Anatomy The Digestive System

The first step in the digestive system can actually begin before the food is even in your mouth.
When you smell or see something that you just have to eat, you start to salivate in anticipation of
eating, thus beginning the digestive process. Food is the body's source of fuel. Nutrients in food
give the body's cells the energy they need to operate. Before food can be used it has to be broken
down into tiny little pieces so it can be absorbed and used by the body. In humans, proteins need
to be broken down into amino acids, starches into sugars, and fats into fatty acids and glycerol.
During digestion two main processes occur at the same time:

 Mechanical Digestion: larger pieces of food get broken down into smaller pieces while being
prepared for chemical digestion. Mechanical digestion starts in the mouth and continues in to the
stomach.
Chemical Digestion: several different enzymes break down macromolecules into smaller
molecules that can be more efficiently absorbed. Chemical digestion starts with saliva and
continues into the intestines. The digestive system is made up by the alimentary canal, or the
digestive tract, and other abdominal organs that play a part in digestion such as the liver and the
pancreas. The alimentary canal is the long tube of organs that runs from the mouth (where the
food enters) to the anus (where indigestible waste leaves). The organs in the alimentary canal
include the esophagus, stomach and the intestines. The average adult digestive tract is about
thirty feet (30') long. While in the digestive tract the food is really passing through the body
rather than being in the body. The smooth muscles of the tubular digestive organs move the food
efficiently along as it is broken down into absorbable atoms and molecules. During absorption,
the nutrients that come from food (such as proteins, fats, carbohydrates, vitamins, and minerals)
pass through the wall of the small intestine and into the bloodstream and lymph. In this way
nutrients can be distributed throughout the rest of the body. In the large intestine there is
reabsorption of water and absorption of some minerals as feces are formed. The parts of the food
that the body passes out through the anus is known as feces.
Mastication
Digestion begins in the mouth. A brain reflex triggers the flow of saliva when we see or even
think about food. Saliva moistens the food while the teeth chew it up and make it easier to
swallow. Amylase, which is the digestive enzyme found in saliva, starts to break down starch
into simpler sugars before the food even leaves the mouth. The nervous pathway involved in
salivary excretion requires stimulation of receptors in the mouth, sensory impulses to the brain
stem, and parasympathetic impulses to salivary glands. Swallowing your food happens when the
muscles in your tongue and mouth move the food into your pharynx. The pharynx, which is the
passageway for food and air, is about five inches (5") long. A small flap of skin called the
epiglottis closes over the pharynx to prevent food from entering the trachea and thus choking.
For swallowing to happen correctly a combination of 25 muscles must all work together at the
same time. Salivary glands also produce an estimated three liters of saliva per day.
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Esophagus
The esophagus (also spelled oesophagus/esophagus) or gullet is the muscular tube in vertebrates
through which ingested food passes from the throat to the stomach. The esophagus is continuous
with the laryngeal part of the pharynx at the level of the C6 vertebra. It connects the pharynx,
which is the body cavity that is common to both the digestive and respiratory systems behind the
mouth, with the stomach, where the second stage of digestion is initiated (the first stage is in the
mouth with teeth and tongue masticating food and mixing it with saliva). After passing through
the throat, the food moves into the esophagus and is pushed down into the stomach by the
process of peristalsis (involuntary wavelike muscle contractions along the G.I. tract). At the end
of the esophagus there is a sphincter that allows food into the stomach then closes back up so the
food cannot travel back up into the esophagus.
Stomach
The stomach a thick walled organ that lies between the esophagus and the first part of the small
intestine (the duodenum). It is on the left side of the abdominal cavity; the fundus of the stomach
lying against the diaphragm. Lying beneath the stomach is the pancreas. The greater omentum
hangs from the greater curvature. A mucous membrane lines the stomach which contains glands
(with chief cells) that secrete gastric juices, up to three quarts of this digestive fluid is produced
daily. The gastric glands begin secreting before food enters the stomach due to the
parasympathetic impulses of the vagus nerve, making the stomach also a storage vat for that
acid. The secretion of gastric juices occurs in three phases: cephalic, gastric, and intestinal. The
cephalic phase is activated by the smell and taste of food and swallowing. The gastric phase is
activated by the chemical effects of food and the distension of the stomach. The intestinal phase
blocks the effect of the cephalic and gastric phases. Gastric juice also contains an enzyme named
pepsin, which digests proteins, hydrochloric acid and mucus. Hydrochloric acid causes the
stomach to maintain a pH of about 2, which helps kill off bacteria that comes into the digestive
system via food. The gastric juice is highly acidic with a pH of 1-3. It may cause or compound
damage to the stomach wall or its layer of mucus, causing a peptic ulcer. On the inside of the
stomach there are folds of skin call the gastric rugae.
Gastric rugae make the stomach very extendable, especially after a very big meal. The stomach is
divided into four sections, each of which has different cells and functions. The sections are: 1)
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Cardiac region, where the contents of the esophagus empty into the stomach, 2) Fundus, formed
by the upper curvature of the organ, 3) Body, the main central region, and 4) Pylorus or atrium,
the lower section of the organ that facilitates emptying the contents into the small intestine.
Two smooth muscle valves, or sphincters, keep the contents of the stomach contained.
They are the: 1) Cardiac or esophageal sphincter, dividing the tract above, and 2) Pyloric
sphincter, dividing the stomach from the small intestine. After receiving the bolus(chewed food)
the process of peristalsis is started; mixed and churned with gastric juices the bolus is
transformed into a semi-liquid substance called chyme. Stomach muscles mix up the food with
enzymes and acids to make smaller digestible pieces. The pyloric sphincter, a walnut shaped
muscular tube at the stomach outlet, keeps chyme in the stomach until it reaches the right
consistency to pass into the small intestine. The food leaves the stomach in small squirts rather
than all at once. Water, alcohol, salt, and simple sugars can be absorbed directly through the
stomach wall. However, most substances in our food need a little more digestion and must travel
into the intestines before they can be absorbed. When the stomach is empty it is about the size of
one fifth of a cup of fluid. When stretched and expanded, it can hold up to eight cups of food
after a big meal.
Gastric Glands
There are many different gastric glands and they secret many different chemicals. Parietal cells
secrete hydrochloric acid; chief cells secrete pepsinogen; goblet cells secrete mucus; argentaffin
cells secrete serotonin and histamine; and G cells secrete the hormone gastrin.
Vessels and nerves
Arteries: The arteries supplying the stomach are the left gastric, the right gastric and right
gastroepiploic branches of the hepatic, and the left gastroepiploic and short gastric branches of
the lineal. They supply the muscular coat, ramify in the submucous coat, and are finally
distributed to the mucous membrane.
Capillaries: The arteries break up at the base of the gastric tubules into a plexus of fine
capillaries, which run upward between the tubules, anatomizing with each other, and ending in a
plexus of larger capillaries, which surround the mouths of the tubes, and also form hexagonal
meshes around the ducts. Veins: From these the veins arise, and pursue a straight course
4

