Vibrio cholera
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Motility - Single flagella, "vibrating" or "fast-moving"Adherence - Pili Mucinase Toxin - Cholera toxin, AB type, stimulates AC Etiology/Pathogenesis Rapid onset, 2-3 days after inoculationVomiting and massive watery diarrhea Dehydration and electrolyte loss Transmission Fecal-routeCarriers Avoid eating raw oysters Clinical ID Stool TCBS medium Oxidase + Test O Antigen Markers
Enterotoxigenic E. coli (ETEC)
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Adhesion - "colonizing factors" Pili Exotoxins - Heat labile toxin (LT) is an AB toxin, Heat stable toxin (ST) Etiology/Pathogenesis Contaminated food and drinksHighest incidence in tropics and young children Incubation period = 1-2 days Vomiting, weakness, dizziness, nausea, abdominal pain, watery diarrhea Transmission Fecal-Oral route Clinical ID ELISA Agglutination tests for presence of toxins DNA probes for LT or ST genes
Enteropathogenic E. Coli (EPEC)
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors "Bundle-forming pilus" "Effacement" Type III secretion Etiology/Pathogenesis Dehydration and electrolyte imbalance Fatal Malabsorptive diarrhea Transmission Fecal-oral route Daycare centers Always remember to wash hands! Clinical ID ELISA Multiplex PCR
C. botulinum
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Botulinal toxin, AB type Etiology/Pathogenesis Highly heat resistant Food, infant, wound botulism No diarrhea Prolonged recovery period Blocks presynaptic release of ACh Transmission Fecal-Oral Clinical ID Anaerobic Gram+, spore-forming bacillus Grow in oxygen-free lab environment Immuno assay for toxin in food, gastric substances or blood
Staphylococcus aureus
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Enterotoxin Heat stable toxins Etiology/Pathogenesis? Projectile vomiting, Nausea Stimulates neural receptors Diarrhea less common, no fever or chills Transmission Fecal-oral Clinica l ID Coagulase test, Catalase test, Beta-hemolytic test, Susceptibility test
Bacillus cereus
Virulence factors? Etiology/Pathogenesis? Transmission?
Emetic (vomiting) form Virulence factors Heat stable enterotoxin Etiology/Pathogenesis Rapid onset Short incubation period, 1-6 hoursN/V, abdominal cramps Transmission Ingestion of fried rice that has been cooked and left at warm temperatures for several hours Diarrheal form Virulence factors Heat-labile enterotoxinEtiology/Pathogenesis Slow onsetSevere abdominal cramps and diarrhea Activates inetstinal AC and causes intestinal fluid secretionTransmission Ingestion of meat or vegetable-containing foods that has been cooked and left above room temperature for several hours
C. perfringens
Virulence factors? Etiology/Pathogenesis? Transmission?
Virulence factors Enterotoxin Type A Etiology/Pathogenesis Abdominal cramps and watery diarrhea without fever, nausea, or vomiting Transmission Ingestion of temperature abuse of prepared food
Giardia lamblia
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Flagellated enteric protozoan - motility and attachment Adhesion to upper small intestine Etiology/Pathogenesis Incubation period of 7-10 days Watery diarrhea, abdominal cramps, bloating, flatulence, weight loss Chronic diarrhea with weight loss is less common Transmission Ingestion of food or water contaminated with cysts Clinical ID Microscopic exam of stool, duodenal aspiration, or duodenal biopsy Antigen test for G. lamblia in stool String test
Cryptosporidium parvum
Etiology/Pathogenesis? Transmission? Clinical ID?
Etiology/Pathogenesis Severe, watery, prolonged diarrhea in immunocompromised patients Mild diarrhea in immunocompetent patients Transmission Fecal-oral route Ingestion of oocysts in contaminated water Clinical ID Small coccidian protozoan parasites
Describe Microsporia spp.
Obligate intracellular, spore forming protists
What is the etiology/pathogenesis of Cyclospora cayetanesis?
Prolonged diarrhea (up to 7 weeks) and is more severe in AIDS patients
What is Isospora belli the most similar to clinically, and how does it present?
