Vibrio cholera and E. coli (ETEC) Proteus, UPEC, Klebsiella and Helicobacter pylori MM (3/1/18) Flashcards
which pathogenic E. Coli can lead to water diarrhea that lasts for weeks
Enteroaggregative
Toxin-produce bacterial pathogens
Vibrio Spp
Enterotoxigenic E coli(
calling signs of toxin-producting bacterial pathogens
small intestine location lots of water in stool no blood in stool no leukocytes in stool no tissue damage
morphology of vibrio
curved, gram-
highly motile
location of vibrio
saltwater
4 species of Vibrio
- V. cholerae - diarrhea, “cholera gravis”
- V. parahaemolyticus - diarrhea
- V. vulnificus - tissues and blood
- V. alginolyticus - tissues and blood
pH of Vibrio Cholerae
8-9.5
what toxin does vibrio cholerae form
cholera toxin
two main biotypes that can cause cholera
classical
el tor - o1 antigen, and 0139 (New)
what does vibrio cholerae form in environment
biofilms
virulence factors for V. cholerae
flagella
pili to adhere to mucosal tissue
cholera toxin
why would V. cholerae express the pili and toxin
shift from salt to the body (lower ions) cause pili to come out and produce toxin
main regulator of pathogenicity island of V. cholerae
ToxR
where the cholera toxin comes from
phage encoded
what is the cholera toxin
A-B type ADP-ribosylating toxin
Cholera tox lead to what
excessive accumulation of cAMP which cuase hypersecretion of chloride, potassium and bicarbonate followed by water by osmotic pressure
how is cholera spread
contaminated water and by humans
under cooked crab/shrimp
incubation period of cholera
2 days
inoculum needed to fcause disease in cholera
high number
Colonize location of cholera
small intestine
what types of cholera produce CT
o1 and o139, rest dont cause cholera
Cholera leads to
loss of water(liters) per day
Rice water stools
hypokalemia and metabolic acidosis : large amound of k and bicarb is loss with water
can kill
cholera immunity
Nonspecific important
SIga against O antigen, B subunit of cholera toxin, and toxin coregulated pilus
why use selective media to look at cholera
lots of stuff in your poo
use addition biochem tests to ID strain
treating cholera
Oral and IV solution of glucose and physiological concentration of Na and Cl, and higher levels of K and HCO3
early intervention is key
also can use antibiotics to decrease time
what is the leading cause of morbidity and mortality in children under 2 in developing countires, ie travelers diarrhea
Enterotoxigenic E. Coli (ETEC)
how is Enterotoxigenic E. Coli (ETEC) spread
contaminated food/water (usually human orign)
uncooked/undercooked foods at greatest risk
inoculum of Enterotoxigenic E. Coli (ETEC)
10^8 to 10^10 in adults
where does Enterotoxigenic E. Coli (ETEC) colonize
proximal small intestine
adhere to cause disease
Virulence factors of Enterotoxigenic E. Coli (ETEC)
colonizing factor pili
toxins: heat-labile toxin (LT) and Heat-Stable toxin (ST)
What is HEat-Labile toxin (LT) from Enterotoxigenic E. Coli (ETEC)
A-B toxin
leads to secretion of Cl, and block of NaCl reabsorption in enterocytes
what is Heat stable toxin (ST) in Enterotoxigenic E. Coli (ETEC)
Binds to cells, leading to signal cascade that ends with fluid and electrolite section
immunity to Enterotoxigenic E. Coli (ETEC)
LT and CF-specific SIgA with no inflammation/tissue destructure
how to identify secretary diarrhea aganets
Rule out V. Cholera
Innoculate plates with diluted stool samples
not very rich medium, so fastidious G- wont grow
aerobic incubation kills anaerobes
how to rule out Vibrio cholera from diarrhea agents
check if eaten shelfish or in endemic area
Thiosulfate-Citrate - bile-sucrose (TCBS) agar)
Agglutination test (EI Tor strain)
Serological testing
how to treat secretory diarrhea
oral rehydration: mix of sugar and water
antibiotics shorten duration and reduce serverity(tetracyclines for vibrio infections, 2nd gen flouroquinolones for ETEC)
Bacterial of invasive bacterial pathogens
Salmonella spp, and shigella spp
Characteristics of invasive bacterial pathogens
large intestine small volume of stool bloody stool leukocytes in stool tissue ulcerations
bacteria that are toxin producing bacterial pathogen
vibrio spp (primarily v. cholerae) and Entertoxigenic E coli (EtEC)
characterisitcs of Toxin-Producing bacterial pathogens
Small intesine lost of watery stool blood in stool no leukocytes in stool no tissue damage
characteristics of Enterohemorrhagicic E coli and Enteropathogenic E coli
Lower small intestine/upper large intesting
Colonization causes attaching and effacing lesion
blood in stool (also urin with EHEC)
most common form of bacterial infection of an organ system
UTI (not including adults
inflammation in the bladder
cytis
who is more likely to get a UTI
women (shorter uethra so bacteria have to travel less far)
Uncomplicated UTI
all normal defenses intake
no recent hospital admission
in lower urinary tract
usually EPEC or other commensal E. COli
Complicated UTI
