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Anatomy of Lower GI Tract
SMALL INTESTINE
• Extends from pylorus to
ileocecal junction
• ~6m long, ÷ to 3 parts:
duodenum, jejunum, ileum
• Proximal: ~25 cm duodenum,
fixed part
• Remaining long part freely
mobile: ÷2 jejunum & ileum
• Jejunum + ileum = principally
concerned w/ digestion &
absorption of digested food =
small intestine proper
Arterial Supply
• Jejunal & ileal branches of superior mesenteric
artery (12-15 in #)
• Arise from left side of superior mesenteric artery
& enter mesentery to reach intestine
• Terminal part of ileum supplied by ileal branches
of ileocolic branch of superior mesenteric artery
• Enters mesentery break up into smaller
branches anastomosing w/ each other arterial
arcades terminal arcades small parallel
straight vessels vasa recta opposite surface of
small intestine
Venous Drainage
• Correspond to branches of superior mesenteric artery
drain to portal vein carries products of proteins & carbs to
liver
Lymphatic drainage
• Pass through mesenteric nodes drain to superior
mesenteric nodes around origin of artery
Nerve supply
• Sympathetic supply: T10-T11 spinal segment through
splanchnic nerves & superior mesenteric plexus
– Pain from jejunum & ileum reffered to umbilical region
– Motor to gut sphincter
• Parasympathetic: vagus nerve through celiac & superior
mesenteric plexuses
– Stimulate peristalsis & inhibitory to sphincter
Mesentery of Small Intestine
• Broad fan-shaped fold of
peritoneum
• Suspend small intestine
(jejunum & ileum) from
posterior abdominal wall
• Root (attached margin) and
free margin (intestinal margin)
• Root attached to oblique line
across posterior abdominal
wall extending from duodenal
flexure ileocecal junction
– Duodenal flexure: left side of
L2
– Ileocecal junction: right
sacroiliac joint
Development
• Jejunum & ileum dev from U-
shaped midgut loop w/
cephalic & caudal limbs
– Cephalic jejunum & upper
part of ileum
– Caudal lower part of ileum
• Apex midgut loop
communicates w/ yolk sac
through vitello-intestinal
duct
• Vitelline duct fenerally
obliterated by 6th wk of
intrauterine life
Meckel’s diverticulum (ileal diverticulum)
• Persistent prox part of embryonic vitello-intestinal duct
Normal: symptomless
May cause clinical problems:
• Intestinal obstruction
• Ectopic gastric mucosa or pancreatic tissue may
ulcerate, perforate, bleed (mimic acute abdomen)
LARGE INTESTINE
• ~1.5 m long
• Extends from caecum in right iliac fossa to anus in
perineum
• Apart from transverse & sigmoid colon, it is more
fixed in position than small intestine
• Parts:
– Caecum & appendix
– Colon
– Rectum
– Anal canal
DISTINGUISHING FEATURES OF
COLON:
• Taenia coli
– Ribbon-like bands of longitudinal
muscle coat
– Distally become continuous w/
longitudinal muscle coat of
rectum
– ✓ until caecum
• Appendices epiploicae
– Small bags of visceral
peritoneum = fats
– ✗ in appendix, rectum & anal
canal
– Most on side of sigmoid colon &
posterior surface of transverse
colon
• Sacculation (haustrations)
– Pouches/dilatation in walls of
cecum & colon b/w taenia
– Due to length of taenia that is
shorter
– Puckered appearance in LI
CAECUM
• Large dilated blind sac at proximal end of LI
• Location: Right iliac fossa above lateral ½ of
inguinal ligament
• At birth: conical in shape, vermiform appendix
attached at its apex growth results in 2
saccules right saccule > left apex of caecum
& base of appendix pushed toward left & nearer
to ileocaecal junction base of appendix is
attached at posteromedial wall of caecum
• On basis of growth, 4 types of caecum maybe found in
adult:
– Conical type/fetal type (2%)
• Conical & appendix attached in apex
– Infantile type (3%)
• Quadrate shape (right = left saccule) & appendix attached at
depressed bottom
– Normal type (80-90%)
• Right > left appendix on posteromedial ~2cm below ileocaecal
junction
– Exaggerated type (4-5%)
• Right >>> (exaggerated growth), left saccule ✗
• Appendix attached just below ileocaecal junction
INTERIOR OF CAECUM
• 2 orifice: ileocecal orifice (prominent feature)
& appendicular orifice
– Valve of Gerlach: semicircular fold of mucous
membrane guarding appendicular orifice
Blood supply & Lymphatic Drainage
• Caecum: anterior & posterior
caecal branches of ileocolic artery
branch of superior mesenteric
artery
• Vein: follow arteries superior
mesenteric vein portal system
• Lymph vessels caecum ileocolic
lymph nodes sueprior
mesenteric of pre-aortic lymph
nodes
Nerve supply
• Sympathetic nerve: T11-L1
through sup mesenteric plexus
• Parasympathetic nerve: vagus
nerve
Vermiform Appendix
• Narrow worm-like
diverticulum arise from
posteromedial wall of
caecum ~2cm below
ileocaecal junction
– Length: children > adults
• Surface anatomy:
– 2 cm below intersection b/w
transtubercular plane & right
midclavicular line
– Clinicians equate surface
marking of appendix to
McBurney’s point
Arterial Supply
• Appendicular artery, branch of inferior division of ileocolic artery