Giardiasis, cryptosporidiosis and microsporidiosis Diarrhea without blood or leukocytes Infects entire intestines More severe in AIDS patients
Clostridium difficile
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Enterotoxin - Toxin A, accumulation of viscous, bloody fluid Cytotoxin - Toxin B, disrupts actin polymerization and cytoskeletal architecture, decreases cellular protein synthesis Etiology/Pathogenesis "Antibiotic associated colitis" Asymptomatic, mild diarrhea or pseudomembranous colitis Transmission Endogenous or nosocomial Clinical ID? Spore-forming, anaerobic, Gram+ rod CCFA selective medium EIA test on stool
Enterohemorrhagic E. coli (EHEC)
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Adhesins - binds to mucosal cells Toxins - Shiga toxin, AB type toxin Type III secretion O, H, and K antigens Etiology/Pathogenesis Colonize the intestinal tracts of cattle (other farm animals) Small number of organisms can cause infection Incubation period : 3-4 daysSevere abdominal pain, copious watery, bloody diarrhea with little or no fever Transmission Ingestion of contaminated meat, milk, or apple cider Avoid eating rare or "bloody" hamburger meat Clinical ID Serotype O157:H7 does not ferment sorbitol Serogroup with specific anti-O157:H7 serum Cytoxic activity with Vero Cells DNA probe for detection of Shiga-toxin genes
Shigella
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Invasion - Attach to M cells on apical surface Type III secretion "Actin-based" motility Bacillary dysentery, invasion of intestinal mucosa Etiology/Pathogenesis Cause inflammatory response - loosening of tight junctions, follow PMNs between cells and make their way to basolateral surfaceSpread from cell-to-cell Remains at mucosal layer Bacillary dysentery (blood and mucus in stool) Highly infectious Serogroups - Group A (S. dysenteriae ) is largest producer of toxin, Group B (S. flexneri ), Group C (S. Boydii ), Group D (S. sonnei ) is most common Multiply in small intestine 0-12 hrs : abdominal pain, cramping, and fever12-72 hrs : No longer detectable in upper intestine, fever decreases, but pain becomes more severe and localizes to lower quadrantsTransmission Person-to-person Clinical ID Non-motile Gram- bacilliLactose negative colonies on MacConkey or Hektoen selective media Oxidase negative Serotyping of groups
How is Enteroinvasive E. coli (EIEC) distinct from Shigella ?
Similar to Shigella , but does not produce any Shiga toxin; spreads cell-to-cell
Salmonella
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Adherence and Invasion - invades M cells and epithelial cells Type III secretion - actin rearrangement, "ruffling" of mucosal membrane, engulfed and multiply inside vesicle Endotoxin - Lipid A of LPS, invades and causes systemic infection O and H antigens Etiology/Pathogenesis Large inoculum needed Replictates inside vacuole of mucosal cells Gastroenteritis, bacteremia, enteric fever (typhoid fever) Exits cells via basolateral side and is picked up by macrophages (and dendritic cells), entering the blood stream Systemic/Septic Transmission Ingestion of food (poultry meat or eggs) that is contaminated with eggs, eating "raw" cookie dough Clinical ID Motile, facultative anaerobic, non-spore forming, Gram- bacilli Gastroenteritis - stool cultures Bacteremia - blood and stool cultures Typhoid fever - blood culture (early stage), Stool culture (late stage)
Campylobacter
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Flagella Enterotoxins, endotoxins (LPS) and cytotoxins Protein S - capsid Autoimmune-mediated attack against nerve tissue Etiology/Pathogenesis ID of 500-1,000,000 Fever, malaise, abdominal pain and cramps Profuse watery and/or bloody diarrhea, mucosal inflammation Incubation period : 1-7 daysVariety of syndromes Transmission Ingestion of contaminated chicken, milk or water Clinical ID Small motile, non-spore forming, comma-shaped, Gram- bacilli Oxidase positive Gastroenteritis - stool smear Selective medium culture Microaerophilic and capnophilic
Describe Vibrio parahemolyticus in terms of transmission, virulence and location prevalence.
