Know all about

Infectious Diarrhea

Dr. Arun Aggarwal,

M.D.
 Etiology
 Diarrhea: noninflammatory and
inflammatory.
 Enteropathogens elicit
noninflammatory diarrhea
through enterotoxin production
by some bacteria, destruction
of villus (surface) cells by
viruses, adherence by parasites,
and adherence and/or
translocation by bacteria.
 Inflammatory diarrhea:
caused by bacteria that invade
the intestine directly or produce
cytotoxins.
 Causative Agents of Gastroenteritis
 BACTERIA
 Aeromonas
 Bacillus cereus
 Campylobacter jejuni
 Clostridium perfringens
 Clostridium difficile
 Escherichia coli
 Plesiomonas
 shigelloides
 Salmonella
 Shigella
 Staphylococcus aureus
 Vibrio cholerae 01 and 0139
 Vibrio parahaemolyticus
 Yersinia enterocolitica
 VIRUSES
 Astroviruses
 Caliciviruses
 Norovirus
 Enteric adenoviruses
 Rotavirus
 Cytomegalovirus
 Herpes simplex viruses
PARASITES
• Balantidium coli
•Blastocystis hominis
•Cryptosporidium parvum
•Cyclospora cayetanensis
•Encephalitozoon intestinalis
•Entamoeba histolytica
•Enterocytozoon b bieneusi
•Giardia lamblia
•Isospora belli
•Strongyloides stercoralis
•Trichuris trichiura
 Chronic or persistent diarrhea lasting 14 days or more
may be due to
 an infectious agent such as Giardia lamblia,
Cryptosporidium parvum, and enteroaggregative
or enteropathogenic E. coli
 any enteropathogen that infects an

immunocompromised host
 residual symptoms due to damage to the intestine

by an enteropathogen after an acute infection.

Indications for stool examination for
O&P
 Pt have a history of recent
travel to an endemic area,
stool cultures are negative
for other enteropathogens,
and diarrhea persists for
more than 1 wk
 part of an outbreak of
diarrhea
 immunocompromised.
 Epidemiology
Agent

Salmonella Poultry, egg, peanut butter, reptiles

Campylobacter Raw poultry

E. Coli Beef, spinach, milk

Yersinia Pork, iron overload (thallasemia)

V. Cholerae Iron overload ( thallassemia)

 Factors that increase susceptibility to
infection with enteropathogens include:
 Young age
 Immune deficiency
 Measles
 Malnutrition
 Travel to an endemic area
 Lack of breast-feeding
 Exposure to unsanitary conditions
 Ingestion of contaminated food or water
 Level of maternal education
 Attendance at a childcare center.
 Immune-Mediated Extraintestinal Manifestations of
Enteric Pathogens
Manifestation Related Enteric Pathogen(s)
Reactive arthritis Salmonella, Shigella, Yersinia,
Campylobacter, Cryptosporidium,
Clostridium difficile
Guillain-Barré syndrome Campylobacter