downward, between the tubules, to the submucous tissue; they end either in the lineal and
superior mesenteric veins, or directly in the portal vein.
Lymphatics: The lymphatics are numerous: They consist of a superficial and a deep set, and
pass to the lymph glands found along the two curvatures of the organ.
Nerves: The nerves are the terminal branches of the right and left urethra and other parts, the
former being distributed upon the back, and the latter upon the front part of the organ. A great
number of branches from the celiac plexus of the sympathetic are also distributed to it. Nerve
plexuses are found in the submucous coat and between the layers of the muscular coat as in the
intestine. From these plexuses fibrils are distributed to the muscular tissue and the mucous
membrane.
Control of secretion and motility
The movement and the flow of chemicals into the stomach are controlled by both the nervous
system and by the various digestive system hormones. The hormone gastrin causes an increase in
the secretion of HCL, pepsinogen and intrinsic factor from parietal cells in the stomach. It also
causes increased motility in the stomach. Gastrin is released by G-cells into the stomach. It is
inhibited by pH normally less than 4 (high acid), as well as the hormone somatostatin.
Cholecystokinin (CCK) has most effect on the gall bladder, but it also decreases gastric
emptying. In a different and rare manner, secretin, produced in the small intestine, has most
effects on the pancreas, but will also diminish acid secretion in the stomach. Gastric inhibitory
peptide (GIP) and enteroglucagon decrease both gastric motility and secretion of pepsin. Other
than gastrin, these hormones act to turn off the stomach action. This is in response to food
products in the liver and gall bladder, which have not yet been absorbed. The stomach needs only
to push food into the small intestine when the intestine is not busy. While the intestine is full and
still digesting food, the stomach acts as a storage for food.
Small Intestine
Diagram showing the small intestine The small intestine is the site where most of the chemical
and mechanical digestion is carried out. Tiny projections called villi line the small intestine
which absorbs digested food into the capillaries. Most of the food absorption takes place in the
jejunum and the ileum. The functions of a small intestine is, the digestion of proteins into
5

