Journal of Gastroenterology and Hepatology (2002) 17 (Suppl.) S54–S71 Guideline for the management of acute diarrhea in adults
SATHAPORN MANATSATHIT,* HERBERT L DUPONT,† MICHAEL FARTHING,‡
CHOMSRI KOSITCHAIWAT,§ SOMCHAI LEELAKUSOLVONG,* BS RAMAKRISHNA,¶
ADERBAL SABRA,** PETER SPEELMAN†† AND SURAPOL SURANGSRIRAT‡‡
*Division of Gastroenterology, Siriraj Hospital, §Division of Gastroenterology, Ramathibodi Hospital,‡‡Division of Gastroenterology, King Pramonkut Hospital, Bangkok, Thailand, †St. Luke’s Episcopal Hospital,Houston, Texas, **International Center for Interdisciplinary Studies of Immunology, and Department ofPediatrics, Georgetown University Medical Center,Washington DC, United States of America, ‡Faculty ofMedicine, University of Glasgow, Glasgow, United Kingdom, ¶Department of Intestinal Science, ChristianMedical College and Hospital,Vellore, India, ††Amsterdam Medical Center, Amsterdam, The NetherlandsINTRODUCTION
provide a complete document that would be applicableto the case management of diarrhea. However, some
Acute diarrhea in adults is one of the most common
explanation and amplification is necessary to clarify the
diagnoses in general practice,1,2 and is responsible for
terms and phrases that have been used, as well as to
considerable morbidity around the world.3–5 While
explain the basis for certain decision pathways in the
acute diarrhea is perceived as a major cause of child-
hood mortality in developing countries, adult mortality
Adult: The definition of ‘adult’ varies from one
from diarrhea is also not uncommon particularly during
country to another. As applied in this guideline, the
epidemics of diarrhea. Contaminated food and water,
term ‘adult’ refers to someone who is of age 12 years or
together with unhygienic eating habits, account for the
continuing high prevalence of acute diarrhea in adults. Acute diarrhea: This is defined as the passage of three
In industrialized countries, the incidence of acute
or more than three loose or watery stool in 24 h, or
diarrhea is estimated to average 0.5–2 episodes per
passage of one or more bloody stool. Acute diarrhea
person per year, and the corresponding figure could be
refers to illness not lasting longer than 14 days.
much higher in developing and underdeveloped coun-
Other conditions that may present as acute diar-
tries. In the USA, with a population of around 200
rhea: ‘Acute diarrhea’ is a clinical syndrome that is
million, about 99 million episodes of acute diarrhea
commonly understood to refer to infective gastroen-
occur every year in adults. Twenty-five percent of hos-
teritis. However, as defined, acute diarrhea may be a
pitalizations in the USA were due to diarrhea and 85%
symptom of other intra-abdominal or systemic illnesses.
of the mortality associated with diarrhea occurred in the
These other clinical conditions may require particular
elderly (> 65 years old).6 It accounts for a large amount
investigations and management, and will need to be
of economic loss and a waste of a country’s resources
recognized and excluded at the outset. Careful history
and labor forces in caring for this group of patients.7 It
and physical examination is necessary to exclude these
is hoped that the development of this guideline will be
conditions from the commonly understood ‘acute diar-
able to provide measures for general practitioners and
rhea’. Special attention should be paid to exclude signs
health care workers around the world to effectively care
of peritonism or peritonitis, which will indicate serious
for adult diarrhea patients so that the mortality and
illnesses that might require surgical care. Examples
of these diverse clinical conditions are presented in Table 1. Specific conditions of acute diarrhea that require Algorithm and definition special consideration: Although the term ‘acute diarrhea’ commonly refers to infectious, toxin-induced
The final algorithm that was developed for the manage-
and drug-induced diarrhea, there are specific acute
ment of adult diarrhea was the result of intensive
diarrhea syndromes that may need a specifically tailored
discussion among the experts. It particularly empha-
approach and management, and where the general algo-
sized simplicity, feasibility and availability of options.
rithm may need to be modified. For example, during
It tries to be as general as possible without sacrificing
epidemic acute diarrhea such as cholera, it is important
the basic principles and theoretical background of
to quickly identify the organism in the first patients pre-
sound management. The algorithm, in itself, should
senting with illness, and to initiate public health mea-
Correspondence: Dr S Manatsathit, Division of Gastroenterology, Department of Medicine, Siriraj Hospital, Mahidol
University, Bangkok, Thailand. Email: [email protected]Specific diarrhea requiring special consideration - Acute diarrhea in the elderly (age > 65 years) Other conditions which
- Hemorhagic colitis (due to EHEC or STEC)
may present as acute diarrhea (see Table Vomiting Diarrhea Watery Diarrhea Bloody Diarrhea In Cholera-endemic area
∑ Consider antidiarrheals for 48 hrs.
Algorithm developed for the management of adult diarrhea. 1Stool examination and culture methods depend on
availability, affordability, and local practice of each community or country. 2Strongly recommended for severly ill patients (selectantibiotics according to sensitivity of local antibiogram). PE, Physical examination; DFM*, dark field microscopy (if not available, look for ‘shooting bacteria’ under light microscopy); ATB, antibiotics; ORT, oral rehydration therapy; IVF, intravenousfluid.
Conditions presenting as acute diarrhea with or
HISTORY AND PHYSICAL
without signs of peritonitis that should be excluded in a
Acute diarrhea is a complex symptom that may be
caused by any of a number of diseases, both infectious
and non-infectious. A proper history and physicalexamination is therefore necessary in these patients.
Special attention should be paid to excluding
Peritonitis secondary to bowel perforation
conditions that may require a different approach and
Systemic infections: for example malaria, measles, typhoid,
Inflammatory bowel diseaseIschemic enterocolitisMesenteric artery/venous occlusion
In the history, it is essential to gather the followinginformation: age, onset and duration of diarrhea, char-
sures that will stop the outbreak. Acute diarrhea in the
acter of the stool (watery, loose or bloody), frequency
elderly needs to be treated in a different manner from
and volume of stool, progression of severity of diarrhea,
that of younger people because of the possibility of com-
presence and severity of vomiting, presence of fever, its
plications relating to compromised cardiac and cerebral
severity and duration, abdominal pain and its location
circulation. A number of these clinical entities are listed
and character, cramps, and tenesmus. The severity of
in Table 2, and these are discussed in greater detail in
diarrhea may be assessed in adults by the degree of dis-
turbance of daily life and activities, debility, thirst, dizzi-
ness, and syncope. The time of last urination should be
the character of stool and accurately assess the type of
noted in patients with dehydrating diarrhea.
diarrhea, whether it is watery or bloody. This is partic-
Occurrence of diarrhea after eating a contaminated
ularly helpful in situations in which patients, especially
meal, the time interval between ingestion and develop-
the elderly or those with poor eyesight, might not be
ment of diarrhea, and the occurrence of illness in others
who also partook of the meal are pointers to a bacter-ial cause of the illness.8 The source of water supply maybe helpful as evidence of a common-source outbreak.9
MAJOR PRESENTATION: VOMITING
The location in which the patient develops diarrhea maybe predictive of the causative organism, for example at
Diarrhoea is the predominating symptom in most
home, in hospital or in an institution. History of recent
patients presenting as ‘acute diarrhea’. Having excluded
travel and the area travelled, may also be helpful. If
the other conditions listed in Tables 1 and 2, we are left
there is research to suggest that specific pathogens are
with a group of illnesses that comprise what is com-
more common during a specific season, this is an addi-
monly understood as ‘acute diarrhea’. These are further
tional factor of which to remain aware.
classified, on the basis of the stool character, as having
It is always worthwhile to exclude the non-infectious
either watery diarrhea or bloody diarrhea. This is one
causes of acute diarrhea and osmotic diarrhea, for
of the decision points in the algorithm, and is discussed
example drugs and toxins. One should inquire if the
further. On the other hand, there are some patients with
patient has recently been taking medications or sub-
‘acute diarrhea’ in whom vomiting overshadows
stances that can cause diarrhea, for example laxatives,
diarrhea as a symptom. In these patients, one should
antacids containing calcium or magnesium, colchicines,
suspect that the illness is caused either by food poison-
antibiotics, alcoholic beverages and sorbitol containing
ing (induced by preformed bacterial toxin) or viral
gums. If such a history is obtained, the suspected
offending substance should be stopped before proceed-ing to any further evaluation.
In addition, it is important to take into account any
underlying diseases that may be present, such as dia-
Bacterial toxin induced food poisoning
betes, hypertension, heart disease, chronic lung disease,chronic renal failure or cirrhosis, because these could
In patients with bacterial preformed heat-stable toxin
complicate the management of diarrhea. Any condition
induced food poisoning, the incubation period is
that affects the patient’s immune status should be called
usually 6–24 h, diarrhea occurs 2–7 h after eating the
to the physician’s attention, such as practices that
contaminated food. These patients usually present with
may predispose the patient to HIV infection, history of
intense nausea and severe vomiting as the major symp-
administration of immunosuppressive drugs, steroids,
toms. Diarrhoea may follow and usually is not so severe.
Abdominal pain may also be present and is usuallycolicky in nature. Most patients are afebrile and notseverely dehydrated unless vomiting or diarrhea isintense. Clostridium perfringens is also a food-borne
disease with a characteristic incubation period of8–14 h. C. perfringens differs clinically from food poi-
In the adult with diarrhea, it is important to look for
soning due to Staphylococcus aureus and Bacillus cereus
signs of dehydration, including examination of the
in the longer incubation period and in clinical symp-
pulse, blood pressure (standing and sitting), jugular
toms. Vomiting is unusual in C. perfringens food-borne
venous pressure, skin turgor, mucosal dryness, for
disease and it is the most important clinical finding in
example in the mouth and lips, evidence of sunken eye
the other forms of food poisoning. Foods that are likely
to be contaminated with toxin or infectious organisms
It should be stressed that, regardless of the severity
of diarrhea, abdominal examination is strongly recom-mended for every patient. Both light and deep palpa-
Specific acute diarrhea syndromes that require
tion should be carefully performed to exclude signs of
peritonitis. Although minimal tenderness to deep pal-pation can be found in dysentery, it should be seriously
Acute diarrhea in the elderly (age ≥ 65-years-old)
observed and these patients must be closely monitored,
because some surgical or serious medical conditions, for
example appendicitis, diverticulitis, adnexitis, pan-
Hemorrhagic colitis (due to enterohaemorrhagic E. coli,
creatitis and ischemic colitis, may present as acute
EHEC or Shiga-toxin producing E. coli, STEC)
diarrhea. In acute diarrhea, guarding, rigidity and re-
bound tenderness should not be present. If they are
Acute diarrhea in immunocompromised hosts
present at all, further investigations and appropriate
Rectal examination should be part of the initial exam-
ination in every case, especially in patients over 50 years
Acute diarrhea in septicemia prone conditions
of age.10 This allows the physician to see with certainty
are cake, bread and cooked rice that have been left for
Enteropathogens responsible for infectious diarrhea
a period of time. Bacteria that could produce such
toxins include S. aureus, B. cereus, C. perfringens, etc. Most symptoms subside within 48–72 h.11 Symptomatic
and supportive treatment is usually sufficient. If the
patient can drink, oral rehydration therapy is highlyencouraged. If vomiting is severe and dehydration is sig-
nificant, intravenous therapy may be necessary. Anti-
emetics, such as metocloparmide, are not effective if
given orally, but intramuscular injection may be effi-
cient. Abdominal cramping pain may respond to anti-
spasmodics, for example hyoscine, hyoscyamine and
Bacteria Viral gastroenteritis
The Norwalk virus is the most common cause of viral
gastroenteritis in adults.12 However, rotavirus and other
viruses, for example astrovirus, calicivirus, coronavirus,
enterovirus, and small round virus-like particles, may
also be the cause. The illness has an incubation period
of between 18 and 72 h, and is characterized by the
abrupt onset of nausea and abdominal cramps followed
by vomiting and/or diarrhea. Low-grade fever (above
37.5°C or 99.5°F) develops in about half of affectedindividuals. Headache, myalgias, upper respiratory tract
symptoms and abdominal pain are common. Red and
white cells are not normally found in the stool. The
illness is usually mild and self-limiting, lasting 24–48 h.
