# 17 - 138 Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning

### 138 Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning

of enteric organisms including aerobic and anaerobic gram-negative 
bacilli is usually isolated from psoas abscesses in the United States. 
S. aureus is most likely to be isolated when a psoas abscess arises from 
hematogenous spread or a contiguous focus of osteomyelitis; a mixed 
enteric flora is the most likely etiology when the abscess has an intraab­
dominal or pelvic source. Patients with psoas abscesses frequently pres­
ent with fever, lower abdominal or back pain, or pain referred to the 
hip or knee. CT is the most useful diagnostic technique.

TREATMENT
Psoas Abscesses
Treatment includes surgical drainage and the administration of an 
antibiotic regimen directed at the inciting organism(s).
Pancreatic Abscesses 
See Chap. 359.
■
■FURTHER READING
Biggins SW et al: Diagnosis, evaluation, and management of ascites, 
spontaneous bacterial peritonitis, and hepatorenal syndrome: 2021 
practice guidance by the American Association for the Study of Liver 
Diseases. Hepatology 74;1014.2021.
De Pascale G et al: Poor timing and failure of source control are risk 
factors for mortality in critically ill patients with secondary peritonitis. 
Intensive Care Med 48:1593, 2022.
Li PK et al: ISPD peritonitis recommendations: 2016 update on prevention 
and treatment. Perit Dial Int 36:481, 2016.
Oliver A et al: Role of rifaximin in spontaneous bacterial peritonitis 
PART 5
Infectious Diseases
prevention. South Med J 111:660 2018.
Roediger R, Lisker-Melman M: Pyogenic and amebic infections of 
the liver. Gastroenterol Clin North Am 49:361, 2020.
Ross JT et al: Secondary peritonitis: Principles of diagnosis and 
intervention. BMJ 361:k1407, 2018.
Van Hooste W et al: Infections caused by hypervirulent Klebsiella 
pneumoniae in non-endemic countries: Three case reports and 
review of the literature. Acta Clin Belg 78:229, 2023.
Ana A. Weil, Regina C. LaRocque

Acute Infectious 

Diarrheal Diseases and 

Bacterial Food Poisoning
Diarrheal disease mortality has decreased substantially in the past 
three decades. Nevertheless, acute diarrheal disease is still a leading 
cause of illness globally and is associated with an estimated 1.57 million 
deaths per year. Across low-income and middle-income countries, one 
in ten deaths among children <5 years of age is attributable to diar­
rhea, with substantial variation in incidence and mortality between 
countries. The morbidity from diarrhea also is significant. Recurrent 
intestinal infections are associated with physical and mental stunting, 
wasting, micronutrient deficiencies, and malnutrition. In short, diar­
rheal disease is a driving factor in global morbidity and mortality.
The wide range of clinical manifestations of acute gastrointestinal 
illnesses is matched by the wide variety of infectious agents involved, 
including viruses, bacteria, and parasites (Table 138-1). This chapter 
discusses factors that enable gastrointestinal pathogens to cause dis­
ease, reviews host defense mechanisms, and delineates an approach 
to the evaluation and treatment of patients presenting with acute 

diarrhea. Individual organisms causing acute gastrointestinal illnesses 
are discussed in detail in subsequent chapters.
PATHOGENIC MECHANISMS
Enteric pathogens have developed a variety of tactics to overcome 
host defenses. Understanding the virulence factors employed by these 
organisms is important in the diagnosis and treatment of clinical 
disease.
■
■INOCULUM SIZE
The number of microorganisms that must be ingested to cause disease 
varies considerably from species to species. For Shigella, enterohemor­
rhagic Escherichia coli, Giardia lamblia, or Entamoeba, as few as 10–100 
bacteria or cysts can produce infection, while 105−108 Vibrio cholerae 
organisms must be ingested to cause disease. The infective dose of Sal­
monella varies widely, depending on the species, host, and food vehicle. 
The ability of organisms to overcome host defenses has important 
implications for transmission; Shigella, enterohemorrhagic E. coli, Ent­
amoeba, and Giardia can spread by person-to-person contact, whereas 
under some circumstances, Salmonella may need to grow in food for 
several hours before reaching an effective infectious dose.
■
■ADHERENCE
Many organisms must adhere to the gastrointestinal mucosa as an 
initial step in the pathogenic process; thus, organisms that can com­
pete with the normal bowel flora and colonize the mucosa have an 
important advantage in causing disease. Specific cell-surface proteins 
involved in attachment of bacteria to intestinal cells are important 
virulence determinants. V. cholerae, for example, adheres to the brush 
border of small-intestinal enterocytes via specific surface adhesins, 
including the toxin-coregulated pilus and other accessory coloniza­
tion factors. Enterotoxigenic E. coli, which causes watery diarrhea, 
produces an adherence protein called colonization factor antigen 
that is necessary for colonization of the upper small intestine by the 
organism prior to the production of enterotoxin. Enteropathogenic 
E. coli, an agent of diarrhea in young children, and enterohemor­
rhagic E. coli, which causes hemorrhagic colitis and the hemolyticuremic syndrome, produce virulence determinants that allow these 
organisms to attach to and efface the brush border of the intestinal 
epithelium.
■
■TOXIN PRODUCTION
The production of one or more exotoxins is important in the pathogen­
esis of numerous enteric organisms. Such toxins include enterotoxins, 
which cause watery diarrhea by acting directly on secretory mecha­
nisms in the intestinal mucosa; cytotoxins, which cause destruction of 
mucosal cells and associated inflammatory diarrhea; and neurotoxins, 
which act directly on the central or peripheral nervous system.
The prototypical enterotoxin is cholera toxin, a heterodimeric pro­
tein composed of one A and five B subunits. The A subunit contains 
the enzymatic activity of the toxin, while the B subunit pentamer 
binds holotoxin to the enterocyte surface receptor, the ganglioside 
GM1. After the binding of holotoxin, a fragment of the A subunit is 
translocated across the eukaryotic cell membrane into the cytoplasm, 
where it catalyzes the adenosine diphosphate ribosylation of a guano­
sine triphosphate (GTP)–binding protein and causes persistent activa­
tion of adenylate cyclase. The result is an increase of cyclic adenosine 
monophosphate in the intestinal cell, which increases Cl– secretion and 
decreases Na+ absorption, leading to a loss of fluid and the production 
of diarrhea.
Enterotoxigenic strains of E. coli may produce a protein called heatlabile enterotoxin (LT) that is like cholera toxin and causes secretory 
diarrhea by the same mechanism. Alternatively, enterotoxigenic strains 
of E. coli may produce heat-stable enterotoxin (ST), one form of which 
causes diarrhea by activation of guanylate cyclase and elevation of 
intracellular cyclic guanosine monophosphate. Some enterotoxigenic 
strains of E. coli produce both LT and ST.
Bacterial cytotoxins, in contrast, destroy intestinal mucosal cells 
and produce the syndrome of dysentery, with bloody stools containing