peptides and amino acids principally occurs in the stomach but some also occurs in the small
intestine. Peptides are degraded into amino acids; lipids (fats) are degraded into fatty acids and
glycerol; and carbohydrates are degraded into simple sugars. The three main sections of the small
intestine is The Duodenum, The Jejunum, The Ileum.
The Duodenum
In anatomy of the digestive system, the duodenum is a hollow jointed tube connecting the
stomach to the jejunum. It is the first and shortest part of the small intestine. It begins with the
duodenal bulb and ends at the ligament of Treitz. The duodenum is almost entirely retro
peritoneal. The duodenum is also where the bile and pancreatic juices enter the intestine.
The Jejunum
The Jejunum is a part of the small bowel, located between the distal end of duodenum and the
proximal part of ileum. The jejunum and the ileum are suspended by an extensive mesentery
giving the bowel great mobility within the abdomen. The inner surface of the jejunum, its
mucous membrane, is covered in projections called villi, which increase the surface area of tissue
available to absorb nutrients from the gut contents. It is different from the ileum due to fewer
goblet cells and generally lacks Preyer's patches.
The Ileum
Its function is to absorb vitamin B12 and bile salts. The wall itself is made up of folds, each of
which has many tiny finger-like projections known as villi, on its surface. In turn, the epithelial
cells which line these villi possess even larger numbers of micro villi. The cells that line the
ileum contain the protease and carbohydrate enzymes responsible for the final stages of protein
and carbohydrate digestion. These enzymes are present in the cytoplasm of the epithelial cells.
The villi contain large numbers of capillaries which take the amino acids and glucose produced
by digestion to the hepatic portal vein and the liver. The terminal ileum continues to absorb bile
salts, and is also crucial in the absorption of fat-soluble vitamins (Vitamin A, D, E and K). For
fat-soluble vitamin absorption to occur, bile acids must be present.

Large Intestine
The large intestine (colon) extends from the end of the ileum to the anus. It is about 5 feet long,
being one-fifth of the whole extent of the intestinal canal. It's caliber is largest at the
commencement at the cecum, and gradually diminishes as far as the rectum, where there is a
dilatation of considerable size just above the anal canal. It differs from the small intestine in by
the greater caliber, more fixed position, sacculated form, and in possessing certain appendages to
its external coat, the appendices epiploic. Further, its longitudinal muscular fibers do not form a
continuous layer around the gut, but are arranged in three longitudinal bands or tni. The large
intestine is divided into the cecum, colon, rectum, and anal canal. In its course, describes an arch
which surrounds the convolutions of the small intestine. It commences in the right iliac region, in
a dilated part, the cecum. It ascends through the right lumbar and hypochondriac regions to the
under surface of the liver; here it takes a bend, the right colic flexure, to the left and passes
transversely across the abdomen on the confines of the epigastric and umbilical regions, to the
left hypochondriac region; it then bends again, the left colic flexure, and descends through the
left lumbar and iliac regions to the pelvis, where it forms a bend called the sigmoid flexure; from
this it is continued along the posterior wall of the pelvis to the anus. There are trillions of
bacteria, yeasts, and parasites living in our intestines, mostly in the colon. Over 400 species of
organisms live in the colon. Most of these are very helpful to our health, while the minority are
harmful. Helpful organisms synthesize vitamins, like B12, biotin, and vitamin K. They
breakdown toxins and stop proliferation of harmful organisms. They stimulate the immune
system and produce short chain fatty acids (SCFAs) that are required for the health of colon cells
and help prevent colon cancer. There are many beneficial bacteria but some of the most common
and important are Lactobacillus Acidophilus and various species of Bifidobacterium. These are
available as "probiotics" from many sources.