Transmission - Ingestion of contaminated food Virulence - Invades intestinal cells, produces heat stable cytotoxin, halophilic ("salt loving") Location prevalence - Japan
What is the most common Yersinia enterocolitica infection and describe its etiology/pathogenesis and mode of transmission?
Enterocolitis is most common Yersinia enterocolitica infection Etiology/Pathogenesis Bloody diarrhea, fever, abdominal pain Duration : 1-2 weeksMesenteric lymphadenitis, most common in children Transfusion-related septicemia, grows at lower temperatures and can multiply to toxic levels in refrigerated blood stored for sevral weeks Transmission Ingestion of contaminated food, water or blood products from livestock, rabbits, and rodents
Entamoeba histolytica (amebic dysentery)
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Cyst stage Trophozoite stage Adherence to luminal surface of bowel Proteolytic (Cytolytic) enzymes Etiology/Pathogenesis Found worldwide Life cycle : ingestion of cyst and breakdown of cyst wall in small intestine > trophozoites colonise colon > erosion of colonic mucosa beginning at base of crypts > trophozoites may enter venules of colon wall and be carried to liver and lead to amebic liver abscessTransmission Ingestion of cysts Clinical ID Microscopic exam of stool Irregular shedding of organisms in stool Cyst and/or trophozoite ultra-structure
Helicobacter pylori
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors Urease, converts urea to ammonia and carbon dioxide Flagella Cytotoxin and mucinase Etiology/Pathogenesis Stomach colonization Duodenal and gastric ulcers Chronic Type B Gastritis, may progress to gastric adenocarcinoma Transmission? Fecal-oral route Clinical ID Small Gram-, microaerophilic, curved bacilli Enriched medium in 6-8% oxygen at 37 degrees Celsius Incubation period : 3-7 daysGastric biospy for culture Urease test (CLOtest)
Listeria monocytogenes
Virulence factors? Etiology/Pathogenesis? Transmission? Clinical ID?
Virulence factors? Bacterial surface protein (internalin) Listeriolysin O (LLO) Actin-mediated motility Lipoteichoic acid (LTA) Etiology/Pathogenesis? Decreased motility at room temperature and non-motile at 37 degrees Celsius Ubiquitous in nature Highest infection rate in infants, or in patients with lypmhomas, AIDS, organ transplantations, or those receiving corticosteroid therapy Pregnant women account for about 30% of all cases Incubation period : 11-70 daysCrosses mucosal barrier and enters bloodstream through M cells Transmission? Ingestion of contaminated soil, decaying vegetation and fecal flora of animals, raw foods Clinical ID? Small, facultatively anaerobic, non-spore forming Catalase positive, oxidase negative, beta-hemolytic, Gram+ bacillus
What are the preformed intoxicating food borne infections?
C. botulinum B. cereusS. aureus
C.B.S.!
What are the intoxicating food borne infections that are formed in the intestine?
V. cholerae B. cereusE. coli (ETEC, EHEC) C. perfringens
V.B.E.C.!
Ascaris lumbricoides
Etiology/Pathogenesis? Transmission?
Etiology/Pathogenesis Larval stages passes through lungs, adults inhabit lumen of small intestine Asypmtomatic in low infestation, or may experience GI upset, colic or loss of appetitie Heavy infection the adults ball up in small intestine and cause obstructionVery common, found worldwide Transmission Ingestion of viable eggs from contaminated soil or food
Enterobius vermicularis (pinworm)
Etiology/Pathogenesis? Transmission?
Etiology/Pathogenesis Worldwide distribution Most commone helminth Lives in cecum Female deposits eggs at night in the perineal area Severe itching of the perianal area Transmission Fecal-oral route
Ancylostoma duodenale and Necator americanus (hookworms)
Etiology/Pathogenesis? Transmission?
