DERS 07 - GIT Infections 3 Flashcards
What is gastroenteritis and what are its symptoms?
Inflammation of the stomach and intestines, typically resulting from bacterial toxins or viral infection
Vomiting and Diarhea
What are the causes of epigastric pain we’re concerned with? What are the more common causes?
- Esophagitis
- Gastritis
- Peptic Ulcer Disease
Commonest causes are indigestion, acid reflux. overeating, lactose intolerance, alcohol, etc.
What are the symptoms of esophagitis?
- Dysphagia
- Odynophagia
- Visible esophageal lesions
- Dry mouth
- Nausea
- Vomiting
- Weight loss (from not eating)
- Epigastric/Chest pain
What are the major causes of infectious esophagitis and what do their lesions look like?
- Candida spp. - “cottage cheese” like white lesions/plaques
- HSV1 - multiple, small discrete, superficial ulcers
- CMV - flat ulcers that appear like volcanoes
See image
What type of organisms are candida spp. and how are they diagnosed
They are a dimorphic yeast that produces pseudohyphae (hyphae are buds that become a cylindrical stalk, pseudohyphae are buds that dont separate from the stalk but dont become perfectly cylindrical either)
Diagnosis is based on appearance of lesions and presence of pseudohyphae in biopsy
What are the major risk factor for candida esophagitis?
- HIV
- Organ transplant
- Alcoholism
- Diabetes
Answer the followin about HSV1:
- Large, medium, or small
- Enveloped or not
- Type of genome
- Where does it establish latent infections
- What patients is HSV1 esophagitis most commonly found and why
Large enveloped dsDNA virus
Establishes latent infections in neurons
HSV1 esophagitis is commonly seen in AIDS and transplant patients because cell-based immunity is what controls HSV1 infections.
Answer the followin about CMV:
- Large, medium, or small
- Enveloped or not
- Type of genome
- Where does it establish latent infections
- What patients is CMV esophagitis most commonly found and why
Large enveloped dsDNA virus
Establishes latent infections in monocytes, granulocytes, and lymphocytes
Most commonly seen in solid organ transplant patients and AIDS patients because cell-based immunity is important for controlling infection
What are the potential outcomes of an H pylori infection?
- Gastritis
- Peptic ulcer disease (PUD)
- ulcerative lesions in stomach or duodenum
- Gastric cancer
Answer the following about H. pylori:
- Gram negative or positive
- Motile or non-motile
- Most relevant enzyme test and result for diagnosis
- Gram negative
- Motile
- Urease +ve
Describe the toxic damage caused by H. pylori LPS?
H. pylori LPS is relatively non-toxic
List the H. pylori virulence factors we need to know and what they do.
- 5-6 flagella help navigate through stomach acid to mucosa
- Urease converst urea to CO2 and NH3. The NH3 both helps neutralize the acid and cause mucosal injury
- LPS and other outer proteins adhere to host cells
- The exotoxin vacuolating toxin A (vacA) causes mucosal injury
- Secretory enzymes (mucinase, protease, lipase) cause mucosal injury
- It has pili-like structures that can inject effectors into host cells
Facts to know about the different H. pylori strains
Strains that have more Cag A+ (an effector) are more likely to cause ulcers and cancer
Strains that have more Vacuolating toxin (VacA) are more likely to cause gastritis and cell death
Diagnostic tests for H. pylori
- Non-invasive
- H. pylori urea breath test - C13 urea pill is given to patient. If they have an active infection, urease will convert the urea into C13 CO2 which is detectable in breath
- H. pylori fecal antigen test - ELISA
- Serology - cheaper than the above two but only indicates previous exposure
- Invasive
- Endoscopy and biopsy for histology, PCR, and rapid urease test (detects pH change from ammonia)
What is the primary type of peritonitis? What is its usual pathogenesis? What microbes are normally involved?
- Spontaneous bacterial peritonitis (SBP) which peritonitis with no obvious source of the bacterial infection (e.g. - injury)
- Something causes the GI flora to transverse the intestinal wall and colonize the mesenteric lymph nodes. Usually caused by GI overgrowth or increased intestinal permeability. Usually E.coli, non-Strep pneumoniase spp, or klebsiella pneumoniae
- Either the lymphatics rupture or the bacteria travels to the liver and leaks into ascitic fluid
