Acute Infectious Diarrheal

Diseases and Bacterial Food

Poisoning

Jose Carlo Valencia, MD, FPCP, FPSMID

Introduction

• Acute diarrheal illness is the leading cause of illness globally and

associated with 1.7 million deaths
• Morbidity from diarrhea is also significant
• Recurrent intestinal infections are associated with physical and
mental stunting, wasting, micronutrient deficiencies and
malnutrition
Pathogenic Mechanism
• Inoculum Size
• The number of organisms that must be ingested to cause disease
varies considerably from species to species
• Shigella, EHEC, Giardia or Entamoeba: as few as 10-100 bacteria or
cyst
• can spread from person-to-person contact
• Vibrio cholerae: 105-108
• The infective dose of Salmonella varies widely, depending on the
species, host, and food vehicle
Pathogenic Mechanism
• Adherence
• Many organism must adhere to the GI mucosa as initial step in the
pathogenic process
• Organisms that can compete with normal bowel flora and colonize
the mucosa have an important advantage causing disease
• Specific cell-surface proteins are important virulence determinants
Pathogenic Mechanism
• Toxin Production
• Enterotoxins which cause watery diarrhea by acting
directly on the secretory mechanism in the intestinal
mucosa
• Cytotoxins which cause destruction of mucosal cells and
associated inflammatory diarrhea
• Neurotoxins act directly on central or peripheral nervous
system
Pathogenic Mechanism
• Toxin Production
• Cholera toxin: increase of cyclic adenosine monophosphate (CAMP)
in the intestinal cell, which increases Cl- secretion and decrease Na+
absorption leading to a loss of fluid and the production of diarrhea
• ETEC: Heat-labile enterotoxin (LT): causes watery diarrhea as cholera
toxin
Heat-stable enterotoxin (ST): elevation cGMP
• Bacterial endotoxins destroy mucosal cells and produce the
syndrome of dysentery with bloody stools containing inflammatory
cells
Pathogenic Mechanism
• Invasion
• Dysentery may result not only from the production of cytotoxins
but from bacterial invasion and destruction of intestinal mucosal
cells
• Infections with Shigella, enteroinvasive E coli are characterized by
invasion of mucosal epithelial cells, intraepithelial multiplication
and subsequent spread to adjacent cells
• Salmonella causes inflammatory diarrhea by invasion of bowel
mucosa but is not associated with destruction of enterocyte
Host Defenses
• Intestinal Microbiota
• Important host defense mechanism
• Prevents colonization of potential enteric pathogens
• Persons with fewer intestinal bacteria like infants or patients receiving antibiotics are
at significantly higher risk

• Gastric Acid
• Acidic pH is an important barrier
• Increased frequency of infections due to Salmonella, Giardia have been reported
among patients who have undergone gastric surgery or are achlorhydric
Host Defenses
• Intestinal Motility
• Normal peristalsis is major mechanism of clearance of bacteria
• When impaired, the frequency of bacterial overgrowth and infection of the small bowel is
increased

• Intestinal Mucin
• A complex layer of mucus covers the stomach, small and large intestines separates the
commensal microbiota from the epithelium

• Immunity
• Humoral immunity to enteric pathogens consists of igG and IgM, as well as secretory IgA
• First line of defense
Approach to Patients
• History
• Narrows down potential causes and help
determine whether treatment is needed
Approach to Patients
• Physical Examination
• Examine for signs of dehydration- severity of illness and the need
for rapid therapy
• Mild- thirst, dry mouth, decreased axillary sweat, decreased urine
output, slight weight loss
• Moderate- orthostatic hypotension, skin tenting, sunken eyes
• Severe- lethargy, obtundation, feeble pulse, hypotension, frank
shock
Approach to Patients
• Diagnostic Approach
• Distinguish inflammatory from non inflammatory diarrhea
• Stool examination
• Grossly bloody or mucoid stool suggest inflammatory process
• Test for stool WBC can suggest inflammatory diarrhea
• Fecal lactoferrin is more sensitive
Epidemiology
• Travel History
• Traveler’s diarrhea is the most common travel-related infection
• Time of onset is usually 3 days to 2 weeks after the traveler’s
arrival in resource-poor area
• Most cases begin within the first 3-5 days
• Self-limiting, lasting 1-5 days
• Related to ingestion of contaminated food or water
Epidemiology
• Location
• Closed and semi closed communities, day-care centers, schools, residential facilities,
cruise ships are important settings for outbreaks

• Age
• Morbidity and mortality involves children < 5 years

• Host Immune Status

• Defects in cell-mediated immunity at higher risk of invasive enteropathies
• Infectious diarrhea can be life-threatening among the Immunocompromised
Bacterial Food Poisoning
• If the history and stool examination indicate a non-inflammatory
etiology of diarrhea and there is evidence of a common-source
outbreak
• Ask for ingestion of specific food
• Time of onset of diarrhea after meal
Treatment
• Mainstay of treatment is ADEQUATE HYDRATION
• The use of oral rehydration solution (ORS) has reduced the mortality
rate of cholera from 50% to <1%
• Patient who are severely dehydrated or in whom vomiting precludes
ORS, should receive IV solutions