Etiology/Pathogenesis Infects 24% of world's population Larvae pass through lungs, adults live in small intestines Withdraws up to 0.2 ml of blood/day Necator is found in worldwide tropics and N. AmericaAncylostoma is found in temperate zonesTransmission Through skin from infected soil or from drinking contaminated water
Taenia saginata (beef tapeworm)
Etiology/Pathogenesis? Transmission?
Etiology/Pathogenesis Adult is 3-10 meters in length Inhabits small intestine Worldwide distribution Transmission Ingestion of uncooked beef
Taenia solium (pork tapeworm)
Etiology/Pathogenesis? Transmission?
Etiology/Pathogenesis? Inhabits small intestine Invade gut wall and migrate to various tissues Can cause cysticerocosis Transmission? Ingestion of uncooked pork
What are the 8 ways in which the GI tract protects itself from invading organisms?
1) Stomach acid 2) Bile salts 3) Rapid flow through the small intestine 4) Secretion of sIgA 5) CD4+ T cells 6) Macrophages 7) Dendritic cells 8) Production of mucus
Which family of Gram- bacilli is the only one that is negative for oxidase?
Enterobacteriaceae
Which family of Gram- bacilli is the only one that will not grow in MacConkey agar?
Campylobacteriaceae
Which family of Gram- bacilli is positive for oxidase, grows in MacConkey agar, and has fermentative metabolism?
Vibronaceae
Which family of Gram- bacilli is positive for oxidase, grows in MacConkey agar, and has oxidative metabolism?
Pseudomonadaceae
In the oxidase reaction of cytochrome C, what gets reduced? Oxidized?
Water gets reduced; cytochrome C gets oxidized
What color should lactose fermentors appear on a MacConkey agar plate?
Pinkish-red
What color should lactose non-fermentors appear on a MacConkey agar plate?
Clear
Compare and contrast oxidative, fermentative, and inert metabolism.
Oxidative Use oxygen as terminal electron acceptor Fermentative Use an element other than oxygen as a terminal electron acceptor Inert Do not produc acid from carbohydrates
Which of the following cause bacterial enterotoxigenic secretory diarrhea:
A) E. coli
B) G. lamblia
C) C. parvum
D) B. cereus
E) C. botulinum
F) S. aureus
G) V. cholera
H) Shigella
A) E. coli B) Shigella C) V. cholera
Which of the following cause bacterial neurotoxic secretory diarrhea:
A) V. cholera
B) Shigella
C) G. lamblia
D) S. aureus
E) C. parvum
F) E. coli
G) B. cereus
H) C. botulinum
H) C. botulinum E) B. cereus F) S. aureus
Which of the following cause non-inflammatory parasitic secretory diarrhea:
A) C. parvum
B) Shigella
C) C. botulinum
D) B. cereus
E) G. lamblia
F) E. coli
G) V. cholera
H) S. aureus
E) G. lamblia H) C. parvum
What is the infection progression of G. lamblia ?
Ingestion of cysts (ID <10) > trophozoites released in duodenum > attachment via sucker disk > reproduction via binary fission > may revert to cyst and shed in stool
Compare and contrast gastroenteritis, bacteremia and enteric fever (Typhoid fever) caused by Salmonella .
Gastroenteritis Most common form Mild diarrhea to fulminate, low grade fever, N/V/D Incubation period : 8-48 hrsAbrupt onset Duration : 2-5 daysBlood cultures (-) Stool cultures (+) Bacteremia RARE, develops after gastroenteritis, high spiking fever, maybe GI symptoms (not common), 2nd infection can occur anywhere Incubation period : variableOnset and duration are variable Blood cultures (+) Stool cultures (-)/(+) Enteric fever (Typhoid fever) Most severe Salmonella infection Infection cycle : invade macrophages in lamina propria > replicate in membrane-bound vacuoles > reticuloendothelial system, blood stream > other organs > re-enter intestinal tract > sepsis develops after 10-14 days > intetstinal symptoms develop after re-entry into intestinal tractIncubation period : 7-20 daysInsidious onset Gradual increase in fever then hits a plateau Duration : weeksEarly sonstipation; late diarrhea Blood cultures (+) at weeks 1 and 2 Stool cultures (-) early stage, (+) late stage