Download Gastointestinal Infections I

Microbiology: Intra-Abdominal Infections I
NORMAL FLORA OF INTESTINAL TRACT:

Mouth: thousands of bacteria in the mouth; many more anaerobes (100:1); main reservoir for introduction into
intestinal tract

Stomach: acidic environment where most oral bacteria killed; similar bacteria to those in mouth and throat

Stomach to Small Intestine: mostly Gram positive
Enterococcus: can live in the presence of bile salts (highest concentration in duodenum)

Colon: beneficial bacteria; mostly anaerobes (1000:1)
400-500 different species (mainly strict anaerobes; therefore cannot be cultured)
Do not cause disease in the environment (only if they get into normally sterile parts of the body)
PROTECTION OF THE INTESTINAL TRACT:

Mucous Membranes:
Goblet Cells: produce mucus
o Lubricant to protect mucous membrane
o Physical barrier to trap bacteria that is expelled by peristalsis
M Cells: aid in presentation of antigens to underlying cells of the immune system (in Peyer’s patches)
o Phagocytose bacteria and other Ags and pass to macrophages under the M cell
Absorptive Cells (Enterocytes): some of the most rapidly dividing cells in the body
o Bacteria that reach mucosal cells have to deal with rapid turnover
o Mucosal cells formed in crypts, move up the villous surface, and are released into the lumen as new
cells replace them

Other Protective Mechanisms:
sIgA
Stomach acid
Bile salts
Rapid flow of material through small intestine (washes bacteria out of SI)
Slow rate of material through colon with dense bacterial population (protective normal flora)

Infection occurs when organisms with virulence mechanisms overcome the protective mechanism of the GI tract
IDENTIFICATION OF GRAM NEGATIVES:

Oxidase Reaction: detects presence of cytochrome oxidase (transfers electrons to O2)

Growth on MacConkey agar: selective for Gram negative

Metabolism: oxidative, fermentive or inert
Family
Oxidase
MacConkey Growth/Color
Metabolism
Enterobacteriaceae
Negative
Yes/Varies by species
Fermentation
Vibrionaceae
Positive
Yes/Colorless to light pink
Fermentation
Campylobacteriaceae
Positive
No growth
Inert
Pseudomonadaceae
Positive
Yes/Colorless
Oxidative

Note: enterobacteriaceae family includes E.coli, Klebsiella, Salmonella, Shigella, Yersinia, Proteus
All are Gram negative rods and facultative anaerobes
BACTERIAL AND PARASITIC GI INFECTIONS:

Terms:
Secretory: watery, non-inflammatory
Non-inflammatory: no leukocytes in the stool
Inflammatory: presence of leukocytes in the stool
Invasive: organism can invade into the epithelial cells
Non-Invasive: bacteria stay in the lumen, but may cause disease by secreting toxins
Enterotoxin: toxin released by a microorganism in the intestine
Neurotoxin: toxin that acts directly on neurons
Cytotoxin: toxin having a specific toxic action on cells of special organs

Overview:
Secretory Diarrhea (Non-Invasive and Non-Inflammatory): caused by toxogenic bacteria, noninvasive parasites,
or virus
o Bacterial Enterotoxigenic Diarrhea: Enterobacteriaceae and Vibrionaceae
o Bacterial Neurotoxin Group: ingested organisms produce a neurotoxin (usually the preformed toxin is
ingested); C.botulinum, B.cereus, S.aureus
o Non-Inflammatory Parasitic: G.lamblia, C.parvum
-
-
Invasive/Tissue Damaging Diarrhea (Inflammatory):
o Bacterial Cytotoxin Caused Inflammation: C.difficile, EHEC
o Bacterial Invasive Infection: Shigella, Salmonella, EIEC
o Parasitic Invasive: E.histolytica
Miscellaneous Intestinal Infections:
o Gastric and duodenal ulcers: H.pylori
o Food-borne bacteremia and meningoencephalitis: L.monocytogenes
o Parasitic GI Helminths
SECRETORY DIARRHEA (NON-INVASIVE AND NON-INFLAMMATORY):
Bacterial Enterotoxigenic Diarrhea:

Vibrio Cholerae (O1 and O139):
Basics:
o Gram negative
o Oxidase positive
o Comma shaped motile rod
o Grows in freshwater ponds and brackish water (can colonize shellfish)
Virulence Factors:
o Motility: single polar flagellum
o Adherence: pili and other adhesins (most important VF)