Glomerulonephritis Shigella, Campylobacter, Yersinia

IgA nephropathy Campylobacter

Erythema nodosum Yersinia, Campylobacter, Salmonella

Hemolytic anemia Campylobacter, Yersinia

HUS S. dysenteriae , E. coli

Specific Pathogens
 Cholera
 Gram negative, slightly curved rod.
 V. cholera O1 and O139 are responsible for causing
disease.
 The two biogroups (or biotypes) of V. cholerae O1
are differentiated as classic and El Tor
 V. cholerae O1 has two major O antigenic types
(Ogawa and Inaba) and an unstable intermediate
type (Hikojima).
 V. cholerae O139 is closely related to the El Tor
biotype
 Epidemiology
 Transmission is usually by fecal-oral spread with
contaminated water.
 Humans are the only known reservoirs of V. cholerae.
 Colonization usually requires the ingestion of a large
number of viable vibrios (>108 viable units), in part,
because the organisms are killed by acid environments
including the normal stomach.
 The primary mechanism of fluid loss is activation of
adenylyl cyclase at the cytoplasmic surface of the
basolateral membrane by the enterotoxin, cholera toxin.
 Clinical Features
 Profuse, painless, watery
diarrhea with a rice-water
consistency and a fishy
odor, sometimes with flecks
of mucus but no blood.
 Fecal leukocytes are not
present because V. cholera
does not invade the mucosa.
 Diagnosis is primarily
clinical.
 The gold standard for
cholera diagnosis remains
stool culture on TCBS
medium.
 Treatment
 Rehydration is the most
important treatment.
 Antibiotics are useful in
shortening the duration of
illness, reducing the period of
excretion of the organisms,
and decreasing the
requirements for fluid
replacement.
 Doxycycline is drug of choice,
Bactrim can be used for <8
yrs, quinolones are effective.
 Complications
 Lethargy, seizures, altered consciousness, fever,
hypoglycemia, hyperglycemia, and death.
 Inadequate fluid and electrolyte replacement may lead to
acute tubular necrosis.
 Hypokalemic arrhythmia can cause sudden death.
 Children with low potassium levels can develop paralytic
ileus and abdominal distention that can make oral
rehydration impossible.
 Pulmonary edema occurs in some children, probably
because of fluid overload during rehydration.
 Vaccine
 Phenol-killed organisms administered parenterally as a two-
dose primary series followed by boosters every 6 mo to
maintain immunity.
 Vaccine has about 50% efficacy by 3–6 mo after vaccination,
does not protect against O139 vibrios, and is highly
reactogenic (i.e., pain, erythema, local induration, fever,
headaches).
 Vaccine should be used only in very high-risk persons (e.g.,
those with achlorhydria) with a very high probability of
exposure.
 It is not recommended for children <6 mo of age.
Salmonella
 Gram negative rod, don’t ferment lactose, grow aerobically.
 Poultry and poultry products (mainly eggs) cause about half of
the common-source outbreaks.
 Meats, especially beef and pork, cause about 13% of the
outbreaks, and raw or powdered milk and dairy products are
the source of about 5% of the outbreaks.
 The estimated number of bacteria that must be ingested to
cause disease is 106–108 organisms.
 Ingested Salmonella organisms reach the stomach, where acid
is the first protective barrier.
 Achlorhydria, buffering medications, rapid gastric emptying
after gastrectomy or gastroenterostomy, and a large inoculum
enable viable organisms to reach the small intestine.
 In the small and large intestines, salmonellae have to
compete with normal bacterial flora to multiply and
cause disease; prior antibiotic therapy disrupts this
competitive relationship.
 After multiplication within the lumen, the organisms
penetrate through the Peyer patches, typically at the
distal part of the ileum and the proximal part of the
colon.
 Children with sickle cell disease are prone to
Salmonella septicemia and osteomyelitis.
 Clinical manifestations
 The most common clinical presentation is acute enteritis.
 After an incubation period of 6–72 hr (mean, 24 hr), there
is an abrupt onset of nausea, vomiting, and crampy
abdominal pain primarily in the periumbilical area and
right lower quadrant, followed by mild to severe watery
diarrhea and sometimes by diarrhea containing blood and
mucus.
 Fever (temperature of 101–102°F [38.5–39°C]).
 The stool typically contains a moderate number of
polymorphonuclear leukocytes and occult blood.
 Symptoms subside within 2–7 days in healthy children.
 Conditions That Increase the Risk of Salmonella
Bacteremia During Salmonella Gastroenteritis
 Neonates and young infants (≤3 mo of age)
 AIDS, chronic granulomatous disease, and other immuno deficiencies
 Malignancies, especially leukemia and lymphoma
 Immunosuppressive and corticosteroid therapy
 Hemolytic anemia, including sickle cell disease, malaria, and
bartonellosis
 Collagen vascular disease
 Inflammatory bowel disease
 Gastrectomy or gastroenterostomy
 Achlorhydria or antacid medication use
 Impaired intestinal motility
 Schistosomiasis
 Malnutrition
 Diagnosis: stool culture, rectal swab, latex
agglutination, serological assays
 Treatment: correction of dehydration and
electrolyte disturbances.
 Antibiotics: ampicillin, bactrim, cefotaxime,
ceftriaxone, quinolones
 In patients with gastroenteritis, antimicrobial agents do not
shorten the clinical course, nor do they eliminate fecal
excretion of Salmonella.
 By suppressing normal intestinal flora, antimicrobial agents
may prolong the excretion of Salmonella and increase the risk
of creating the chronic carrier state.
 Antibiotics therefore are not indicated routinely in treating
Salmonella gastroenteritis.
 They should be used in infants (≤3 mo of age) and other
children who are at increased risk of a disseminated disease .
(previous table)
Shigella
 Four species of Shigella are responsible for shigellosis:
S. dysenteriae (serogroup A), S. flexneri (serogroup B), S.
boydii (serogroup C), and S. sonnei (serogroup D).
 Contaminated food (often a salad or other item requiring
extensive handling of the ingredients) and water are
important vectors.
 Person-to-person transmission is probably the major
mechanism of infection.
 Shigellae require very low inocula to cause illness.
Ingestion of as few as 10 S. dysenteriae serotype 1
organisms can cause dysentery.
 The basic virulence trait shared by all shigellae
is the ability to invade intestine.
 The pathologic changes of shigellosis take
place primarily in the colon.
 Secretory IgA and serum antibodies develop
within days to weeks after infection with
Shigella. (protection is serotype specific).
 Incubation period: 12 hr to several days.
 Severe abdominal pain, high fever, emesis, anorexia,
generalized toxicity, urgency, and painful defecation
characteristically occur.
 Physical examination may show abdominal distention
and tenderness, hyperactive bowel sounds, and a
tender rectum on digital examination.
 The diarrhea may be watery and of large volume
initially, evolving into frequent small-volume, bloody
mucoid stools.
 Neurologic findings occur in as many as 40% of
hospitalized infected children.
 Convulsions, headache, lethargy, confusion, nuchal
rigidity, or hallucinations may be present before or
after the onset of diarrhea.
 The most common complication of shigellosis is
dehydration.
 S. dysenteriae serotype 1 infection is commonly
complicated by hemolytic-uremic syndrome.
 This syndrome is caused by Shiga toxin–mediated
endothelial injury.
 Diagnosis: clinical picture, stool examination, rectal
swab, blood cultures
 Treatment: fluid and electrolytes
 Antibiotics: azithromycin, ampicillin, bactrim, cefixime,
nalidixic acid, quinolones.
E. coli
 ETEC EIEC EPEC STEC/ EAggEC
EHEC