In some cases, diarrhea and vomiting may persist for a
week or longer.13 In general, oral rehydration treatment
is adequate and only in rare cases intravenous rehydra-
tion may be needed.14 Bismuth subsalicylate has been
shown to improve the clinical symptoms of viral
MAJOR PRESENTATION: Helminths DIARRHEA
ETEC, enterotoxigenic Escherichia coli; EPEC, enteropath-
Watery diarrhea, that is, stool of decreased form from
ogenic E. coli; EAggEC, enteroaggregative E. coli; EIEC,
normal-looking, semiformed to loose or watery, without
enteroinvasive E. coli; EHEC, enterohaemorrhagic E. coli.
the presence of blood, is often the clinical presentationof enterotoxin induced diarrhea. Examples of such diar-rhea include cholera caused by Vibrio cholerae andVibrioO139, and diarrhea due to non-O1 vibrios, enterotoxi-
Bloody diarrhea is the clinical presentation of severe
genic Escherichia coli, and enteropathogenic E. coli.
bacterial colitis, which is caused by invasive enteric
Some cases of infection with Vibrio parahemolyticus,
pathogens, for example Shigella spp., Salmonella spp.,
Salmonella, Aeromona spp., Pleisiomona spp., Campy-Campylobacter jejuni, Yersinia enterocolitica, enteroinva-
lobacter jejuni, Yersinia enterocolitica and Clostridium dif-
sive E. coli, enterohemorrhagic E. coli, Entamoeba his-ficile may also present as watery diarrhea, especially in
tolytica and Balantidium coli. Some cases of Vibrio
the initial stages of their course (see Table 3). parahemolyticus, Aeromona spp., and Plesiomona spp. may also present as bloody diarrhea, especially later inthe course of acute diarrhea (see Table 3). Bloody diarrheaDiarrhoea where the stool on macroscopic observationcontains blood mixed up with feces or inseparable from
the stool is classified as bloody diarrhea. Microscopi-cally, the feces generally contain numerous red blood
For the purpose of this guideline, the term ‘clinical
dehydration’ refers to moderate and/or severe dehydra-
tion, and does not include mild diarrhea or mild
other features are also important, for example the very
abrupt onset of acute diarrhea that occurs in a matter
All cases of acute diarrhea would have dehydration
of hours, the rapid progression to profound dehydra-
due to loss of fluid and electrolytes. Even mild diarrhea
tion, the absence of fever and abdominal pain, and the
would have some degree of dehydration, but this may
presence of muscle cramps.16,21,22 In the obvious cases,
be difficult to assess quantitatively. Adults normally
stools are often greenish-yellow clear watery with very
have better compensatory mechanisms than children
little food residue. Signs of dehydration should be
through the larger body fluid reserve, the better kidney
present and sometimes are very prominent. Dark field
compensatory mechanisms, and better response to
microscopy (DFM) and stool culture should be done
correct thirst. Together with poorer tissue elasticity
in all cases. Stool examination with fine microscopic
and slower shift of extra cellular fluid, the clinical
adjustment could also reveal shooting bacteria, but
signs of dehydration in adults would be less obvious
there are no red blood cells or white blood cells. In
than in children. Severity of dehydration does not
nonendemic areas, once DFM or stool culture is posi-
always correlate with severity of diarrhea. Some may
tive for cholera, notification of the area health author-
rely on the subjective symptoms alone to classify
ity should be done as soon as possible.
severity of diarrhea while it is more reliable to evaluate
It should be noted that in endemic areas, during out-
the severity of dehydration from objective signs. The
breaks or seasonal epidemics of cholera, watery diarrhea
proper assessment of severity of dehydration should
of all severity should be treated as cholera and stool
utilize both subjective and objective evidence (see
culture should be done to confirm in all cases (see
Treatment: The treatment of watery diarrhea should Watery diarrhea with clinical dehydration
focus mainly on fluid and electrolyte replacement. In
In general, severe watery diarrhea with severe dehydra-
patients with mild dehydration, and with little or no
tion is mostly caused by V. cholerae serogroup O1. There
vomiting, oral rehydration therapy using oral rehydra-
are also other organisms that cause a similar clinical
tion salts solution (ORS) should be administered at
picture as cholera. They are Vibrio O139,16 other-
approximately 1.5 times the volume of stool loss in
Non-O1 vibios17 and sometimes Vibrio parahemolyticus,
24 h without discontinuing dietary intake.23 In moder-
ate to severe dehydration, prompt aggressive intra-
Although diarrhea caused by these organisms is often
venous fluid repletion and supportive care can obviate
milder than cholera, more severe cases may occur,
the high mortality that is associated with the disease.
which should be treated in the same fashion as severe
Also if vomiting is severe and the deficit cannot be
watery diarrhea. On the other hand, it should be noted
replaced solely by ORS, intravenous fluids in the form
that during epidemics, or even in an endemic area for
of Ringer lactate will be required. In moderate to severe
cholera, patients with cholera may be found to have only
diarrhea, at least half of the calculated deficit should be
mild diarrhea, and they should be managed differently
replaced within 4 h and the rest is to be replaced within
from the suggested algorithm (see Appendix).
24 h.24 Evaluation of fluid and electrolyte deficit is
Although severe profuse watery diarrhea alone is
crucial in calculating the amount of fluids to replace.
highly suggestive of cholera, it should be stressed that
Hence, stool volume loss should be closely monitored
Classification of severity of dehydration
Subjective Objective signs
and, if possible, weighed or accurately measured. In
cells/HPF.27 These cases usually are not accompanied
those patients who are not sick enough and still can go
to toilets on their own, it may be difficult to estimateaccurately the amount of deficit and ongoing loss. Where culturally acceptable the use of ‘cholera cots’ can
Treatment: As dehydration is often mild, the need for
be very helpful to monitor the amount of ongoing loss.
fluid and electrolytes replacement may be less pressing
If cholera cots are not available, it may be safer to
than in the group with clinical dehydration. Neverthe-
replace twice the amount of estimated loss and closely
less, rehydration remains the mainstay of treatment in
monitor the status of hydration of the patient.
this group of patients. As the disease is dynamic and
Antibiotics, when given to cholera patients, reduce
mild dehydration may progress to more severe dehy-
stool volume loss and shorten the clinical course.25 If
dration, early hydration with oral rehydration therapy
there is recent epidemiological data available, the
(ORT) should be encouraged to prevent fluid deficits.
empiric antibiotics should be given according to the
Intravenous fluid replacement is often not needed.
sensitivity of Vibrio cholerae in the region. In cases where
Administration of antibiotics is unnecessary and not
antibiogram is not available, tetracycline 2 g daily for
recommended. Antidiarrheals can be allowed and lop-
3 days should be the treatment. Alternatively, doxycy-
eramide has been recommended for use as self-
cline 300 mg as a single oral dose, or 100 mg twice
medication in adults with mild acute diarrhea.28 (A brief
daily for 3 days, and ciprofloxacin 500 mg twice daily
review of scientific information regarding efficacy, side-
for 3 days (especially in regions where resistance
effects and precautions for the use of these antidiar-
to tetracycline is greater than 20%), have all been
recommended. For pregnant women, furazolidone
Particular attention should be paid to geriatric
400 mg/day for 3 days has been suggested. Antidiarrheal
patients over the age of 65 years, immunocompromised
drugs may be somewhat effective in reducing enteric
patients, and patients with conditions predisposing to
symptoms, but they play a minor role in the treatment
septicemia. Patients in these categories will need antibi-
of watery diarrhea and cannot be routinely recom-
otics, usually orally administered but sometimes sys-
mended. (Loperamide is not indicated for patients with
severe watery diarrhea, for example cholera, but forwatery diarrhea in travelers, loperamide can be veryhelpful). Treatment should rely only on rehydrationtherapy and antibiotics only. Recently the use of resis-tant starch has been shown to be of benefit in reducing
stool volume loss and shortening the clinical course inadult patients with cholera.26
Most acute bloody diarrhea is caused by Shigella spp. and Campylobacter jejuni. Shigella dysenteriae and Shigellaflexneri, often produce a more severe disease with high
Watery diarrhea without dehydration
fever, while Shigella boydii and Shigella sonnei usually
Patients in this group comprise the majority of cases of
cause a milder disease. Other enteric pathogens pro-
acute diarrhea in adults. They are often mild and are
ducing bloody diarrhea include Salmonella enteritidis,
not accompanied with signs of dehydration.They repre-
Yersinia enterocolitica, Clostridium difficile, EHEC and
sent acute gastroenteritis that are usually caused by
EIEC. Sometimes Aeromonas hydrophila and Ple-
enteric pathogens which have a self-limited course
siomonas shigelloides that have severe enough diarrhea
and generally does not need antibiotics (except in
may also produce bloody diarrhea.29 Entamoeba his-
patients with extreme ages), for example Non-O1
tolytica infections commonly present as chronic diar-
vibrios, Vibrio parahemolyticus, Aeromonas spp., Ple-
rhea, but they may sometimes present as acute bloody
siomonas spp., Edwardsiella spp., Salmonella spp. It may
also include the milder and uncomplicated forms of
Bloody diarrhea is often accompanied by fever that
diarrhea from Vibrio cholerae, Vibrio O139, Shigella
may persist for longer than 2 days and may be higher
boydii, Shigella sonnei, Campylobacter spp., Yersinia spp.,
than 38.5°C. Initially, these patients may pass watery
and all groups of Escherichia coli.