TABLE 138-1  Gastrointestinal Pathogens Causing Acute Diarrhea
MECHANISM
LOCATION
ILLNESS
STOOL FINDINGS
EXAMPLES OF PATHOGENS INVOLVED
Noninflammatory 
(enterotoxin)
Proximal 
small bowel
Watery 
diarrhea
No fecal leukocytes; mild 
or no increase in fecal 
lactoferrin
Inflammatory 
(invasion or 
cytotoxin)
Colon or 
distal small 
bowel
Dysentery or 
inflammatory 
diarrhea
Fecal polymorphonuclear 
leukocytes; substantial 
increase in fecal 
lactoferrin
Penetrating
Distal small 
bowel
Enteric fever
Fecal mononuclear 
leukocytes
Abbreviations: LT, heat-labile enterotoxin; ST, heat-stable enterotoxin.
inflammatory cells. Enteric pathogens that produce such cytotoxins 
include Shigella dysenteriae type 1, Vibrio parahaemolyticus, and Clos­
tridioides difficile. S. dysenteriae type 1 and Shiga toxin–producing 
strains of E. coli produce potent cytotoxins and have been associated 
with outbreaks of hemorrhagic colitis and hemolytic-uremic syndrome.
Neurotoxins are usually produced by bacteria outside the host and 
therefore cause symptoms soon after ingestion. Included are the staph­
ylococcal and Bacillus cereus toxins, which act on the central nervous 
system to produce vomiting.
■
■INVASION
Dysentery may result not only from the production of cytotoxins but 
also from bacterial invasion and destruction of intestinal mucosal cells. 
Infections due to Shigella and enteroinvasive E. coli are characterized by 
the organisms’ invasion of mucosal epithelial cells, intraepithelial mul­
tiplication, and subsequent spread to adjacent cells. Salmonella causes 
inflammatory diarrhea by invading the bowel mucosa but generally is 
not associated with the destruction of enterocytes or the full clinical 
syndrome of dysentery. Salmonella enterica serovar Typhi and Yersinia 
enterocolitica can penetrate intact intestinal mucosa, multiply intra­
cellularly in Peyer patches and intestinal lymph nodes, and then dis­
seminate through the bloodstream to cause enteric fever—a syndrome 
characterized by fever, headache, relative bradycardia, abdominal pain, 
splenomegaly, and leukopenia.
HOST DEFENSES
Given the enormous number of microorganisms ingested with every 
meal, the normal host must combat a constant influx of potential 
enteric pathogens. Studies of infections in patients with alterations in 
defense mechanisms have led to a greater understanding of the variety 
of ways in which the normal host can protect itself against disease.
■
■INTESTINAL MICROBIOTA
The large numbers of bacteria that normally inhabit the intestine (the 
intestinal microbiota) act as an important host defense mechanism, 
preventing colonization by potential enteric pathogens. Mechanisms of 
colonization resistance are not fully understood but include geographic 
and nutritional exclusion at the mucosal surface. Persons with fewer 
intestinal bacteria, such as infants who have not yet developed normal 
enteric colonization or patients receiving antibiotics, are at greater risk 
of developing infections with enteric pathogens. The bacterial com­
munity composition of the intestinal microbiota is as important as 
abundance of organisms present. More than 99% of the normal colonic 
microbiota is made up of anaerobic bacteria, and the acidic pH and 
volatile fatty acids produced by these organisms appear to be critical 
elements in resistance to colonization.
■
■GASTRIC ACID
The acidic pH of the stomach is an important barrier to enteric patho­
gens, and an increased frequency of infections due to Salmonella, 

