Yu- GI Bacteria X4- Melissa** Flashcards
How many species of bacteria colonize the human GI tract?
How was this determined?
1000 different species in human gut (determined by 16s rRNA sequencing)
How many species of bacteria colonize the human BODY?
100 trillion (10^13) bacteria in human body (more bacteria than human cells)
How does the micro biome shift between healthy patients and patients with bowel disease? (2)
- # pathogenic ‘proteobateria’ like e. coli ^ in patients with IBD + Necrotizing enterocolitis
- patients with DM2 have more bacteriodetes
What is the function of the microbiota in the GI tract?
What is one factor that can dramatically change GI microiota?
Describe the layers of the GI tract from the lumen outward.
- Microbiota identified by immune system as non-foreign early in life; Provides barrier to colonization by foreign bacteria
- Microbiota dramatically changed by ABX use
- Microbiota–> Mucus layer–> Epi–> Mucosa
Three important bacteria in the stomach microbiome
- Lactobacillus
- Streptococcus
- H. pylori (associated with PUD)
Two important bacteria in the duodenum and jejunum microbiome, also found in standard probiotics?
- Streptococcus
- Lactobacillus
How does the micro biome change at the point of the ileum through the colon?
- *Overall increase in # of species
* *Overall increase in anaerobic species (Clostridium, Bacteroides, etc)
In the colon, what is a vital function of the microbiome outside the realm of immunologic defense?
**Many anaerobes that ferment polysaccharides and oligosaccharides (used by epi cells)
Segmented Filamentous Bacteria (SEM): What are these bacteria and what purpose do they serve?
- Spore forming anaerobic bacteria (like clostridium)
- Live in mucus layer on top of lymphoid tissue
- Enter M cells; Stimulate B and T cells to induce maturation of T17 cells; modulate gut immunity in animal models
4 mechanisms of bacterial gastroenteritis:
Also: what is the point of methylene blue staining of poop?
1) Toxin mediated (endo/exo)
2) Superficial invasion local inflammation
3) Deep invasion of blood or lymph
4) Mechanical trauma +/- abscess
Methylene blue: detects leukos in poop; + in INVASIVE diarrhea
(Shigella, salmonella, campy)
H. Pylori:
Gram/ motility/ O2 ?
Oxidase and Catalase present or absent?
Optimal pH?
Gram (-) curved rod Motile (unipolar flagella) Microaerophillic Oxidase, catalase, and ALK phos + Lives at pH 7--> 8; dies at pH 4.
H. pylori: 6 important virulence factors
- Sheathed flagellae
- Urease (+) –> ^ NH3, neutralize stomach acid
- VacA (vacuolating toxin)
- CagA (pathogenicity gene islands, passed bw strains)
- Phospholipase
- Protease
How common is H. pylori infection?
How does H. pylori induce infection?
What are 4 possible sequelae of H. pylori infection?
1 stomach infection
Normal microbiota overgrowth in mucin layer–>
Adhesion + cytotoxin–> Gastric atrophy–>
Class I carcinogen
1) Chronic gastritis
2) Peptic Ulcer Disease
3) MALT Lymphoma
*will shrink with irradication of the pathogen
4) Stomach Adenocardinoma
E.Coli/ EHEC (O157H7):
Gram/ MacConkeys/ Fermentation? Disease?
ETEC:
Fermentation and disease?
Gram (-) rod Pink = MacConkey’s EHEC: (Lactose +, Sorbatol -) Bloody diarrhea and HUS ETEC: Lactase and sorbitol fermenting; watery diarrhea
E.Coli/ EHEC (O157H7): most importnat virulent factor?
-Shiga Like Toxin (SLT) on phage stops protein synthesis
E.Coli/ EHEC (O157H7): Mechanism of infection and sequelae of disease (3)
Ingest LOW infectious load in undercooked meet–> Attachment-Effacement in Large intestine = ruffling of membranes–>
Bacteria make SLT–>
SLT penetrates cells–>
Pediatric Hemorrhagic colitis +/- HUS +/- Renal failure
***EHEC DOES NOT enter the cell; other e. coli might…
Shigella:
Gram, McConkeys, fermentation, motility?
Gram (-) rod
White = MacConkey’s
(Lactose -; produces no gasses)
Nonmotile
NO GAS. NO FERMENTATION. NO MOBILITY.
Two important shigella virulence factors:
- Shiga Toxin (Binds GB3-R,cleaves 28s rRNA in 60s subunit)
- Type III secretion system
Pathogenesis of shigella gastroenteritis + sequelae of disease? Which population is infected?
INVASIVE.
