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Food Poisoning: a 2013

comprehensive review
Food poisoning is relevant to toxicology and public health largely ! "
because of adulterant contamination. Food poisoning is usually
caused by infectious agents but other ingested toxic compounds can cause
diarrhea, vomiting, and abdominal pain as well. It also has direct relevance to
community acquired disease, assessments for such diseases, and
surveillance. The following review article was recently published online in
emedicine #175569.

Food poisoning is defined as an illness caused by the consumption of food or water

contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The
symptoms, varying in degree and combination, include abdominal pain, vomiting, diarrhea,
and headache; more serious cases can result in life-threatening neurologic, hepatic, and
renal syndromes leading to permanent disability or death.

Most of the illnesses are mild and improve without any specific treatment. Some patients
have severe disease and require hospitalization, aggressive hydration, and antibiotic
treatment.[1]

A food-borne disease outbreak is defined by the following 2 criteria:

1. Similar illness, often GI, in a minimum of 2 people

2. Evidence of food as the source

The pathogenesis of diarrhea in food poisoning is classified broadly into either

noninflammatory or inflammatory types.

Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory

mechanisms of the mucosa of the small intestine, without invasion. This leads to large
volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally,
profound dehydration may result. The enterotoxins may be either preformed before
ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae,
enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus,[2]Staphylococcus
organisms , Giardia lamblia, Cryptosporidium,rotavirus, norovirus (genus Norovirus,
previously called Norwalk virus), and adenovirus.

Inflammatory diarrhea is caused by the action of cytotoxin on the mucosa, leading to

invasion and destruction. The colon or the distal small bowel commonly is involved. The
diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile
and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea
because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test
indicates an inflammatory process, and sheets of leukocytes indicate colitis.

Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic
tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio
parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica,
Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigellaspecies.

In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a

toxin acting on the central nervous system. The clinical syndrome of botulismresults from
the inhibition of acetylcholine release in nerve endings by the botulinum.

The pathophysiological mechanisms that result in acute GIsymptoms produced by some of

the noninfectious causes of food poisoning (naturally occurring substances
[eg,mushrooms, toadstools] and heavy metals [eg, arsenic, mercury, lead]) are not well
known.

Epidemiology: United States

Initially, food-borne diseases were estimated to be responsible for 6-8 million illnesses and
as many as 9000 deaths each year.[3, 4] However, the change in food supply, the
identification of new food-borne diseases, and the availability of new surveillance data have
changed the morbidity and mortality figures. The US Centers for Disease Control and
Prevention (CDC) estimates 1 in 6 Americans (48 million people) are affected by foodborne
illness annually. The estimates suggest 128,000 people are hospitalized and 3,000 die.[5]
The 31 known pathogens account for an estimated 9.4 million annual cases, 55,961
hospitalizations, and 1,351 deaths. Unspecified agents account for 38.4 million cases,
71,878 hospitalizations, and 1,686 deaths.[6]

Overall, food-borne diseases appear to cause more illnesses but fewer deaths than
previously estimated.[7]

The most common pathogens are as follows:[5]

Norovirus – 5,461,731 cases

Salmonella – 1,027,561
C perfringens – 965,958
Campylobacter species – 845,024
Staphylococcus aureus – 241,148

The most common pathogens responsible for hospitalizations are as follows:[5]

Salmonella – 19,336 hospitalizations

Norovirus – 14,663 hospitalizations
Campylobacter species – 8,463 hospitalizations
Toxoplasma gondii – 4,428 hospitalizations
E coli – 2,138 hospitalizations
The pathogens most commonly associated with death are as follows:
Salmonella – 378 deaths
T gondii – 327 deaths
Listeria monocytogenes – 255 deaths
Norovirus – 149 deaths
Campylobacter species – 76 deaths

In March 2012, the CDC reported a rise in foodborne disease outbreaks caused by
imported food in 2009 and 2011. Nearly 50% of the outbreaks implicated food that was
imported from regions not previously associated with outbreaks. Outbreaks reported to
CDC’s Foodborne Disease Outbreak Surveillance System from 2005-2010 implicated 39
outbreaks and 2,348 illnesses that were linked to imported food from 15 countries. Within
this 5-year period, nearly half (17) occurred in 2009 and 2010. Fish (17 outbreaks) were the
most common source of implicated imported foodborne disease outbreaks, followed by
spices (6 outbreaks including 5 from fresh or dried peppers). Approximately 45% percent of
the imported foods causing outbreaks came from Asia.[8]