Population >1 Yr & >1 yr <2 yr 6mo- 10 <1 yr &

at risk travellers yr travellers

Watery +++ + +++ + +++

diarrhea

Bloody --- ++ --- +++ ---

diarrhea (HUS)

Duration Acute Acute Acute/ Acute Acute/

persistent persistent
Camplylobacter
 Human campylobacterioses most commonly
result from ingestion of contaminated food or
water, from direct contact with environmental
sources (i.e., a pet), or from person-to-person
transmission.
 Patients may have loose, watery stools or bloody and
mucus-containing stools (dysentery).
 Fever, vomiting, malaise, and myalgia are common.
 The abdominal pain is periumbilical.
 Abdominal pain may mimic appendicitis or
intussusception.
 Persistent infection may mimic chronic IBD.
 Diagnosis: stool culture, rectal swab, serological studies.
 The optimum incubation temperature for C. jejuni and C.
coli is 42 to 43ºC; as a result, the term "thermophilic"
campylobacters is sometimes applied to these species.
 Treatment:
 Fluid replacement

 Correction of electrolytes

 Antibiotics: azithromycin, aminoglycosides,

doxycycline, trimethoprim
 Antibiotics are recommended for patients with the
dysenteric form of the disease, high fever, or a severe
course and for children who are immunosuppressed or
have underlying diseases.
Yersinia
 Y. enterocolitica is transmitted to humans through
food, water, animal contact, and contaminated blood
products.
 The organisms most often enter by the alimentary
tract and cause mucosal ulcerations in the ileum.
Necrotic lesions of Peyer patches and mesenteric
lymphadenitis occur.
 Presentation: enterocolitis with diarrhea, fever, and
abdominal pain.
 Acute enteritis is more common among younger
children, and mesenteric lymphadenitis that may
mimic appendicitis.
 Diagnosis: stool culture, rectal swab.
 Treatment: self-limiting disease and no benefit of
antibiotic therapy is established.
 Patients with systemic infection and very young
children in whom septicemia is common should be
treated.
 Yersinia strains are sensitive to trimethoprim-
sulfamethoxazole, aminoglycosides, third-generation
cephalosporins, and quinolones.
 Patients on deferoxamine should discontinue
iron chelation therapy during treatment for Y.
enterocolitica, especially if they have
complicated gastrointestinal infection or
extraintestinal infection.
C. difficile
 C difficile–associated diarrhea, also known as
pseudomembranous colitis or antibiotic-associated
diarrhea, is a major cause of nosocomial diarrhea.
 C. difficile is a ubiquitous spore-forming gram-
positive anaerobic bacillus.
 The organism produces two toxins: toxin A
(enterotoxin) acts on the intestinal mucosa to
produce diarrhea; toxin B (cytotoxin) increases
vascular permeability in low doses and is lethal to
experimental animals in high doses.
 Virtually all known antibiotics have been implicated;
penicillins, broad-spectrum cephalosporins, and
clindamycin are the most frequent offenders.
 Newborns are often colonized with C. difficile during
the first weeks of life. Carriage decreases to the adult
rate of 1–3% by 2 yr of age.
 Illness is unusual in neonates and infants; the basis
for this remains unknown.
 The classic picture of pseudomembranous colitis is
diarrhea with blood and mucus accompanied by
fever, cramps, abdominal pain, nausea, and vomiting.
Disease occurs during and as long as weeks after
antibiotic therapy.
 The diagnosis is confirmed by detecting C. difficile or
its toxin in the stool.
 Findings at sigmoidoscopy or colonoscopy include
pseudomembranous nodules and plaques
characteristic of toxin-related colitis. Fecal leukocytes
are present in approximately one half of cases; occult
or frank blood is common.
 The first and essential step in treatment is the
discontinuation of the current antibiotics, if possible.
 If symptoms persist, antibiotics cannot be discontinued,
or the illness is severe, then oral metronidazole (20–
40 mg/kg/24 hr divided q 6–8 hr PO) or vancomycin
(25–40 mg/kg/24 hr divided q 6 hr PO) should be given
for a 7–10 day course.
 The initial response rate is >95%, but 5–30% of patients
