancers [11 ,12].
Enteroaggregative Escherichia coli
EAEC is a noninvasive but inflammatory pathogen
involving the distal ileum and colon. EAEC strains
are important causes of diarrhea in children
throughout the world and have been recognized
to cause persistent diarrhea of young children in
developing regions. The organism is the second most
common cause of travelers diarrhea and is known
to cause diarrhea in patients with HIV infection.
A recent outbreak of foodborne disease in Germany
affecting more than 1500 people and causing dys-
enteric illness and HUS was caused by an E. coli strain
that was a hybrid of STEC and EAEC strains.
Enteroinvasive Escherichia coli
Strains of EIEC have been identified as an endemic
cause of dysentery in certain countries of South
America and Eastern Europe and the organism has
been a rare cause of foodborne outbreaks in the
United States that can be quite extensive. This organ-
ism should be suspected in large outbreaks of diarrhea
with fever in which a number of those affected are
passing grossly bloody stools and the laboratory is
unable to identify a pathogen.
Aeromonas spp.
Diarrhea-producing Aeromonas strains cause diarrhea
most commonly in the tropics. Persistent diarrhea,
with illness lasting 2 weeks or longer, is common
with Aeromonas diarrhea and dysentery is frequently
reported in those infected by this organism.
Noncholera Vibrio spp.
A noncholera Vibrio should be suspected in the
presence of a seafood (often shellfish) associated
outbreak in which a proportion of those affected
are passing grossly bloody stools.
Enterotoxigenic Bacteroides fragilis
Enterotoxigenic Bacteroides fragilis is a recently
described cause of inflammatory diarrhea in adults
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Approach to the patient with infectious colitis DuPont
and children in developing countries [13] and a
&&
cause of travelers diarrhea [14 ]. Characteristics
of the disease are poorly described and need further
study.
Clostridium difficile
C. difficile is the most important definable cause
when patients in the hospital receive antibiotics
stools per day), febrile dysenteric diarrhea, toxic
dilatation of the colon, otherwise unexplained
leukocytosis (white blood count >10 000 per ml)
or patients are found to have characteristic white
yellow mucosal lesions including pseudomembra-
nous colitis on colonoscopy. CDI not infrequently
complicates IBD in which pseudomembranous
&&
colitis may be found on colonoscopy [15 ]. When
IBD is complicated by CDI, antibiotic treatment of
the enteric infection should occur before initiating
anti-IBD therapy [16].
Entamoeba histolytica
Amebiasis should be suspected in people living
under conditions with reduced hygiene often in
developing tropical or semi-tropical areas. Occasion-
ally international travelers and people living in the
USA acquire intestinal amebiasis. The diagnosis may
be difficult to make because E. histolytica cysts and
trophoizoites may be erroneously diagnosed as fecal
leukocytes. Commercial E. histolytica serology is
a valuable tool for making a diagnosis of intestinal
or hepatic amebiasis.
Schistosoma mansoni
Intestinal schistosomiasis caused by S. mansoni is
a recognized cause of dysentery among travelers to
endemic areas. The disease may be mistakenly
diagnosed as IBD [17]. Endoscopic diagnosis may
be required to establish an etiologic diagnosis of
&
colitis due to S. mansoni [2 ].
Viral pathogens
Common viral causes of diarrhea, noroviruses and
rotaviruses, do not cause colitis. Cytomegalovirus
(CMV) in an immunocompromised patient may
produce colitis. CMV colitis has been seen in the
elderly without obvious immunosuppression [18].
CMV also has been shown to complicate the course
&&
of IBD [19 ]. It is important to suspect CMV in
such patients and seek an etiologic diagnosis
because specific therapy is needed to control
symptoms and eradicate the acute infection.
www.co-gastroenterology.com 43
 Large intestine
Colonoscopy and mucosal biopsy is the preferred
way to diagnose CMV colitis.
CLINICAL CONSIDERATIONS
Infectious colitis should be suspected in subjects
with acute diarrhea complicated by fever, systemic
toxicity, or dysentery. It should also be suspected in
patients with positive stool examination for one of
the common causes of infectious colitis listed in
Table 1. When patients present with dysentery,
the medical and epidemiologic histories can then
provide other clues as to the etiologic diagnosis.
