ACUTE DIARRHEA

By Kumar Mukesh
 Leading cause of illness gobally

Associated with 1.7 M deaths/year

INTRODUCTION
Among children, diarrheal disease is 2nd
only to lower respiratory tract infection as
the most common cause of death

Recurrent infection is associated with

physical and mental stunting, wasting,
micronutrient deficiencie and malnutrition

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• Inoculum size
• Adherence
• Toxin production
• Invasion

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Inoculum size
• The number of microorganisms that must be ingested to cause disease varies from species to
species.

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Adherence
• Many organisms must adhere to the
gastrointestinal mucosa as an initial
step in the pathogenic process.
• Specific cell surface proteins
• V. cholerae – toxin coregulated
pilus or other accessory
colonization factors
• Enterotoxigenic E. coli –
colonization factor antigen
• Enteropathogenic and
enterohemorrhagic – produce
virulence determinants that allow
attachment
Invasion
• Shigella and enteroinvasive E. coli –
characterized by ability to:
• invade mucosal epithelial cells
• intraepithelial multiplication
• and subsequent spread to adjacent
cells
• Salmonella and Yersinia
enterocolitica
• Penetrate the intact intestinal
mucosa
• Multiply intracellularly in the Peyer’s
patches ad intestinal lymph nodes
• Disseminate in the blood stream to
cause ENTERIC fever – fever,
headache, relative bradycardia,5
Toxin Production
• Enterotoxin – directly acting on the
secretory mechanism
• Cholera toxin
• A subunit – enzymatic activity
of the toxin
• B subunit – binds to the
enterocyte
• Increase in cAMP in the intestinal
wall ! ↑Cl- secretion, ↓ Na
absorption ! loss of fluid !
diarrhea
• Enterotoxigenic strains of E. coli
• Heat labile enterotoxin (LT)
• Heat stabile enterotoxin (ST)
• Cytotoxin – destruction of cell and
associated inflammatory diarrhea
• Shigella dysenteriae type 1,
Vibrio parahaemolyticus and
Clostridium difficile
• Neurotoxins – central and
peripheral nervous system
• Staphylococcal and Bacillus
cereus toxins
• Vomiting
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 • Intestinal microbiota
• Gastric acid
HOST DEFENCES • Intestinal motility
• Intestinal mucin
• Immunity
• Genetic determinants

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Intestinal microbiota Gastric acid

• Prevents colonization of potential • Barrier to enteric pathogens

enteric pathogens • Salmonella and G. lamblia and a variety
• Infants receiving antibiotics are in of helminth infections increased in
significantly greater risk those with gastric surgery or are
achlohydric
• More than 99% of normal colonic
• Rotavirus – highly stable in acidity
microbiota is made up of anaerobic
bacteria and the acidic pH and the
volatile fatty acids produced
appear to be critical elements in the
resistance to colonization

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Intestinal motility
• Normal peristalsis is the major
mechanism of clearance of bacteria
• Some patients whose treatment for
Shigella infection consists of
diphenoxylate HCl with atropine
experience prolonged fever and
shedding of oragnisms
• Patients with Salmonella
gastroenteritis treated with opiates
have higher frequency of bacteremia
Intestinal mucin
• Separates the microbiota from the
epithelium
• The thickness and constituents of the
mucus barriers vary throughout the GIT
• Rapid turnover
• Antimicrobial molecules
• Secreted immunoglobulin
• Pathogens bypass this by:
• Secreting enzymes to degrade
mucus or through flagella mediated
motility
• Shigella secrete toxins that can
diffuse through the mucus and
disrupt the epithelium
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Immunity
determinants
• Humoral immunity
• IgG, IgM, secretory IgA
• Mucosal immune system
• First line of defense
Genetic
• O blood group have increased
susceptibility to
• V. cholerae
• Shigella
• E. coli O157
• novovirus
• Polymorphisms of genes encoding
inflammatory mediators have been
associated with outcomes of infections
with enteroaggregative E. coli,
enterotoxin-producing E. coli,
Salmonella, C. difficile, V. cholerae
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EPIDEMIOL
OGY
Travel History
Location
Age
Host Immune Status
Bacterial Food Poisoning