G. lamblia, and a variety of helminths has been reported among patients 
who have undergone gastric surgery or are achlorhydric for some 
other reason. Neutralization of gastric acid with antacids, proton pump 

Vibrio cholerae, enterotoxigenic Escherichia coli (LT and/or ST), enteroaggregative 
E. coli, Clostridium perfringens, Bacillus cereus, Staphylococcus aureus, Aeromonas 
hydrophila, Plesiomonas shigelloides, rotavirus, norovirus, enteric adenoviruses, 
Giardia lamblia, Cryptosporidium spp., Cyclospora spp., microsporidia
Shigella spp., Salmonella spp., Campylobacter jejuni, enterohemorrhagic E. coli, 
enteroinvasive E. coli, Yersinia enterocolitica, Listeria monocytogenes, Vibrio 
parahaemolyticus, Clostridium difficile, A. hydrophila, P. shigelloides, Entamoeba 
histolytica, Klebsiella oxytoca
Salmonella Typhi, Y. enterocolitica
inhibitors, or H2 blockers—a common practice in the management of 
hospitalized patients—similarly increases the risk of enteric coloniza­
tion. In addition, some microorganisms can survive the extreme acid­
ity of the gastric environment; rotavirus and Shigella, for example, are 
highly stable to acidity.
■
■INTESTINAL MOTILITY
Peristalsis is the major mechanism for clearance of bacteria from the 
proximal small intestine. When intestinal motility is impaired (e.g., by 
treatment with opioids or other antimotility drugs, anatomic abnor­
malities, or hypomotility states), the frequency of bacterial overgrowth 
and infection of the small bowel with enteric pathogens is increased. 
Some patients whose treatment for Shigella infection consists of 
diphenoxylate hydrochloride with atropine (Lomotil) experience pro­
longed fever and shedding of organisms, while patients treated with 
opioids for mild Salmonella gastroenteritis have a higher frequency of 
bacteremia than those not treated with opioids.
CHAPTER 138
■
■INTESTINAL MUCIN
A complex layer of mucus, produced by specialized secretory cells, 
covers the stomach, small intestine, and large intestine, and separates 
the lumenal commensal microbiota from the epithelium. The thickness 
and constituents of this mucus barrier vary throughout the gastro­
intestinal tract. The mucus barrier turns over rapidly and comprises 
glycoproteins and a range of antimicrobial molecules and secreted 
immunoglobulins directed against specific microbial antigens. Enteric 
pathogens have evolved a wide range of strategies to overcome this 
barrier and thus to reach the underlying epithelium and cause disease. 
For example, pathogens can penetrate the mucus layer by secreting 
enzymes to degrade the mucus or through flagella-mediated motil­
ity. Some organisms, such as Shigella, secrete toxins that can diffuse 
through the mucus layer and disrupt the underlying epithelium. The 
resulting reduction of mucus production allows the pathogen to reach 
the cell surface.
Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning  
■
■IMMUNITY
Both cellular immune responses and antibody production play impor­
tant roles in protection from enteric infections. Humoral immunity to 
enteric pathogens consists of systemic IgG and IgM as well as secre­
tory IgA. The mucosal immune system may be the first line of defense 
against many gastrointestinal pathogens. The binding of bacterial 
antigens to the lumenal surface of M cells in the distal small bowel and 
the subsequent presentation of antigens to subepithelial lymphoid tis­
sue leads to the proliferation of sensitized and specialized lymphocytes. 
These lymphocytes circulate and populate all of the mucosal tissues of 
the body as IgA-secreting plasma cells.
■
■GENETIC DETERMINANTS
Host genetic variation influences susceptibility to diarrheal dis­
eases. People with blood group O show increased susceptibility to 
disease due to V. cholerae, Shigella, E. coli O157, and norovirus. 
Polymorphisms in genes encoding inflammatory mediators have been 
associated with the outcome of infection with enteroaggregative E. coli, 
enterotoxin-producing E. coli, Salmonella, C. difficile, and V. cholerae.

APPROACH TO THE PATIENT
Infectious Diarrhea or Bacterial Food Poisoning
The approach to the patient with possible infectious diarrhea or 
bacterial food poisoning is shown in Fig. 138-1. 
HISTORY
Diarrhea is defined as the passage of loose or watery stools that 
conform to the shape of a container three or more times in a 24-h 
period. The answers to questions with high discriminating value 
can quickly narrow the range of potential causes of diarrhea and 
help determine whether treatment is needed. Important elements 
of the narrative history are detailed in Fig. 138-1. 
Diarrhea, Nausea, or Vomiting
Symptomatic therapy
Oral rehydration therapy
  (see Table 138-5)
Assess:
  Duration (>1 day)
  Severity (see text)
Yes
PART 5
Infectious Diseases
Obtain history:
  Duration1
  Fever2
  Appearance of stool3
  Frequency of bowel
    movements4
  Abdominal pain5
Tenesmus6
Vomiting7
Common source8
Antibiotic use9
Travel10
and
  