have clinical relapse, usually within 1–2 wk of treatment.
 These patients should be re-evaluated and treated again;
most will respond to a second course of the original
treatment.
 A few patients develop multiple recurrences, with short-
lived responses to repeated treatment.
 Treatment strategies for these patients include oral
cholestyramine, oral bacitracin, oral immunoglobulin,
reconstitution of bowel flora with oral lactobacilli or
baker's yeast, or instillation of fecal flora by tube feeding
or enemas (faeces transplant).
Rota Virus
 Rotavirus causes 3 million cases of diarrhea, 50,000
hospitalizations, and 20–40 deaths annually in the
United States.
 Disease tends to be most severe in patients 3-24
months of age.
 Infants younger than 3 mo of age are relatively
protected by transplacental antibody and possibly
breast-feeding.
 The virus is shed in stool at very high concentration
before and for days after the clinical illness.
 Very few infectious virions are needed to cause disease in
a susceptible host.
 The gastric mucosa is not affected despite the commonly
used term “gastroenteritis.
 Selective viral infection of intestinal villus tip cells thus
leads to
 an imbalance in the ratio of intestinal fluid absorption
to secretion
 malabsorption of complex carbohydrates, particularly
lactose.
 Clinical manifestations: incubation period: <48 hrs
 mild to moderate fever and vomiting followed by the
onset of frequent, watery stools.
 Diagnosis: Enzyme immunoassays, which offer
approximately 90% specificity and sensitivity, are
available for detection of group A rotavirus and
enteric adenovirus in stool samples.
 Laboratory findings: Isotonic dehydration with
acidosis.
 Treatment
 Avoiding and treating dehydration are the main goals
in treatment of viral enteritis.
 A secondary goal is maintenance of the nutritional
status of the patient.
 Controlled studies have shown no benefit from
antiemetics or antidiarrheal drugs.
 Therapy with probiotic organisms such as
Lactobacillus species has been shown to reduce
somewhat the intensity and duration of illness.
 Vaccine
Amebiasis
 Infection is established by ingestion of parasite cysts.
 Cysts are resistant to environmental conditions such
as low temperature and the concentrations of chlorine
commonly used in water purification; the parasite can
be killed by heating to 55°C.
 Infection is not transmitted by trophozoites because
of their rapid degeneration outside the body or in the
low pH environment of normal gastric contents.
 Food or drink contaminated with Entamoeba cysts
and direct fecal-oral contact are the most common
means of infection.
 Once E. histolytica trophozoites invade the intestinal
mucosa, they produce tissue destruction (ulcers).
 The organisms multiply and spread laterally
underneath the intestinal epithelium to produce
characteristic flask-shaped ulcers.
 These lesions are commonly seen in the cecum,
transverse colon, and sigmoid colon.
 Amebae may produce similar lytic lesions if they
reach the liver; these lesions are commonly called
abscesses.
 Clinical presentations range from asymptomatic cyst
passage to amebic colitis, amebic dysentery,
ameboma, and extraintestinal disease.
 colicky abdominal pains and frequent bowel
movements (6–8/day).
 Stools are blood stained and contain a fair amount of
mucus.
 Hepatic Amebiasis
 Fever is the hallmark of amebic liver abscess.
 abdominal pain
 distention, and enlargement and tenderness of the liver.
 Changes at the base of the right lung, such as elevation of
the diaphragm and atelectasis or effusion, may also occur.
 Laboratory examination findings are a slight leukocytosis,
moderate anemia, high ESR and nonspecific elevations
of hepatic enzyme (particularly alkaline phosphatase).
 Stool examination for amebae yields negative results.
 Diagnosis is based on detecting the organisms in stool
samples, sigmoidoscopically obtained smears, tissue
biopsy samples, or, rarely, aspirates of a liver abscess.
 The most sensitive serologic test, indirect
hemagglutination, yields a positive result years after
invasive infection.

