GI Infections - Diarrhea Flashcards
Why does diarrhea kill?
Immediate: Fluid and electrolyte imbalance
a) Fluid loss - impacts children much more so due to their lower blood volume
Delayed: Malnutrition
a) Increase flow of nutrients (not being able to be absorbed)
b) Inflammation of the absorptive mucosa - no exchange
c) repair mechanisms: no proteins being absorbed = no repair mechanism = leads to further malnutrition
What is the association between Diarrhea and Malnutrition?
1) Increased Energy Loss:
a) Diarrhea and vomiting - energy expensive processes
b) Increased metabolic needs - due to immune response]
2) Decreased Intake
a) absorptive processes not functional - inflammation?
b) With-holding of food: the thought that food/breast milk caused the diarrhea (Breast milk is a good mechanism to help with diarrhea)
Where does the majority of fluid uptake occur?
In the small intestine (upto 8.5 L / day). It also secretes water.
What role does the LI have in water reabsorption?
Absorbs the remaining water from the SI - approx 1.5L. It also has a reserve capacity (5L).
How do the rates of absorption differ between the SI and LI?
Small Intestine - faster rate of absorption
Large Intestine - slower rate of absorption
What kind of diarrhea do you get if the origin is in the SI? LI?
SI - diffuse watery diarrhea, high frequency; overwhelms the reserve capacity of the LI.
LI - small amounts of water, usually a dysentery - blood, pus, mucus
What kind of bacteria/virus/protozoa diarrheal distribution do you seen in: developing vs developed countries?
- Developing: bacteria>viral>protozoa
2. Developed: viral>bacteria>protozoa
Name the Diarrheal Syndromes:
NDF TPH CE
Non-specific Gastroenteritis, Dysentery, Foodborne, Traveller’s, Pseudomembranous Colitis, Hemmorhagic, Cholera-Like, Enteric Fever
Name the 2 types of Dysentery and their causes
- Bacillary Dysentery: Shigella Dysenteria/EIEC
2. Amoebic Dysentery: Amoebia Histolytica
What are the prominent causes of food borne ill-ness?
S2V2C3 BELY
Salmonella (most common cause), Staph. Aureus (S.Ag), Vibrio Cholera, Viruses (Nora/Rota), Ciguatoxin (fish), Clostridium, Campylobacter (Chicken), Bacillus, EHEC, Listeria Yessinia
How does Salmonella act? Where is it found?
Salmonella: Type 3 secretory pathway –> actin modification
Found in uncooked meats, protected by creamy products
How does Staph. Aureus Act? How is it found in food?
Produces an enterotoxin that is a super antigen. Usually preformed in foods. Acts on the CNS to cause diarrhea and vomiting. Some action on the gut.
How does Rotavirus Function?
Disrupts the microvilli
How does Vibrio Cholera Function?
enterotoxin activates Gs → diarrhea
Where is Camplyobacter found?
Zoonosis: carried by chickens. Can be contaminated after cooking – if placed on the same cutting board.
How does Ciguatoxin function? Where is it found?
not infective, found in fish, lowers the threshold of the sodium gated voltage channels → leading to paralysis
How does Clostridium function?
Spores are ingested - sporulation - toxin release
How does Bacillus function?
Produces a toxin similar to cholera toxin.
What is EHEC? Where is it found? What is its infective dose?
- Carried by cows, fecal content not destroyed due to improper cooking technique
- Low infective dose –> small number of bacteria needed to cause an infection.
What agents cause Traveller’s Diarrhea?
50% of traveller’s diarrhea is caused by ETEC
What is pseudomembranous colitis? What causes it? How is it caused? What toxins are involved?
i. Severest form of antibiotic associated diarrhea
ii. 20 – 33 % of the population get diarrhea due to antibiotics. Could be due to the disruption of the protective microflora OR toxic effects of the AB.
iii. C. Difficile (found in 3% of the population) takes advantage of the lack of microbiota.
iv. Produces Toxin A → binds to the brush border and Toxin B → cystoskeleton disruption leading to pseudomembranous colitis.
What is Hemmorhagic colitis? What causes it? How is it caused? What toxins are involved?
EHEC, Shigella Dysteria
i. EHEC produces Shigella Toxin
ii. The stool contains mostly blood with minimal amounts of pus and mucus.
iii. Shigella can produce both dysentery and H. colitis; the other 3 shigellas only produce dysentery
iv. Shigella: Chromosomally encoded toxin
v. EHEC: plasmid encoded (phage infects the E.Coli with shiga gene)
What is the difference between Shigella and EHEC?
Shigella: Chromosomally encoded toxin
EHEC: plasmid encoded (phage infects the E.Coli with shiga gene)
What is Cholera Like Diarrhea? What causes it? How is it caused? What toxins are involved?
i. Vibrio: epidemic cholera caused by O1 and O139. O2-O138 are serotypes that don’t cause epidemics.
Vibrio Choleri: Phage encoded toxin
ii. Non-Vibrio: ETEC
How is the toxin encoded in vibrio cholera?
Phage encoded toxin
How are the different E.coli distinguished?
Different virulence factors
What virulence factors are found on EPEC? How does it illicit its pathogenicity?
Bundle Forming Pili (BFP), intimins, Translocated Intimin Receptor
a. Attachment/Effacing Pathway: attachment to microvilli, actin deformation, malformation of the microvilli
b. Stage 1: Plasmid mediated: BFP allows for attachment at the microvilli
c. Stage 2: Chromosomally mediated: LEE – Pathogenicity Island
• Type 3 Secretory System: secretes TiR into the host cell via a bridge into the bacteria→ intimin binds to TiR → change in actin cytoskeleton → tight binding
What virulence factors are found on EHEC? How does it illicit its pathogenicity?
a derivative of EPEC, intimins, Shiga Toxin
What virulence factors are found on ETEC? DO they invade the mucosa?
Colonization Fimbrial Adhesions (CFA)
a. Attach to the mucosa, don’t invade, secrete enterotoxins:
• LT: labile
• ST: heat stable: increase cAMP → H20 secretion
What virulence factors are found on EIEC? How does it illicit its pathogenicity?
Shigella like pathogenesis, IpaC
a. Plasmid encoded genes promote endocytosis → cleavage within the endosome → bacteria does damage internally
Which bacteria are:
i. Adhesive enterotoxigenic:
ii. Adhesive with brush border:
iii. Invasion restricted to mucosa:
iv. Invasion of Submucosa:
v. Systemic Invasion:
i. Cholera/ETEC: no invasion
ii. EP/HEC – intimin
iii. Shigella (cell to cell mvmt)
iv. Salmonella, Campylobacter
v. Salmonella
