MICR_041213 Chol, Campy, Helico Flashcards
What are some characteristics of vibrio cholerae?
gram (-), motile, polar flagellum
What are some of the virulence factors that vibrio cholerae produce? (5)
1) endotoxins (O, H, neuraminidase), 2) exotoxins (Cholera toxin (enterotoxin)), 3) TCP (toxin coregulated pilus)
What is the major colonization factor of vibrio cholerae?
TCP - toxin coregulated pilus
What is the major virulence factor that vibrio cholerae produces that is responsible for the massive, watery diarrhea?
cholera toxin (an entero-/exo-toxin)
Which serotype of vibrio cholerae causes epidemic cholera?
serogroup O1
What is the mechanism of pathogenesis of vibrio cholerae?
1) oral ingestion, 2) bypasses stomach to reach small intestines, 3) forms microcolonies in intestinal crypts, 4) secretes CHOLERA TOXIN, which binds Gm1 gangliosides on enterocytes. 4) NEURAMINIDASE converts other gangliosides to GM1 ganglioside (to increase the number of toxin-binding sites). 5) CHOLERA TOXIN enters cells via endocytosis, 6) increases cAMP production via adenylate cyclase, 7) decreases Na/Cl/HCO3 reabsorption, 8) massive intestinal fluid loss
What are the clinical features of vibrio cholerae infection?
painless, odorless watery diarrhea (leads to volume loss, dehydration, low blood pressure “shock”)
What are the treatments for vibrio cholerae infection?
1) ORT, 2) antibiotics: doxycycline and azithromycin
What antibiotics are used to treat vibrio cholerae?
doxycycline and azithromycin
Vibrio cholerae is prevalent in which countries?
poverty/inadequate sanitation (developing countries: Asia, Africa, South America)
What is the mortality rate of vibrio cholerae?
1%.
Where is the newest epidemic of vibrio cholerae?
Haiti - caused by UN workers who brought it in from Nepal
What vaccines are available to treat vibrio cholerae?
PARENTERAL: ineffective. ORAL: 1) inactivated vaccine - 70% effective and is currently being used in Haiti, 2) live-attenuated vaccine - effective in north-American volunteers, but yet to be proven in endemic populations
What is the most common etiologic agent of diarrhea in the world?
campylobacter
What are some characteristics of campylobacter?
gram (-), microaerophile
What are the common causative agents of campylobacter?
C. jejuni, C. coli, and C. fetus
What is the mechanism of pathogenesis of campylobacter?
1) intake of contaminated food/water (chicken/unpasteurized milk), 2) bypass stomach to enter intestines, where it 3) initiates an inflammatory process that causes 4) diarrhea.
What are the clinical features of campylobacter?
incubation period of 3-5d, followed by prodromal symptoms (fever, malaise, headache, fever), followed by abdominal pain and diarrhea
What is a complication of campylobacter infection? Who is most at risk?
1:1000 people develop autoimmunity to nerves, leading to paralysis (Guilliam Barre Syndrome); increased risk in immunocompromised patients
What is the infectious dose of campylobacter?
500
How do you diagnose campylobacter?
stool culture on selective media (campy-BAP with cephalothin), incubated at 5-10% O2 at 37 or 42˚C
How do you treat campylobacter?
fluids or antibiotics (erythromycin or ciprofloxacin)
Which two antibiotics are used to treat campylobacter?
erythromycin or ciprofloxacin
What are some characteristics of helicobacter?
gram (-), spiral shaped
Where does helicobacter live?
stomach and duodenum
How can helicobacter survive the acidic environment of the stomach?
it lives in the thick, protective mucous layer and it produces urease (urea -> bicarbonate/ammonia), which makes the environment more hospitable
What are the 3 big virulence factors that helicobacter produce?
adhesins: 1) BabA, 2) CagA, 3) VacA
What is BabA?
virulence factor of helicobacter. binds to lewis B antigens on stomach epithelial cells
What is CagA?
virulence factor of helicobacter. injected into stomach epithelial cells and disrupts the cytoskeleton, cell polarity, adherence, and other cellular activities
What is VacA?
virulence factor of helicobacter. vacuolating cytotoxin A - further damages the epithelial lining
What is the pathogenesis of helicobacter?
1) oral ingestion, 2) invades mucous layer in stomach, 3) neutralizes acid via UREASE, 4) colonizes the mucous layer, 5) mucosal damage by bacterial MUCINASE, 6) mucosal cell death by CYTOXINS, AMMONIA, and SUPEROXIDE RADICALS, 7) inflammation via gastric acid, proteases, and effector molecules of the immune system, 8) gastritis
What are the complications of helicobacter infection?
peptic ulcer or gastric cancer
What changes occur during the transition between gastritis to gastric cancer?
intestinal metaplasia, where there is a malignant change to become MALT lymphomas
What are the clinical features of helicobacter?
abdominal pain, bleeding in GI tract
What is the infectious dose of helicobacter?
unknown
What antibiotics are used to treat helicobacter?
1) amoxicillin, 2) clarithromycin, 3) tetracycline, and 4) metronidazole – all taken with bismuth salts (ie pepto bismol)
What is the epidemological features of helicobacter?
it’s present in 50% of the world population, with the highest rates in developing countries.
What vaccines are available to treat helicobacter?
none
What are the 5 tests that are used to diagnose helicobacter?
1) carbon-urea breath test, 2) stool culture, 3) seroconversion test, 4) PCR, 5) endoscopy
How does the carbon urea breath test work to detect helicobacter?
it’s a non-invasive, sensitive test that measrues presence of UREASE. If the radiolabeled urea is cleaved by urease, the C14 is relased as an aerosol and is measured
Why is the stool cuture accompanied by the urease test in the detection of helicobacter.
to differentiate between campylobacter and helicobacter
What does the seroconversion test measure in the diagnosis of helicobacter?
(+) response against helicobacter antigens
What samples would you do a PCR on in the diagnosis of helicobacter?
stool sample or dental scraping
What usually accompanies the endoscopy in the diagnosis of helicobacter?
biopsy or culture for a definitive diagnosis.