– Passes behind terminal part of ileum enters
mesoappendix runs in free margin to reach tip of appendix
(least vascular part)
– Appendicular artery = end artery; in appendicitis: artery
thrombosed gangrenous change in tip may perforate
Venous drainage
• Correspond to artery superior mesenteric vein portal vein
Lymphatic drainage
• Ileocolic lymph nodes appendicular nodes in mesoappendix
Nerve supply
• Sympathetic; carries pain sensation: T10 via splanchnic & sup
mesenteric plexus umbilical region
• Parasympathetic: vagus nerve
Histology of Lower GIT
SMALL INTESTINE
3 Segments: Duodenum, Jejunum, Ileum
MUCOSA
• Permanent Circular folds (plicae circulares Kerckringi)
– Consisting mucosa & submucosa
– Best developed in jejunum
• Simple columnar epithelium of absorptive cells: enterocytes w/ many
goblet cells
• Villi projecting to lumen covering entire mucosal outgrowth
– Finger or leaff-like projections
• Each villus has core:
– Loose connective tissue from lamina propria
– Contain: fibroblast, Smfibers, lymphocytes, plasma cells, fenestrated
capillaries, central lymphatic (lacteal)
• b/w vili: openings of short tubular gland (crypts of Lieberkuhn)
Each villus continuous w/ intervening glands & – Large eosinophilic secretory granules in
pluripotent stem cells: apical cytoplasm
• Enterocytes: – Release lysozome, phospholipase A2,
– absorptive cells, tall columnar w/ oval hydrophobic peptides defensins break
nucleus in basal down bacterial cell walls
– Apical end w/ brush border (microvilli – Innate immunity & regulate
covered w/ glycocalyx) = nutrients taken microenvironment of crypts
into cells • Enteroendocrine cells:
• Cylindrical protrusion – Secrete peptide hormones
• Contain actin filaments & enclosed – Has chemoreceptor similar to taste buds
by cell membr • M (microfold) cells
Villi, microvilli, plicae = mucosal surface area – Specialized epith cells in mucosa of ileum
important for absorption overlying lymphoid follicles of Peyer
• Goblet cells: patches
– Interspersed among absorptive – Basal membrane invaginations or
enterocytes pockets containing many intraepithelial
– Secrete glycoprotein mucins hydrated lymphocytes & APC
mucus protect & lubricate lining of – Endocytose Ag & transport them to
intestine underlying lymphocytes & dendritic cells
• Paneth cells: lymph nodes immune response
– Basal portion of intestinal crypts below
stem cells
– Exocrine cells
MUCOSAL LAMINA PROPRIA
• Contains extensive BV & LV, nerve fibers, SMC,
diffuse lymphoid tissue
• SM fibers extending from muscularis mucosae
produce rhythmic movements of vili
absorption efficiency
• Produce local movements of plicae circulares
propel lymph from lacteals to submucosal &
mesenteric lymphatics
SUBMUCOSA
• Larger BV & LV & diffuse interconnected
neurons = Meisnner nerve plexus
• Proximal duodenum: Brunner glands
• In ileum, both lamina propria & submucosa
contain well dev MALT (mucosa-associated
lymphid tissue) of lymphoid aggregates Peyer
patches underlying M cells
LARGE INTESTINE
• Absorption of H2O & electrolytes from
indigestible materials to feces
• Regions:
– Short cecum w/ ileocecal valve & appendix
– Ascending, transverse, descending, sigmoid colon
– Rectum to store feces for defecation
• ✗ villi in mucosa
• Rectum ✗ major folds
• <1/3 lonf from SI, diameter: 6-7 cm
• Wall of colon puckered to large sacs: haustra
MUCOSA significant component of MALT
• Tubular intestinal gland Muscularis of colon
• Lumen lined by goblet + absorptive • Taenia coli: muscularis; fibers of
cells outer layer gathered in 3 separate
• # of enteroendocrine cells longitudinal bands
• Columnar absorptive cells • Serosa
colonocytes • Descending colons are tunica
adventitia
• Goblet cells produce mucus #
along colon & rectum DISTAL GI TRACT
• Epith stem cells in 1/3 bottom each Anus: distal end of GI tract (3-4 cm)
gland • Rectoanal junction: simple
Lamina propria columnar stratified squamous
• Rich lymphoid cells & lymph epithelium
nodules extending to mucosa • Circular layer of rectum’s
• MALT due to bacteria # muscularis internal anal
Appendix ✗ absorptive function but sphincter
Physiology of Lower GIT
SMALL INTESTINE
• Most digestion & absorption takes place
– In large intestine ✗ further digestion; only small # absorption of H2O
& salt
• Lies coiled w/in abdominal cavity
• Divided to 3 segments:
– Duodenum
• 1st portion: duodena cap/bulb
• At ligament of Treitz (in duodenojejunal flexure) bends
– Jejunum
• Upper 40% SI below duodenum
– Ileum
• Lower 60%
• Shorter during life than cadavers
• Mucosa contains solitary lymphatic nodules (esp ileum); Peyer’s patch
• Brunner’s gland in duodenum & goblet cells in mucosa secrete intestinal
mucus throughout GIT
Motility, 3 types
• Segmentation
– Mixes & slowly propels chyme
– Oscillating
• Ring like contraction along length w/in
seconds
• Contracted segment relax & previously
relaxed area contract mixing chyme w/in
SI lumen
• Initiation: BER (basic Electrical rhythm)