structural abnormality in urinary tract
recently in hospital
will spread to kindney
other enterobacteriacea
natural defenses of urinary tract
complete voidance of bladder peristalsis ureterovesicle valves mucous layer pH
cause of pyelonephrities
Cystitis spread to kidney via retrograde flow from bladder to kidney -neurological disorders -ureteroviscle valves not fully formed -pregnancy hormones change peristalsis Urethral catheters Urinary tract stones
what cuase 90% of infectious cystists and pyelonephritis in US
E. Coli (oringate from intesnite) (Uropathogenic E. Coli)
virulence of UPE
type 1 pili
P pili for ascending infection
invade superficial epithelial cells
alpha-hemolysin and cytotoxic necrotizing factors cause injury
Proteus causes what type of UTI’s
uncomplicated and nosocomical infections
usually for abnormal urinary tract strucutre
P. mirabilis UTI vs. E. Coli UTI severity
P. mirabilis more severe(more virulence)
virulence factors of P. mirabilis
Flagella Adhesion on fimbriea for urinary eptihelium hemolysins IgA protease Urease
roll of Urease
raise pH of urin to create Nh3 and Co2 and grows better in less acidic encironment
Urease effect on renal cells
toxic and creates cystals for identification clincally
diagnosis of UTI
hard to positively ID causative agent of UTI
count bacteria
healthy individual bacteriuria
less than 10^5 CFU/ml
CFU with individual with dysuria
greater than 10^2
what is dysuria
painful urination
what is pyuria
WBC/pus in urin
Proteus can be diagnoses by
Consistently alkaline urine
Production of urease
treating a UTI
antimicrobials (trimethoprim-sulgamethoxazole first choice) 3 days for acute cystitis 10-14 days for polynephritis prophylactic treatment asymptomatic bacteriuria(pregnant)
morphology of Klebsiella
nonmotile, capsule
how does klebsiella adhere
pili
capsule with colonies of Klebsiella
large mucoid colonies (interferes with complement activation
where does Klebsiella infect
respiratory and urinary epithelium
klebsiella virulence factors
pili (type 1 and type 3 )
enterotoxin similar to ST and LT
aerobactin
Antiphagocytic capsule
roll of type 1 pili
adherence to urinary tract epithelial cells
roll of type 3 pili
important for adherence to respirator tract epithelial cells
enterotoxin of Klebsiella leads to
similar to ST and LT to induce secretory diarrhea
roll of aerobactin
iron sequestering PR
the primary virulence factory
antiphagocytic capsule
Klebsiella antibiotic resistance
very resistant, especially type 258
Klebsiella resistance to antibiotics is implicated where
hospital acquired respirator, UTI and Bloodstream Infections
what was Helicobacter pylori originally classified as
campylobacter (motile, curved, G- rod)
microaerophilic
growth of Helicobacter pylori
slow growth (3-5 days) but infection can last for days
where does Helicobacter pylori colonize
in stomach, secreting urease to raise pH
how does Helicobacter pylori cause apoptosis of host cell
Vacuolating cytotoxin
how is helicobacter pylori transmitted
likely feca-oral and even oral-oral
where si Helicobacter pylori found
30-50% of people in developing countries, and nearly all of devlping nations
Helicobacter pylori is the precursor of
Gastritis, gastric ulcer, and duodenal ulcar
the only class one carcinogen
Helicobacter pylori
how does Helicobacter pylori act as a class I carcinogen
Cag+ strains lead to the developmeny of gastric adenocarinoma by triggering growth-promoting oncogenic signals
Infection cycle of H. Pylori
- H. pylorisecretes urease in order to raise the pH in the stomach (via ammoniaproduction).
- Uses flagella to propel itself into the mucus layer where it secretes more urease.
- Outer membrane proteins are used to adhere to gastric epithelial cells.
- Type IV secretion system injects VacAand Cag into gastric epithelial cells.
- Inflammatory response likely contributes to epithelial cell death and ulcer formation.
how to kill H. Pylori
readily killed by gastric acid
IL-8 come because of inflammatory effector moelcules
what all causes the problem with H. pylori ulcer
inflammation, cytotoxin, and downregulation of domatostatin-producing D cells
what can H. pylori infection lead to
peptide ulcer
chronic supericical gasritis
lymphoproliterative disease
chronic astrophic gastritis
clinical manifestation of H. Pylori
can be silent of nausea and upper ab pain belching heartburn dysphagia globus sensation
best way to test for H. Pylori
Urea breath test: injest labeled urea
urease in stomach break it down into a labeled CO2 that is exhauled and quantified
probelm with treating H> pylori
intense with many side effects
how to treat H. pylori
First Line
•Proton pump inhibitor
•Antibiotic cocktail
•usually clarithromycin and metronidazole or amoxicillin
•250-1000 mg twice a day for 7-10 days
Second Line
•Proton pump inhibitor
•bismuth subsalicylate
•tetracycline 500 mg four times a day for 14 days
•metronidazole 500 mg three times a day for 14 days