INTRODUCTION
Ranging from mild annoyances during vacations to devastating dehydrating illnesses that
can kill within hours, acute gastrointestinal illnesses rank second only to acute upper respiratory
illnesses as the most common diseases worldwide. In children <5 years old, attack rates range
from 23 illnesses per child per year in developed countries to as high as 1018 illnesses per
child per year in developing countries. In Asia, Africa, and Latin America, acute diarrheal
illnesses are not only a leading cause of morbidity in childrenwith an estimated 1 billion cases
per yearbut also a major cause of death. These illnesses are responsible for 46 million deaths
per year, or a sobering total of 12,600 deaths per day. In some areas, >50% of childhood deaths
are directly attributable to acute diarrheal illnesses. In addition, by contributing to malnutrition
and thereby reducing resistance to other infectious agents, gastrointestinal illnesses may be
indirect factors in a far greater burden of disease.
The wide range of clinical manifestations of acute gastrointestinal illnesses is matched by
the wide variety of infectious agents involved, including viruses, bacteria, and parasitic
pathogens (Table 22-1). This chapter discusses factors that enable gastrointestinal pathogens to
cause disease, 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, enterohemorrhagic Escherichia coli, Giardia lamblia, or
Entamoeba, as few as 10100 bacteria or cysts can produce infection, while 105108 Vibrio
cholerae organisms must be ingested orally to cause disease.The infective dose of Salmonella
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, Entamoeba, and Giardia can spread by person-to-person contact,

whereas under some circumstances Salmonella may have to grow in food for several hours
before reaching an effective infectious dose.
9

Adherence
Many organisms must adhere to the gastrointestinal mucosa as an initial step in the
pathogenic process; thus, organisms that can compete 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 colonization 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 enterohemorrhagic E. coli, which causes hemorrhagic colitis and the
hemolytic-uremic 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 pathogenesis of numerous
enteric organisms. Such toxins include enterotoxins, which cause watery diarrhea by acting
directly on secretory mechanisms 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 protein 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 ADP-ribosylation of a GTP-binding protein
and causes persistent activation of adenylate cyclase. The end result is an increase of cyclic AMP
in the intestinal mucosa, which increases Cl secretion and decreases Na+ absorption, leading to
loss of fluid and the production of diarrhea.

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Enterotoxigenic strains of E. coli may produce a protein called heat-labile enterotoxin

(LT) that is similar to 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 GMP. 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 inflammatory cells. Enteric pathogens
that produce such cytotoxins include Shigella dysenteriae type 1, Vibrio parahaemolyticus, and
Clostridium difficile. S. dysenteriae type 1 and Shiga toxinproducing strains of E. coli produce
potent cytotoxins and have been associated with outbreaks of hemorrhagic colitis and hemolyticuremic syndrome.
Neurotoxins are usually produced by bacteria outside the host and therefore cause
symptoms soon after ingestion. Included are the staphylococcal 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
multiplication, and subsequent spread to adjacent cells. Salmonella causes inflammatory diarrhea
by invasion of the bowel mucosa but generally is not associated with the destruction of
enterocytes or the full clinical syndrome of dysentery. Salmonella typhi and Yersinia
enterocolitica can penetrate intact intestinal mucosa, multiply intracellularly in Peyers patches
and intestinal lymph nodes, and then disseminate through the bloodstream to cause enteric fever,
a syndrome characterized by fever, headache, relative bradycardia, abdominal pain,
splenomegaly, and leukopenia.