• Slightly/asent b/w meals, vigorous
immediately after meal
– Duodenum & ileum start to segment
simultaneously when meal 1st enter SI
• Focal distention by chyme duodenum
starts to segment
– Ileum: gastrin secreted in response to
chyme in stomach (gastroileal reflex)
– Extrinsic nerve:
• Parasymphatics segmentation
• Symphatics segmentation
Function of segmentation
– Mixing chyme & digestive juices
– Exposing chyme to all absorptive surfaces of SI
mucosa
– Freq of segmentation along length of SI
– Pacemaker in duodenum spontaneous depol
faster than farther down
• Duodenum: 12/min
• Ileum: 9/min
⌃chyme pushed forward
Slow movement: allows digestive & absorptive processes
Content move ~3-5 hrs through SI
• Migrating Motility Complex (MMC)/Intestinal
housekeeper
– b/w meals
– Weak, repetitive peristaltic wave starting at
stomach intestine
– ~100-150 min
– Sweeps remnants of preceding meal +mucosal
debris & bacteria colon
– End of SI cycle begins again until next meal
– Regulated by hormone Motilin, secreted during
unfed state by SI mucosa endocrine cells
ILEOCECAL JUNCTURE
• b/w SI & LI, last part of ileum
empties to cecum
• Region as a barrier. 2 factors
contributing:
– Valve-like folds of tissue; protrude
from ileum lumen of cecum
• Ileal contents pushed ileocecal
valce easily opened
• Folds forcibly closed when cecal
content attempt to move
backwards
– Smooth muscles w/in several cm
of ileal wall thickened sphincter
under neural & hormonal control
• Ileocecal sphincter remains mildly
constricted (intrinsic plexus)
• Distention ileal side sphincter
relax
• pressure in cecal side contract
more
Primary role of SI: ABSORPTION
• Most in duodenum & jejunum, little in ileum
• 50% SI can be removed w/out interference in
absorption except:
– Terminal ileum removed vit b12 & bile salts ✗
abs
• Transport mechanism is here
• Special absorptive function:
– Large surface area
– Epithelial cells have variety or specialized
transport mech
• Adaptation SI SA:
– Inner surface: circular folds (3x )
– Finger like villi (10x )
– Smaller hairlike projection: brush
border/microvilli (20x )
– 3000-6000 microvilli/epith cells
– Enzymes w/in brush border
DIARRHEA Causes:
• Secretion & absorption ✗ • Excess SI motility:
parallel each other – irritation of gut wall by
• Acid – base abnormalities infections or emotional
stress
• Loss of fluid
– ✗ time for adequate
• ly fluid fecal matter ( absorption of fluid
freq of defecatio) • Excess osmotically active
• Beneficial: rapid particles; fluidity of
emptying/elimination of feces
harmful materials in body • Toxins of bacterium
• Excessive loss: V.cholera excess # of
dehydration, nutrients, fluid by mucosa
metabolic acidosis (loss Th/: oral rehydration
oh HCO3-)
LARGE INTESTINE
• Consist of: colon, rectum, cecum, appendix
– Cecum: forms blind-end pouch at ileocecal valve
– Appendix: fingerlike projection: lymphoid tissue
– Colon: not coiled, 3 straight parts
• End part: S shaped: sigmoid straightened rectum
• Primarily a drying & storage organ
COLON
• Main function of colon: absorption of H2O, Na+, minerals
• Receives ~500 mL chyme from SI/day
• Consist of: indigestible food residues (cellulose), unabsorbed biliary
components, remaining fluid
• Main motility: haustral contraction initiated by autonom rhythmicity of
colon SMC (~30 min b/w contraction)
• MASS MOVEMENT
– 3-4x/day after meals
motility during
drive feces 1/3 – ¾ Distal part of LI,
contraction of ascending
length of colon in few materials stored until
& transverse colon
seconds defecation
simultaneously
Next mass
movement
Urge Urge
propels more
feces to rectum
Protein
Absorption
&
Utilization
CARBOHYDRATES
• By hydrolysis
– Liberate oligo/polysaccharide di/monosaccharide
• Amylase catalyzes hydrolysis of starch
– Salivary & pancreatic amylase
• Hydrolysis of α(1 4) glycoside bonds
• Dissaccharidase are brush border enzyme
– Dissacharidase, maltase, sucrase/isomaltase (hydrolysis of sucrose &
isomaltose), lactase, trehalase (located in brush border of intestinal
mucosal cells) resultant: monosaccharide are absorbed
• Lactose gradually through adolescence lactose
intolerance
– Lactose remains in interstitial lumen as substrate for bacterial fermentation to
lactate discomfort + diarrhea
2 Mechanism of absorption of Monosaccharide
in small intestine
• Glucose & galactose
absorption by Na-dependent
process
Transport prot: SGLT1,
competing w/ each other
for intestinal absorption
• Other monosaccharide
absorbed by carrier-mediated
diffusion
✗ actively transported,
eg: fructose & alcohols
only absorbed down the
[] gradient after
moderately intake
Some remains in lumen
(substrate for bacterial
fermentation)
Indigestible Carbohydrates
• Fiber, some oligosaccharides and resistant starch
– Resistant starch: escaped digestion in small intestine
of healthy individual due to cooking & process altering
its digestibility
• Foods high in starch:
– Legumes, unripe bananas, cold cooked potatoes, rice,
pasta