With dysentery of acute onset associated with fever
or if the dysenteric illness follows travel to a tropical
or semitropical region, the invasive bacterial patho-
gens should be suspected. If it occurs in a person
on antibiotics, especially if confined or recently
confined to a hospital or a nursing home, C. difficile
is a likely diagnosis. With an outbreak of acute
dysenteric illness, especially in the absence of a
substantial fever (greater than 1028F) in those
affected, STEC should be strongly considered. When
patients report previous bouts of diarrhea with or
without dysentery, IBD should be considered. In
a US hospital Emergency Department among a large
group of subjects presenting with acute dysentery
the relative importance of pathogens identified
from most common to least were: Shigella,
&&
Campylobacter, Salmonella, and then STEC [20 ].
In developing regions among endemic populations,
the same pathogens are found but additionally
Aeromonas spp. and E. hystolytica may be found.
DIAGNOSIS
Infectious colitis should be suspected in persons
with diarrhea who have any of the following:
fever, dysentery, fecal inflammatory markers found
by the laboratory (including leukocytes, lactoferrin
and/or calprotectin), or mucosal inflammation on
colonoscopy.
In many settings diagnostic laboratories
routinely perform tests aimed at documenting pres-
ence of colitis. The fecal leukocyte test looks for the
presence of white blood cells (WBCs) providing
semiquantitative information after looking at a
number of microscope fields and reporting the value
as negative, few, moderate, or many. A wood appli-
cator stick is moved through a diarrhea stool looking
for strands of mucus to which leukocytes can be
expected to adhere if present in abundant numbers.
Dilute methylene blue is the optimal stain for leuko-
cytes [21] and can be used in a wet mount preparation
under the high dry objective of the microscope or
the sample can be heat fixed before staining with
the dilute methylene blue and examined under oil
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emersion. When there are many WBCs the patient is
likely to have either diffuse colonic inflammation or
proctitis. When focal colitis is present, the WBCs will
be either absent or few in number because of their
dilution in luminal contents. The finding of many
WBCs does not differentiate between infectious
colitis and IBD. Lactoferrin and calprotectin are
constituents in polymorphonuclear leukocyte
granules. Fecal lactoferrin is a much more sensitive
indicator of gut inflammation than the fecal leuko-
cyte test but is not readily available in diagnostic
laboratories. Fecal calprotectin has been used to
differentiate between patients with IBD and func-
&
tional bowel disease [22 ], shown to correlate with
endoscopic score for Crohns disease [23], and used to
determine whether a patient should undergo endo-
&
scopy to evaluate for the presence of IBD [22 ].
Screening stools with fecal calprotectin has been used
in limited study as a screen for bacterial diarrhea
[24] and to differentiate between bacterial and viral
pathogens in children with gastroenteritis [25]. Find-
ing inflammatory markers in stool of patients with
acute diarrhea is an indication for performing stool
culture to identify an infectious cause, or performing
colonoscopy when IBD is suspected because of a
more protracted history.
When a patient presents with acute bloody
diarrhea it can be assumed to be a case of bacterial
colitis. Obtaining a stool for microbiologic culture
should be routinely performed. If a stool sample is
sent to the laboratory for culture, Shigella, Salmonella,
and Campylobacter will be the agents routinely
sought. If STEC, a noncholera Vibrio, or Yersinia is
suspected (see Table 1 for clinical clues) the labora-
tory should be alerted to look for these pathogens
because specialized methods must be employed.
When a parasite (E. histolytica or S. mansoni) or
CMV is in the differential diagnosis, specialized
laboratory tests should be employed (see Table 1).
TREATMENT
Patients with infectious colitis usually will benefit
by receiving an antimicrobial drug directed against
the causative agent. Laboratory study will be import-
ant to identifying the cause of the colitis.