Obtain stool to be examined for WBCs
  (and, if >10 days, for parasites)
Inflammatory (WBCs;
see Table 138-1)
Examine stool
for parasites
Noninflammatory
(no WBCs; see
Table 138-1)
Continue
  symptomatic therapy
  (Table 138-5);
  further evaluation
  if no resolution
Culture for: Shigella, Salmonella,
  Campylobacter jejuni
Consider:
  Clostridioides difficile cytotoxin
Consider: Empirical
antimicrobial therapy
(Table 138-5)
FIGURE 138-1  Clinical algorithm for the approach to patients with community-acquired infectious diarrhea or bacterial food poisoning. Key to superscripts: 1. Diarrhea 
lasting >2 weeks is generally defined as chronic; in such cases, many of the causes of acute diarrhea are much less likely, and a new spectrum of causes needs to be 
considered. 2. Fever often implies invasive disease, although fever and diarrhea may also result from infection outside the gastrointestinal tract, as in malaria. 3. Stools 
that contain blood or mucus indicate ulceration of the large bowel. Bloody stools without fecal leukocytes should alert the laboratory to the possibility of infection with 
Shiga toxin–producing enterohemorrhagic Escherichia coli. Bulky white/gray stools suggest a small-intestinal process that is causing malabsorption. An acute illness with 
profuse “rice-water” stools, with an appearance of water after rice has been cooked, suggests cholera or a similar toxigenic process. 4. Frequent stools over a given period 
can provide the first warning of impending dehydration. 5. Abdominal pain may be most severe in inflammatory processes like those due to Shigella, Campylobacter, and 
necrotizing toxins. Painful abdominal muscle cramps, caused by electrolyte loss, can develop in severe cases of cholera. Bloating is common in giardiasis. An appendicitislike syndrome should prompt a culture for Yersinia enterocolitica with cold enrichment. 6. Tenesmus (painful rectal spasms with a strong urge to defecate but little passage 
of stool) may be a feature of cases with proctitis, as in shigellosis or amebiasis. 7. Vomiting implies an acute infection (e.g., a toxin-mediated illness or food poisoning) but 
can also be prominent in a variety of systemic illnesses (e.g., malaria) and in intestinal obstruction. 8. Asking patients whether anyone they know is sick is a more efficient 
means of identifying a common source than is constructing a list of recently eaten foods. If a common source seems likely, specific foods can be investigated. See text for 
a discussion of bacterial food poisoning. 9. Current antibiotic therapy or a recent history of treatment suggests Clostridioides difficile diarrhea (Chap. 139). Stop antibiotic 
treatment if possible and consider tests for C. difficile toxins. Antibiotic use may increase the risk of chronic intestinal carriage following salmonellosis. 10. See text (and 
Chap. 130) for a discussion of traveler’s diarrhea. (From The New England Journal of Medicine. Bacterial and Protozoal Gastroenteritis. RL Guerrant, DA Bobak 325:327-340. 
Copyright @1991 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.)

PHYSICAL EXAMINATION
The examination of patients for signs of dehydration provides 
essential information about the severity of the diarrheal illness and 
the need for rapid therapy. Mild dehydration is indicated by thirst, 
dry mouth, decreased axillary sweat, decreased urine output, and 
slight weight loss. Signs of moderate dehydration include an ortho­
static fall in blood pressure, skin tenting, and sunken eyes (or, in 
infants, a sunken fontanelle). Signs of severe dehydration include 
lethargy, obtundation, feeble pulse, hypotension, and shock. 
DIAGNOSTIC APPROACH
After assessing severity of illness, the clinician must distinguish 
between inflammatory and noninflammatory disease. Using the 
Resolution
No
Continued illness
Specific antiparasitic
therapy

history and epidemiologic features of the case, the clinician can 
then rapidly evaluate the need for further efforts to define a specific 
etiology and for therapeutic intervention. Examination of a stool 
sample may supplement the narrative history. Grossly bloody or 
mucoid stool suggests an inflammatory process. A test for fecal 
leukocytes (preparation of a thin smear of stool on a glass slide, 
addition of a drop of methylene blue, and examination of the wet 
mount) can suggest inflammatory disease in patients with diarrhea, 
although the predictive value of this test is still debated. A test for 
fecal lactoferrin, which is a marker of fecal leukocytes, is more 
sensitive and is available in latex agglutination and enzyme-linked 
immunosorbent assay formats. Stool culture or molecular testing is 
useful for diagnosing a causative organism, particularly in patients 
with severe illness or high-risk comorbidities. Causes of acute infec­
tious diarrhea, categorized as inflammatory and noninflammatory, 
are listed in Table 138-1. 
POST DIARRHEA COMPLICATIONS
Short- or long-term complications may follow the resolution of an 
acute diarrheal episode. The clinician should inquire about prior 
diarrheal illness if the conditions listed in Table 138-2 are observed.
EPIDEMIOLOGY
■
■TRAVEL HISTORY
Of the several million people who travel from temperate industrialized 
countries to tropical regions of Asia, Africa, and Central and South 
America each year, 20–50% experience a sudden onset of abdominal 
cramps, anorexia, and watery diarrhea; thus, traveler’s diarrhea is the 
most common travel-related infectious illness (Chap. 130). The time 
of onset is usually 3 days to 2 weeks after the traveler’s arrival in a 
resource-poor area; most cases begin within the first 3–5 days. The 
illness is generally self-limited, lasting 1–5 days. The high rate of diar­
rhea among travelers is related to the ingestion of contaminated food 
or water.
The pathogens that cause traveler’s diarrhea vary considerably with 
location (Table 138-3), as does the pattern of antimicrobial resistance. 
In all areas, enterotoxigenic and enteroaggregative E. coli are the most 
common pathogens among persons with the classic secretory traveler’s 
diarrhea syndrome. Infection with Campylobacter jejuni is especially 
common in areas of Asia.
■
■LOCATION
Closed and semi-closed communities, including day-care centers, 
schools, residential facilities, and cruise ships, are important settings 
TABLE 138-2  Postdiarrhea Complications of Acute Infectious 
Diarrheal Illness
COMPLICATION
COMMENTS
Chronic diarrhea (diarrhea lasting 

