Final; Toxin-Producing Pathogens of Mucosal Surfaces Flashcards
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
Where in the intestine are the toxin producing bacteria
small intestine
What are the species of vibrio
V. cholerae; cholera
V. parahaemolyticus; dirrhea
V. vulcificus; tissues and blood
V. alginolyticus; tissues and blood
True or False
V. cholera are highly motile
True
What are the two typs of cholera
nonpathogenic and pathogenic
What is the strain of cholera that emerged in 1992
a “new” El Tor
What is specific about the new El Tor strain
mutated O antigen
new LPS serotype
now encapsulated
affected all age groups
What are three virulence factors of V. cholerae
flagella
pili to adhere to mucosal tissues
cholera toxin; phage encoded
What causes the expression of pili and toxin in V. cholerae
a shift from saltwater to reduced ion levels found in the body
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
How many different strains of E.coli are there
thousands; but many are commensal
These strains of E.coli cause secretory diarrhea
ETEC (enterotoxigenic E.coli)
EPEC (enteropathogenic E.coli)
This strain of E. coli cause dystenery-like symptoms
EHEC (enterohemorrhagic E.coli)
This strain of E.coli causes urinary tract infections
UPEC (uropathogenic E.coli)
This is responsible for 30-45% of cases of traveler’s diarrhea (when traveling to Mexico)
ETEC
ETEC requires what kind of infectious dose
large
What helps ETEC adhere to mucosal tissues
colonization factor antigens (cfa) on fimbrae
What toxins does ETEC produce
heat-labile toxin (LT)
heat-stable toxin (ST)
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
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
What are the treatments for secretory diarrhea
oral rehydration; mix or sugar and salt
antibiotics can help shorten the duration/severity
What are considered the hybrid “misfits” where they do not fall into either the toxin producing or invasive pathogens
EPEC
EHEC
What does colonization of the hybrids do
causes attaching and effacing lesion; reorganization of epithelial cells
What is special about the stool following a EHEC infection
blood in still (and possible the urine)
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