#1 effective GI pathogen (similar to invasive e. coli)
Type III secretion system–>
Membrane ruffling–>invades M cells in Colon–>
Cell to cell spread via actin tail–>
Mucosal abscess/cell–>
Host cell apoptosis–> Pediatric Dysentery
Dx/ Tx/ Px for shigella infection?
Dx: Methylene Blue stain of feces
Tx/Px: FLUIDS +/- FQN (Cipro) for close contact px
Salmonella Typhi/Paratyphi: gram?
Gram (-) rod
Salmonella Typhi/Paratyphi: Invasive or non-invasive? Gasses produced? Fermentation? 3 virulence factors? Intracellular or Extracellular? How common?
- Invasive
- H2S (+); no fermentation
- O, H Antigen, Vi Capsular antigen
- Facultative intracellular
- Salmonella: #1 food borne infection
Describe the pathogenesis of typhoid (enteric) fever induced by salmonella typhi infection:
6-30 days incubation–>
Endocytosis by M cells of Peyers Patches
–> MQs in Liver, GB, spleen–>
Intracellular proliferation + septicemia–>
Flu sx +/- rose spotted rash; Bloody, watery diarrhea–> Asx. Carrier state (phagosomes of MQs)
Describe the pathogenesis of enercolitis induced by salmonella typhi/paratyphi infection:
Fecal Oral w ^ infective dose–>
INVADES epi/subepi of intestines–>
PMN response–> Infection limited to gut
Asx. Carrier state (phagosomes of MQs)
How do we treat salmonella infection?
ABX + symptomatic relief
S. Typhii vaccine moderately effective (short lasting immunity)
C. Difficile:
Gram, spore, MacConkeys, fermentation, O2?
Gram (+) Spore former White = MacConkey’s (Lactose -) Strict Anaerobe
C. Difficile: most important virulence factor?
Toxin production
Enterotoxin A: neutro chemotaxis
Cytotoxin B: depolymerization of actin
Describe the two mechanism of C. diff infection.
How is the infection treated?
1) Nosicomial SPORE ingestion
2) ABX (originally Asstd w clynda)–> kill normal flora–> C.diff overgrowth
Tx: Metronizazole then Oral Vanc; Relapse is common, give poop in a pill
Campylobacter Jejuni:
Gram, shape, O2, Motility, catalase, oxidase, urease, growth temp?
Gram (-) Small, comma shaped Microaerophilic Motile Catalase (+) Oxidase (+) Urease (-) 42 C
Campylobacter Jejuni:
Mechanism of infection and sequelae of disease in immunocompromised vs. immunocompetent host?
Ingestion of contaminated + undercooked chicken–> Invades Illeum Colon (like salmonella)–>
Immunocompetent Host:
Ulcerative Gastroenteritis; Bloody, watery diarrhea +/- Abscess**
Immunocompromised Host: Guillian Barre
Treatment for campylobacter jejuni infection:
Tx: Self limited in mmunocompetent hosts (fluids);
Erythromycin = DOC ; Aminoglycosides if disseminated
Possible non-GI sequelae of campylobacter jejune infection?
Associated with Guillian Barre Syndrome: common cause in young adults
(I have had this question multiple times on RX! Me too!!)
Yersiniae entercolitica + Yersiniae Pseudoptuberculosis:
Gram, MacConkeys, Lactose, O2, Temp, Oxidase?
Gram (-) rod White= MacConkey’s (Lactose -) Facultative Anaerobic; likes cold Oxidase (-)
Yersiniae: 2 virulence factors
- Plasmids w virulence
- Protein capsule in Y. PESTIS
Yersiniae entercolitica + Yersiniae Pseudoptuberculosis: Describe the three manifestations of infection?
In which geographic regions is this infection more common?
Y. PESTIS infection?
*Infections more common in colder regions
1) Entercolitis similar to Shigella or Salmonella (bloody)
2) Mesenteric adenitis (presents like acute appendicitis)
3) Intestinal abcesses (Acute = pesudotuberculosis; Chronic= entercolitica)
PESTIS: plague
Foodborne Outbreak Defined:
2+ individuals develop similar sx. After ingesting common food (Mary Hanks and Melissa Saab go to cookout, eat a burger, almost die on the same day…)
Incubation clues: How is timing relevant to dx pathogen?
What is the most common food borne illness in US?
- > > 15 hrs viral; remember intracellular pathogens
Most common foodborne illness in US is salmonella; remember this bc the chicken industry is disgusting.
Common Contributing factors to food borne illness (3)
- Industrialization of food prep/ widespread distribution of food
- Improper storage 97%
- Dirty handlers
Three Mechanisms to induce Gastroenteritis:
- Attachment-effacement and interfere w secretory/ absorbance in gut
- Enterocyte invasion
- Invasion of MALT (i.e. M cells MQs)
V. Cholerae O1, O139 (El tor, Cholerae):
Gram, O2, Fermentation, Oxidase, Motility, Habitat?