>4 weeks)
• Lactase deficiency
• Small-bowel bacterial overgrowth
• Malabsorption syndromes (tropical 
Occurs in ~1% of travelers with acute 
diarrhea
Protozoa account for approximately 
one-third of cases
and celiac sprue)
Initial presentation or exacerbation of 
inflammatory bowel disease
May be precipitated by traveler’s 
diarrhea
Irritable bowel syndrome
Occurs in ~10% of travelers with 
traveler’s diarrhea
Reactive arthritis
Particularly likely after infection 
with invasive organisms (Shigella, 
Salmonella, Campylobacter, Yersinia)
Hemolytic-uremic syndrome (hemolytic 
anemia, thrombocytopenia, and renal 
failure)
Follows infection with Shiga 
toxin–producing bacteria 
(Shigella dysenteriae type 1 and 
enterohemorrhagic Escherichia coli)
Guillain-Barré syndrome
Particularly likely after Campylobacter 
infection

TABLE 138-3  Causes of Traveler’s Diarrhea
APPROXIMATE 
PERCENTAGE OF 
CASES
COMMENTS
ETIOLOGIC AGENT
Bacteria
50–75
Enterotoxigenic 
Escherichia coli
10–45
Single most important agent
Enteroaggregative E. coli
5–35
Emerging enteric pathogen with 
worldwide distribution
Campylobacter jejuni
5–25
More common in Asia
Shigella
0–15
Major cause of dysentery
Salmonella
0–15
—
Others
0–5
Including Aeromonas, 
Plesiomonas, and Vibrio 
cholerae
Viruses
0–20
Norovirus
0–10
Associated with cruise ships
Rotavirus
0–5
Particularly common among 
children
Parasites
0–10
Giardia lamblia
0–5
Affects hikers and campers who 
drink from freshwater streams
Cryptosporidium
0–5
Resistant to chlorine treatment 
of water sources
Entamoeba histolytica
<1
—
Cyclospora
<1
—
CHAPTER 138
Other
0–10
Acute food poisoninga
0–5
—
No pathogen identified
10–50
—
aFor etiologic agents, see Table 138-4.
Source: After DR Hill et al: The practice of travel medicine: Guidelines by the 
Infectious Diseases Society of America. Clin Infect Dis 43:1499, 2006.
Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning  
for outbreaks of enteric infections. Norovirus, which is highly con­
tagious and robust in surviving on surfaces, is the most common 
etiologic agent associated with outbreaks of acute gastroenteritis. 
Other common organisms, often spread by fecal–oral contact in such 
communities, are Shigella, C. jejuni, and Cryptosporidium. Rotavirus 
is rarely a cause of pediatric diarrheal outbreaks in the United States 
since rotavirus vaccination was broadly recommended in 2006. Simi­
larly, hospitals are sites in which enteric infections are concentrated. 
Diarrhea is one of the most common manifestations of nosocomial 
infections. C. difficile is the predominant cause of nosocomial diar­
rhea among adults in the United States, and outbreaks of norovirus 
infection are common in health care settings. Klebsiella oxytoca has 
been identified as a cause of antibiotic-associated hemorrhagic colitis. 
Enteropathogenic E. coli has been associated with outbreaks of diarrhea 
in nurseries for newborns. One-third of elderly patients in chronic-care 
institutions develop a significant diarrheal illness each year; more than 
one-half of these cases are caused by cytotoxin-producing C. difficile. 
Antimicrobial therapy can predispose to pseudomembranous colitis by 
altering the normal colonic microbiota, which then permits the multi­
plication of C. difficile (Chap. 139).
■
■AGE
Globally, most morbidity and mortality from enteric pathogens involve 
children <5 years of age. Breast-fed infants are protected from patho­
gens in contaminated food and water and derive some protection from 
maternal antibodies, but their risk of infection rises dramatically when 
they begin to eat solid foods. Exposure to rotavirus is universal, with 
most children experiencing their first infection in the first or second 
year of life if not vaccinated. Older children and adults are more com­
monly infected with norovirus. Other organisms with higher attack 
rates among children than among adults include enterotoxigenic, 
enteropathogenic, and enterohemorrhagic E. coli; Shigella; C. jejuni; 
and G. lamblia.

■
■HOST IMMUNE STATUS
Immunocompromised hosts are at elevated risk of acute and chronic 
infectious diarrhea. Individuals with defects in cell-mediated immu­
nity (including those with AIDS) are at particularly high risk of 
invasive enteropathies, including salmonellosis, listeriosis, and cryp­
tosporidiosis. Individuals with hypogammaglobulinemia are at par­
ticular risk of C. difficile colitis and giardiasis and can develop chronic 
infections with viral pathogens such as norovirus. Patients with 
cancer are more likely to develop C. difficile infection due to chemo­
therapy-associated antibiotic exposure and frequent hospitalizations. 
Infectious diarrhea can be life-threatening in immunocompromised 
hosts, with complications including persistent infection, bacteremia, 
and metastatic seeding of infection. Furthermore, dehydration may 
compromise renal function and increase the toxicity of immunosup­
pressive drugs.