• 90% is infectious in cause

• Associated with vomiting, fever,
abdominal pain 11
Travel History

• Travelers to tropical regions of Asia,

Africa and Central/South America
experience sudden onset abdominal
cramps, anorexia, and watery
dairreha; traveler’s diarrhea
• Onset usually 3 – 14 days
• Generally self limited, lasting 1-5 days
• Ingestion of contaminated food/water
• Exterotoxigenic, enteroaggregative
strains of E. coli – classic traveler;’s
diarrhea
• C. jejuni – Asia
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Location Age

• Closed and semi closed • Usually children < 5 years

communities are important sources • Breast fed are protected due to the
of outbreaks maternal antibodies
• Norovirus is the most common • But risk increases when they start
taking solid food
cause of outbreaks
• First or 2nd year of life – rotavirus
• Rotavirus not as common due to
• Older children - norovirus
vaccination
• Diarrhea is one of the most common
manifestation of nosocomial
infection
• C. diffile, norovirus
• Antibiotic associated hemorrhagic
colitis
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• Klebsiella oxytoca
Host immune status Bacterial Food
Poisoning
• Cell mediated immunity
• Invasive enteropathies including
salmonellosis, listeriosis,
cryptosporidiosis
• Hypogammaglobulinemia
• C. difficile, giardiasis
• Cancer
• C. diffile

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APPROACH TO A
PATIENT WITH
INFECTIOUS
DIARRHEA

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Laboratory Evaluation
• Many cases of non inflammatory
diarrhea are self limited or be
treated empirically
• E coli cannot be distinguished from
normal flora
• Enterotoxins detection tests are not
available in most clinics
• Cholera – cultured on selective
media such as thiosulfate-citrate-bile
salts-sucrose (TCBS) or tellurite
tacurocholate gelatin (TTG) agar
• Rotavirus – latex agglutination
• Norovirus – PCR
• All patient with fever and signs of
inflammatory disease should be
evaluated for salmonella, shigella, and
camphylobacter.
• Salmonella, shigella – MacConkey agar
(colorless colonies), Selenite
enrichment broth
• Nosocomial diarrhea – C. difficile
• Toxins A and B – latex agglutination
test or PCR
• C. jejuni – culture under microaerophilic
atmosphere
• Amoebiasis – microscopy or rapid
antigen detection assay
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 TREATMENT
In many cases, specific diagnosis is
not necessary or available to guide
treatment, hence many are treated
empirically.
MAINSTAY – rehydration

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Treatment
• ORS
• ↓ mortality from >50% to <1%
• Contents: 3.5g NaCl, 2.5g
NaHCO3, or 2.9g of Na citrate,
1.5 g of KCl, and 20g of glucose
or 40g of sucrose per liter of
water
• Those severely dehydrated should
receive IV solutions such as
Ringer’s lactate
• Traveler’s diarrhea – usually
supportive management
• Antibiotics may decrease the
illness from 3-4 days to 1-2 days
• Dysentery should be empirically be treated
with antibiotics (fluoroquinolone, macrolide)
pending analysis of stool.
• Shigellosis – 3-7 day course
• Due to widespread resistance of
Camphylobacter to fluoroquinolones,
macrolides are preferred
• Salmonellosis –usually at high risk of
disseminated salmonellosis
• Infants
• With prosthetic device
• >50 years old
• Immunocompromised
• Antibiotics may increase risk of hemolytic
uremic syndrome and renal failure in
enterohemorrhagic E. .coli infection –18
bloody diarrhea with low fever or none at all
POST DIARRHEAL
COMPLICATIONS

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 • Hygiene
• YES! Hot cooked food, boiled or treated water
• NO! raw food, ice
• Bismuth subsalicylate is an inexpensive prophylaxis for
traveler’s diarrhea
PROPHYLAXIS
• 2 tablets (525mg) 4x a day
• Safe to treat up to 3 weeks
• Darkening of the tongue, tinnitus
• Probiotics decrease risk by 15%
• Prophylactic antibiotics are not recommended except
when the traveler is immunocompromised or have an
underlying disease that increase their risk for infection
• Rifaxmin
• Vaccination
• S. typhi, V. cholerae, rotavirus

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