stools that rapidly progresses to bloody diarrhea and
In general, diarrhea is characterized by the passage of
dysentery. Dysentery is characterized by the frequent
loose or loose watery stools with some food residue in
passage (usually 10–30 times a day) of small-volume
the feces. These patients normally pass 4–8 stools a day
stools consisting of blood, mucus and pus; this diarrhea
without or with minimal signs of dehydration. There
is accompanied by abdominal cramps and tenesmus,
should be no gross blood or bloody mucoid material in
the painful straining at stool that may lead to rectal
the stool. Fever could be present but is often mild and
prolapse. Diagnosis is enhanced if microscopically RBC
does not last longer than two days. Abdominal pain and
and WBC are found in the stool.27,30 It is essential to
vomiting may be severe in the first few days but grad-
exclude amoebic colitis by examining fresh stool for
ually subsides in the following days. Abdominal tender-
trophozoites. Seizures are rare in adults with bloody
ness should be absent, both to light and deep palpation.
diarrhea. Mild dehydration is common and severe dehy-
If stool microscopic examination is available, it charac-
dration is very rare. The hemolytic uremic syndrome
teristically shows no ova or parasites, RBC or WBC.
rarely complicates bloody diarrhea. Bacteremia is asso-
However, small numbers of RBC and WBC are some-
ciated with higher-than-usual mortality and is more
times present microscopically, but do not exceed 20
common among elderly patients31–33 (see Appendix). Treatment: The mild dehydration in bloody diarrhea
uals, the diarrhea will probably subside before the
can be readily corrected with ORT and intravenous
culture results become available.38,39 Stool culture is
therapy is often not needed. The use of antibiotics in
advisable in patients with bloody diarrhea, moderate to
most patients with bloody diarrhea reduces the dura-
severe diarrhea with objective evidence of dehydration,
tion of illness and can shorten the carrier stage. For
and those with diarrhea that does not subside after a
practical purpose, after having excluded amoebic colitis
few days.40 In the situation of an outbreak, nosocomial
and EHEC or STEC by careful stool examination, it is
diarrhea, or the specific conditions of acute diarrhea
acceptable to start empiric therapy with antibiotics
listed in Table 2, extensive work up with stool culture
rather than waiting for stool culture results. If the local
should be encouraged (see Appendix).
antibiogram of Shigella spp. is known, the preferred
‘Routine’ culture techniques vary from country to
antibiotics can be selected. But if no information is
country and hospital to hospital, depending on the
available, one of the fluoroquinolones is preferred. Nor-
availability, feasibility and local practice. When diarrhea
floxacin 800 mg/day, ciprofloxacin 1000 mg/day or lev-
is non-specific or indeterminate and there are limita-
ofloxacin 500 mg/day for 3–5 days should be adequate
tions of resources and facilities, routine stool culture
for healthy adults. For geriatric patients, or septicemic
with MacConkey agar is the minimal requirement.
prone conditions, ofloxacin or ciprofloxacin is pre-
Because most laboratories in the USA do not culture
ferred. It is imperative not to administer antimotility
routinely for Vibrio cholerae or other Vibrio spp., clini-
agents, such as loperamide, diphenoxylate, atropine and
cians should request appropriate cultures for clinically
codeine, as the drugs are suspected of enhancing the
suspected cases.When cholera is suspected from a posi-
severity of disease by delaying excretion of organisms
tive DFM or presence of shooting bacteria from
and thus facilitating further invasion of the mucosa.
light microscopy, thiosulfate-citrate-bile-salt-sucrose(TCBS) agar should be added to the routine Mac-Conkey agar to detect Vibrio group organisms. Further
identification for Vibrio cholerae
serogrouping should be done, together with the identi-
Although fresh stool examination under light
fications of Vibrio O139, Non-O1 Vibrio cholerae
microscopy should be encouraged in every case,34 it
and Vibrio parahemolyticus. When bloody diarrhea is
may not always be practicable or possible. In real life
suspected, selective media for Shigella, for example
situations, assessment of patients with acute diarrhea
salmonella-shigella agar or XLD agar should be added
may have to rely solely on history and physical exami-
to the routine MacConkey agar. Micro-aerophilic cul-
nation. Hence, in the algorithm, stool examination is
tivation technique with inhibitory media to detect
recommended in patients with watery diarrhea with
Campylobacter and special media for Yersinia should be
dehydration and in patients with bloody diarrhea, but
added to the routine culture.41,42 If traveler’s diarrhea is
not considered as essential in patients with watery diar-
diagnosed, culture for all bacterial causes should be per-
rhea without dehydration. Depending on the avail-
formed. For suspected EHEC associated diarrhea, Sor-
ability, feasibility and local practice, stool examination
bitol-MacConkey agar should be added to the routine
may be done early in some cases and when it is done,
culture.43 For antibiotic-associated enterocolitis, detec-
the detection of microscopic RBC and WBC > 20
tion of C difficile Toxin A and B using ELISA or tissue
cells/HPF by early stool examination may have some
culture assay should be done (see Appendix).
predictive value in detecting early cases of bloody
Fresh stool specimens should always be used when
diarrhea. In patients with gross bloody diarrhea, stool
possible to ensure that fastidious organisms that decom-
examination can provide essential information for
pose easily are detected before they degenerate. Stool
differentiating shigellosis from amebiasis.35 In addition,
specimens should be transported to the microbiology
dark-field microscopy (DFM) is strongly recommended
department ideally within 2 h after the passage, but
in all patients with watery diarrhea with dehydra-
8–12 h would also be acceptable.44 In cases in which
tion.36,37 A positive DFM for shooting bacteria should
stool specimens are not available, rectal swabs should
indicate the high possibility of Vibrio spp., especially
be obtained and put in transport media until culture. Vibrio cholerae, and appropriate antibiotics to eradicateVibrio cholerae should be promptly initiated. In situa-tions in which DFM is not available, fine adjustment oflight microscopic examination to look for active motile
‘shooting’ bacteria can be a helpful alternative to diag-nose Vibrio spp. as a cause of diarrhea. Presence of stool
All patients who do not improve after rehydration, with
ova and parasites in the stool should lead to appropri-
or without antidiarrheals and/or empiric antibiotics,
should require re-evaluation after 3–5 days, dependingon the severity of the continuing illness. Such patientsshould be informed to bring along his or her ‘fresh’ stool
specimen for microscopic re-examination and/or re-culture at their next visit. They should be advised to
In general, stool culture is probably not necessary in
observe their stool. They should also be advised to
patients who present to physicians with mild diarrhea
consult their physician for re-evaluation if the stool
without obvious signs of dehydration, and within the
character changes and becomes more watery or bloody,
first few days of onset of illness. In most such individ-
if they develop high fever (> 38.5°C), if their stage of
clinical dehydration does not improve, or if their
as possible. Selection of antibiotics for corresponding
abdominal pain becomes more intense or persistent.
enteropathogens should follow the antibacterial sensi-
When the patient comes for the second visit, stool
tivity of the pathogen that was isolated. In situations
examination and culture should be done especially if
where an antibiogram is not available, antibiotics selec-
they were not performed in the first visit. In cases of
tion should follow the available local or regional data
bloody diarrhea without an identifiable pathogen, which
regarding antibiotic susceptibility in that region or
do not improve after empiric treatment, further
country. If no such information is available, the use of
investigation by doing sigmoidoscopy or colonoscopy
conventional recommended antibiotics (as shown in
together with biopsy is usually necessary.
Table 5) is recommended. It must be noted that anti-biotics are not recommended for some entero-pathogens, as there is no information to confirm the
efficacy of antibiotic use or the available informationsuggests that antibiotic use in this particular situation
Patients who were managed along the scheme of the
may actually be deleterious. Again, it should be stressed
algorithm or have bloody diarrhea in spite of empiric
that dehydration needs to be properly corrected in all
antibiotics, and did not improve, should be further
cases, no matter the result of the stool culture.
investigated by sigmoidoscopy or colonoscopy. Colonicbiopsy together with culture should be performed eventhough the mucosa may look normal endoscopically.45
Oral rehydration Selective antibiotics for known pathogens
In this article, the term ORS (Oral Rehydration SaltsSolution) and ORT (Oral Rehydration Therapy) are
Whenever stool examination and culture results are
used.To avoid confusion, clarification of these terms are
available, treatment should be as selective and specific
Recommended antibiotics against specific enteric pathogens
Doxycycline, 300 mg single doseTMP-SMZ, 160–800 mg b.i.d. ¥ 3 dFluoroquinolone* ¥ 3 d
Doxycycline, 300 mg single doseTMP-SMZ, 160–800 mg b.i.d. ¥ 3 dFluoroquinolone* ¥ 3 d
Antibiotics are usually not required, except in
Antibiotics are usually not required, except in
Gentamicin#, 80 mg ¥ 5–7 dCefotaxime#, 1 g q.i.d. ¥ 5–7 d
Ceftriaxone#, 1 g b.i.d. ¥ 5–7 dAzithromycin 250 mg single dose
Antibiotics are usually not required, except in
Antibiotics are usually not required, except in
Antibiotics are usually not required, except in
Antibiotics are usually not required, but may be
Fluoroquinolone* ¥ 3 dTMP-SMZ, 160–800 mg b.i.d. ¥ 3 d
Antibiotics have no established therapeutic
value and are usually not required, except in
Antibiograms are needed. (Mostly in children)
Antibiotics are usually not required, except in
Enteroaggregative Fluoroquinolone* ¥ 3 d
Role of antibiotics is unclear and administration
should be avoided as they may be harmful.