■
■BACTERIAL FOOD POISONING
If the history and the stool examination indicate a noninflammatory 
etiology of diarrhea and there is evidence of a common-source out­
break, questions concerning the ingestion of specific foods and the 
time of onset of diarrhea after a meal can provide clues to the bacterial 
cause of the illness. Potential causes of bacterial food poisoning are 
shown in Table 138-4.
Bacterial disease caused by an enterotoxin elaborated outside the 
host, such as that due to Staphylococcus aureus or B. cereus, has the 
shortest incubation period (1–6 h) and generally lasts <12 h. Most cases 
of staphylococcal food poisoning are caused by contamination from 
Staphylococcus-infected human carriers. Staphylococci can multiply 
at a wide range of temperatures; thus, if food is left to cool slowly and 
remains at room temperature after cooking, the organisms will have the 
opportunity to form enterotoxin. Outbreaks following picnics where 
potato salad, mayonnaise, and cream pastries have been served offer 
classic examples of staphylococcal food poisoning. Diarrhea, nausea, 
vomiting, and abdominal cramping are common, while fever is rare.
PART 5
Infectious Diseases
B. cereus can produce either a syndrome with a short incuba­
tion period—the emetic form, mediated by a staphylococcal type 
of enterotoxin—or one with a longer incubation period (8–16 h)—the 
diarrheal form, caused by an enterotoxin resembling E. coli LT, in which 
TABLE 138-4  Bacterial Food Poisoning
INCUBATION PERIOD, 
ORGANISM
SYMPTOMS
COMMON FOOD 
SOURCES
1–6 h
Staphylococcus aureus
Nausea, vomiting, 
diarrhea
Ham, poultry, potato or 
egg salad, mayonnaise, 
cream pastries
Bacillus cereus
Nausea, vomiting, 
diarrhea
Fried rice
8–16 h
Clostridium perfringens
Abdominal cramps, 
diarrhea (vomiting rare)
Beef, poultry, legumes, 
gravies
B. cereus
Abdominal cramps, 
diarrhea (vomiting rare)
Meats, vegetables, dried 
beans, cereals
>16 h
Vibrio cholerae
Watery diarrhea
Shellfish, water
Enterotoxigenic 
Escherichia coli
Watery diarrhea
Salads, cheese, meats, 
water
Enterohemorrhagic 

E. coli
Bloody diarrhea
Ground beef, roast beef, 
salami, raw milk, raw 
vegetables, apple juice
Salmonella spp.
Inflammatory diarrhea
Beef, poultry, eggs, dairy 
products
Campylobacter jejuni
Inflammatory diarrhea
Poultry, raw milk
Shigella spp.
Dysentery
Potato or egg salad, 
lettuce, raw vegetables
Vibrio parahaemolyticus
Dysentery
Mollusks, crustaceans

diarrhea and abdominal cramps are characteristic but vomiting is 
uncommon. The emetic form of B. cereus food poisoning is associated 
with contaminated fried rice; the organism is common in uncooked 
rice, and its heat-resistant spores survive boiling. If cooked rice is not 
refrigerated, the spores can germinate and produce toxin. Frying before 
serving may not destroy the preformed, heat-stable toxin.
Food poisoning due to Clostridium perfringens also has a slightly 
longer incubation period (8–14 h) and results from the survival of 
heat-resistant spores in inadequately cooked meat, poultry, or legumes. 
After ingestion, toxin is produced in the intestinal tract, causing mod­
erately severe abdominal cramps and diarrhea; vomiting is rare, as is 
fever. The illness is self-limited, rarely lasting >24 h.
Not all food poisoning has a bacterial cause. Nonbacterial agents 
of short-incubation food poisoning include capsaicin, which is found 
in hot peppers, and a variety of toxins found in fish and shellfish 
(Chap. 471).
■
■LABORATORY EVALUATION
Many cases of noninflammatory diarrhea are self-limited or can be 
treated empirically, and in these instances, the clinician may not 
need to determine a specific etiology. Potentially pathogenic E. coli 
cannot be distinguished from normal fecal flora by routine culture, 
and tests to detect enterotoxins are not available in most clinical 
laboratories. In situations in which cholera is a concern, stool should 
be cultured on selective media such as thiosulfate–citrate–bile 
salts–sucrose (TCBS) or tellurite–taurocholate–gelatin (TTG) agar; 
rapid diagnostic tests are also available. A latex agglutination test 
has made the rapid detection of rotavirus in stool practical for many 
laboratories, while reverse-transcriptase polymerase chain reaction 
(PCR) and specific antigen enzyme immunoassays have been devel­
oped for the identification of norovirus. Stool specimens should be 
examined by immunofluorescence-based rapid assays, PCR, or (less 
sensitive) standard microscopy for Giardia cysts or Cryptosporidium 
if the level of clinical suspicion regarding the involvement of these 
organisms is high.
All patients with fever and evidence of inflammatory diarrhea 
acquired outside the hospital should be evaluated for Salmonella, 
Shigella, and Campylobacter. Salmonella and Shigella can be selected on 
MacConkey agar as non-lactose-fermenting (colorless) colonies or can 
be grown on Salmonella–Shigella agar or in selenite enrichment broth, 
both of which inhibit most organisms except these pathogens. Evalua­
tion of nosocomial diarrhea should initially focus on C. difficile; stool 
culture for other pathogens in the hospital setting is extremely low 
yield and is not cost-effective. Toxins A and B produced by pathogenic 
strains of C. difficile can be detected by rapid enzyme immunoassays, 
latex agglutination tests, or PCR (Chap. 139). Isolation of C. jejuni 
requires inoculation of fresh stool onto selective growth medium and 
incubation at 42°C in a microaerophilic atmosphere. In many labora­
tories in the United States, E. coli O157:H7 is among the most common 
pathogens isolated from visibly bloody stools. Shiga-toxin containing 
strains of this enterohemorrhagic serotype can be identified by PCR 
or in specialized laboratories by serotyping, but also can be identified 
presumptively as lactose-fermenting, indole-positive colonies of sor­
bitol nonfermenters (white colonies) on sorbitol MacConkey plates. If 
the clinical presentation suggests the possibility of intestinal amebiasis, 
stool should be examined by a rapid antigen detection assay or by (less 
sensitive and less specific) microscopy. Multiplex nucleic acid amplifi­
cation methods for detection of many stool pathogens (viral, bacterial, 
and parasitic) are increasingly being used in clinical microbiology 
laboratories to decrease the time to detection of a pathogen. These tests 
are more sensitive and rapid than standard culture methods and may 
detect multiple pathogens, which may lead to challenges in interpreta­
tion. For bacterial enteric infections, the lack of a microbial isolate 
prevents determination of antimicrobial susceptibility and typing of 
strains by public health authorities in order to detect and respond to 
common-source outbreaks. For this reason, the Centers for Disease 
Control and Prevention suggests that diagnosis of an enteric bacterial 
infection by a nucleic acid amplification method should be followed by 
attempted isolation of the pathogen by culture.