The CDC recognized the following outbreaks and sources in 2012:[5]

E coli – Spinach and spring mix, raw clover sprouts at Jimmy John’s restaurants
Salmonella – Peanut butter, Frescolina Marte brand ricotta salata cheese, mangoes,
cantaloupe, ground beef, live poultry, dry dog food, raw scraped ground tuna product,
small turtles, raw clover sprouts

International
Transnational trade; travel; and migration and globalization of food production,
manufacturing, and marketing pose greater risk of cross-border transmission of infectious
diseases and food-borne illness.[9] A travel history should be obtained because traveler's
diarrhea is the leading cause of travel-related illness. Onset occurs 3 days to 2 weeks after
arrival. Illness is self-limiting within 5 days. Enterotoxigenic E coli is the most common
isolate.

Mortality/Morbidity
Symptoms vary in degree and combination. They may include abdominal pain, vomiting,
diarrhea, headache, and prostration. More serious cases can result in life-threatening
neurologic, hepatic, and renal syndromes leading to permanent disability or death.

Age
Morbidity and mortality are higher in elderly individuals. The reasons for this increased
susceptibility in elderly populations include age-associated decrease in immunity,
decreased production of gastric acid and intestinal motility, malnutrition, lack of exercise,
habitation in a nursing home, and excessive use of antibiotics. Elderly persons are more
likely to die from infection with C perfringens; E coli O157; and Salmonella, Campylobacter,
and Staphylococcus organisms.

Causes:

The CDC found that 5 bacterial enteric pathogens (Campylobacter, E coli 0157 ,
Salmonella, Shigella, and Y enterocolitica) caused 291,162 illnesses annually in children
younger than 5 years.[10] This resulted in 102,746 doctor visits, 7,830 hospitalizations, and
64 deaths. Rates of illness remain higher in children.

History:

A detailed history, including the duration of the disease, characteristics and frequency of
bowel movements, and associated abdominal and systemic symptoms, may provide a clue
to the underlying cause. The presence of a common source, types of specific food, travel
history, and use of antibiotics always should be investigated.

The presenting complaints, typical features and pathogenesis of various causative agents,
and diagnosis and treatment information can be found in Table 1 in the Causes section.

The following are some of the salient features of food poisoning:

Acute diarrhea in food poisoning usually lasts less than 2 weeks. Diarrhea lasting 2-4
weeks is classified as persistent. Chronic diarrhea is defined by duration of more than
4 weeks.
The presence of fever suggests an invasive disease. However, sometimes fever and
diarrhea may result from infection outside the GI tract, as in malaria.
A stool with blood or mucus indicates invasion of the intestinal or colonic mucosa.
When vomiting is the major presenting symptom, suspect Staphylococcus aureus, B
cereus, or Norovirus.[11]
Reactive arthritis can be seen with Salmonella, Shigella, Campylobacter, and Yersinia
infections.
A profuse rice-water stool suggests cholera or a similar process.
Abdominal pain is most severe in inflammatory processes. Painful abdominal muscle
cramps suggest underlying electrolyte loss, as in severe cholera.
A history of bloating should raise the suspicion of giardiasis.
Yersinia enterocolitis may mimic the symptoms of appendicitis.
Proctitis syndrome, seen with shigellosis, is characterized by frequent painful bowel
movement containing blood, pus, and mucus. Tenesmus and rectal discomfort are
prominent features.
Consumption of undercooked meat/poultry is suspicious for Salmonella,
Campylobacter, Shiga toxin E coli, and C perfringens.
Consumption of raw seafood is suspicious for Norwalk-like virus, Vibrio organism, or
hepatitis A.
Consumption of homemade canned foods is associated with C botulinum.
Consumption of unpasteurized soft cheeses is associated with Listeria, Salmonella,
Campylobacter, Shiga toxin E coli,and Yersinia.
Consumption of deli meats notoriously is responsible for listeriosis.
Consumption of unpasteurized milk or juice is suspicious for Campylobacter,
Salmonella, Shiga toxin E coli,and Yersinia.
Salmonella has been associated with consumption of raw eggs

The physical examination should focus on assessing the severity of dehydration.

A dry mouth, decreased axillary sweat, and decreased urine output indicate mild
dehydration, whereas orthostasis, tachycardia, and hypotension indicate more severe
volume depletion.
A rectal examination always should be performed to directly visualize the stool, to test
occult blood, and to palpate the rectal mucosa for any lesions.
Rose spot macules on the upper abdomen and hepatosplenomegaly may be seen
in Salmonella typhi infection.
Erythema nodosum and exudative pharyngitis are suggestive of Yersinia infection.
Patients with Vibrio vulnificus or Vibrio alginolyticus may present with cellulitis and otitis
media.