(may predispose to hemolytic uremic syndrome
Antibiotics are usually not required, except in
Antibiotics are usually not required, except in
Offending antibiotics should be withdrawn if
Vancomycin 125–250 mg q.i.d. ¥ 10-14 d
Metronidazole, 250–500 mg q.i.d. ¥ 10–14 d
aantibiotics may be required in septicemic prone conditions e.g. cirrhosis, or immunocompromised hostsbantibiotics may be required in severely ill patients, or traveler’s diarrhea, or septicemic prone conditions e.g. cirrhosis, uncon-
trolled diabetes mellitus, or immunocompromised hosts
cantibiotics may be required in severely ill patients, or age < 6 months or > 65 year old, or immunocompromised hosts, or sep-
ticemic prone conditions e.g. patients with prosthesis, valvular heart disease, or severe atherosclerosis, or malignancy, or uremia,or uncontrolled diabetes mellitus.
dantibiotics may be required in severely ill patients, or immunocompromised hostseantibiotics may be required in severely ill patients, traveler’s diarrhea, or immunocompromised hosts, or septicemic prone
conditions, or uncontrolled diabetes mellitus.
fantibiotics may be required in severely ill patients, traveler’s diarrheagantibiotics may be required in severely ill patients, or associated bacteremia, or when bacteremia is suspected, or immuno-
*fluoroquinolone, for example 300 mg ofloxacin, 400 mg norfloxacin, or 500 mg ciprofloxacin b.i.d. #antibiotics for suspected septicemic cases
Oral rehydration salts solution (ORS)
also refers to non-ORS measures of rehydration, includ-
Oral rehydration salts solution refers to the oral rehy-
ing various natural or formulated electrolyte containing
dration salts formula that is recommended by WHO. It
contains sodium chloride 3.5 g, sucrose 40 g (or glucose
Adult patients with watery diarrhea and clinical dehy-
20 g), trisodium citrate dihydrate 2.9 g (or sodium
dration should receive the proper WHO-recommended
bicarbonate 2.5 g) and potassium chloride 1.5 g in one
ORS formula to correct their dehydration, especially in
litre of clean drinking water. This combination should
endemic areas of cholera. In other parts of the world
give the concentration of sodium 90 mEq/L, potassium
where cholera is not a problem, a milder formula may
be accepted. Patients with mild dehydration or patients
with all types of diarrhea without obvious evidence of clinical dehydration can also use the WHO ORSformula in conjunction with intermittent free waterdrinking. In adults, the chance of having hyponatremia
or hypernatremia may be much greater in the elderly.31
Oral rehydration therapy in the context of these guide-
Hence, ORT or usage of lower sodium concentration of
lines refers to the use of informal oral rehydration
ORS, may be more appropriate in elderly patients. In
formulas or electrolyte packages with lower sodium
geriatric patients, periodic assessment of serum elec-
concentration than the one recommended by WHO. It
trolytes may be necessary. The super ORS, which
contain glycine or starch (cereal-based formulations)
oping world, where diarrhea is very prominent. In
are receiving increased attention.51 Because of their
industrialized countries, the antidiarrheal compounds
lower osmolarity, they may reduce stool output and
may be cost effective and useful in returning people
better enhance electrolytes absorption. The use of resis-
more quickly to work and school during a bout of
tant starch to provide colonic short chain fatty acids
There is a wide variety of antidiarrheal drugs avail-
In general, ORS or ORT should be taken by mouth
able on the market. Physicians in each region of the
slowly and intermittently by ‘sipping’ little by little, not
world will have to keep in mind the cost-risk-benefit
‘drinking’ in large amount in a short period of time.The
ratios and make their own judgment in selecting or
amount to be taken should be approximately 1.5–2
recommending the antidiarrheals. In the following
times the estimated amount of deficit plus concurrent
paragraphs the evidence supporting the use of each
antidiarrheal drug is briefly reviewed, so that physicianscan decide which to use by judging from their efficacy,side-effects, indications and contra-indications basedon the available literature. Antidiarrheal drugs are
Intravenous fluid replacement
grouped and discussed under the following topics.
For initial management of severely dehydrated or hypo-volemic shock patients, immediate intravenous fluid
Antiperistaltics or antimotility drugs
replacement is essential. Patients with moderate ormilder degree of dehydration may also need intravenous
Most available antiperistalic agents act by altering
fluid replacement if they have severe vomiting and are
intestinal motility. Some also may have mild pro-
unable to drink ORS properly. Patients with dull con-
absorptive or antisecretory activity. They include
sciousness, who may harbor the risk of aspiration,
loperamide, diphenoxylate, codeine, tincture opium and
should also be rehydrated intravenously. Ringer’s lactate
other opiates. They may be helpful in secretory diarrhea
is best recommended for all forms of acute diarrhea in
of mild to moderate severity by reducing the frequency
adults, as it contains potassium 4 mEq/L, which can
and volume of stools.53–55 Among all antimotility drugs,
be replaced rapidly in large amounts according to the
loperamide is the most commonly recommended agent
severity of deficit. The total fluid deficit in severely
for use in uncomplicated diarrhea.28,56 However, such
dehydrated patients can be replaced safely within the
antimotility agents are contraindicated in diarrhea
first 4 h of therapy, half within the first hour.52 The
caused by invasive pathogens because the induced
volume of fluid to be administered is determined by the
intestinal stasis may enhance tissue invasion by the
rate of stool losses and the degree of pre-existing dehy-
organisms or delay their clearance from the bowel.
dration. Meanwhile, oral therapy usually can be initi-
Hence, bloody diarrhea with high fever, immunocom-
ated with the goal of maintaining fluid intake equal to
promised host and septicemic prone conditions with
the ongoing loss. However, patients with continued
diarrhea should not be given this group of drugs.
large-volume diarrhea might require prolonged intra-
Some of these drugs may cause addiction, if they are
venous treatment to keep up with gastrointestinal fluid
to be administered for a long period. Suppression of res-
losses. It should also be used with additional potassium
piration is significant in children and may be harmful
supplements by mouth. The oral route of rehydration
in elderly people with chronic lung disease. The newer
and potassium replacement is safer than the intravenous
loperamide preparation, loperamide oxide, may be the
route and is physiologically regulated by thirst and urine
drug in this group with the least side-effects.57 Response
to loperamide can vary from one person to another.Theaim should be to reduce the frequency of diarrhea, notto ‘stop’ diarrhea. Antidiarrheal drugs
While every effort should be made to identify andcorrect the specific causes of diarrhea, in many cases,
They include atropine, hyoscine, hyoscyamine and dicy-
causes that are specific and potentially treatable are
clomine. They are not effective in reducing the fre-
often not identifiable. Identification is not possible and
quency and volume of stools, but may have some value
symptomatic therapy alone is commonly indicated.
in selected cases in reducing pain from abdominal
Although most diarrheas are self-limited, some
cramps.58 High dose of anticholinergics may cause dry
antidiarrheal drugs may help in reducing amount of
mouth, urinary retention, blurred vision, palpitation,
fluid loss, frequency and consistency of stool, or shorten
the clinical course of diarrhea. The addition of antidiar-rheal drugs improves the quality of life to a certainextent at the financial cost of the drugs.The cost-benefit
ratio of using various antidiarrheal agents has not
There are a variety of drugs in this group, for example
been properly studied. As acute diarrhea is a very
activated charcoal, kaolin, pectin, dioctahedral smectite,
common condition affecting large numbers of people,
attapulgite (anhydrous aluminum silicate), aluminum
the routine usage of antidiarrheals could mean a great
hydroxide and tannic acid. Theoretically these medica-
financial burden to countries, especially in the devel-
tions adsorb toxins produced by toxigenic bacteria and
act by preventing their adherence to intestinal mem-
controlling motility and secretion of the gut. As 5HT
branes. To be effective, they have to be given very early
is also a neurotransmitter found in the brain and
before the toxins are fixed to intestinal mucosa. Their
the enteric nervous system (ENS). The antagonists of
efficacy depends on their potency to adsorb toxins,
5HT3 receptor were found to inhibit extrinsic sensory
some preparations, for example dioctahedral smectite,
neuron stimulation (which can inhibit nausea, vomit-
attapulgite and bismuth preparations are more effective
ing, stomach pain and bloating) and reduce peristalsis
in adsorbing toxins than others.59–61 In clinical trials,
and secretory reflex. As a result, they help to reduce
they can increase stool consistency and decrease stool
stool volume and improve stool consistency. Another
frequency, but cannot reduce the amount of fluid loss.
newer antisecretory agent is oral enkephalinase
They only mask its extent and dehydration is not pre-
inhibitor (Racecadotril). It prevents the degradation of
vented.When prescribing these medications, it is impor-
endogenous opioids (enkephalins), thereby reducing
tant to maintain adequate hydration and proper diet,
hypersecretion of water and electrolytes into the intesti-
especially in the elderly. Adsorbents are not effective in
nal lumen. Clinical trials that show the efficacy of these
patients with febrile bloody diarrhea. In rare instances,
drugs in the management of acute diarrhea in children
they may cause constipation. Prolonged use may inter-
and adults are being validated.73,74 Octreotide, which is
fere with some medications, for example theophylline
a long-acting synthetic analog of somatostatin, has a sig-
and digoxin. Psyllium and other hydrophilic agents are
nificant antisecretory effect.75 It is expensive and has to
bulk forming agents, which absorb water and thereby
be administered subcutaneously. It is more reasonable
enhance stool consistency. Commonly, they are used in
to prescribe in otherwise refractory cases of chronic
chronic diarrhea and irritable bowel syndrome, not in
There are an enormous numbers of herbal medicines
Probiotics are non-pathogenic organisms, for example
around the world that are claimed to be effective in
Lactobacillus acidophilus and Saccharomyces boulardii,
treating diarrhea. However, there is very little scientific
which multiply in the patient’s intestine and produce
data to support or confirm the efficacy of these medi-
metabolites, which increase acidity of stool and prohibit
cines, or if results are available, they are mostly incon-
the growth of enteropathogens. They prevent the inva-
clusive and anecdotal. However, they are cheap and
sion of bacteria in intestine tissue, and produce short
locally available. Administration of herbal medicine that
chain fatty acids that are beneficial for intestine recov-
is shown to be harmless in mild watery diarrhea without
ery, and increase the rate of fluid and electrolyte absorp-
dehydration can be locally accepted, provided that the
tion. In children, there are studies which show that the
dehydration is properly corrected and patients with
use of probiotics could reduce the clinical course of
febrile dysentery are properly managed. Herbal medi-
acute diarrhea.62–64 In adults, they are used mainly in
cines should not be recommended in severe diarrhea no
chronic diarrhea and relapse of antibiotic associated
There are many drugs in everyday use that have anti-secretory effects in vitro, for example phenothiazine,
Acute diarrhea in adults is a common every-day condi-
chlorpromazine, aspirin, indomethacin, lithium car-
tion all over the world. Besides acute infectious diar-
bonate, and calmodulin-inhibitors. They work by a
rhea, the definition also encompasses many intestinal
variety of different mechanisms including inhibition of
conditions that may present as acute diarrhea. Stool
prostaglandins and effects on cyclic AMP, calmodulin
examination and culture results are often not available,
inhibition,66 inhibition of gut hormones and encephali-
and proper hydration together with empiric treatment
nase inhibition of chloride channels.67 But some of these
has to be initiated. A practical approach for the man-
drugs have to be administered in very high doses to give
agement of adult patients with acute diarrhea is pre-
effective antisecretory effects in vivo. Hence, their drug-
sented in an algorithmic diagram. After careful history
related side-effects preclude them from being used
taking and a physical examination to exclude other con-
effectively.68,69 This group of drugs is more physiologic
ditions that may present as acute diarrhea, and other
in approach and may become the ideal agents for use
specific situations of acute diarrhea that deserve to be
in acute diarrhea. Bismuth salts preparations, according
approached differently, patients are classified as having
to their mode of action, are also an antisecretory agents.
predominately diarrhea or predominately vomiting.The
They are found to be as effective as loperamide, and
diarrhea predominant group is further classified into
reduce the number of stools passed by about 50%, with
watery diarrhea and bloody diarrhea subgroups by their
improvement in other associated symptomatology.70,71
gross stool appearance. The watery diarrhea subgroup
The untoward side-effects of bismuth preparations are
with clinical dehydration will have to exclude cholera by
blackened stool, blackened tongue, tinnitus and fecal
stool examination with dark field microscopy confirmed
later by stool culture. The watery diarrhea without clin-
Recently, drugs that affect 5-hydroxytryptamine
ical dehydration subgroup is managed by ORT with or
(5HT) or serotonin were found to have a pivotal role in
without antidiarrheals.The bloody diarrhea subgroup is
treated with antibiotics either empirically or after stool
15 Stenhoff MC, Douglas RGJ, Greenberg HB, Callahan
examination and culture to rule out EHEC or STEC.