TREATMENT
Infectious Diarrhea or Bacterial Food Poisoning
In many cases, a specific diagnosis is not necessary or not available 
to guide treatment. The clinician can proceed with the informa­
tion obtained from the history, stool examination, and evaluation 
of dehydration severity. Empirical regimens for the treatment of 
traveler’s diarrhea are listed in Table 138-5.
The mainstay of treatment is adequate rehydration. The treat­
ment of cholera and other dehydrating diarrheal diseases was 
revolutionized by the development and promotion of oral rehydra­
tion solution (ORS), the efficacy of which depends on the fact that 
glucose-facilitated absorption of sodium and water in the small 
intestine remains intact in the presence of cholera toxin. The use of 
ORS has reduced cholera mortality rates from >50% (in untreated 
cases) to <1%. Several ORS formulas have been developed and 
tested. Initial preparations were based on the treatment of patients 
with cholera and included a solution containing 3.5 g of sodium 
chloride, 2.5 g of sodium bicarbonate (or 2.9 g of sodium citrate), 
1.5 g of potassium chloride, and 20 g of glucose (or 40 g of sucrose) 
per liter of water. Such a preparation can still be used for the treat­
ment of severe cholera. Many causes of secretory diarrhea, however, 
are associated with less electrolyte loss than occurs in cholera. 
Beginning in 2002, the World Health Organization recommended 
a reduced-osmolarity/reduced-salt ORS that is better tolerated and 
TABLE 138-5  Treatment of Traveler’s Diarrhea on the Basis of Clinical 
Featuresa
CLINICAL SYNDROME
SUGGESTED THERAPY
Watery diarrhea (no blood in stool, 
no fever), 1 or 2 unformed stools 
per day without distressing enteric 
symptoms
Oral fluids (oral rehydration solution, 
Pedialyte, Lytren, or flavored mineral 
water) and saltine crackers
Watery diarrhea (no blood in stool, 
no fever), 1 or 2 unformed stools 
per day with distressing enteric 
symptoms
Bismuth subsalicylate (for adults): 30 mL 
or 2 tablets (262 mg/tablet) every 30 min 
for 8 doses; or loperamideb: 4 mg initially 
followed by 2 mg after passage of each 
unformed stool, not to exceed 8 tablets 
(16 mg) per day (prescription dose) or 4 
caplets (8 mg) per day (over-the-counter 
dose); drugs can be taken for 2 days. 
Antibacterial drugc can be considered in 
selected circumstances.
Dysentery (passage of bloody 
stools) or fever (>37.8°C)
Antibacterial drugc
Vomiting, minimal diarrhea
Bismuth subsalicylate (for adults; see dose 
above)
Diarrhea in infants (<2 years old)
Fluids and electrolytes (oral rehydration 
solution, Pedialyte, Lytren); continue 
feeding, especially with breast milk; seek 
medical attention for moderate dehydration, 
fever lasting >24 h, bloody stools, or 
diarrhea lasting more than several days
aAll patients should take oral fluids (Pedialyte, Lytren, or flavored mineral water) 
plus saltine crackers. If diarrhea becomes moderate or severe, if fever persists, 
or if bloody stools or dehydration develops, the patient should seek medical 
attention. bLoperamide should not be used by patients with fever or dysentery; its 
use may prolong diarrhea in patients with infection due to Shigella or other invasive 
organisms. cThe recommended antibacterial drugs are as follows:
If the level of suspicion is low for fluoroquinolone-resistant Campylobacter:
Adults: (1) A fluoroquinolone such as ciprofloxacin, 750 mg as a single dose or 500 
mg bid for 3 days; levofloxacin, 500 mg as a single dose or 500 mg qd for 3 days; or 
norfloxacin, 800 mg as a single dose or 400 mg bid for 3 days. (2) Azithromycin, 1000 
mg as a single dose or 500 mg qd for 3 days. (3) Rifaximin, 200 mg tid or 400 mg bid 
for 3 days (not recommended for use in dysentery).
Children: Azithromycin, 10 mg/kg on day 1, 5 mg/kg on days 2 and 3 if diarrhea persists.
If fluoroquinolone-resistant Campylobacter is suspected (for example, following 
travel to Southeast Asia):
Adults: Azithromycin (at above dose for adults). Children: Same as for children 
traveling to other areas (see above).
Source: After DR Hill et al: The practice of travel medicine: Guidelines by the 
Infectious Diseases Society of America. Clin Infect Dis 43:1499, 2006.

