Final; Toxin-Producing Pathogens of Mucosal Surfaces Flashcards by Courtney Kast

What are the symptoms of a toxin producing bacterial invasion

copious amounts of watery stool
no blood in stool
no leukocytes in stool
no tissue damage

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Where in the intestine are the toxin producing bacteria

small intestine

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What are the species of vibrio

V. cholerae; cholera
V. parahaemolyticus; dirrhea
V. vulcificus; tissues and blood
V. alginolyticus; tissues and blood

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True or False

V. cholera are highly motile

True

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What are the two typs of cholera

nonpathogenic and pathogenic

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What is the strain of cholera that emerged in 1992

a “new” El Tor

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What is specific about the new El Tor strain

mutated O antigen
new LPS serotype
now encapsulated
affected all age groups

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What are three virulence factors of V. cholerae

flagella
pili to adhere to mucosal tissues
cholera toxin; phage encoded

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What causes the expression of pili and toxin in V. cholerae

a shift from saltwater to reduced ion levels found in the body

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What does the cholera toxin do to the cells

it enters through epithelial cells
activated adenylate cyclase
forming cAMP
which turn off adenylate cyclase
but the toxin produces negative feedback causing cAMP to build up
lots of cAMP causes the cell to stop absorbing Na and secreting Cl drawing the water to the intestinal lumen
watery stool

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How many different strains of E.coli are there

thousands; but many are commensal

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These strains of E.coli cause secretory diarrhea

ETEC (enterotoxigenic E.coli)

EPEC (enteropathogenic E.coli)

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This strain of E. coli cause dystenery-like symptoms

EHEC (enterohemorrhagic E.coli)

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This strain of E.coli causes urinary tract infections

UPEC (uropathogenic E.coli)

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This is responsible for 30-45% of cases of traveler’s diarrhea (when traveling to Mexico)

ETEC

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ETEC requires what kind of infectious dose

large

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What helps ETEC adhere to mucosal tissues

colonization factor antigens (cfa) on fimbrae

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What toxins does ETEC produce

heat-labile toxin (LT)

heat-stable toxin (ST)

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What are the similarities and differences of the ETEC colonization of cells to cholera

same pathway with adenylate cyclase but uses cGMP and guanulate cyclase

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What is the first step in diagnosing secretory diarrhea agents

rule out V. cholera with tests like;
inoculation of plates
tiosulfate-citrate-bile-sucrose agar
aerobic incubation kills anaerobes

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What are the treatments for secretory diarrhea

oral rehydration; mix or sugar and salt

antibiotics can help shorten the duration/severity

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What are considered the hybrid “misfits” where they do not fall into either the toxin producing or invasive pathogens

EPEC

EHEC

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What does colonization of the hybrids do

causes attaching and effacing lesion; reorganization of epithelial cells

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What is special about the stool following a EHEC infection

blood in still (and possible the urine)

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This infection is prevalent in newborns

EPEC

What type of diarrhea does EPEC cause

noninflammatory secretory diarrhea

Where in the small intestine does EPEC infect

distal small intestine

Does EPEC require a small or large infectious dose

large

What is characteristic of the exotoxins of EPEC

there is an absence of traditional exotoxins

What type of lesion does EPEC cause

characteristic intimate adherence pattern (an attaching and effacing lesion)

What is the first stage of intimate adherence by EPEC and EHEC

bundle-forming pili (bfp) assist in adherence from relative long distance; like a "syringe"

What is the second stage of intimate adherence by EPEC and EHEC

syringe-like secretion system (called type III secretion) injects Tir (translocated intimin receptor) into host cell

What is the third stage of intimate adherence by EPEC and EHEC

Tir bind to intimin on E.coli resulting in pedestal (receptor) formation

What is the overall goal of intimate adherence

to inject the receptor into host cell and the host cell expresses the receptor binding the E.coli to the cell

What causes diarrhea due to EPEC

no toxin but malabsoprtion due to microvili disruptions and of epithelial tight junctions

EHEC has a set of genes which does what

EPEC genes (eae genes) which produces an attaching effacing lesion and a toxin that can lead to uremic syndrome