DR. Bismuth subsalicylate therapy of viral gastro-
If patients do not improve after the first visit and spe-
enteritis. Gastroenterology 1980; 78: 1495–9.
cific pathogens causing diarrhea are identified, specific
16 Bhattacharya SK, Bhattacharya MK, Nair GB et al.
antibiotics should be administered according to the sen-
Clinical profile of acute diarrhoea cases infected with the
sitivity results or data from the community. Further
new epidemic strain of Vibrio cholerae O139: designation
investigation by repeating stool examination and culture
of the disease as cholera. J. Infect. 1993; 27: 11–15.
together with sigmoidoscopy or colonoscopy are essen-
17 Campos E, Bolanos H, Acuna MT et al. Vibrio mimicus
tial if the patient does not get better. There are special
diarrhoea following ingestion of raw turtle eggs. Appl.
situations in acute diarrhea that require special consid-
Environ. Microbiol. 1996; 62: 1141–4.
erations and these are discussed in detail.
18 Alabi SA, Odugbemi T. Occurrence of Aeromonas
species and Plesiomonas shigelloides in patients with andwithout diarrhoea in Lagos, Nigeria. J. Med. Microbiol.REFERENCES
1990; 32: 45–8.
19 Sack RB, Gorbach SL, Banwell JG, Jacobs B, Chatterjee
1 Stone DH, Mitchell S, Packham B,Williams J. Prevalence
BD, Mitra RC. Enterotoxigenic Escherichia coli isolated
and first-line treatment of diarrhoeal symptoms in the
from patients with severe cholera-like disease. J. Infect.
community. Public Health 1994; 108: 61–8. Dis. 1971; 123: 378–85.
2 van Berkestijn LG, Kastein MR, Lodder A, de Melker
20 Sack DA, McLaughlin JC, Sack RB, Orskov F, Orskov I.
RA, Bartelink ML. How well are patients treated in
Enterotoxigenic Escherichia coli isolated from patients
family practice? Quality of consultations for non-acute
at a hospital in Dacca. J. Infect. Dis. 1977; 135: 275–80.
abdominal complaints. Int. J. Qual. Health Care 1998; 10:
21 Keen MF, Bujalski L. The diagnosis and treatment of
cholera. Nurse Pract. 1992; 17: 53–6.
3 World Health Organization. The World Health Report
22 Fukuda JM,Yi A, Chaparro L, Campos M, Chea E. Clin-
1996: Fighting disease, fostering development. Geneva:
ical characteristics and risk factors for Vibrio cholerae
infection in children. J. Pediatr. 1995; 126: 882–6.
4 Cohen ML. Epidemiology of diarrhoeal disease: infec-
23 Bojalil R., Guiscafre H, Espinosa P et al. A clinical train-
tious diarrhoea. Infect. Dis. Clin. North Am. 1988; 2:
ing unit for diarrhoea and acute respiratory infections:
an intervention for primary health care physicians in
5 Feldman R., Banatvala N. The frequency of culturing
Mexico. Bull.World Health Organ. 1999; 77: 936–45.
stools from adults with diarrhoea in Great Britain.
24 Seas C, DuPont HL, Valdez. LM et al. Practical guideline
Epidemiol. Infect. 1994; 113: 41–4.
for treatment of cholera. Drugs 1996; 51: 966–73.
6 Gangarosa RE, Glass RI, Lew JF, Boring JR. Hospital-
25 Mahalanabis D, Molla AM, Sack DA. Clinical manage-
izations involving gastroenteritis in the United States,
ment of cholera. In: Barua D, Greenough WB eds.
1985 the special burden of the disease among the elderly. Cholera. New York: Plenum, 1992; 253. Am. J. Epidemiol. 1992; 135: 281–90.
26 Ramakrishna BS, Venkataraman S, Srinivasan P, Dash P,
7 Thoren A, Lundberg O, Bergdahl U. Socioeconomic
Young G, Binder H. Amylase-resistant starch plus oral
effects of acute diarrhoea in adults. Scand. J. Infect. Dis.
rehydration solution for cholera. N. Engl. J. Med. 2000;
1988; 20: 317–22. 342: 308–13.
8 CDC. Diagnosis and Management of Foodborne Ill-
27 Alvarado T. Fecal leucocytes in patients with infectious
nesses. A Primer for Physicians. Morb. Mortal.Wkly Rep.
diarrhoea. Trans. R. Soc.Trop. Med. Hyg 1983; 77: 316–20.
2001; 50: 1–70.
28 Wingate D, Phillips SF, Lewis SJ et al. Guidelines for
9 Ramakrishna BS, Kang G, Rajan DP, Mathan M, VIM.
adults on self-medication for the treatment of acute diar-
Isolation of Vibrio cholerae O139 from the drinking water
rhea. Aliment Pharmacol. Ther. 2001; 15: 773–82.
supply during an epidemic of cholera. Trop. Med. Int.
29 Kain KC, Kelly MT. Clinical features, epidemiology, and
Health 1996; 6: 854–8.
treatment of Plesiomonas shigelloides diarrhea. J. Clin.
10 Reardon M, Coleman P, Twomey C, Hyland CM. Rectal
Microbiol. 1989; 27: 998–1001.
examination in hospital patients. Ir. Med. J. 1995; 88:
30 Siegel D, Cohen PT, Neighbor M et al. Predictive value
of stool examination in acute diarrhea. Arch. Pathol. Lab.
11 Tauxe RV, Hughes JM. Foodborne disease. In: Mandel,
Med. 1987; 111: 715–8.
GF Bennett, JE Dohr, R. eds. Principles and Practices of
31 Bennett RG, Greenough WB. Approach to acute diarrhea
Infectious Diseases. 4th edn. New York: Churchill Living-
in the elderly. Gastroenterol. Clin. North Am. 1993; 22 (3):
12 Kapikian AZ, Estes MK, Chanock RM. Norwalk group
32 Lew JF, Glass RI, Gangarosa RE, Cohen IP, Bern C, Moe
of viruses. In: Fields BN, Knipe DM, Howley PM,
CL. Diarrheal deaths in the United States, 1979 through
eds. Fields Virology, 3th edn. Philadelphia, Pennsylvania:
1987. A special problem for the elderly. JAMA 1991; 265:
13 Tallett S, MacKenzie C, Middleton P, Kerzner B, Hamil-
33 Ramakrishna BS. Gastrointestinal infections in the
ton R. Clinical, laboratory, and epidemiologic features of
elderly. In: Sharma OP ed. Geriatrics and. Gerontology:
a viral gastroenteritis in infants and children. Pediatrics
ANB Publishers. New Delhi, 1999; 186–95.
1977; 60: 217–22.
34 Thorne GM. Diagnosis of infectious diarrheal diseases:
14 Blacklow NR, Greenberg HB, Engl N. Viral gastroen-
infectious diarrhea. Infect. Dis. Clin. North Am. 1988; 2:
teritis. J. Med. 1991; 325: 252–61.
35 Speelman P, McGlaughlin R., Kabir I, Butler T. Differ-
52 Rahman O, Bennish ML, Alam AN et al. Rapid intra-
ential clinical features and stool findings in shigellosis
venous rehydration by means of a single polyelectrolyte
and amoebic dysentery. Trans. Roy Soc. Trop Med. Hyg.
solution with or without dextrose. J. Pediatr. 1988; 113:
1987; 81: 549–51.
36 Benenson AS, Islam MR, Greenough WB. Rapid identi-
53 Multicentre general practice comparison of loperamide
fication of Vibrio cholerae by darkfield microscopy. Bull.
and diphenoxylate with atropine in the treatment of acute
WHO 1964; 30: 827–31.
diarrhoea in adults. Br. J. Clin. Pract. 1979; 33: 77–9.
37 Pryor WM, Bye WA, Curran DH, Grohmann GS. Acute
54 Bergstrom T, Alestig K, Thoren K, Trollfors B. Sympto-
diarrhoea in adults: a prospective study. Med. J. Aust.
matic treatment of acute infectious diarrhoea: loperamide
1987; 147: 490–3.
versus placebo in a double-blind trial. J. Infect. 1986; 12:
38 Koplan JP, Fineberg HV, Ferraro MJB, Rosenberg ML.
Value of stool cultures. Lancet 1980; 2: 413–6.
55 van Loon FP, Bennish ML, Speelman P, Butler C.
39 Roncoroni AJ, de Cortigianni MR, Garcia Damiano MC.
Double blind trial of loperamide for treating acute watery
Cost and effectiveness of fecal culture in the etiologic
diarrhoea in expatriates in Bangladesh. Gut 1989; 30:
diagnosis of acute diarrhea. Bol. Oficina Sanit. Panama
1989; 107: 381–7.
56 Hughes IW. First-line treatment in acute non-dysenteric
40 Bauer TM, Lalvani A, Fahrenbach J et al. Derivation and
diarrhoea. clinical comparison of loperamide oxide,
validation of guidelines for stool cultures for enteropath-
loperamide and placebo. [UK Janssen Res. Group
ogenic bacteria other than Clostridium difficile in hospi-
General Practitioners]. Br. J. Clin. Pract. 1995; 49: 181–5.
talized adults. JAMA 2001; 285: 313–9.
57 Dettmer A. Loperamide oxide in the treatment of acute
41 Tabibian N, Clarridge JE, Smith JL, Alpert E, Shaw I,
diarrhoea in adults. Clin. Ther. 1994; 16: 972–80.
Graham DY. Clinical impact of stool cultures for Campy-
58 Reves R., Bass P, DuPont HL, Sullivan P, Mendiola J.
lobacter in adults with acute or chronic diarrhoea. South
Failure to demonstrate effectiveness of an anticholiner-
Med. J. 1987; 80: 709–11.
gic drug in the symptomatic treatment of acute travelers’
42 Feeney GF, Kerlin P, Sampson JA. Clinical aspects of
diarrhea. J. Clin. Gastroenterol. 1983; 5: 223–7.
infection with Yersinia enterocolitica in adults. Aust. NZ J.