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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.
Normal Flora
The large numbers of bacteria that normally inhabit the intestine act as an important host
defense by preventing colonization by potential enteric pathogens. Persons with fewer intestinal
bacteria, such as infants who have not yet developed normal enteric colonization or patients
receiving antibiotics, are at significantly greater risk of developing infections with enteric
pathogens. The composition of the intestinal flora is as important as the number of organisms
present. More than 99% of the normal colonic flora 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 pathogens, 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 or H2 blockersa common
practice in the management of hospitalized patientssimilarly increases the risk of enteric
colonization. In addition, some microorganisms can survive the extreme acidity of the
gastric environment; rotavirus, for example, is highly stable to acidity.
Intestinal Motility
Normal peristalsis is the major mechanism for clearance of bacteria from the proximal
small intestine. When intestinal motility is impaired (e.g., by treatment with opiates or other
antimotility drugs, anatomic abnormalities, 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
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with atropine (Lomotil) experience prolonged fever and shedding of organisms, while patients
treated with opiates for mild Salmonella gastroenteritis have a higher frequency of bacteremia
than those not treated with opiates.
Immunity
Both cellular immune responses and antibody production play important roles in
protection from enteric infections. The wide spectrum of viral, bacterial, parasitic, and fungal
gastrointestinal infections in patients with AIDS highlights the significance of cell-mediated
immunity in protection from these pathogens. Humoral immunity is also important and consists
of systemic IgG and IgM as well as secretory IgA. The mucosal immune system may be the first
line of defense against many gastrointestinal pathogens. The binding of bacterial antigens to
the luminal surface of M cells in the distal small bowel and the subsequent presentation of
antigens to subepithelial lymphoid tissue lead to the proliferation of sensitized lymphocytes.
These lymphocytes circulate and populate all of the mucosal tissues of the body as Ig
Asecreting plasma cells.
Genetic Determinants
The mechanisms underlying genetic variation in host susceptibility remain poorly
understood. People with blood group O show increased susceptibility to cholera, shigellosis,
and norovirus infection. A polymorphism in the interleukin 8 gene is associated with
increased risk of diarrhea from enteroaggregative E. coli.
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. 22-1.

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HISTORY 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. 22-1.
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 orthostatic fall in 231

14

blood pressure, skin tenting, and sunken eyes (or, in infants, a sunken fontanelle). Signs of severe
dehydration range from hypotension and tachycardia to confusion and frank shock.
DIAGNOSTIC APPROACH After the severity of illness is assessed, the clinician must
distinguish between inflammatory and noninflammatory disease. Using the history and
epidemiologic features of the case as guides, 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. Causes of acute infectious diarrhea, categorized as inflammatory and
noninflammatory, are listed in Table 22-1.
POST-DIARRHEA COMPLICATIONS Chronic complications may follow the resolution of
an acute diarrheal episode. The clinician should inquire about prior diarrheal illness if the
conditions listed in Table 22-2 are observed.

15

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, 2050% experience a
sudden onset of abdominal cramps, anorexia, and watery diarrhea; thus travelers diarrhea is the
most common travel-related illness. The time of onset is usually 3 days to 2 weeks after the
travelers arrival in a tropical area; most cases begin within the first 35 days. The illness is
generally selflimited, lasting 15 days. The high rate of diarrhea among travelers to
underdeveloped areas is related to the ingestion of contaminated food or water.
The organisms that cause travelers diarrhea vary considerably with location (Table 223). In all areas, enterotoxigenic and enteroaggregative E. coli are the most common isolates from
persons with the classic secretory travelers diarrhea syndrome.