• Affects GI motility, type of intestinal microflora,
nutrient absorption & # of intestinal gas
• Stimulate GI motility
– vol of material in lumen of intestine bulk of
material in feces
– + water from soluble fibers & resistant stach to intestine =
easier evacuation of stool
– healthy bowel function: extra bulk stimulates peristalsis
muscle of colon works extra, becomes stronger,
function better
• Promote healthy microflora
– Serve as food source for microflora
– Breakdown of these carbs SCFA + acidification of colonic
contents SCFA as fuel source for cells in colon & body
tissues regulates cellular process
• Acid inhibits growth of undesirable bacteria & favor growth of
Lactobacili & Bifidobacteria
– SCFA help prevent & treat inflammation in bowel (causes
of diarrhea) & protect against colon cancer
• Slow nutrient absorption
– vol of intestinal contents & absorb water
viscous solutions slow nutrient absorption
# of contact b/w nutrients & absorptive surface
of SI & enzymes and foods
– Fiber causes distention & slows emptying in
stomach
– Slows absorption of glucose fluctuation in
blood glucose in SI
– Binds cholesterol & bile absorption
blood cholesterol & risk of CVD
• Intestinal Gas
http://www.cmrinstitute.org/nni/content/module2/groups/44.html
LIPIDS
• Major lipids in diet: Triacylglycerol,
phospholipids (lesser in extent)
• Hydrophobic mol., therefore have to be
emulsified to very small droplets (micelles)
before they can be absorbed
• Fat sol., vits & other lipids (chol.) are absorbed
dissolved in micelles
– Absorption of vitamins are impaired on a very low
fat diet
• Hydrolysis of triacylglycerol initiated by lingual &
gastric lipases
– Attack sn-3 ester bond forming (C1 & C3) 1,2-
diacylglycerol + F.A (aiding emulsification)
• Pancreatic lipases secreted to small intestine, then
requires further pancreatic proteins (colipase) for
activity
– Specific for primary ester link position 1 & 3 in
triacylglycerol 2-monoacylglycerol & FFA (major end
product)
– Monoacylglycerol (poor substrates for hydrolysis), so <25%
of ingested triacylglycerol is completely hydrolyzed to
glycerol + F.A
• Bile salts by liver, secreted in bile
– Permits emulsification of products of lipid digestion into
micelles (together w/ phospolipid & chol. from bile)
Diffusion
Allow Permit close
(transported
Because product of contact w/ Allow uptake
thru aq.
micelles are digestion brush border into
Environment
soluble (includes of mucosal epithelium
of intestinal
vitamin) cells
lumen
Background document: The diagnosis, treatment and prevention of typhoid fever. Communicable Disease Surveillance & Response Vaccines & Biologicals. WHO
The Disease
typhoid organisms
S. typhi multiplies in
Ingestion in food or pass through the
mononuclear
water pylorus and reach the
phagocytic cells.
small intestine
pathogen reaches an
intracellular haven
(resides) within 24
hours after ingestion general circulation
enter the thoracic
throughout the silent primary
duct
organs of bacteraemia
reticuloendothelial
system (spleen, liver,
bone marrow, etc.)
Inoculation: the introduction of a pathogen or antigen into a living organism to stimulate the production of antibodies
Symptoms & Factors
• Mild illness with low-grade fever, malaise, and slight dry cough Severe clinical
picture with abdominal discomfort and multiple complications
Harrison's 18th
Epidemiology
• Acute gastroenteritis is a common cause of morbidity and mortality
worldwide.
• Diarrhea is in the top 5 causes of deaths worldwide, with most occurring
in young children in nonindustrialized countries.
• In industrialized countries, diarrheal diseases are a significant cause for
morbidity across all age groups.
• Etiologies include bacteria, viruses, parasites, toxins, and drugs.
(Viruses are the most often, in all ages)
• Sporadic gastroenteritis in infants, which most frequently is caused by
rotavirus.
• Epidemic gastroenteritis, which occurs either in semiclosed communities
(eg, families, institutions, ships, vacation spots) or as a result of classic
food-borne or water-borne pathogens. Most of these infections are
caused by caliciviruses.
• Sporadic acute gastroenteritis of adults, which most likely is caused by
caliciviruses, rotaviruses, astroviruses, or adenoviruses.
Harrison's 18th
Diarrhea Classification
• Acute Diarrhea
– lasts two weeks or less
– self-limited
– requiring no diagnostic work-up
– symptomatic treatment only (fluids)
– Acute diarrhea should be investigated only if there is
• evidence of tissue invasion such as blood or pus in the stool
• fever
• leukocytosis
• severity that produces significant fluid and electrolyte loss�
• Chronic diarrhea
– lasts longer than two weeks
– or is intermittent over months or years
– This form requires a diagnostic work-up and a treatment strategy
Pathophysiology of Diarrhea
• Osmotic diarrhea
– Diarrheal stools promptly regress with discontinuation of the offending nutrient, and the
stool ion gap is high, exceeding 100 mOsm/kg.