59 Wakinson MA. A lack of therapeutic response to kaolin
Med. 1987; 17: 216–9.
in acute childhood diarrhoea treated with glucose
43 Tarr PINM, Clausen CR, Watkins SL, Christie DL,
electrolyte solution. J. Trop. Pediatr. 1982; 28: 308.
Hickman RO. Escherichia coli 0157. H7 and the hemolytic
60 Leber W. A new suspension form of smectite (Liquid
uremic syndrome: importance of early cultures in estab-
‘Diasorb’) for the treatment of acute diarrhoea: a
lishing the etiology. J. Infect. Dis. 1990; 162: 553–6.
randomized comparative study. Pharmatherapeutica 1988;
44 Lew JF, LeBaron CW, Glass RI et al. Recommendations
for collection of laboratory specimens associated with
61 Zaid MR, Hasan M, Khan AA. Attapulgite in the treat-
outbreaks of gastroenteritis. Morb. Mortal. Wkly Rep.
ment of acute diarrhoea: a double-blind placebo-
1990; 39: 14.
controlled study. J. Diarrhoeal Dis. Res. 1995; 13: 44–6.
45 Bellaiche G, Le Pennec MP, Slama JL et al. The value
62 Kaila M, Isolauri E, Saxellin M, Arvilommi H, Vesikari
of rectosigmoidoscopy and the bacteriologic culture of
T. Viable versus inactivated lactobacillus strain GG in
colon biopsies in the etiologic diagnosis of acute diar-
acute rotavirus. Arch. Dis. Child 1995; 72: 51–3.
rhoea of adults. A prospective study of 65 patients. Ann.
63 Elmer GW, Surawicz CM, McFarland LV, Biotherapeu-
Gastroenterol. Hepatol. (Paris) 1996; 32: 11–17.
tic agents. A neglected modality for the treatment and
46 Safrin S, Morris JG, Adams M et al. Non-O1 Vibrio
prevention of selected intestinal and vaginal infections.
cholerae bactermia. case report and review. Rev. Infect.JAMA 1996; 275: 870–6. Dis. 1988; 10: 1012–17.
64 Guandalini S, Pensabene L, Zikri MA et al. Lactobacil-
47 Hally RJ, Rubin RA, Fraimow HS et al. Fatal Vibrio para-
lus GG administered in oral rehydration solution to chil-
hemolyticus septicemia in a patient with cirrhosis. Dig.
dren with acute diarrhea: a multicenter European trial. Dis. Sci. 1995; 40: 1257–60. J. Pediatr. Gastroenteol. Nutr. 2000; 30: 50–60.
48 Wanke CA, Gerrior J, Blais V, Mayer H, Acheson D. Suc-
65 McFarland LV, Surawicz CM, Greenberg RN et al.
cessful treatment of diarrhoeal disease associated with
Prevention of beta-lactam-associated diarrhea by
enteroaggregative Escherichia coli in adults infected with
Saccharomyces boulardii compared with placebo. Am. J.
human immunodeficiency virus. J. Infect. Dis. 1998; 178: Gastroenterol. 1995; 90: 439–48.
66 Okhuysen PC, DuPont HL, Ericsson CD et al. Zaldaride
49 Centuori S, Mati L, Foto E, Gellili L, Tamburlini G.
maleate (a new calmodulin antagonist) versus lop-
Success and constraints in the implementation of WHO
eramide in the treatment of traveler’s diarrhoea: ran-
guidelines for the management of diarrhoea in Albania.
domized, placebo-controlled trial. Clin. Infect. Dis. 1995;
Minerva Pediatrica 1998; 50: 57–61. 21: 341–4.
50 Bahl R., Bhandari N, Bhan MK. Reduced-osmolarity
67 Roge J, Baumer P, Berard H, Schwartz JC, Lecomte JM.
oral rehydration salts solution multicentre trial: implica-
The enkephalinase inhibitor, acetorphan, in acute diar-
tions for national policy. Indian J. Pediatr. 1996; 63:
rhoea. A double- blind, controlled clinical trial versus
loperamide. Scand. J. Gastroenterol. 1993; 28: 352–4.
51 Molla AM, Molla A, Nath SK, Khatun M. Food-based
68 Castor B, Thoren A, Barkenius G. Failure of aspirin in
oral rehydration salt solutions for acute childhood diar-
symptomatic treatment of acute diarrhoea. J. Diarrhoeal
rhoea. Lancet 1989; 2: 429–31. Dis. Res. 1991; 9: 29–32.
69 Islam MR, Sack DA, Holmgren J, Bardhan PK, Rabbani
88 Karmali MA, Petric M, LIMC et al. The association
GH. The use of chlorpromazine in the treatment of
between idiopathic hemolytic uremic syndrome and
cholera and other severe acute watery diarrheal diseases.
infection by verotoxin-producing Escherichia coli. J. Infect.Gastroenterology 1982; 82: 1335–40. Dis. 1985; 151: 775–82.
70 DuPont HL. Nonfluid therapy and selected chemopro-
89 Bender JB, Hedberg CW, Besser JM, Boxrud DJ, Mac-
phylaxis of acute diarrhoea. Am. J. Med. 1985; 78
Donald KL, Osterholm MT. Surveillance by molecular
subtype for Escherichia coli O157: H7 infections in Min-
71 Johnson PC, Ericsson CD, DuPont HL, Morgan DR,
nesota by molecular subtyping. N. Engl. J Med. 1997; 337:
Bitsura JA, Wood LV. Comparison of loperamide with
bismuth subsalicylate for the treatment of acute travel-
90 Su C, Brandt LJ. Escherichia coli O157: H7 infection in
ers’ diarrhoea. JAMA 1986; 255: 757–60.
humans. Ann. Intern. Med. 1995; 123: 698–714.
72 DuPont HL, Flores Sanchez J, Ericsson CD et al.
91 Bell BP, Goldoft M, Griffin. PM, et al. A multistate out-
Comparative efficacy of loperamide hydrochloride and
break of Escherichia coli O157: H7-associated bloody
bismuth subsalicylate in the management of acute diar-
diarrhoea and hemolytic uremic syndrome from ham-
rhoea. Am. J. Med. 1990; 88 (Suppl.): 15S–19S.
burgers. The Washington experience. JAMA 1994; 272:
73 Hamza H, Ben Khalifa H, Baumer P, Berard H, Lecomte
JM. Racecadotril versus placebo in the treatment of acute
92 Seigler RL, Milligan MK, Burningham TH et al.
diarrhoea in adults. Aliment Pharmacol. Ther. 1999; 13
Long-term outcome and prognostic indicators in the
hemolytic–uremic syndrome. J. Pediatr. 1991; 118:
74 Salazar-Lindo E, Santisteban-Ponce J, Chea-Woo E,
Gutierrez M. Racecadotril in the treatment of acute
93 Fitzpatrick MM, Shah V, Trompeter RS, Dillon MJ,
watery diarrhea in children. N. Engl. J. Med. 2000; 343:
Barratt TM. Long-term renal outcome of childhood
haemolytic uraemic syndrome. BMJ 1991; 303: 489–92.
75 Abbas Z, Moid I, Khan AH et al. Efficacy of octreotide
94 Walterspiel JN, Ashkenazi S, Morrow AL et al. Effect of
in diarrhoea due to Vibrio cholerae: a randomized, con-
subinhibitory concentrations of antibiotics on extracellu-
trolled trial. Ann. Trop. Med. Parasitol. 1996; 90: 507–13.
lar Shiga-like toxin I. Infection 1992; 20: 25–9.
76 Pentland B, Pennington CR. Acute diarrhoea in the
95 McFarland LV. Epidemiology of infectious and iatrogenic
elderly. Age Ageing 1980; 9: 90–2.
nosocomial diarrhoea in a cohort of general medicine
77 Alapati SV, Mihas AA. When to suspect ischemic colitis.
patients. Am. J. Infect. Control 1995; 23: 295–305.
Why is this condition so often missed or misdiagnosed?
96 Cunha BA. Nosocomial diarrhoea. Crit. Care Clin. 1998;
Postgrad. Med. 1999; 105: 177–87. 14: 329–38.
78 Stek M. Traveler’s diarrhoea in the Mediterranean basin.
97 Mylotte JM, Graham R., Kahler L,Young L, Goodnough
Mil. Med. 1980; 145: 628–9.
S. Epidemiology of nosocomial infection and resistant
79 Taylor DN, Houston R., Shlim DR, Bhaibulaya M,
organisms in patients admitted for the first time to an
Ungar BL, Echeverria P. Etiology of diarrhea among trav-
acute rehabilitation unit. Clin. Infect. Dis. 2000; 30:
elers and foreign residents in Nepal. JAMA 1988; 260:
98 Cartmill TD, Shrimpton SB, Panigrahi H, Khanna V,
80 Haberberger RL, Mikhail IA, Burans JP et al. Travelers’
Brown R., Poxton IR. Nosocomial diarrhoea due to a
diarrhea among United States military personnel during
single strain of Clostridium difficile: a prolonged
joint American-Egyptian armed forces exercises in Cairo.
outbreak in elderly patients. Age Ageing 1992; 21: 245– Egypt. Mil. Med. 1991; 156: 27–30.
81 Beller M, Schloss M. Self-reported illness among
99 Centers for Disease Control and Prevention. Foodborne
travelers to the Russian Far East. Public Health Rep. 1993;
outbreaks of enterotoxigenic Escherichia coli. Rhode Island108: 645–9. New Hampshire, 1993 [published erratum appears in
82 Ericsson C, DuPont HL. Travelers’ diarrhea: approaches
MMWR Morb. Mortal.Wkly Rep. 1994; 43: 127] MMWR
to prevention and treatment. CID 1993; 16: 616–26. Morb. Mortal.Wkly Rep. 1994; 43: 81–9.
83 Larson SC. Traveler’s diarrhea. Emer. Med. Clin. North
100 Daniels NA, Bergmire-Sweat DA, Schwab KJ et al. A
Am. 1997; 15: 179–89.
foodborne outbreak of gastroenteritis associated with
84 Peltola H GS. Travelers’ diarrhea epidemiology and
Norwalk-like viruses: first molecular traceback to deli
clinical aspects. Hamilton, Ontario: BC Decker Inc,
sandwiches contaminated during preparation. J. Infect.Dis. 2000; 181: 1467–70.