The CDC estimates that 97% of all cases of food poisoning result from improper food
handling; 79% of cases result from food prepared in commercial or institutional
establishments and 21% of cases result from food prepared at home.[5]

The most common causes are as follows: (1) leaving prepared food at temperatures that
allow bacterial growth, (2) inadequate cooking or reheating, (3) cross-contamination, and
(4) infection in food handlers. Cross-contamination may occur when raw contaminated food
comes in contact with other foods, especially cooked foods, through direct contact or
indirect contact on food preparation surfaces.

Bacteria are responsible for approximately 75% of the outbreaks of food poisoning and for
80% of the cases with a known cause in the United States.[3] As many as 1 in 10
Americans has diarrhea due to food-borne infection each year.

Table 1.Causes of Food Poisoning. (Open Table in a new window)

Causative Agents Source and Pathogenesis Diagnosis and

Clinical Features Treatment

Staphylococci Improperly stored Enterotoxin acts Symptomatic

foods with high salt or on receptors in gut treatment
sugar content favor that transmit
growth of impulses to
staphylococci. medullary centers

Intense vomiting and

watery diarrhea start 1-
4 hafter ingestion and
last as long as 24-48 h

B cereus Contaminated fried Emetic enterotoxin Symptomatic

rice (emetic) (short incubation treatment
and duration) -
Poorly understood

Meatballs (diarrheal)

Diarrheal
enterotoxin (long
Emetic: Duration is 9 incubation and
h, vomiting and duration) -
cramps Increasing
intestinal secretion
by activation of
adenylate cyclase
Diarrheal: Lasts for 24 in intestinal
h epithelium

Mainly vomiting after

1-6 hand mainly
diarrhea after 8-16
hafter ingestion; lasts
as long as 1 d

C perfringens Inadequately cooked Enterotoxin Culture of clostridia

meat, poultry, or legumes produced in the in food and stool
gut, and food
causes
hypersecretion in
Acute onset of abdominal the small intestine Symptomatic
cramps with diarrhea treatment
starts 8-24 hafter
ingestion.

Vomiting is rare. It lasts

less than 1 d.

Enteritis necroticans
associated with C
perfringens type C in
improperly cooked pork
(40% mortality)

C botulinum Canned foods (eg, Toxin absorbed Toxin present in

smoked fish, from the gut food, serum, and
mushrooms, blocks the release stool.
vegetables, honey) of acetylcholine in
the neuromuscular
junction
Respiratory support
Descending weakness
and paralysis start 1-4
dafter ingestion,
followed by Intravenous
constipation. trivalent antitoxin
from CDC

Mortality is high

Listeria Raw and pasteurized Highly motile, CSF or blood

monocytogenes milk, soft cheeses, raw heat-resistant, culture
vegetables, shrimp gram-positive
organism

Must treat with

Systemic disease antibiotics if
associated with bacteremic
bacteremia

Intestinal symptoms
precede systemic
disease

Can seed meninges,

heart valves, and other
organs

Highest mortality
among bacterial food
poisonings

Enterotoxic E coli(eg, Contaminated water Enterotoxin Supportive

traveler's diarrhea) and food (eg, salad, causes treatment
cheese, meat) hypersecretion in
small and large
intestine via
guanylate cyclase No antibiotics
Acute-onset watery activation
diarrhea starts 24-48
hafter ingestion

Concomitant vomiting
and abdominal cramps
may be present. It
lasts for 1-2 d

EnterohemorrhagicE Improperly cooked Cytotoxin results Diagnosis with stool

coli (eg, E hamburger meat and in endothelial culture
coliO157:H7) previously spinach damage and leads
to platelet
aggregation and
microvascular Supportive
Most common isolate fibrin thrombi treatment
pathogen in bloody
diarrhea starts 3-4
dafter ingestion
No antibiotics

Usually progresses
from watery to bloody
diarrhea. It lasts for 3-8
d

May be complicated by
hemolytic-uremic
syndromeor thrombotic
thrombocytopenic
purpura

Enteroinvasive E coli Contaminated Enterotoxin Supportive

imported cheese produces treatment
secretion

Usually watery No antibiotics

diarrhea (some may Shigalike toxin
present with facilitates invasion
dysentery)