Allow bacteria to adhere tightly to the epithelium of the SI

Tcp pili= toxin co-regulated pili (long, filamentous pili)
o Cholera Toxin (Choleagen): A-B type ADP-ribosylating toxin

A subunit: enzymatic; only 1 subunit

B subunit: binding; 5 identical subunits
Adherence and Toxin Production:
o Toxin attaches to the surface of a mucosal cell (binds GM1 gangliosides)
o A1 subunit is released from the toxin and enters the host cell

ADP-ribosylates membrane protein Gs (turns on adenylate cyclase constitutively)
 Normal: GDP + Gs= no activation; GTP + Gs= transient activation

Adenylate cyclase causes an increase in cAMP

Increase in cAMP causes ion imbalance that results in water loss
 Hypersecretion of fluids and chloride ions
 Inhibition of sodium absorption
Etiology/Pathogenesis:
o Rapid onset 2-3 days after inoculation

Need to ingest a lot because of sensitivity to gastric acids (~108 cfu)

Replicates to very high numbers

Attachment to epithelial cells in the small intestine (flagella and pili help)

Produces and secretes CTX toxin
o Initial Clinical Manifestations:

Vomiting

Massive watery diarrhea with mucous flecks (rice-water stools)

No PMNs in stool
o Rapid dehydration and electrolyte loss
Transmission:
o Fecal-Oral: via water, fish, and shellfish
o Carriers: recovered patients can still shed the organism (important in endemic regions)
Clinical Identification:
o Stool specimen only
o Lab Tests: oxidase positive, curved Gram negative rod
o Special Medium: thiosulfate citrate bile sucrose (TCBS)
o O Antigens: O1 and O139 are markers for strains that produce cholera toxin (the others do not, and
therefore only produce non-epidemic diarrhea and extra-intestinal infections)

Epidemic Cholera via O1 and O139:
 Classic
 El Tor (worse)

Enterotoxigenic E.Coli (ETEC):
Basics:
o Most common cause of Traveler’s diarrhea
o Highest incidence in the tropics and in the young
Virulence Factors:
o Adherence:

Adhesins: colonization factors on pili (bind epithelial cells in SI)

Bundle-forming pilus: similar to Tcp pili in V.cholerae
o Exotoxins:

Heat Labile Toxin (LT): inactivated at 100 degrees C for 30 minutes
 Shares ~75% aa sequence with cholera toxin
 5B:1A subunit (same structure as cholera toxin)
 Binds same receptor (GM1 ganglioside) and has the same MOA as cholera toxin
 Difference from CT: LT is not secreted (localized in periplasm)

Heat Stable Toxin (ST): not inactivated at 100 degrees C for 30 minutes
 Family of small molecules (not a single toxin)
 MOA: binds a guanylate cyclase in the membrane of the host cell, resulting in
activate and increase in cGMP
 Result: fluid and electrolyte loss
Etiology/Pathogenesis:
o Colonizes the SI with adhesins
o Production of LT and ST leads to diarrhea
o Clinical Manifestations: incubation period of 1-2 days

Starts as: nausea, vomiting, weakness, dizziness and abdominal pain; also a low grade fever

Progresses to: watery diarrhea (mild to severe)
Transmission:
o Contaminated food and beverages are the major vehicles of transmission
Identification of Organism:
o ELISA or agglutination tests for presence of toxins
o DNA probes for LT or ST genes

Enteropathogenic E.Coli (EPEC):
Basics:
o Causes severe (often fatal) watery diarrhea in infants and children in developing
o Previously associated with outbreaks in nurseries in developed countries
o Can cause Traveler’s diarrhea in adults
Virulence Factors:
o Attaching and Effacing Lesion:

Non-intimate binding: occurs via the bundle-forming pilus

Intimate binding: mediated by bacterial proteins (Tir and intimin)

Effacement of the cell membrane: loss of microvilli and the formation of a pedestal-like
structure beneath the organism
o Type III Secretion: proteins injected right into the cell so that Abs to the proteins never see them

Injects a receptor for itself into the cell (allows it to bind any cell)
Etiology/Pathogenesis:
o Dehydration and electrolyte balance can cause death
o Malabsorptive Diarrhea: most likely caused by a loss of absorptive capacity of mucosal cells due to
damage of the host cell surface
o Symptoms:

Watery diarrhea (non-bloody, mucous-filled)

Fever

N/V
Transmission:
o Fecal-oral route
Identification:
o ELISA and multiplex PCR
Bacterial Neurotoxin Group:

Clostridium botulinum:
Virulence Factors:
o Botulinal Toxin: neurotoxin; usually ingested as a preformed toxin and travels in the bloodstream to
neurons, resulting in flaccid paralysis (death usually due to respiratory collapse)

AB Toxin: B portion binds ganglioside receptors on nerve cells;
 Toxin internalized and blocks presynaptic release of ACh at the NMJ (prevents
muscle contraction)
 Can be inactivated by boiling for 10-15 minutes
Etiology/Pathogenesis:
o Spores are heat resistant: can withstand 100 degrees Celsius for 3-5 hours
o Spore Locations: found in animal feces, soil and lake sediment
o Types of Botulism:

Food Botulism: spore germinates in foods, resulting in bacterial growth and toxin production
(food needs to be anaerobic, like canned goods)
 Ingestion of preformed toxin, which is absorbed in the stomach and enters the
bloodstream; Sx occur 12-36 hours later

Infant Botulism: C.botulinum can colonize the infant colon (ie. spores in honey), and since
they are without complete colonic microflora, it can grow and produce toxin
 Rare cause of Sudden Infant Death Syndrome

Wound Botulism: spores colonize deep wounds (anaerobic), grow and produce toxin that
enters the bloodstream
o Not associated with diarrhea
o Recovery period is long: affected nerve endings need to regenerate
Identification of Organism:
o Anaerobic, Gram negative, spore-forming bacillus
o Organism can be grown in oxygen free lab environment
o Laboratory confirmation by immunoassay for toxin in food, gastric contents or blood

Staphylococcus aureus:
Basics: most common form of food poisoning
Virulence Factors:
o Pre-formed toxin (enterotoxin): ingested and absorbed into the gut, stimulating neural receptors

Stimulus transferred to the vomiting center in the CNS
Symptoms:
o Vomitting (projectile) within hours
o Diarrhea less frequently
Tranmission:
o Can multiply/make toxins in foods that are unrefrigerated for extended periods of time
o Re-heating the food does not destroy the heat-stable enterotoxins

Bacillus cereus:
Emetic (Vomiting) Form:
o Cause: ingestion of pre-formed heat stable enterotoxin ingested in reheated foods

Often associated with Chinese restaurants (fried rice)
o Short incubation period: 1-6 hours (rapid onset)
o Symptoms: N/V and abdominal cramps (similar to S.aureus food poisoning)
o Duration: usually 24 hours or less
Diarrheal Form:
o Cause: heat-labile toxin formed in vivo, which activates adenylate cyclase and causes intestinal fluid
secretion

Associated with meat or vegetable containing foods after cooking (food held above room
temperature for a prolonged period)
o Long incubation period: 8-16 hours
o Symptoms: severe abdominal cramps and diarrhea (ma be a small volume or profuse and watery)
o Duration: usually 24 hours or less

C.perfringens:
Basics: very similar to B.cereus diarrheal form
Cause:
o Temperature abuse of prepared foods (meat, meat products, gravy)
o Contaminated with enterotoxin producing C.perfrigens type A (toxin produced in GI tract)
Onset: 8-24 hours after ingestion of contaminated meat
Symptoms: abdominal cramps and watery diarrhea
o Without fever, nausea or vomiting
Non-Inflammatory Parasitic:

Giardia lamblia:
Basics: flagellated, enteric protozoan
Virulence Factors:
o Life Cycle: two stages- trophozoite (free living) and cyst (infective)
o Adhesion: via sucking/adhesive disk on the trophozoite; adheres to upper SI mucosal surface
o Flagella: motility and attachment
Etiology/Pathogenesis:
o Infection: due to oral ingestion of cysts (trophozoites destroyed by gastric activity)

Often associated with drinking contaminated water (cysts can survive in water up to 3
months)
o Incubation: 7-10 days
o Symptoms:

Acute onset of watery diarrhea

Abdominal cramps, bloating and flatulence

Some patients progress to chronic diarrhea with malabsorption (weight loss common)
Identification of Organism:
o Microscoping examination of stool, duodenal aspiration or duodenal biopsy
o Antigen testing for G.lamblia in the stool
o String test (swallowing a string to obtain a sample from the upper part of the small intestine)

Cryptosporidium parvum:
Basics: small coccidian protozoan parasite
Symptoms:
o Immunocompromised: severe, watery, prolonged diarrhea
o Immunocompetent: mild diarrhea
Life Cycle:
o Oocyst ingested in contaminated water
o Sporozoite released in intestine
o Sporozoite enters intestinal epithelial cells (infects the microvilli)
o Undergoes sexual and asexual replication
o Oocysts produced (infective stage) which are then shed in the feces

Other Non-Inflammatory Diarrhea Parasites:
Microsporidia (Microspora): group of obligate, intracellular, spore forming protists
Cyclospora cayetanesis: have cyanobacterium-like bodies
o Cause prolonged diarrhea (up to 7 weeks)
o More severe in AIDs patients
Isospora belli: clinically indistinguishable from giardiasis, cryptosporidiosis and microsporodiosis
o Diarrhea without blood or leukocytes
o Infects entire intestine
o More severe in AIDS patients
INVASIVE AND TISSUE-DAMAGING DIARRHEA (INFLAMMATORY):
Bacterial Cytotoxin Induced Inflammation:

Clostridium difficile:
Basics: normal flora in ~5% of healthy adults; can cause acute inflammation of the colonic mucosa in some cases
Virulence Factors:
o Toxin-A Enterotoxin: causes accumulation of viscous, bloody fluid

Chemotactic for PMNs, resulting in cell lysis

Cell lysis causes release of inflammatory mediatiors, which causes:
 Fluid secretion
 Altered membrane permeability
 Hemorrhagic necrosis of mucosa
o Toxin B Cytotoxin:

Disrupts the actin polymerization and cytoskeletal architecture

Decreases cellular protein synthesis (similar to diphtheria toxin)
Etiology/Pathogenesis:
o Source: endogenous or from the environment (nosocomial infections)
o Cause of Diarrhea: altered intestinal flora from a course of antibiotics (antibiotic associated colitis)
o Symptoms: variable

Asymptomatic carrier

Mild diarrhea

Pseudomembranous colitis:
 Pseudomembranes/plaques consist of fibrin, mucus, necrotic epithelial cells, and
leukocytes adherent to the underlying inflamed mucosa
Identification:
o Characteristics: spore forming, anaerobic, Gram positive rod
o Selective Media: CCFA (cycloserine, cefoxitin, fructorse agar); culturing organism not helpful
o Tests: toxin tests in stool are the most useful clinically (EIA test)

Enterohemorrhagic E.Coli (EHEC):
Basics:
o Also called Shiga-toxin E.coli (STEC) or Verocytotoxin E.Coli (VTEC)
o Causes: diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS)
Virulence Factors:
o Adhesins: tight binding to mucosal cells, mediated by Tir and intimin
o Shiga Toxin: AB type toxin

B subunit binds Gb3 ganglioside on host cell

A subunit enzymatically modifies 28S ribosomal RNA of the 60S-ribosomal subunit
 Blocks proteins synthesis
 Eventually leads to cell death

Causes: capillary thrombosis and associated inflammation of the colonic mucosa (leads to
hemorrhagic colitis)

Types: strains may carry one or both; encoded by bacteriophages
 Shiga Toxin I (StxI)
 Shiga Toxin II (StxII)
o Type III Secretion: inserts toxin and its own receptor into the host cell; causes attaching and effacing
lesions like EPEC
Etiology/Pathogenesis:
o Cause: Shiga-toxin producing strains colonize the intestinal tract of cattle and other farm animals

Outbreaks occur from contaminated meat (hamburger), milk and apple cider

Only a small number of organisms required for infection
o Incubation Period: 3-4 days
o Symptoms:

Severe, crampy abdominal pain

Copious watery diarrhea that develops into grossly bloody diarrhea

Little to no fever*

Hemolytic Uremic Syndrome: develops in 5-10% of patients (esp. young kids)
 Acute renal failure, thrombocytopenia and hemolytic anemia
 Caused by Shiga toxin damage to endothelial cells of renal glomeruli
-
Identification:
o Serotyping:

O Antigens: outer region 1 of LPS (endotoxin) polysaccharide Ag

H Antigens: flagella proteins

K Antigens: extracellular polysaccharide Ags
o Serotype O157:H7: causes 50-80% of infections

Does not ferment sorbitol (almost all other strains do)

However, sorbitol positive strains may also produce Shiga toxins
o Other Methods:

Anti-O157:H7 serum

Demonstrate cytotoxicity with Vero Cells

DNA probe for detection of Shiga toxin genes
Bacterial Invasive Infection:

Shigella:
Basics: produces bacillary dysentery (blood and mucus in stool)
Virulence Factors:
o Invasion: enters through M cells only

Superficial: very rare penetration beyond mucosa

Primary virulence characteristic of Shigella is invasiveness
o Type III Secretion: used to induce actin rearrangements causing pseudopods at the basolateral surface
of epithelial cells in order to take up bacteria
o Actin-Based Motility: once in the cell, causes rapid polymerization and depolymerization of actin at
one pole, causing the bacteria to be propelled through the cell to invade adjacent ones

Invaded cells die and slough off (surface erosion of gut wall)

Results in the formation of shallow ulcers (ulcerative colitis)
o Bacillary Dysentery: local inflammation with abundant neutrophils, RBCs and mucus in the stool

Shigellae promotes cytokine release and an inflammatory response to cause damage to the
epithelium, allowing more invasion by bacteria
o Shiga Toxin: one species (S.dysenteriae type 1) produces Shiga toxin; plays a role n local destruction of
the mucosa in this case
Etiology/Pathogenesis:
o Spread: only human to human (by food, fingers, feces and flies)
o Highly Infectious: only need <103 organisms for infection
o Four Serotypes:

Group A: S.dysenteriae (Shiga bacillus- largest producer of toxin)

Group B: S.flexneri* (causes the rest of US cases)

Group C: S.boydii

Group D: S. sonnei* (causes 60-80% of US cases)
o Disease: organisms multiply in the lumen of the small intestine, with higher numbers occurring in the
lower intestine

First 12 Hours: abdominal pain, cramping, and fever (while bacteria localized in SI)

12-72 Hours:
 Organism no longer detectable in upper intestine
 Fever decreases
 Pain becomes more severe (localizes to lower quadrants)
 Dysentery develops (cramps, tenesmus and lethargy)
 Bloody, low volume diarrhea with large number of PMNs in mucoid stool
Identification of Organism:
o Basics: non-motile, Gram negative bacillus
o Lab Tests: lactose negative, oxidase negative
o Serological identification of serogroups

Enteroinvasive E.Coli (EIEC):
Basics: relatively rare
Virulence Factors:
o Behaves like Shigella (no Shiga toxin)
o Infects and spreads cell-to-cell similar to Shigella

Salmonella:
Basics: found in almost all animal species
o Exceptions: some found in only humans (S.typhi)
Virulence Factors:
o Adherence and Invasion: organism binds microvilli and can invade M cells or epithethial cells

Bacteria engulfed in a vesicle (remain inside the phagosome and replicate)
o Type III Secretion: extensive actin rearrangement where the bacteria attaches leads to ruffling and
bacterial-mediated endocytosis
o Endotoxin: Lipid A of LPS released upon lysis

Induces inflammatory response that contributes to mucosal damage
Etiology:
o Transmission: usually by contaminated food (poultry meat or eggs)
o Many Serotypes: over 2400 based on O and H Ags
o Not as infectious as Shigella: requires a large inoculum for infection
Pathogenesis: causes 3 main clinical syndromes
o Gastroenteritis (Enterocolitis): most common form

Incubation Period: 8-48 hours

Onset: abrupt

Fever: usually low

Duration: 2-5 days

GI Symptoms: N/V/D at onset

Blood Culture: negative

Stool Culture: positive for several weeks
o Bacteremia: rare event that sometimes develops after gastroenteritis; secondary infection can occur

Incubation Period: variable

Onset: abrupt

Fever: rapid rise and spike (septic)

Duration: variable

GI Symptoms: often absent

Blood Culture: positive during fever

Stool Culture: infrequently positive
o Enteric (Typhoid) Fever: classically associated with S.typhi or S.paratyphi (others may also cause)