more effective than classic ORS. This preparation contains 2.6 g 
of sodium chloride, 2.9 g of trisodium citrate, 1.5 g of potassium 
chloride, and 13.5 g of glucose (or 27 g of sucrose) per liter of water. 
ORS formulations containing rice or cereal as the carbohydrate 
source may be even more effective than glucose-based solutions. 
Patients who are severely dehydrated, are unable to drink, or in 
whom vomiting precludes oral therapy should receive IV solutions 
such as Ringer’s lactate in addition to ORS when the patient can 
ingest it safely.

Most cases of traveler’s diarrhea (usually due to enterotoxigenic 
or enteroaggregative E. coli or to Campylobacter) can be treated 
effectively with rehydration, bismuth subsalicylate, or antiperistal­
tic agents. Antimicrobial agents can shorten the duration of illness 
from 3–4 days to 24–36 h but may be associated with the acquisi­
tion of multidrug-resistant organisms; their use should therefore be 
reserved for severe cases. Changes in diet have not been shown to 
have an impact on the duration of illness, and the efficacy of probi­
otics to hasten recovery continues to be debated. Most individuals 
who present with dysentery (bloody diarrhea and fever) should be 
treated empirically with an antimicrobial agent (e.g., a fluoroquino­
lone or a macrolide, depending on local antimicrobial susceptibility 
patterns) pending diagnostic testing. Individuals with shigellosis 
should receive a 3- to 7-day course. Patients with severe or pro­
longed Campylobacter infection often benefit from antimicrobial 
treatment. Because of widespread resistance of Campylobacter to 
fluoroquinolones, especially in parts of Asia, a macrolide antibiotic 
such as erythromycin or azithromycin is preferred for this infection.
Treatment of salmonellosis must be tailored to the individual 
patient. Since administration of antimicrobial agents often prolongs 
intestinal colonization with Salmonella, these drugs are usually 
reserved for individuals at high risk of complications from dis­
seminated salmonellosis, such as infants, patients with prosthetic 
devices, patients over age 50, and immunocompromised persons. 
Antimicrobial agents should not be administered to individuals 
(especially children) in whom enterohemorrhagic E. coli infection 
is suspected. Laboratory studies of enterohemorrhagic E. coli strains 
have demonstrated that many antibiotics induce replication of Shiga 
toxin–producing lambdoid bacteriophages, thereby significantly 
increasing toxin production by these strains. Clinical studies have 
supported these laboratory results, and antibiotics may increase by 
20-fold the risk of hemolytic-uremic syndrome and renal failure 
during enterohemorrhagic E. coli infection. A clinical clue in the 
diagnosis of the latter infection is bloody diarrhea in a patient with 
a low-grade fever or who is afebrile.
CHAPTER 138
Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning  
PROPHYLAXIS
Improvements in safe water infrastructure to limit fecal–oral spread of 
enteric pathogens will be necessary if the prevalence of diarrheal dis­
eases is to be significantly reduced in resource-poor countries. Travelers 
can reduce their risk of diarrhea by eating only hot, freshly cooked food; 
by avoiding raw vegetables, salads, and unpeeled fruit; and by drinking 
only boiled or treated water and avoiding ice. Historically, few travelers 
to tourist destinations adhere to these dietary restrictions, even after 
pretravel counseling. Bismuth subsalicylate is an inexpensive agent for 
the prophylaxis of traveler’s diarrhea; it is taken at a dosage of 2 tablets 
(525 mg) four times a day. Treatment appears to be effective and safe 
for up to 3 weeks, but adverse events such as temporary darkening of 
the tongue, constipation, and tinnitus can occur. A meta-analysis sug­
gests that probiotics may lessen the likelihood of traveler’s diarrhea by 
~15%, but further studies are needed. Prophylactic antimicrobial agents, 
although effective, are not generally recommended for the prevention 
of traveler’s diarrhea except when travelers are immunosuppressed or 
have underlying illness that places them at high risk for morbidity from 
gastrointestinal infection. If prophylaxis is indicated, the nonabsorbed 
antibiotic rifaximin can be considered.
The possibility of exerting a major impact on the worldwide mor­
bidity and mortality associated with diarrheal diseases has led to inten­
sive efforts to develop effective vaccines against common bacterial and