85 Aronsson B, Mollby R, Nord CE. Antimicrobial agents
101 Gupta DN, Sen D, Saha MR et al. Report of an outbreak
and Clostridium difficile in acute enteric disease:
of diarrhoeal disease caused by cholera followed by
epidemiological data from Sweden, 1980–82. J. Infect.
rotavirus in Manipur. Indian J. Public Health 1990; 34: Dis. 1985; 151: 476–81.
86 Boyce TG, Swerdlow DL, Griffin PM. Escherichia coli
102 Hedberg CW, Levine WC, White KE et al. An interna-
0157. H7 and the hemolytic–uremic syndrome. N. Engl.
tional foodborne outbreak of shigellosis associated with
J. Med. 1995; 333: 364–8.
a commercial airline. JAMA 1992; 268: 3208–12.
87 Carter AO, Borczyk AA, Carlson JA et al. A severe out-
103 Khuri-Bulos NAAK, Shehabi A, Shami K. Foodhandler-
break of Escherichia coli 0157: H7–associated hemor-
associated Salmonella outbreak in a University hospital
rhagic colitis in a nursing home. N. Engl. J Med. 1987;
despite routine surveillance cultures of kitchen employ-
ees. Infect. Control Hops. Epidemiol. 1994; 15: 311–4.
104 Reves RRMA, Bartlett AV et al. Child day care increases
122 Bircks W, Reidemeister C, Sadony V, Schulte HD, Tarbiat
the risk of clinic vistis for acute diarrhoea and diarrhoea
S. Diagnostic and therapeutic problems of septicemia
due to rotavirus. Am. J. Epidemiol. 1993; 137: 97–107.
after valvular replacement. J. Cardiovasc Surg. (Torino)
105 Bacillus cereus food poisoning associated with fried rice
1972; 13: 385–9.
at two child day care centers-Virginia 1993. MMWR
123 Aksnes J, Abdelnoor M, Berge V, Fjeld NB. Risk factors
Morb. Mortal.Wkly Rep. 1994; 177–8.
of septicemia and perioperative myocardial infarction in
106 Emont SL, Cote TR, Dwyer DM, Horan JM. Gastroen-
a cohort of patients supported with intra-aortic balloon
teritis outbreak in a Maryland nursing home. Md Med.
pump (IABP) in the course of open heart surgery. Eur.J. 1993; 42: 1099–103. J. Cardiothorac Surg. 1993; 7: 153–7.
107 Sims RV, Hauser RJ, Adewale AO et al. Acute gastroen-
teritis in three community-based nursing homes. J. Gerontol. Biol. Sci. Med. Sci. 1995; 50: M252–6.
108 Asplund S, Gramlich TL. Chronic mucosal changes of
the colon in graft-versus-host disease. Mod. Pathol. 1998; 11: 513–5.
The following specific conditions of acute diarrhea are
109 van Kraaij MG, Dekker AW,Verdonck LF et al. Infectious
specifically mentioned here as there are theoretical basis
gastro-enteritis. an uncommon cause of diarrhoea in
and scientific information to warrant special consider-
adult allogeneic and autologous stem cell transplant
ations. They should be managed differently from the
recipients. Bone Marrow Transplant 2000; 26: 299–
suggested algorithm in this report. These conditions
110 Yeomans A, Davitt M, Peters CA, Pastuszek C, Cobb S.
Efficacy of chlorhexidine gluconate use in the preventionof perirectal infections in patients with acute leukemia. Acute diarrhea in the elderly Oncol. Nurs. Forum 1991; 18: 1207–13.
111 Kraus A, Guerra-Bautista G, Alarcon-Segovia D. Salmo-
Acute diarrhea that occurs in patients aged over 65
nella arizona arthritis and septicemia associated with
years is associated with higher mortality.31,32,76 Diarrhea
rattlesnake ingestion by patients with connective tissue
is a common problem among the elderly that can have
diseases. A dangerous complication of folk medicine. J.
catastrophic results. Atherosclerosis predisposes older
Rheumatol. 1991; 18: 1328–31.
adults to morbid sequelae from dehydration resulting
112 Poulos JE, Cancio M, Conrad P, Nord HJ, Altus P. Non
from diarrhea. Ischemic colitis is a serious differential
0–1 Vibrio cholerae septicemia and culture negative neu-
diagnosis especially in developed countries.77 Deaths
trocytic ascites in a patient with chronic liver disease. J.
related to diarrheal illnesses are recognized among older
Fla. Med. Assoc. 1994; 81: 676–8.
adults living in the community as well as among those
113 Merlin M, Gandara S, Iannicillo H et al. Acute and
confined to nursing homes. Outbreaks have most often
chronic diarrhoea in AIDS. Study 435 (HIV+) Patients,
been associated with excess deaths from diarrhea
Buenos Aires. Acta Gastroenterol. Latinoam 1996; 26:
among nursing-home patients. Although most cases of
dehydration from diarrhea result from gastrointestinal
114 Weber R., Ledergerber B, Zbinden R. et al. Enteric infec-
infections, non-infectious causes of diarrhea related to
tions and diarrhoea in human immunodeficiency virus-
prescription of laxatives, side-effects of medications and
infected persons: prospective community-based cohort
use of enteral feedings are common. Clostridium difficile
study. Swiss HIV Cohort Study. Arch. Intern. Med. 1999;
infection is particularly common among older adults in
hospitals and nursing homes, and relapsing disease in
115 Du Pont HL, Marshall GD. HIV-associated diarrhea and
these groups may be more frequent than among
wasting. Lancet 1995; 346: 352–6.
younger adults. The approach to an elderly patient with
116 Ramakrishna BS. Prevalence of intestinal pathogens in
diarrhea is to ensure proper hydration using available
HIV patients with diarrhea: implications for treatment.
oral rehydration solutions, proceed with diagnostic tests
Indian J. Pediatr. 1999; 66: 29–36.
likely to yield a positive result, avoid the use of harmful
117 Levine GI. Sexually transmitted parasitic diseases. Prim.
antiperistaltic drugs, and provide adequate follow-up of
Care 1991; 18: 101–28.
the nutritional state. Antibiotics should be administered
118 Gagarin VV. Acute disorders of the mesenteric circula-
in acute diarrhea due to invasive bacteria, especially
tion among heart defect patients. Kardiologiia 1984; 24:
119 Chan TY, Chow DP, Ng KC, Pang KW, McBride GA.
Vibrio vulnificus septicemia in a patient with liver cirrhosis. Southeast Asian J.Trop Med. Public Health 1994;
Traveler’s diarrhea 25: 215–16.
120 Christenson B, Soler M, Nieves L, Souchet LM. Sep-
This is a specific entity that occurs after a person has
ticemia due to a non-0: 1, non-0: 139 Vibrio cholerae.
traveled from an industrialized country to a developing
Bol. Asoc. Med. P. R. 1997; 89: 31–2.
country and experienced acute diarrhea. The risk
121 Chan HL, Ho HC, Kuo TT. Cutaneous manifestations
increases if the traveler consumes food from street
of non-01 Vibrio cholerae septicemia with gastroenteritis
vendors rather than from a restaurant or a hotel. Symp-
and meningitis. J. Am. Acad. Dermatol. 1994; 30: 626–
toms and severity depend on the prevalence of common
pathogens endemic in the developing country.
The common causes of acute traveler’s diarrhea vary
tissue culture assay technique in confirming diagnosis.
from one geographical area to another.78–84 The most
Sigmoidoscopy or colonoscopy may reveal normal,
frequently identified pathogen causing traveler’s diar-
minimally erythematous colonic mucosa with some
rhea is toxigenic Escherichia coli, although in some parts
edema, or granular, friable, or hemorrhagic mucosa
of the world (notably North Africa and South-east
with typical pseudomembrane formation.
Asia), Campylobacter infections appear to predominate.
The course is highly variable. In patients with clini-
Other common causative organisms include enteroag-
cally mild disease, withdrawal of offending antibiotics
gregative E. coli, Salmonella spp., Shigella spp., rotavirus
usually leads to prompt resolution of symptoms. Those
and the Norwalk agent. Except for giardiasis, cryp-
who have more protracted diarrhea usually need spe-
tosporidium and cyclosporidium, parasitic infections
cific therapy. Oral rehdyration therapy is the mainstay
are uncommon causes of traveler’s diarrhea.
treatment to correct dehydration. Intravenous fluid may
The disease is usually short-lived, self-limited,
be required in severe cases. Empiric metronidazole
however, many of them are amenable to antibiotics.
250–500 mg four times daily should be administered
Choice of antibiotics depends on epidemiologic data.
while waiting for the result of a cytotoxin study,
The same principle should apply in correcting dehy-
and should be continue for 10–14 days. If cytotoxin
dration from other types of diarrhea. Antidiarrheal
study is positive and the patient does not get better
drugs can be given in conjunction with antibiotics.
after a week of metronidazole, then vancomycin
A growing problem for travelers is the development
125–250 mg/day should be substituted. Relapses or
of antibiotic resistance in many bacterial pathogens;
reinfections are common and occur in as many as 20%
examples include strains of Campylobacter resistant
of cases. These patients can be treated with the same
to quinolones and strains of E. coli, Shigella, and Sal-
treatment as given for the primary infection. Subse-
monella resistant to trimethoprim-sulfamethoxazole.
quent recurrences of antibiotic associated enterocolitisare best managed with vancomycin plus rifampicin. Antidiarrheal drugs have no advantage in treatingantibiotic-associated enterocolitis, except cholestyra-
Antibiotic associated enterocolitis
mine and probiotics, which can be helpful in chronic orrelapsing disease.