 Two types of drugs are used to treat infection with E.
histolytica.
 The luminal amebicides, such as iodoquinol, paromomycin,
and diloxanide furoate, are primarily effective in the gut
lumen.
 Metronidazole or other nitroimidazoles, chloroquine, and
dehydroemetine are effective in the treatment of invasive
amebiasis.
 All individuals with E. histolytica trophozoites or cysts in
their stools, whether symptomatic or not, should be treated.
 Invasive amebiasis of the intestine, liver, or other organs
requires the use of metronidazole (30–50 mg/kg/24 hr
divided tid PO for 10 days.
Giardia
 Giardia lamblia (also referred to as G. intestinalis
and G. duodenalis) is a flagellated protozoan that
infects the duodenum and small intestine.
 Clinical manifestations range from asymptomatic
colonization to acute or chronic diarrhea and
malabsorption.
 Giardia is a particularly significant pathogen in
people with malnutrition, certain
immunodeficiencies, and cystic fibrosis.
 The life cycle of Giardia is composed of two stages:
trophozoites and cysts.
 Giardia infects humans after ingestion of as few as 10–100
cysts.
 Cysts are passed in stools of infected individuals and
may remain viable in water for as long as 2 mo.
 Giardia cysts are relatively resistant to chlorination
and to ultraviolet light irradiation. Boiling is effective
for inactivating cysts.
 Clinical Signs and Symptoms of
Giardiasis
Symptoms Frequency
 Diarrhea  64–100
 Malaise, weakness  72–97
 Abdominal distention  42–97
 Flatulence  35–97
 Abdominal cramps  44–81
 Nausea  14–79
 Foul-smelling, greasy stools  15–79
 Anorexia  41–73
 Weight loss  53–73
 Vomiting  14–35
 Fever  0–28
 Constipation  0–27
 A definitive diagnosis of giardiasis is established by
documentation of trophozoites, cysts, or Giardia
antigens in stool specimens or duodenal fluid.
 Diagnostic testing include the use of polyclonal
antisera or monoclonal antibodies against Giardia
organism–specific antigens in EIA or
immunofluorescent assays.
 PCR and gene probe–based detection systems
specific for Giardia have been used in environmental
monitoring.
 Asymptomatic excreters generally are not treated
except in specific instances such as in
 outbreak control

 for prevention of household transmission by

toddlers to pregnant women

 patients with hypogammaglobulinemia or cystic
fibrosis
 in situations requiring oral antibiotic treatment