– The fecal osmolality in this circumstance is accounted for not only by the electrolytes
but also by the unabsorbed nutrient(s) and their degradation products.
• Secretory diarrhea
– The epithelial cells’ ion transport processes are turned into a state of active secretion.
– The most common cause of acute-onset secretory diarrhea is a bacterial infection of the
gut.
– Colonization enteric pathogens may adhere to or invade the epithelium produce
enterotoxins or cytotoxins trigger release of cytokines attracting inflammatory cells &
prostaglandins or platelet-activating factor.
– Features of secretory diarrhea include a high purging rate, a lack of response to fasting,
and a normal stool ion gap (ie, 100 mOsm/kg or less), indicating that nutrient absorption
is intact.
Etiology
Viruses : Enterovirus, adenovirus, rotavirus
Enteral Infection
Bacteria : Vibrio, E. coli, Shigella,
Salmonella, Campylobactr,
Yersinia, Aeromonas
Infection Protozoa : G. Lamblia, E.
Histolitica, Isospora belli
Helmin : Ascaris,
Parasites
Trichuris, Oxyyuris,
Caused of Strongyloides
diare
Fungal : Candida albicans
Harrison's 18th
Treatment : Acute Diarrhea
• Fluid and electrolyte replacement.
– Oral sugar-electrolyte : severe
– IV rehydration : infants and elderly
• Moderately severe nonfebrile and nonbloody diarrhea
loperamide
• Bismuth subsalicylate reduce symptoms of vomiting and
diarrhea, may reduce frequency of travelers’ diarrhea
• Antibiotics
– Moderate-severe febrile dysentery empiric quinolone
– Suspect giardiasis empiric metronidazole
– AB prophylaxis immunocompromise, IBD, hemochromatosis, gastric
achlorhydria
– Ciplrofloxacin anf rifaximin reduce bacterial diarrhea in
uncomplicated travelers’ diarrhea
Harrison's 18th
Prevention
• Preventing viral diarrhea
– Wash frequently.
– Use hand sanitizer when washing isn't possible.
• Preventing diarrhea from contaminated food
– Serve food right away or refrigerate it after it has been cooked or reheated.
– Wash work surfaces frequently to avoid spreading germs from one food item
to another.
– Use the refrigerator to thaw frozen items.
• Preventing traveler's diarrhea
– Watch what you eat. Eat hot, well-cooked foods.
– Watch what you drink.
• Drink bottled water, soda, beer or wine served in its original container.
• Avoid tap water and ice cubes.
• Use bottled water even for brushing your teeth. Keep your mouth closed while you
shower.
• Remember that alcohol and caffeine can aggravate diarrhea and dehydration.
– Ask your doctor about using antibiotics.
– Check for travel warnings.
Harrison's 18th
Classification of Dehydration
Mild Dehydration Moderate Dehydration Severe Dehydration
Fluid loss (% from 2-5 % 5-8% 8-10%
body weight)
Symptoms Turgor <<, hoarse, Bad turgor, hoarse, Moderate
preshock preshock or shock dehydration + loss of
consciousness,
muscle stiffness,
cianosis
Plasma density 1.025-1.028 1.028-1.032 1.302-1.040
Harrison's 18th
DIARRHEA
• Passage of abnormally liquid or unformed stools at frequency
• Adults: stool weight >200 g/d considered diarrheal
• Defined based on duration:
– Acute <2 wks
– Persistent 2-4 wks
– Chronic >4 wks
• Stool totaling <200 g/d = pseudodiarrhea: freq passage of small vol
of stools, associated w/ rectal urgency, tenesmus, or feeling
incomplete evacuation, & accompanies IBS or proctitis
• Fecal incontinece: involuntary discharge of rectal contents due to
neuromuscular disorders or strucutral anorectal problems
• Diarrhea & urgency if severe aggravate or cause incontinence
ACUTE DIARRHEA
• >90% cases caused by infectious agents
– + fever, vomiting, abdominal pain
• 10% by non-infectious agents:
– Medications, toxic ingestions, ischemia, food
indiscretions
GASTROENTERITIS
• Inflammatory process of stomach or intestinal
mucosal surface
• Refers to acute infectious diarrhea w/
syndrome of <2 wks duration + fever, nausea,
vomiting, abdominal pain, dehydration,
weight loss
• GIT: efficient at fluid reabsorption
– 1-2 L fluid ingested orally, 7 L enter upper tract from saliva,
gastric, pancreatic, biliary sources
– <200 mL fluid excreted in daily feces
Thus, small in secretory rate or in absorptive rate =
overwhelm intestinal absorptive capacity
• Diarrhea: freq (>3 bowel movements) or vol (>200
mL/day)
• Intestinal infection w/ bacteria, viruses, parasites
gastroenteritis = fecal-oral transmission
– More commonly via ingestion of food or water
contaminated w/ pathogens from human or animal feces
• Acute infection occurs when ingested agent overwhelms
host’s mucosal immune & nonimmune (gastric acid,
digestive enzymes,mucus, peristalsis & suppresive resident
flora) defenses
PRINCIPAL HOST DEFENSES
• Gastric acidity
– <4.0 kill more than 99% ingested
organisms
– Rotavirus & protozoal cysts survive
– Achlorydia or hypochlorhydia risk of dev
infectious diarrhea
• Physical barrier of mucosa
– Disruption; e.g mucositis predispose pts