Diarrhoea that occurs as a result of administered anti-biotics which alter the normal intestinal flora andincrease the proliferation of Clostridium difficile, produceenterotoxin A and B that cause enterocolitis and
Hemorrhagic colitis (due to Enterohaemorrhagic E. coli, EHEC or
antibiotics usage prior to the development of diarrhea
Shiga Toxin Producing E. coli, STEC)
may raise the possibility of antibiotic associated entero-colitis, however, the use after the onset of diarrhea
Hemorrhagic colitis, caused by enterohemorrhagic
usually does not suggest antibiotic associated enter-
Escherichia coli (EHEC), should always be a differential
ocolitis. Onset of symptoms occurs either during anti-
diagnosis in patients who present with acute bloody
microbial administration or within four weeks after
diarrhea, especially during an outbreak of food-borne
treatment. While all antimicrobials may cause the syn-
illness. Patients who present with non-bloody diarrhea
drome, some drugs cause it more commonly than
that progresses to bloody diarrhea should also raise the
others and some only rarely. The common causes of
possibility of EHEC diarrhea. Other prominent com-
antibiotic associated enterocolitis include clindamycin,
plaints include striking abdominal pain and tenderness
ampicillin, and the cephalosporins. The rare causes of
often in the absence of fever. In an outbreak situation,
antibiotic associated enterocolitis are vancomycin,
some patients with EHEC infection may be asympto-
metronidazole, and the aminoglycosides.
matic and are only recognized during epidemiologic
The clinical spectrum of antibiotics-associated ente-
surveillance in association with symptomatic cases. In
rocolitis is diverse. It ranges from mild loose watery
general, the mortality rate is 1–2%,86 although it may
diarrhea to severe colitis causing bloody or dysentery-
be substantially higher in the young and the elderly.87
like diarrhea in the later course of the disease. In the
The most worrisome complication of EHEC infection
first week, diarrhea is usually watery, voluminous and
is the hemolytic–uremic syndrome (HUS),88 which
without gross blood or mucus. Later, it becomes bloody.
most frequently involves children between the ages of
Other symptoms also vary considerably. At one end of
5–10 years.89 Hemolytic-uremic syndrome is character-
the spectrum are many patients with annoying diarrhea
ized by the triad of acute renal failure, microangiopathic
with no severe systemic toxicity; while at the other end
hemolytic anemia, and thrombocytopenia. Patients who
are those with high and prolonged fever with abdomi-
also have fever and neurologic symptoms are considered
nal pain. Abdominal pain can be severe with cramping,
to have the related disorder thrombotic thrombocy-
especially at the left iliac fossa. Vomiting is uncommon
topenic purpura (TTP), which has also been associated
and dehydration is often mild except in very severe
with E. coli O157:H7 infection.86,90 Hemolytic-uremic
cases. Examination of stool may reveal large numbers
syndrome usually begins 5–10 days after the onset of
of red blood cells and some leukocytes. Stool culture
diarrhea.86,90,91 The incidence of subclinical renal dys-
for C. difficile needs anaerobic conditions and may take
function is substantially higher, particularly in patients
several days to perform. It is usually more practical to
with prolonged anuria during the initial presenta-
perform cytotoxin assay in the stool using ELISA, or
tion.92,93 Stool culture using sorbitol-MacConkey agar
should be done in all suspected EHEC diarrhea. The
In the situation in which there is a known outbreak
Centers for Disease Control and Prevention (CDC) has
of an epidemiologically important enteric pathogen,
recommended that all stools from patients with a
for example cholera, salmonella, shigella, campylobac-
history of bloody diarrhea should be screened for E. coli
ter, EHEC (STEC), any acute diarrheas that occur in
O157:H7 or Shiga toxin by direct stool examination.92
the outbreak area should be managed as if they are
E. coli strains presumptively identified as E. coli
caused by the ‘outbreak pathogen’, no matter the sever-
O157:H7 and Shiga toxin-positive stools should be sent
ity of diarrhea. As in an outbreak situation, the disease
to a reference laboratory for confirmation. A number of
spectrum is often highly variable, ranging from very
newer diagnostic approaches for EHEC infection
mild to very severe. All acute diarrhea in the outbreak
focuses on direct detection of Shiga toxins in stool, or
area should be reported to the Area Health Authority
the use of DNA probes for detecting the toxin genes in
and proper epidemiologic investigation should be
fecal isolates. One such assay, the Premier EHEC assay,
employed. Rapid testing or a kit that is helpful in iden-
utilizes an enzyme-linked immunosorbent assay
tifying the ‘outbreak pathogen’ should be used in the
(ELISA) to detect both Shiga toxin 1 and Shiga toxin
field and further confirmation can be done later in a
reference center. Antibiotics that are known to be
The only current treatment of EHEC infection is
effective in eradicating the pathogen should be empiri-
supportive, with monitoring for the development of
cally administered to all acute diarrhea cases in the out-
microangiopathic complications such as HUS. The
break area. The purpose is to contain the spreading
impact of antibiotic therapy on the duration of diarrhea
of the disease, not necessarily to shorten the clinical
or on the subsequent occurrence of systemic complica-
course of diarrhea in that particular case. Epidemiologic
tions is controversial. The use of antibiotics may actu-
surveillance is necessary until the outbreak completely
ally increase the risk of HUS, perhaps by increasing
production or release of toxin.94 A number of newapproaches to therapy of EHEC infection are currentlybeing evaluated, but are not yet proven effective nor
residues given orally and hyperimmune antitoxin
This is acute diarrhea that occurs in persons who stay
in an institution where there is a uniform populationwith the same clinical or social setting, for example anursing home, a day-care center, a refugee camp,
Any single case of acute diarrhea that occurs in an
Nosocomial diarrhea, that is acute diarrhea that occurs
institution should all be investigated by stool examina-
in hospitalized patients, is an important problem in hos-
tion and culture, as there is risk of spreading among
pitals, and in critical care units in particular. Hospital-
inhabitants in the same institution and may progress to
acquired diarrhea may be on an infectious or
an established outbreak of diarrhea. Apart from the
non-infectious basis. Common non-infectious causes of
routine correction of dehydration, there should also be
nosocomial diarrhea include food intolerance, drug
isolation of the patient and an improvement of hygiene
induced diarrhea, drug-induced changes in the fecal
and sanitation in the institution. Early empiric treat-
flora, or changes secondary to enteral hyperalimenta-
ment with antibiotics may help to contain the suspected
tion.95,96 Infectious causes of nosocomial diarrhea are
enteropathogens. In patients with diarrhea due to sal-
due to eating food contaminated with enteric pathogens
monella, empiric antibiotic treatment may increase the
or in outbreak situations. However, the major cause
time of shedding of the organism by one to three weeks.
of sporadic (non-epidemic) nosocomial diarrhea is
Antibiotics are usually not given to otherwise healthy
Clostridium difficile.96 All cases of nosocomial diarrhea
patients with milder forms of non-typhoid salmonel-
should be properly investigated with stool examination,
losis. The young or the elderly and patients with
culture and C. difficile cytotoxin assay.97,98 Proper hydra-
immunocompromised are usually given antimicrobials
tion together with dietary adjustment should immedi-
in intestinal salmonellosis. In confirmed groups, other
ately be employed. If possible, discontinuation of
organisms may produce illness in individuals or as out-
offending drugs or antibiotics should be considered.
breaks. The cause of the illness generally requires labo-
Empiric metronidazole can be started in patients with
a possibility of antibiotic associated enterocolitis. (Seeantibiotic associated enterocolitis for details of thisinfection). Systemic antibiotics may be necessary in
Acute diarrhea in immunocompromised patients
Acute diarrhea that occurs in an immunocompromised
host, who has been treated with immunosuppressiveagents or chemotherapy, or those with HIV infection,
Acute diarrhea that occurs in two or more persons from
autoimmune diseases, malignancy, especially hemato-
the same exposure, assumed to be caused by the same
logic malignancy, and acute graft-versus-host condition
pathogens, is considered an outbreak.99–103
are a special entity.108,109 Acute diarrhea that occurs in
these patients may easily lead to septicemia, hence early
including parasitic protozoans and helminths. The most
antibiotic therapy during their course of diarrhea
common of these parasitic infections are amebiasis,
should be instituted, no matter the type or severity of
caused by Entamoeba histolytica, and giardiasis caused
the diarrhea.110–112 Apart from the hemodynamic
by Giardia lamblia.117 Both entities may cause acute or
support, parenteral antibiotics are often needed. Bloody
chronic diarrhea, as well as other abdominal symptoms.
diarrhea in immunocompromised patients may also be
Most gay men with amebiasis are asymptomatic, and
caused by cytomegalovirus enteric infection.
invasive disease in this group is extremely rare. Both
Acute and chronic diarrhea that occurs in an HIV
amebiasis and giardiasis can be diagnosed on the
infected person should receive special attention in terms
basis of microscopic examination of stool specimens,
of investigation and management.113,114 HIV infected
although duodenal aspiration is occasionally necessary
persons, who are not yet immunocompromised or
to confirm a diagnosis of giardiasis. Metronidazole is
having CD4 count > 500 cell/mm3, can be managed as
efficacious in the treatment of both amoebiasis and gia-
in the suggested algorithm (Fig. 1). But HIV infected
rdiasis. Other common causes of diarrhea in homosex-
persons who are immunocompromised or their CD4
ual males include the spread of the organisms by
counts are < 500 cell/mm3, apart from doing routine
the fecal oral route (e.g. shigella, campylobacter,
stool culture and examination, stool staining for AFB,
salmonella) and those spread by receptive anal inter-
modified AFB, modified trichrome staining and C.
course (e.g. Neisseria gonorrhoeae, Chlamydia trachoma-difficile cytotoxin assay should also be employed. tis, Herpes simplex and Treponema pallidium.)
Blood cultures should be performed since entero-pathogens and Mycobacterium-avium intracellulareoften produce bacteremia in immunocompromisedpatients.115 Empiric treatment can be considered if the
Acute diarrhea in septicemic
nature of enteropathogens infecting these patients is
known.116 Specific treatment with antibiotics, if beingadministered, should be given in a more prolonged
Acute diarrhea that occurs in a person who is prone to
course to ensure the complete eradication of the
septicemia due to the presence of some underlying con-
pathogen and prevent early relapse. Nutritional man-
ditions that are not truly immunocompromised condi-
agement is also required in this group of patients.
tions but were reported to have related higher incidenceof septicemia with diarrhea, or complications whendiarrhea occurs, for example cirrhosis, especially alco-
Gay bowel syndrome
holic cirrhosis, uncontrolled diabetes mellitus, patientswith heart valves, prosthesis, severe atherosclerosis with
This is a specific syndrome of acute diarrhea that occurs
aortic aneurysm, malignancy and uremia.118
in homosexual men who may or may not be infected
There are several reports of-Non-O1 Vibrios sep-
with HIV. Homosexual people are a unique group of
ticemia in patients with cirrhosis.47,119,120 Uncontrolled
patients who are prone to diarrhea due to their sexual
diabetes mellitus patients with diarrhea are prone to
activity, which is the primary method of transmission
gram negative septicemia.121 Patients with heart valve,
for several important enteric parasitic diseases. The
prosthesis, severe atherorosclerosis are prone to salmo-
majority of parasitic sexually transmitted diseases
nella septicemia and lodging of salmonella infection at
involve protozoan pathogens; however, nematode and
the diseased heart valve and prosthesis.122,123 These
arthropod illnesses are also included in this group. Oral-
patients should be aware of the possibility of septicemia
anal and oral-genital sexual practices predispose male
and an early empiric parenteral antibiotic should be
homosexuals to infection with many enteric pathogens,
administered from the first presentation.
SECOND GRADE STANDARDS BASED RUBRIC PHYSICAL SCIENCE Essential Standard: THE MOTION OF OBJECTS CAN BE OBSERVED AND MEASURED. First Trimester: Benchmarks FAR BELOW/BELOW BASIC PROFICIENT ADVANCED Able to make predictions based on Able to explain predictions based sequence of steps, events, and observations. Unable to show understanding that Demonstrate