where Giardia may have produced malabsorption

of the antibiotic.
 Metronidazole is the treatment most often prescribed
in the United States for adults.
 Furazolidone is less effective than metronidazole but
is often prescribed in children because it is available
in liquid form.
 Paromomycin, a nonabsorbable aminoglycoside, is
less effective than other agents but is recommended
for treatment of pregnant women with giardiasis
because of potential teratogenic effects of other
agents.
Approach to diarrhea
 Assess the degree of dehydration and provide fluid
and electrolyte replacement,
 Prevent spread of the enteropathogen
 In select episodes determine the etiologic agent
and provide specific therapy if indicated.
 Information about oral intake, frequency and
volume of stool output, general appearance and
activity of the child, and frequency of urination
must be obtained.
 Data should be obtained about:
 childcare center attendance

 recent travel to a diarrhea endemic area

 use of antimicrobial agents

 exposure to contacts with similar symptoms

 intake of seafood, unwashed vegetables,

unpasteurized milk, contaminated water, or
uncooked meats.
 Duration and severity of diarrhea

 stool consistency

 presence of mucus and blood

 other associated symptomatology, such as fever,

vomiting, and seizures.
 EXAMINATION OF STOOL
 Stool cultures should be obtained as early in
the course of disease as possible from patients
in whom:
 HUS is suspected,

 in patients with bloody diarrhea,

 if stools contain fecal leukocytes,

 during outbreaks of diarrhea

 in persons who have diarrhea and are

immunosuppressed.
 Adjusting Fluid Therapy in Diarrhea
AVERAGE COMPOSITION OF DIARRHEA
 Sodium: 55mEq/L

 Potassium: 25mEq/L

 Bicarbonate: 15mEq/L

APPROACH TO REPLACEMENT OF ONGOING

LOSSES
 Solution: D5 1/4 NS + 15mEq/L bicarbonate +
25mEq/LKCl
 Replace stool mL/mL every 1–6hr
 Adjusting Fluid Therapy for Emesis or
Nasogastric Losses
AVERAGE COMPOSITION OF GASTRIC
FLUID
 Na: 60mEq/L

 K: 10mEq/L

 Cl: 90mEq/L

APPROACH TO REPLACEMENT OF
ONGOING LOSSES
 Solution: D5 1/2 NS + 10mEq/LKCl

 Replace output mL/mL every 1–6hr

 Fluid Management of Dehydration
Restore intravascular volume
 Normal saline: 20mL/kg over 20min (Repeat until
intravascular volume restored)
Calculate 24-hr water needs
 Calculate maintenance water
 Calculate deficit water
Calculate 24-hr electrolyte needs
 Calculate maintenance sodium and potassium
 Calculate deficit sodium and potassium
Select an appropriate fluid (based on total water and
electrolyte needs)
 Administer half the calculated fluid during the first 8hr, first
subtracting any boluses from this amount
 Administer the remainder over the next 16hr
Replace ongoing losses as they occur
 Treatment of Hypernatremic Dehydration
Restore intravascular volume
 Normal saline: 20mL/kg over 20min (Repeat until
intravascular volume restored)
Determine the time for correction based on the
initial sodium concentration
 [Na]: 145–157mEq/L: 24hr
 [Na]: 158–170mEq/L: 48hr
 [Na]: 171–183mEq/L: 72hr
 [Na]: 184–196mEq/L: 84hr
Administer fluid at a constant rate over the time
for correction
 Typical fluids: D5 1/4 NS or D5 1/2 NS (both with
20mEq/L KCl unless contraindicated)
 Typical rate: 1.25–1.5 times maintenance
Solution Glucose Na K Cl Base Osmolality
(mmol/L) (mEq/L (mEq/ (mEq/ (mEq/L) (mOsm/kg)
) L) L)
WHO 111 90 20 80 30 311
solution
Rehydralyte 140 75 20 65 30 310

Pedialyte 140 45 20 35 30 250

Pediatric 140 45 20 35 48 250

Electrolyte
Infalyte 70 * 50 25 45 34 200

Naturalyte 140 45 20 35 48 238

 Prevention.
 Patients who are hospitalized should be placed under
contact precautions, including handwashing before
and after patient contact, gowns when soiling is
likely, and gloves when touching contaminated
material.
 Patients and their families should be educated about
the mode of acquisition of enteropathogens and
methods to decrease transmission.
 Patients who attend childcare centers should be
excluded from the center or cared for in a separate
area until diarrhea has subsided.
 Isolation
STANDARD PRECAUTIONS