to gram 0ve bacteremia
• peristalsis propels organisms along GIT
cough reflex clearing w/ lungs
• Intestinal flora
– SI & colon ~104 – 1011 organisms/mL
respectively
– 99% anaerobes
– Production of fatty acids + acidic pH,
competition for mucosal attachment
prevent colonization of invading organisms
– AB use & extremes of ages alter flora
risk for GE
Virulence factors
Play complementary role in acute
infectious diarrhea
• Most organisms acquire an inoculum
of 105-108 = infection
– Except: Shigella, Giardia,
Cryptosporidium, Entamoeba 10
– 100 organisms ingested ✓
• Production of toxins variety
clinical syndrome
– Enterotoxins: watery diarrhea
– Cytotoxins: dystentery
– Neurotoxins
• Botulinum toxin (classic example)
• Staph.auerus & Bacillus cereus
neurotoxins CNS emesis
• Adherence & invasions factors
facilitate colonization contribute
to virulence
Infectious Agents
• Mostly acquired by fecal-oral transmission
• More commonly via ingestion of food or water
contaminated w/ pathogens from human or
animal feces
• Immunocompetent resident fecal microflora
(>500 species) rarely cause diarrhea actually
play role in growth of ingested pathogen
– Disturbances of flora by AB diarrhea by digestive
function or allows overgrowth of pathogens
• E.g: Clostridium difficile
Indicators of possible infectious
diarrhea
• Travel to dev. Areas
• Day-care center attendance or employment
• Consumption of unsafe foods (raw meats, eggs, shellfish, unpasteurized
milk or juices)
• Swimming in or drinking untreated fresh surface water from (e.g lake or
stream)
• Visiting a farm or petting zoo or having contact w/ reptiles or pets w/
diarrhea
• Knowledge of other ill persons (dormitory or office or social function)
• Certain recent or regular medications (AB, antacids, antimotility agents)
• Underlying medical conditions predisposing infectious diarrhea (AIDS,
medications, prior gastrectomy, extremes of age)
• Receptive anal intercourse or oral-anal sexual contact
• Occupation as food handler or care giver
Clinical
Syndromes
• Acute infectious
diarrhea divided
into:
– Non
inflammatory
– Inflammatory
– invasive
Epidemiology
• Gastroenteritis: major cause of global mortalilty & morbidity
among infants & children
– Peak attack rates: young school children & siblings
– Most case: viral agents
• Rotavirus 10-50%
• Norovirus 10-30%
• Enteric adenovirus 2-5%
– Bacterial <15% disease; severe in Campylobacter spp, E.coli spp,
Salmonella spp, Yersinia spp.
• EHEC O157:H7 = important cause of hemolytic uremic syndrome in
children
• Yersinia = watery diarrhea in children 1-5 yo, mimic appendicitis in older
children & adolescents
• World Health Organization (WHO) & UNICEF:
– ~2 billion cases of diarrheal disease worldwide
every year;
– 1.9 million children <5 years of age perish from
diarrhea each year, mostly in developing
countries.
– 18% of all the deaths of children under the age of
five
– more than 5000 children are dying every day as a
result of diarrheal diseases.
– Of all child deaths from diarrhea, 78% occur in the
African and South-East Asian regions.
• Each child <5 years of age experiences an average of 3
annual episodes of acute diarrhea.
• Globally in this age group, acute diarrhea is the second
leading cause of death (after pneumonia)
– both the incidence and the risk of mortality from diarrheal
diseases are greatest among children in this age group,
particularly during infancy – thereafter, rates decline
incrementally.
• Other direct consequences of diarrhea in children:
– growth faltering, malnutrition, and impaired cognitive
development in resource-limited countries.
Causative agents & pathogenic mechanisms
BACTERIAL AGENTS
In dev countries, enteric bacteria & parasites > viruses
DIARRHEAGENIC E.COLI
• Enterohemorrhagic E.coli (EHEC O157:H7) cause disease more commonly
in dev countries
– Enterotoxigenic E.coli (ETEC) traveler’s diarrhea
– Enteropathogenic E.coli (EPEC) rarely cause disease in adults
– Enterohemorrhagic E.coli (EHEC) bloody diarrhea, severe hemorragic colitis,
hemolytic uremic syndrome (cattle as predominant reservoir)
Pediatric details:
• Enteroaggregative E.coli (EAggEC) watery diarrhea in young children &
persistent diarrhea in children w/ HIV
• Enterotoxigenic E.coli (ETEC) diarrhea in infants & children in dev
countries
• Enteropathogenic E.coli (EPEC) common in children <2 years, persistent
diarrhea in children
Montezuma’s revenge: travelers' diarrhea or other sicknesses contracted by tourists visiting Mexico
Pediatric details:
• Campylobacter is one of the most frequently isolated bacteria from
the feces of infants and children in developing countries,
• peak isolation rates: 2 years of age and younger
SHIGELLA
• Hypoglycemia, occurs more frequently than in other types of
diarrheal diseases
• S. sonnei is common in developed countries, causes mild illness,
and may cause
• institutional outbreaks.