EnteroaggregativeE Implicated in traveler's Bacteria clump on Ciprofloxacin may

coli diarrhea in developing the cell surfaces shorten duration
countries and eradicate the
organism

Can cause bloody

diarrhea

V cholera Contaminated water Enterotoxin Positive stool

and food causes culture finding
hypersecretion in
small intestine

Large amount of Prompt

nonbloody diarrhea replacement of
starts 8-24 hafter Infective dose fluids and
ingestion. It lasts for 3- usually is 107- electrolytes (oral
5d 109organisms rehydration
solution)

Tetracycline (or
fluoroquinolones)
shortens the
duration of
symptoms and
excretion of Vibrio

V parahaemolyticus Raw and improperly Enterotoxin Positive stool

cooked seafood (ie, causes culture
mollusks and hypersecretion in
crustaceans) small intestine

Prompt
replacement of
Explosive watery Hemolytic toxin is fluids and
diarrhea starts 8-24 lethal electrolytes
hafter ingestion

Infective dose is Sensitive to

It lasts for 3-5 d usually 107- tetracycline, but
109organisms unclear role for
antibiotics

V vulnificus Wound infection in salt Polysaccharide Culture of

water or consumption capsule characteristic
of raw oysters bullous lesions or
blood

Growth correlates
Can be lethal in with availability of
patients with liver iron (especially Immediate
disease (50% transferrin antibiotics if
mortality) saturation >70%) suspected (eg,
doxycycline and
ceftriaxone)

C jejuni Domestic animals, Uncertain about Culture in special

cattle, chickens endotoxin media at 42°C
production and
invasion

Fecal-oral Erythromycin for

transmission in invasive disease
humans (fever)

Foul-smelling watery
diarrhea followed by
bloody diarrhea

Abdominal pain and

fever also may be
present;it starts 1-3
dafter exposure and
recovery is in 5-8 d

Shigella Potato, egg salad, Organisms invade Polymorphonuclear

lettuce, vegetables, epithelial cells and leukocytes (PMNs),
milk, ice cream, and produce toxins blood, and mucus
water in stool

Infective dose is
Abrupt onset of bloody 102-103organisms Positive stool
diarrhea, cramps, culture
tenesmus, and fever
starts 12-30 hafter
ingestion. Enterotoxin-
mediated diarrhea Oral rehydration is
followed by mainstay
invasion
Usually self-limited in (dysentery/colitis)
3-7 d
Trimethoprim-
sulfamethoxazole
(TMP-SMX) or
ampicillin for severe
cases

No opiates

Salmonella Beef, poultry, eggs, Invasion but no Positive stool

and dairy products toxin production culture finding
Abrupt onset of
moderate-to-large
amount of diarrhea
with low-grade fever; in Antibiotic for
some cases, bloody systemic infection
diarrhea

Abdominal pain and

vomiting also present,
beginning 6-48 hafter
exposure and lasts 7-
12 d

Yersinia Pets; transmission in Gastroenteritis Polymorphonuclear

humans by fecal-oral and mesenteric leukocytesand
route or contaminated adenitis blood in stool
milk or ice cream

Direct invasion Positive stool

Acute abdominal pain, and enterotoxin culture finding
diarrhea, and fever
(enterocolitis)

No evidence that
antibiotics alter the
Incubation period not course but may be
known Polyarthritis used in severe
and erythema infections
nodosum in children

May mimic
appendicitis

Aeromonas Untreated well or Enterotoxin, Positive stool

spring water hemolysin, and culture
cytotoxin

Diarrhea may be Fluoroquinolones or

bloody TMP/SMX for
chronic diarrhea

May be chronic up to
42 din the United
States

Parasitic Food Source and Clinical Pathogenesis Diagnosis and

Poisoning Features Treatment
E histolytica Contaminated food Invasion of the Criterion standard
and water mucosa by the is colonoscopy with
parasites biopsy

90% asymptomatic
Ova and parasites
may be seen in the
stool but has low
10% dysentery sensitivity

Minority may develop Luminal amebicides

liver abscesses (eg, paromomycin)
Tissue amebicides
(eg, metronidazole)

G lamblia Contaminated ground Unknown Initial diagnostic

water test is stool
enzyme-linked
immunosorbent
Highest assay
Fecal-oral concentration in
transmission in the distal
humans duodenum and
proximal jejunum Duodenal aspiration
or small bowel
biopsy
Mild bloody diarrhea
with nausea and
abdominal cramps
starts 2-3 dafter Cyst in the stool
ingestion; lasts for 1
wk

Metronidazole

May become chronic

Seafood/Shellfish Source and Pathogenesis Diagnosis and

Poisoning

Clinical Features Treatment

Paralytic shellfish Temperate costal Fish acquires General

poisoning areas toxin-producing observation for 4-6
dinoflagellates h

Source - Bivalve
mollusks Maintain patent
airway.