 Standard precautions, formerly known as

universal precautions, are intended to protect
health care workers from blood and body fluids
and should be used whenever providing care.
 Standard precautions involve the use of barriers—
gloves, gowns, masks, goggles, and face
shields—as needed to prevent transmission of
microbes associated with contact with blood or
body fluids.
 Contact precautions include gowns and gloves and
single room isolation.
 Droplet precautions include masks for close contact
(<3 ft) and single room isolation.
 Cohorting of children infected with the same
pathogen is acceptable.
 Airborne precautions include masks and single room
isolation with negative-pressure ventilation.
 Transmission-based precautions are continued for as
long as a patient is considered to be contagious.
Questions
 A 2-year-old child who attends day care
presents with abdominal cramps and severe
bloody diarrhea, which has been present for 2
days. He has no fever. Which infection is most
consistent with this clinical picture:
a. Rotavirus
b. Giardia lamblia
c. E. coli O157:H7
d. Norvovirus infection
e. Shigellosis
 A three year old has just returned from Central
America. You see him after five days of fever;
diarrhea which is described as green, bloody,
foul-smelling, “mucosy”. He has pain on
defecation. The preliminary report on the stool
culture is “non-lactose fermenters” You suspect:
 Pseudomonas
 E. coli
 Salmonella
 Proteus
 Aeromonas
 A 10 week old afebrile infant has bloody
diarrhea. The stool culture grows Salmonella.
You would:
 Perform an LP
 Treat with appropriate antibiotic
 Obtain a bone scan to rule/out osteomyelitis
 Treat only if child has significant toxicity or
severe gastroenteritis
 Rule out HIV infection
 Which of the following is LEAST frequent
with rotavirus infection?
 Fever
 Vomiting
 Coryza preceding the diarrhea
 Blood and mucus in the stool
 Diarrhea lasting more than 48 hours
 A 1 yr old boy is brought to you with vomiting and loose stools for
the past 4 days. Initially, mother gave pedialyte, but for the last 24
hrs, the baby has been vomiting all feeds. Mother doesn’t know
when he last urinated. O/E child is sleepy and responds only when
blood was withdrawn.
Pulse= 142/min, RR: 32/min, wt: 10 kg
Skin turgor is decreased with obvious tenting. Nail beds were pink
with prompt capillary refill.
Which of the following would represent the best choice for initial
fluid orders?
 D5W/ 0.2% NS @100cc/hr. Add 20 meq KCl after urination.
 D5W/ 0.45% NS to run at 150 cc/hr for the next 8 hrs
 D5W/ 0.45% NS @100cc/hr for the next 8 hrs. Add 20 meq KCl
after urination
 NS @ 150 cc/hr for the next 8 hrs
 During teaching rounds you come across a patient
with Rota virus diarrhea. Patient continues to
have diarrhea day 10 after onset. You tell the
residents that the diarrhea is secondary to
malabsorption due to loss of cells lining the villi.
One smart resident asks you how long it would
take for intestinal cells to turn over.
 1 day
 2-3 weeks
 3-5 days
 1-2 months
 8-10 days
 Results of a stool culture from a 2 yr old boy who
has been hospitalized with bloody diarrhea
indicate that the causative agent is Shigella sp.
The boy is allergic to trimethoprim-
sulfamethoxazole.
Of the following the most appropriate
antimicrobial agent to use for this patient is:
 amoxicillin
 azithromycin
 cefdinir
 ciprofloxacin
 linezolid
 Medication that can safely be used in case of
acute diarrhea:
 Loperamide
 Octreotide
 Racecadotril
 All of the above
 None of the above
 Racecadotril: enkephalinase inhibitor
 Enkephalins are endogenous pro- absorptive
agents that directly inhibit the activity of
adenylate cyclase on the enterocyte baselateral
membrane.
 Racecadotril is a synthetic, potent inhibitor of
enkephalinase, devoid of any effect on intestinal
motility, thus without the potential to induce the
bloating that can be associated with
enteropooling.
THINGS TO REMEMBER……..

 New WHO ORS

 Super ORS
 SGLT 1
 Feeding (BRAT)
 Medications
 Probiotics
 Antibiotics (for Shigella, cholera, Giardia,
Yersinia)
 Zinc
 Thanks for Watching

Dr. Arun Aggarwal

Pediatric Gastroenterologist