• S. flexneri is endemic in many developing countries and causes
dysenteric
• symptoms and persistent illness; uncommon in developed
countries.
• S. dysenteriae type 1 (Sd1) — the only serotype that produces Shiga
toxin, as
• does EHEC.
Pediatric details:
• An estimated 160 million episodes occur in developing countries,
primarily in children.
• common in toddlers and older children than in infants
Clinical Microbiology Reviews. American Society for Microbiology. http://cmr.asm.org/content/21/1/134/F1.expansion.html
Pediatric details:
• In children, hypoglycemia can lead to convulsions and
death.
Salmonella
• Enteric fever — Salmonella enterica Typhi and Paratyphi A, B, or C
• (typhoid fever);
– fever lasts for 3 weeks or longer; patients may have normal bowel habits, constipation or
diarrhea.
• Animals are the major reservoir for salmonellae.
• Humans are the only carriers of typhoidal Salmonella.
• In non-typhoidal salmonellosis (Salmonella gastroenteritis):
– Acute onset of nausea
– vomiting,
– Diarrhea: watery
• The elderly & people with immune-compromised status (e.g., hepatic and
lymphoproliferative disorders, hemolytic anemia), appear to be at the greatest
risk.
Pediatric details:
• Infants and children with immune-compromised status (e.g., severe
malnourishment) appear to be at the greatest risk.
• Fever develops in 70% of affected children.
• Bacteremia occurs in 1–5%, mostly in infants.
Viral Agents
In both industrialized and developing countries,
viruses are the predominant cause of acute
diarrhea, particularly in the winter season.
ROTAVIRUS
• 1/3 of diarrhea hospitalizations & 500,000
deaths worldwide
• each year
• Associated with gastroenteritis of above-
average severity.
Pediatric details:
• Leading cause of severe, dehydrating
gastroenteritis among children.
• Nearly all children in both industrialized and
developing countries get infected by the
time they are 3–5 years of age.
• Neonatal infections are common, but often
asymptomatic.
• The incidence of clinical illness peaks in
children b/w 4 and 23 months of age.
HUMAN CALICIVIRUSES (HUCVS):
• Family Caliciviridae—the noroviruses and sapoviruses (previously
• called “Norwalk-like viruses” and “Sapporo-like viruses.”
• Noroviruses: most common cause of outbreaks of gastroenteritis,
affecting all age groups.
Pediatric details:
• Sapoviruses primarily affect children. 2nd most common viral agent
after rotavirus, 4–19% of episodes of severe gastroenteritis in
young children
ADENOVIRUS
• Infections most commonly cause illnesses of the respiratory system.
Pediatric details:
• depending on the infecting serotype, this virus may cause
gastroenteritis especially in children.
Parasitic Agents
http://www.uib.cat/depart/dba/microbiologia/ADSenfcomI/material_archivos/infeccion%20gastrointestinal.pdf
Hookworms can cause some of the
following symptoms:
• anemia (pale skin etc.) and protein
deficiency caused by blood loss
• constipation
• congestive heart failure
• decreased rate of growth and
mental development in children
(caused by protein and iron
deficiency)
• diarrhea
• dizziness
• dyspnea (shortness of breath)
• excessive coughing during larvae
migration
• fatigue (tiredness)
• fever
• loss of appetite
• nausea
• rash or sore and itchy feet after
larval invasion
• stomach or chest pain
• vomiting
• weight loss
Minor infections can be asymptomatic but usually
one or more of the following symptoms occur:
• anemia (for example, pale skin)
• constipation
• cough
• diarrhea
• eosinophilic pneumonitis (during larvae
migration through the lungs)
• nausea
• rashes in waist and buttocks
• stomach ache
• vomiting
• weight loss.
Diphyllobothriasis symptoms
include:
• constipation
• diarrhea
• fatigue
• obstruction of the bowel
• pernicious anemia (caused by
vitamin B12 deficiency) which
can lead to
• subacute combined
degeneration of spinal cord
• stomach pain
• vomiting
• weight loss.
• Migrating proglottids can
cause inflammation of the bile
duct or the gall bladder.
The first symptoms are a rash
or itch during the first few
days.