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Location
Day-care centers have particularly high attack rates of enteric infections. Rotavirus is
most common among children <2 years old, with attack rates of 75100% among those exposed.
G. lamblia is more common among older children, with somewhat lower attack rates. Other
common organisms, often spread by fecaloral contact, are Shigella, Campylobacter jejuni, and
Cryptosporidium. A characteristic feature of infection among children attending day-care centers
is the high rate of secondary cases among family members.
Similarly, hospitals are sites in which enteric infections are concentrated. In medical
intensive care units and pediatric wards, diarrhea is one of the most common manifestations of
nosocomial infections. C. difficile is the predominant cause of nosocomial diarrhea among
adults in the United States. Viral pathogens, especially rotavirus, can spread rapidly in pediatric
wards. Enteropathogenic E. coli has been associated with outbreaks of diarrhea in nurseries for
17

newborns. One-third of elderly patients in chronic-care institutions develop a significant

diarrheal illness each year; more than half of these cases are caused by cytotoxin-producing C.
difficile. Antimicrobial therapy can predispose to pseudomembranous colitis by altering the
normal colonic flora and allowing the multiplication of C. difficile (Chap. 23).
Age
Most of the morbidity and mortality from enteric pathogens involves children <5 years of
age. Breast-fed infants are protected from 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. Infants and younger children are more likely than adults to develop
rotavirus disease, while older children and adults are more commonly infected with norovirus.
Other organisms with higher attack rates among children than among adults include
enterotoxigenic, enteropathogenic, and enterohemorrhagic E. coli; C. jejuni; and G. lamblia. In
children, the incidence of Salmonella infections is highest among those <1 year of age, while the
attack rate for Shigella infections is greatest among those 6 months to 4 years of age.
Bacterial Food Poisoning
If the history and the stool examination indicate a noninflammatory etiology of diarrhea
and there is evidence of a common-source outbreak, questions concerning the ingestion of
specific foods and the time of onset of the diarrhea after a meal can provide clues to the bacterial
cause of the illness. Potential causes of bacterial food poisoning are shown in Table 22-4.

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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 (16 h) and generally lasts
<12 h. Most cases of staphylococcal food poisoning are caused by contamination from 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 less so.
B. cereus can produce either a syndrome with a short incubation periodthe emetic form,
mediated by a staphylococcal type of enterotoxinor one with a longer incubation period (816
h)the diarrheal form, caused by an enterotoxin resembling E. coli LT, in which 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

19

can germinate and produce toxin. Frying before serving may not destroy the preformed, heatstable toxin.
Food poisoning due to Clostridium perfringens also has a slightly longer incubation
period (814 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
moderately 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.
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 thiosulfatecitratebile salts sucrose (TCBS) agar. A
latex agglutination test has made the rapid detection of rotavirus in stool practical for many
laboratories, while reverse-transcriptase polymerase chain reaction and specific antigen enzyme
immunoassays have been developed for the identification of norovirus.At least three stool
specimens should be examined for Giardia cysts or stained for Cryptosporidium if the level of
clinical suspicion regarding the involvement of these organisms is high.
All patients with fever and evidence of inflammatory disease acquired outside the
hospital should have stool cultured for Salmonella, Shigella, and Campylobacter. Salmonella and
Shigella can be selected on MacConkeys 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. Evaluation of nosocomial diarrhea should initially focus
on C. difficile; stool culture for other pathogens in this setting has an 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 and latex agglutination tests (Chap. 23). Isolation of C. jejuni
requires inoculation of fresh stool onto selective growth medium and incubation at 42C in a
microaerophilic atmosphere. In many laboratories in the United States, E. coli O157:H7 is
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among the most common pathogens isolated from visibly bloody stools. Strains of this
enterohemorrhagic serotype can be identified in specialized laboratories by serotyping but also
can be identified presumptively in hospital laboratories as lactose-fermenting, indole-positive
colonies of sorbitol nonfermenters (white colonies) on sorbitol MacConkey plates. Fresh stools
should be examined for amebic cysts and trophozoites.
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 information obtained from the history, stool examination, and
evaluation of dehydration severity. Empirical regimens for the treatment of travelers diarrhea are
listed in Table 22-5.