Onset usually is 30-60

min Administer oxygen,
and assist
ventilation if
necessary
Initial symptoms
include perioral and
intraoral paresthesia
For recent
ingestion, charcoal
50-60 g may be
Other symptoms helpful
include paresthesia of
the extremities,
headache, ataxia,
vertigo, cranial nerve
palsies, and paralysis
of respiratory muscles,
resulting in respiratory
arrest

Neurotoxic shellfish Coastal Florida Fish acquires Symptomatic

poisoning toxin-producing
dinoflagellates

Source - Mollusks

Illness is milder than in

paralytic shellfish
poisoning

Ciguatera Hawaii, Florida, and Fish acquires Symptomatic

Caribbean toxin-producing
dinoflagellates

Anecdotal reports
Source - Carnivorous of successful
reef fish Toxin increases treatment of
intestinal secretion neurologic
by changing symptoms with
intracellular mannitol 1 g/kg IV
Vomiting, diarrhea, and calcium
cramps start 1-6 hafter concentration
ingestion and last from
days to months

Diarrhea may be
accompanied by a
variety of neurologic
symptoms including
paresthesia, reversal
of hot and cold
sensation, vertigo,
headache, and
autonomic
disturbances such as
hypotension and
bradycardia

Chronic symptoms (eg,

fatigue, headache)
may be aggravated by
caffeine or alcohol

Tetrodotoxin Japan Neurotoxin is Symptomatic

poisoning concentrated in
the skin and
viscera of puffer
Source - Puffer fish fish.

Onset of symptoms
usually is 30-40 minbut
may be as short as 10
min;it includes
lethargy, paresthesia,
emesis, ataxia,
weakness, and
dysphagia; ascending
paralysis occurs in
severe cases; mortality
is high.

Scombroid Source - Tuna, mahi- Improper Antihistamines

mahi, kingfish preservation of (diphenhydramine
large fish results 25-50 mg IV)
in bacterial
degradation of
Allergic symptoms histidine to
such as skin flush, histamine H2 blockers
urticaria, (cimetidine 300 mg
bronchospasm, and IV)
hypotension usually
start within 15-90 min

Severe reactions
may require
subcutaneous
epinephrine (0.3-
0.5 mL of 1:1000
solution)

Heavy Metal Source Symptoms Treatment

Poisoning
Mercury Ingestion of inorganic Causes metallic Consult a
mercuric salts taste, salivation, toxicologist
thirst,
discoloration and
edema of oral
mucous Remove ingested
membranes, salts by emesis and
abdominal pain, lavage, and
vomiting, bloody administer activated
diarrhea, and charcoal and a
acute renal failure cathartic

Dimercaprol is
useful in acute
ingestion

Lead Toxicity results from Common Other than

chronic repeated symptoms include activated charcoal
exposure colicky abdominal and cathartic,
pain, constipation, severe toxicity
headache, and should be treated
irritability with antidotes
It is rare after single (edetate calcium
ingestion disodium [EDTA]
and dimercaprol).
Diagnosis is
based on lead
level (>10 mcg/dL)

Arsenic Ingestion of pesticide Symptoms usually Gastric lavage and

and industrial appear within 1 activated charcoal
chemicals hafter ingestion
but may be
delayed as long
as 12 h Dimercaprol
injection 10%
solution in oil (3-5
mg/kg IM q4-6h for
Abdominal pain, 2 d) and oral
watery diarrhea, penicillamine (100
vomiting, skeletal mg/kg/d divided qid
muscle cramps, for 1 wk)
profound
dehydration, and
shock may occur

EVALUATION:

Gram staining and Loeffler methylene blue staining of the stool for WBCs help to
differentiate invasive disease from noninvasive disease.
Perform microscopic examination of the stool for ova and parasites.
Bacterial culture for enteric pathogens, such as Salmonella, Shigella,
and Campylobacter organisms, becomes mandatory if a stool sample shows positive
results for WBCs or blood or if patients have fever or symptoms persisting for longer
than 3-4 days.
Perform blood culture if the patient is notably febrile.
CBC with differential, serum electrolyte assessment, and BUN and creatinine levels
help to assess the inflammatory response and the degree of dehydration.
Assay for C difficile to help rule out antibiotic-associated diarrhea in patients receiving
antibiotics or in those with a history of recent antibiotic use.

