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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 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): 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 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) 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): Taenia saginata (Beef Tapeworm): Worldwide distribution Basics: inhabits the small intestine; adult is 3-10 meters in length Transmission: occurs by eating uncooked beef 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