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The mainstay of treatment is adequate rehydration. The treatment of cholera and other
dehydrating diarrheal diseases was revolutionized by the promotion of oral rehydration solutions,
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 oral rehydration
solutions has reduced mortality due to cholera from >50% (in untreated cases) to <1%. The
World Health Organization recommends a solution containing 3.5 g sodium chloride, 2.5 g
sodium bicarbonate, 1.5 g potassium chloride, and 20 g glucose (or 40 g sucrose) per liter of
water. Oral rehydration solutions containing rice or cereal as the carbohydrate source may be
even more effective than glucose-based solutions, and the addition of L-histidine may reduce the
frequency and volume of stool output. Patients who are severely dehydrated or in whom
vomiting precludes the use of oral therapy should receive IV solutions such as Ringers lactate.
Although most secretory forms of travelers diarrhea usually due to enterotoxigenic
and enteroaggregative E. colican be treated effectively with rehydration, bismuth
subsalicylate, or antiperistaltic agents, antimicrobial agents can shorten the duration of illness
from 34 days to 2436 h.Changes in diet have not been shown to have an impact on the
duration of illness, while the efficacy of probiotics continues to be debated.
Antibiotic treatment for children who present with bloody diarrhea raises special
concerns. Laboratory studies of enterohemorrhagic E. coli strains have demonstrated that a
number of antibiotics induce replication of Shiga toxinproducing lambdoid bacteriophages,
significantly increasing toxin production by these strains. Clinical studies have supported these
laboratory results, and antibiotics are not recommended for the treatment of enterohemorrhagic
E. coli infections in children.
PROPHYLAXIS
Improvements in hygiene to limit fecal-oral spread of enteric pathogens will be necessary
if the prevalence of diarrheal diseases is to be significantly reduced in developing
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. However, an intensive hygienic effort in Jamaica involving government, hotel, and

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tourism agencies led to a decrease in the incidence of travelers diarrhea by 72% from 1996 to
2002.
Bismuth subsalicylate is an inexpensive agent for the prophylaxis of travelers 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. Prophylactic antimicrobial agents, although effective, are not generally
recommended for the prevention of travelers diarrhea, except when travelers are
immunosuppressed or have other underlying illnesses that place them at high risk for morbidity
from gastrointestinal infection.The risk of side effects and the possibility of developing an
infection with a drug-resistant organism or with more harmful, invasive bacteria make it more
reasonable to institute an empirical short course of treatment if symptoms develop. The recent
availability of effective nonabsorbed antibiotics such as rifaximin may lead to new prophylactic
options.
The possibility of exerting a major impact on the worldwide morbidity and mortality
associated with diarrheal diseases has led to intense efforts to develop effective vaccines against
the common bacterial and viral enteric pathogens. Recent research has yielded promising
advances in the development of vaccines against rotavirus, Shigella,V. cholerae, S. typhi, and
enterotoxigenic E. coli.

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Daftar Pustaka
1. Sudoyo Aru W, dkk. 2007. Buku Ajar Ilmu Penyakit Dalam Jilid I Edisi IV. PAPDI.
Jakarta. Hal 408-414
2. Fauci Antony, dkk. 2010. Harrisons Gastroenterology and Hepatology. McGraw-Hill.
United State. Hal 42-48
3. Sudoyo Aru W, dkk. 2007. Buku Ajar Ilmu Penyakit Dalam Jilid II Edisi IV. PAPDI.
Jakarta. Hal 1772-1776
4. Fauci Antony, dkk. 2010. Harrisons Gastroenterology and Hepatology. McGraw-Hill.
United State. Hal 228-237
5. Farthing Prof M, dkk. 2012. Acute Diarrhea in Adults and Children a Global Perspective.

World Gastroenterology Organisation Global Guidelines.

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