http://www.parasitesinhumans.org/
Patient Evaluation
• Most cases of acute GE: self-limited
• Consultation is advised for pts w/
– fever >38.50C,
– dysentery,
– significant abdominal pain,
– dehydration,
– risk factors for disease requiring intervention
(Elder, pregnant, recent AB use)
INITIAL EVALUATION
• History should focus of:
– Severity of disease
– Risk factors for specific types of infectious diarrhea
– Symptoms, duration, fever, abd pain, tenesmus, dehydration
– Freq, vol, blood, pus, mucus in stools
– Diarrhea >2 – 4 wks CHRONIC fully investigated
– Inquiry made into factors at specific subgroup at risk:
• >70 yo, pregnant, recent travel or camping, recent AB use,
immunosuppression (HIV, prednison th/, chemoth/), anal intercourse,
seafood consumption, household contacts of day-care workers or
children, potential common source (friends, realtives w/ similar sympts)
– Short incubation <6 hrs or 6-16 hrs
• enterotoxin S.aureus & B.cereus or Clostridium perfringens
– Vomiting
• dominant w/ viral infections & food poisoning S.aureus, B.cereus, norovirus)
Physical examination
• Helpful to gauge severity of disease
• Orthostasis, Tachycardia, skin turgor, Dry mucous
membranes dehydration
• Fever, abdominal tenderness, skin rash documented
• All patients should undergo rectal exam when rectal bleeding
reported
Screening stool examination
• Based upon history & physical exam
• Fresh-cup specimen – preferred
• Evaluate:
– Fecal leukocytes
• Staining or lactoferrin testing
• Methylene blue stain
• 3 or more leukocytes/high-powered field (at least 4 fields) = +ve
• Lactoferrin latex agglutination = more precise marker
– Fecal occult blood
– Organisms most common associated w/ +ve screening test:
Salmonella, Shigella, E.coli O157, Campylobacter, Yersinia, Aeromonas,
Vibrio, C.difficile
Laboratory Evaluation
• Lab testing & antimicrobial th/ recommended underscored by
overall stool cultures +ve
• Indicated in pts w/ following findings or risks:
– Severe or persistent disease
• Fever >38.50C
• Dehydration
• Grossly bloody stools
• Duration >1 wk
• At risk subpopulations
• +ve stool screening exam
• Lab exam includes:
– CBC
– Serum electrolytes
– Stool processed for bacterial culture
• ✗ cost effective for ova & parasites
• Differentiation of pathogenic & non-pathogenic strains of
E.coli
– Specific serotyping
• Commercial enzyme immunoassay kits for detection of
rotavirus & enteric adenovirus
– Useful in pediatric population & elderly
• Colonoscopy rarely needed
– But appropriate where differential includes: ischemic
colitis, IBD, other etiologies requiring biopsies
(immunocompromised, concern for C.difficile w/ -ve stool
studies)
• Initial evaluation of AIDS-associated diarrhea:
– Stool exam for culture, ova, parasites, acid-fast stain
• Specialized stool studies
– detection of Cryptosporidium, Cyclospora,
microsporidiosis, Cystoisospora belli
• Mucosal biopsies
– diagnosis of CMV & Mycobacterium avium intracellulare
complex
• Sigmoidoscopy
– persistent or severe cases in pts w/ <100/μL CD4 counts &
weight loss
Pediatric details: Identification of a pathogenic bacterium, virus, or parasite in a stool
specimen from a child with diarrhea does not indicate in all cases that it is the cause
of illness.
Management
REHYDRATION that are lost in diarrhea stool.
• Oral rehydration therapy (ORT) is
the administration of appropriate ORT consists of:
solutions by mouth to prevent or • Rehydration—water & electrolytes
correct diarrheal dehydration. administered to replace losses.
• Cost-effective method of managing • Maintenance fluid therapy to take
acute gastroenteritis care of ongoing losses once
• It reduces hospitalization rehydration is achieved (along with
requirements in both developed and appropriate nutrition).
developing countries
• Oral rehydration salts (ORS) contain
specific amounts of important salts
• ORT is contraindicated in:
– initial management of severe dehydration
– in children with paralytic ileus, frequent and persistent
vomiting (more than four episodes per hour)
– painful oral conditions such as moderate to severe thrush
(oral candidiasis)
Nasogastric administration of ORS solution is potentially
lifesaving if IV rehydration not possible & the patient is being
transported to a facility
Pediatric details:
• Breastfed infants and children should continue
receiving food, even during the rehydration phase
• However, for non-breastfed, dehydrated children&
adults, rehydration is the first priority and that can be
accomplished in 2–4 hours
Anti-diarrheal treatment
• Usually unnecessary in acute diarrhea
management, some have sedative effects
ORT difficult
Pediatric details: antidiarrheals have no practical
benefits for children w/ acute or persistent
diarrhea
Doses shown are for oral administration
• Antimicrobials are reliably helpful; routine use is
recommended in the treatment of severe (clinically
recognizable):
– Cholera, shigellosis, typhoid and paratyphoid fevers .
– Dysenteric presentation of campylobacteriosis and
nontyphoidal salmonellosis when they cause persistent
diarrhea, and when host immune status is compromised
for any reason such as severe malnutrition, chronic liver
disease, or lymphoproliferative disorders.
– Invasive intestinal amebiasis
– Symptomatic giardiasis (anorexia and weight loss,
persistent diarrhea, failure to thrive).
• Consider antimicrobial treatment for:
– Shigella, Salmonella, Campylobacter (dysenteric form) or
parasitic infections.
– Nontyphoidal salmonellosis among at-risk populations
(malnutrition, infants and elderly, immunocompromised
patients, and those with liver diseases and
lymphoproliferative disorders), and in dysenteric
presentation.
– Moderate/severe traveler’s diarrhea or diarrhea with fever
and/or with blood stools.
– Antimicrobials are also indicated for associated health
problems such as pneumonia.
Complications
DEHYDRATION
• Loses too much water & salt from the body
• Causes disturbance of electrolytes affect vital organs
• Must be treated to help restore balance of water & salt
• Treated w/ ORS
Asses dehydration
• Restless or irritable
• Sunken eyes
• Skin loses elasticity
• Lethargic or unconcious (if continues)
Acute diarrhea in adults and children: a global perspective. World Gastroenterology organisation Global Guidelines 2012