Incubation Period: 7-20 days

Onset: insidious (gradual)

Fever: gradual, and then high plateau

Duration: several weeks

GI Symptoms: constipation early; bloody diarrhea late

Other Symptoms:
 Early: chills, headache, anorexia, weakness and muscle aches
 Late: fever, swollen LNs, enlargement of the liver and spleen
 Maculopapular Rash (Rose Spots): 1/3 of patients get this on lower trunk

Blood Culture: positive in 1-2 weeks of disease

Stool Culture: negative early; positive after 2 weeks
Other Bacterial Agents of Inflammatory Diarrhea:

Campylobacter:
Virulence Factors:
o Flagella: motility through mucus layer of SI (multiplies in the mucus layer)
o Toxins: enterotoxin, endotoxin (LPS) and cytotoxin destroys intestinal cells (bloody diarrhea)
o Protein S: surface protein functioning as a capsule

Blocks complement binding

Causes serum resistance to phagocytosis
Etiology/Pathogenesis:
o Infective Dose: 500-1,000,000
o Transmission: most commonly associated with eating chicken (milk, water and other meats have also
been implicated)
o Incubation Period: 1-7 days
o
-
Symptoms:

Fever and malaise

Abdominal pain and cramps

Profuse watery or bloody diarrhea (due to mucosal inflammation)

PMNs in the stool
o Guillan-Barre Syndrome: auto-immune mediated attack on nerve tissue 1-3 weeks following infection

Demyelination occurs due to similarities between host myelin and the surface of
Campylobacter organism

Takes months to recover
Identification:
o Basics: motile, non-spore forming, comma-shaped Gram negative bacillus
o Lab Tests: oxidase positive
o Stool Sample: characteristic darting motility of organism
o Culture: selective media (will not grown on MacConkey even though it is Gram negative)

Incubate at 42 degrees C

Microaerophilic and capnophilic

Vibrio parahemolyticus:
Basics: halophilic (grows in brackish water) and contaminates seafood; major problem in Japan
Invasion: invades intestinal cells
Virulence: produces heat stable cytotoxin

Yersinia enterocolitica:
Carriage: carried by livestock (mainly pigs), rabbits and rodents
Transmission: contaminated food, water or blood products
Enterocolitis (Most Common):
o Bloody diarrhea, fever and abdominal pain (1-2 weeks; due to necrosis of Peyer’s patches)
o Mesenteric lymphadenitis (after invasion of terminal ileum; can cause abscesses and can mimic acute
appendicitis; most common in young kids)
Transfusion Related Septicemia: grows at lower temperatures and can multiply to toxic levels in refrigerated
blood stored for several weeks
Parasitic Invasive:

Entamoeba histolytica (Amebic Dysentery):
Virulence Factors:
o Life cycle: cyst stage (infectious stage; environmentally resistant) and trophozoite stage (invasive in
the tissue)
o Galactose-Specific Adhesion: adheres to luminal surface by galactose-inhibitable surface protein
o Proteolytic Enzymes: involved in the dissolution of ECM that anchors cells in tissue structure
o Cytolytic Enzymes
Etiology/Pathogenesis:
o Tranmission: cyst is ingested, and its wall breaks down in the SI; trophozoites form from the nuclei
and cytoplasm of the cyst (colonize the colon)
o Disease Process: begins upon invasion of mucosal surface

Erosion of mucosa begins at base of the crypts and progresses to ulceration

Ulcers can extend into the submucosa to produce flask shaped lesions

Although rare, trophozoites can also enter the venules in the colon wall to be carried to
extraintestinal sites (most commonly the liver- causing amebic liver abscess)
Identification:
o Microscopic examination of stool or colonoscopic sample

Irregular shedding of organisms in stool

Identification based on characteristic ultra-structure of cyst and/or trophozoite
MISCELLANEOUS INTESTINAL INFECTIONS:
Gastric and Duodenal Ulcers:

Helicobacter pylori:
Basics: major etiological agent of chronic gastritis and peptic ulcers; major risk factor for gastric cancer
Virulence Factors:
o Urease: converts urea to ammonia and CO2; protects it from stomach acid (allows bacteria to become
establish in the mucin layer in the stomach)
o Flagella: allow rapid penetration of the gastric mucus
o Cytotoxin and Mucinase: localized destruction of tissue; stimulate infiltration of inflammatory cells
Etiology/Pathogenesis:
o Major cause of ulcers: 90% of duodenal and 70-80% of gastric ulcers
o Pathogenesis: chronic type B gastritis (superficial and atrophic) with possible progression to
adenocarcinoma