- Gram (-), comma shape
- Facultative anaerobe
- Fermentative
- Oxidase (+)
- Motile (single flagella)
- Salt or Fresh H2O; requires low pH
What are the two LPS-O Ags asstd. with the v. cholera infectious to humans?
Which is encapsulated and can form biofilm?
- LPS O-Ags (O1, O139)
- Capsule = O139
What is the most important virulence factor to v. cholera? List 6 others.
1= AB Cholera toxin (CTX)= highly infectious; acid stable, resistant to intestinal motility
- Some hemolytic strains
- (Cfa) Colonization Factor
- (Tcpa) Toxin Regulated Pilus
- (LTA) Labile Toxin
- Adenyate cyclase
- Hemagluttinin
Describe the MOA for CTX: What kind of toxin is this?
AB toxin; highly infectious
B domain binds ganglioside on sm. intestine enterocyte–>
A1 (Active domain) enters cytoplasm–>
ADP ribosylates Gs protein–>
Activates adenylate cyclase–> ^ CAMP–>
^ NaCl absorption, Cl + HCO3- secretion–>
^ Volume H2O in lumen–>
**Sudden onset, MASSIVE Secretory Diarrhea–> Dehydration, acidosis, shock–> DEATH
How much bug is required to cause v. cholera infection?
Describe the characteristic stool.
What can make infection worse?
How do we treat the infection?
Contaminated water ingested w/ HIGH INFECTIOUS LOAD
**Stool characterized as “ricewater” diarrhea w flakes of mucus and infectious bacteria content
**Worse in patients with LOW gastric acidity (need lower infectious dose)
Treatment: Supportive ONLY; oral or IV rehydration + electrolyte replacement
Vibrio vulnificus: Gram?
How does one become infected and what kind of infection does this bug cause?
Gram (-)
Ingest undercooked shellfish or contaminate open wounds while swimming/ cleaning shellfish–>
Rapidly progressive WOUND (swelling/ erythema/ pain vesicles/ bullae–> TISSUE NECROSIS +/- septicemia)
w/ 50% mortality rate!!!
Vibrio parahaemolyticus: Gram?
How does one become infected and what kind of infection does this bug cause?
Which patient populations are vulnerable?
- Gram Neg
- People eat this in sushi on the northern coasts
Problematic for immunocompromised + patients with liver disease gastroenteritis or wound infections
(less severe than v. vulnificus)
Bacillus cereus: Gram, O2, motility?
Gram (+) spore former
Aerobic
Motile
Bacillus cereus: 4 virulence factors
- Lecithinase (PLC)
- Enterotoxins (exotoxin)
- Necrotic toxin (heat labile, permeability)
- Cereolysin (hemolytic disruption of cholesterol cell membrane
Bacillus cereus: Infection caused and how is it treated?
“Bacillus cereal”—you get this from ingesting spores in reheated rice/ grains
1) Emetic or diarrheal food poisoning
2) Eye infections
* *Treat with fluid/ electrolyte replacement if necessary
S. Aureus:
Gram, motility, O2, Fermentation, Catalase, Coagulase, Characteristic growth on agar, where does it colonize on human body?
Gram (+) cocci Nonmotile Facultative Ferments mannitol + glucose Catalase (+) Coagulase (+) Golden yellow on agar Colonizes the nares
List the enterotoxins + one other virulence factor associated with S. aureus; which enterotoxin is most common?
Enterotoxins: #1= A -B, causes enterocolitis (rare) -C, contaminated dairy -D, contaminated dairy -E, contaminated dairy
Other:
TSS—not food Asstd.
Describe the pathogenesis of food poisoning caused by s. aureus; what other diseases can this organism cause?
Causes many suppurative infections, food poisoning, TSS
Ingest bacteria–> 4hr mean incubation–>
Enterotoxins A-E Interact w/ brain vomit center, inhibit H2O absorption in intestine, superAg induction of IL-1–>
24hr n/v/ non-bloody diarrhea (+) cramping, (-) fever
V. Cholerae: pathogenesis of infection + sequelae of disease
Contaminated water ingested–>
Bacteria produce toxin–>
Toxin adheres to epi in Small intestine–>
Secretory Diarrhea w/ leukos (rice water)
What are two treatments for H pylori infection?
What is the most prominent ADR?
1 –> Proton pump inhibitor w/ Clarythro + Amox or Metranidazole 7 days
Tx: ADRs = Diarrhea
*** NOTE: SATATNam has her own version of treatment for H pylori, and since she does pharm, to avoid confusion, I would learn hers. They’re similar.