What is the notorious E.coli of EHEC

O157:H7; primary reservoir is cattle

O157:H7 causes what

attaching effacing lesion (gastroenteritis) | produces a shiga-like toxin causing hemorrhagic colitis and hemolytic uremic syndrome

Shiga-like toxins attack where

heavily vascularized mucosal surfaces like small intestine

How would you diagnose EHEC

clinical manifestations easily recognized; bloodily stool and edema of ascending colon EHEC cannot ferment sorbitol detection of shiga-like toxins

Why would you not use antibiotics to treat EHEC

It makes the toxin more potent by killing the microbes which will release more toxins like LPS and stimulating inflammation

What treatment would you use to treat EHEC

supportive therapy; rehydration if necessary | dialysis of HUS pending

This is the most common form of bacterial infection of an organ system (not including the mouth) and it is also the most frequent cause of physician visits by adults

urinary tract infection

What is cystitis

inflammation of the bladder

When do males usually get UTIs

When the prostate in inactive; early and later in life

What is an uncomplicated UTI

all normal defense mechanisms are intact no recent hospital admissions disease limited to lower urinary tract

What is a complicated UTI

some structural abnormality in urinary tract (immunosuppressive, etc.) recently admitted to hospital disease most likely will spread to kidneys

What are the natural defenses found in the urinary tract

``` complete voidance of bladder peristalsis ureterovesicle valves mucous layer normal microbiota (Lactobacillus spp.) pH ```

UTI can spread to the kidney and cause what

pyelonephritis retorgrade flow of urine from bladder to kidney can be caused by urethral catheters

What bacteria cause urinary tract stones

Proteus spp. it neutralizes pH and causes formation of "struvite" calculi

How does UPEC adhere to uroepithelial cells

through fimbriae | acute cystitis and pyelonephritis are associated with fimbriae expression

UPEC is able to produce what special substances

aerobactin | hemolysin, which lyses host cells

This occurs in uncomplicated and nonsocial infection, abnormal urinary tract structure more likely to have UTI caused by this

Proteus mirabilis

Which UTI is more severe, one caused by E. coli or one caused by P. mirabilis

P. mirabilis

What are the virulence factors of P.mirabilis

``` flagella adhesion of frimbriae hemolysis IgA protease Urease; raising pH of urine ```

Is it easy or hard to positively ID the causative agent of a UTI

difficult | must count the bacteria in the urine ≥ 10^5 CFU/ml = normal

P. mirabilis can be diagnosed by what

consistently alkaline urine | blood/pus in urine

What are the treatment options for UTIs

antimicrobials; trimethoprim-sulfamethoxazole

This pathogen exhibits large mucoid colonies due to large capsule and causes pneumonia

klebsiella

What are the virulence factors of Klebsiella

pili enterotoxin similar to ST or LT (secretory diarrhea) aerobactin; an iron sequestering protein antiphagocytic capsule**

What are the different types of pili

type 1; important for UT epithelial | type 3; important for respiratory tract epithelial

This is among the most prevalent gram-negative GI bugs and is mostly transmitted through oral to oral (and fecal to oral)

helicobacter pylori

Where is H. pylori only found

in the mucous overlying the mucous secreting cells of the stomach

True or False; | H. pylori can lead to many different diseases

True; including gastric adenocarcinoma

How does H. pylori survive in the stomach

produces urease inflammatory effector molecules; cause epithelial cells to produce IL-8 cytotoxin is associated with peptic ulcer disease down regulation of somatostatin-producing D cells but is killed by gastric acid

How would you diagnose an H. pylori infection

mucosal biospies urea breath test serology

Why does H. pylori cause carcinogenesis

H. pylori down regulates somatostatin somatostatin inhibits gastrin when down regulated it allows gastrin to be produced which causes epithelial cells to proliferate if there is a mutation, then problems arise

What are some treatments of H. pylori infection

first line; proton pump inhibitor and antibiotic cocktail | second line; proton pump inhibitor, bismuth subsalicylate, tetracycline and metronidazole