Penetrates the mucus layer of the host and adheres to the gastric mucosa

Produces ammonia using urease to neutralize gastric acid

Proliferate, migrate and finally form infectious focus- results in development an ulcer by
destruction of mucosa, inflammation and cell death

Increase secretion of gastrin and gastric acid stimulated by infection promotes gastric
metaplasia
Identification:
o Basics: Gram negative curved bacillus
o Gastric Biospy: culture or urease test (CLO test)
o Special Media: enriched in 6-8% O2 (microaerophilic); incubate at 37 degrees C for 3-7 days
Food-Borne Bacteremia and Meningoencephalitis:

Listeria monocytogenes:
Basics: usually only cause infections in immunocompromised
Virulence Factors:
o Internalin: bacterial surface protein that induces phagocytosis (intracellular pathogen can then avoid
Ab-mediated defenses)
o Listeriolysin O (LLO): enables bacteria to escape from phagosome and avoid intracellular killing
o Actin Mediated Motility: enables the organism to spread from cell to cell (avoid Abs, complement and
neutrophils)
o Lipotechoic Acid (LTA): causes septic shock
Etiology/Pathogenesis:
o Ubiquitous: found in soil, decaying vegetation and fecal flora of many animals
o Only pathogenic Listeria species in humans
o Cause: most human infection is from food (raw vegetables, raw milk, soft cheeses, fish, poultry, and
meats)
o Immunocompromised: highest infection rates seen in infants, pregnant women (~30% of all cases) and
other immunocompromised individuals
o Incubation Period: 11-70 days (mean ~1 month)
o Disease Process:

Crosses the mucosal barrier through M cells in the intestine and enters the bloodstream

Healthy People: cleared by macrophages

Immunocompromised: hematogenous dissemination can occur to any site (particularly the
CNS and placenta)
 Can cause meningitis and still births/birth defects
Identification:
o Basics: Gram positive, facultative anaerobe, non-spore forming, motile at room-temperature, nonmotile at 37 degrees C
o Lab Tests: oxidase negative, catalase positive, beta-hemolytic
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Summary of Food Borne Disease:
Intoxications:
o Preformed Toxin: C.botulinum, S.aureus, B.cereus
o Toxin Formed in the Intestine: V.cholerae, E.coli (ETEC, EHEC), B.cereus, C.perfringens
Invasions: Salmonella, Shigella, Yersinia enterocolitica, Campylobacter, Listeria, V.parahemolytica
PARASITIC GASTROINTESTINAL HELMINTHS:
Nematodes (Round Worms):
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Ascaris lumbricoides:
Very common: found world wide
Transmission: eating viable eggs from feces-contaminated soil or food
Disease Process:
o Adults live in lumen of SI
o Larvae pass through lungs
Symptoms:
o Low Infestation: asymptomatic in most; can also cause GI upset, colic and loss of appetite
o Heavy Infection: adult worms ball up in SI and result in physical obstruction
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Enterobius vermicularis (pinworm):
Most common helminth: found world wide
Transmission: fecal-oral route (most common in children)
Disease Process:
o Adult lives in cecum
o Female deposits eggs at night in the perianal area, leading to perianal pruritis (severe itching)
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Ancylostoma duodenale and Necator americanus (hookworms):
Infects 24% of the world’s population
o Necator: worldwide tropics and North America
o Ancylostoma: temperate zones
Transmission: through the skin from infected soil or from drinking contaminated water
Disease Process:
o Adult lives in small intestines
o Larvae pass through the lungs
o Each worm can withdraw up to 0.2ml of blood/day
Cestodes (Tapeworms):
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Taenia saginata (Beef Tapeworm):
Worldwide distribution
Basics: inhabits the small intestine; adult is 3-10 meters in length
Transmission: occurs by eating uncooked beef
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Taenia solium (Pork Tapeworm):
Worldwide distribution
Basics: inhabits small intestine; can invade gut wall and migrate to various tissues (such as muscles or brain,
causing cysticeorocosis)
Transmission: occurs by eating uncooked pork