Nonspecific treatment
Patients with infectious colitis such as others
with diarrhea of small bowel origin will benefit by
paying attention to fluid and salt administration to
meet losses from illness and to keep up with
continuing losses. Occasionally intravenous fluid
administration will be needed. Symptomatic
therapy with antimotility therapy (e.g., loperamide)
is generally not indicated in infectious colitis and
Volume 28  Number 1  January 2012

can be dangerous if given without specific treatment
[26]. There is no evidence that the antimotility drugs
are harmful in inflammatory diarrhea if given with
proper antimicrobial treatment designed to treat
& 361:15601569.
the bacterial enteric infection [27 ,28]. For possible
STEC infection in which specific therapy is not
available, antimotility drugs can potentiate the
&&
development of HUS [29 ].
Antimicrobial therapy
In Table 2 recommended antimicrobial therapy for
the various forms of infectious colitis are provided.
Making an etiologic diagnosis (Table 1) is important
for developing a plan for therapy.
CONCLUSION
Infectious colitis, generally caused by a virulent
bacterial enteropathogen, is suspected in a person
with diarrhea and any of the following: fever and/or
dysentery, marker of inflammation in the stool
sample, a positive culture for a mucosally invasive
or inflammatory pathogen or inflamed mucosa by
endoscopy. Some pathogens are found by sending
the sample to the laboratory for routine culture or C.
difficile toxin testing and others must be sought only
after instructing the laboratory to look for a targeted
pathogen. Most forms of infectious colitis have
specific therapy once the etiologic agent is ident-
ified. Infection by STEC is an exception.
Acknowledgements
None.
Conflicts of interest
The work was supported in part by grants from Public
Health Service (grant DK 56338) which funds the Texas
Gulf Coast Digestive Diseases Center.
The author has consulted with, received honoraria for
speaking, and has received research grants administered
through his university from Salix Pharmaceutical Com-
pany and has received research grants administered
through his university from Intercell Corporation and
Santarus Pharmaceutical Company.
None declared.
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The possibility of CDI should be considered in patients with IBD when enteric
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suppressive treatments. CDI is further suggested when pseudomembranous
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19. Kim CH, Bahng S, Kang KJ, et al. Cytomegalovirus colitis in patients without
inflammatory bowel disease: a single center study. Scand J Gastroenterol
&&
2010; 45:12951301.
CMV infection was diagnosed by colonoscopy in 43 patients with CMV colitis.
Many of the patients had spontaneous recovery while biopsies were being
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&& patients presenting to United States emergency departments: prevalence of
Escherichia coli O157:H7 and other enteropathogens. Clin Infect Dis 2001;
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This is one of the few studies evaluating a large number of patients with acute
dysentery visiting a hospital emergency center for cause of illness. The major
causes of bloody diarrhea in order of importance were: Shigella, Campylobacter,
Salmonella, and STEC.
www.co-gastroenterology.com 45
 Large intestine
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& of patients with suspected inflammatory bowel disease: diagnostic meta-
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Fecal calprotectin is a useful screening test to determine who should be evaluated
for IBD by endoscopy.
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46 www.co-gastroenterology.com
Copyright Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
26. DuPont HL, Hornick RB. Adverse effect of lomotil therapy in shigellosis. JAMA
1973; 226:15251528.
27. Koo HL, Koo DC, Musher DM, DuPont HL. Antimotility agents for the
& treatment of Clostridium difficile diarrhea and colitis. Clin Infect Dis 2009;
48:598605.
A thorough evaluation of the literature and post-marking information from the
company suggested that the antimotility agent loperamide was not associated with
worsening of CDI if the patients were also treated with anti-CDI antibiotics.
28. Murphy GS, Bodhidatta L, Echeverria P, et al. Ciprofloxacin and loperamide in
the treatment of bacillary dysentery. Ann Intern Med 1993; 118:582586.
29. Nelson JM, Griffin PM, Jones TF, et al. Antimicrobial and antimotility agent
&& use in persons with shiga toxin-producing Escherichia coli O157 infection in
FoodNet Sites. Clin Infect Dis 2011; 52:11301132.
This report presents the most recent US experience with STEC infection reported
by the FoodNet program. The study found that a high percentage of patients
received antimotility drugs (e.g., loperamide) which is known to predispose to
HUS.
Volume 28  Number 1  January 2012