Flat and upright abdominal radiographs should be obtained if the patient experiences
bloating, severe pain, or obstructive symptoms or if perforation is suggested.

When a stool examination is nondiagnostic, performing sigmoidoscopy/colonoscopy

with biopsy and esophagogastroduodenoscopy (EGD) with duodenal aspirate and
biopsy may be beneficial. This is especially important in patients who are
immunocompromised.
Consider sigmoidoscopy in patients with bloody diarrhea. It can be useful in diagnosing
inflammatory bowel disease, antibiotic-associated diarrhea, shigellosis, and amebic
dysentery.

Treatment:

Because most cases of acute gastroenteritis are self-limited, specific treatment is not
necessary. Some studies have quantified that only 10% of cases require antibiotic therapy.
The main objective is adequate rehydration and electrolyte supplementation. This can be
achieved with either an oral rehydration solution (ORS) or intravenous solutions (eg,
isotonic sodium chloride solution, lactated Ringer solution). Strict personal hygiene should
be practiced during the illness.

Oral rehydration is achieved by administering clear liquids and sodium-containing and

glucose-containing solutions. A simple ORS may be composed of 1 level teaspoon of
salt and 4 heaping teaspoons of sugar added to 1 liter of water.
The use of ORS has reduced the mortality rate associated with cholera from higher
than 50% to less than 1%.
ORS also is indicated in other dehydrating diarrheal diseases.
ORS promotes cotransport of glucose, sodium, and water across the gut epithelium, a
mechanism unaffected in cholera.
The World Health Organization (WHO) recommends a solution containing 3.5 g of
sodium chloride, 2.5 g of sodium bicarbonate, 1.5 g of potassium chloride, and 20 g of
glucose per liter of water.

Intravenous solutions are indicated in patients who are severely dehydrated or who have
intractable vomiting.

Absorbents (eg, Kaopectate, aluminum hydroxide) help patients have more control over the
timing of defecation. However, they do not alter the course of the disease or reduce fluid
loss.

An interval of at least 1-2 hours should elapse when using other medications with
absorbents.
Antisecretory agents, such as bismuth subsalicylate (Pepto-Bismol), may be useful.
The dose is 30 mL every 30 minutes, not to exceed 8-10 doses.
Antiperistaltics (opiate derivatives) should not be used in patients with fever, systemic
toxicity, or bloody diarrhea or in patients whose condition either shows no improvement
or deteriorates.
Diphenoxylate with atropine (Lomotil) is available in tablets (2.5 mg of diphenoxylate)
and liquid (2.5 mg of diphenoxylate/5 mL). The initial dose for adults is 2 tablets 4
times a day (ie, 20 mg/d). The dose is tapered as diarrhea improves.
Loperamide (Imodium) is available over the counter as 2-mg capsules and as a liquid
(1 mg/5 mL). It increases the intestinal absorption of electrolytes and water and
decreases intestinal motility and secretion. The dose in adults is 4 mg initially, followed
by 2 mg after each diarrhea stool, not to exceed 16 mg in a 24-hour period.

If symptoms persist beyond 3-4 days, the specific etiology should be determined by
performing stool cultures. If symptoms persist and the pathogen is isolated, specific
treatment should be initiated.

Empiric treatment should be initiated in patients with suspected traveler's diarrhea or

dysenteric or systemic symptoms. Treatment with an agent that covers Shigella
andCampylobacter organisms is reasonable in patients with diarrhea (>4 stools/d) for more
than 3 days and with fever, abdominal pain, vomiting, headache, or myalgias. A 5-day
course of a fluoroquinolone (eg, ciprofloxacin 500 mg PO bid, norfloxacin 400 mg PO bid)
is the first-line therapy. TMP/SMX (Bactrim DS 1 tab qd) is an alternative therapy, but
resistant organisms are common in the tropics. Infection with either V choleraeor V
parahaemolyticus can be treated either with a fluoroquinolone or with doxycycline (100 mg
PO bid).

In the absence of dysentery, do not administer antibiotics until a microbiologic diagnosis is

confirmed and E coli O157:H7 is ruled out.

During episodes of acute diarrhea, patients often develop an acquired disaccharidase

deficiency due to washout of the brush-border enzymes. For this reason, avoiding milk,
dairy products, and other lactose-containing foods is advisable.