L5- GI Infections I (esophagitis, H. pylori) Flashcards
Gastroenteritis is defined as (1) typically resulting from (2) causing (3) symptoms.
1- inflammation of stomach and intestines
2- bacterial toxins, viral infection
3- v/d
GI microbiota varies with the following factors…
- site (oral, stomach, SI, LI, ect)
- age (inc diversity with age, starting at newborn through childhood)
- diet
most GI microbiota are found in the (1) segment
list the GI segments and the associated flora
(least flora, 10^2/mL)
- Stomach: Candida peptostreptococcus, Strep. lactobacillus
- duodenum thru proximal ileum: Strep. lactobacillus
(medium flora, 10^8/mL)
-Distal ileum: clostridium, bacteroides, corynebacterium
(most flora, 10^12/mL)
Colon: clostridium, bacteroides, bifidobacterium, enterobacteriaceae
list the DDxs for epigastric pain w/o diarrhea (suspecting infectious cause)
- esophagitis
- gastritis / peptic ulcer disease / gastric cancer
[non-infectious: GERD, indigestion, overeating, lactose intolerance, alcohol, hiatal hernia, Barrett’s, gallbladder issue, pregnancy]
Esophagitis:
- (1) definition
- (2) most common cause
- (3) risk factors
1- esophagus inflammation
2- GERD (non-infectious cause)
3- cancer chemotherapy, transplantation, HIV, diabetes
Esophagitis:
- (1) common infectious causes
- (2) hallmark Sxs
- (3) Dx
1- Candida, HSV, CMV
2- odynophagia, dysphagia
3- *endoscopy, double-contrast esophagram, brushing and biopsy
list all the possible symptoms in esophagitis (non-specific to causal agent)
- lesions
- dysphagia
- dry mouth
- n/v
- weight loss
- chest pain
match the symptoms with the causal agent of esophagitis:
- (1) multiple, small discrete superficial ulcers
- (2) flat (ovoid, elongated, diamond shaped) ulcers
- (3) ‘cottage-cheese’ like white plaque / lesion that can bleed if scraped
1- HSV
2- CMV
3- Candida spp.
describe the specific symptoms related to esophagitis specific to the following:
- (1) Candida spp.
- (2) HSV
- (3) CMV
1- ‘cottage-cheese’ like white plaque / lesion that can bleed if scraped
2- multiple, small discrete superficial ulcers
3- flat (ovoid, elongated, diamond shaped) ulcers
(1) is the most common cause of infectious esophagitis, particularly in (2) populations and also has (3) property in terms of general distribution. Other risk factors beyond (2) include (4).
1- Candida spp.
2- immuno-compromised, HIV (11%)
3- 40% healthy people carry it in oropharynx
4- organ transplant, DM, antibiotics, malnourished, cancer
Candidasis = (1) of mucous membranes:
- (2) general characteristics
- (3) oropharyngeal features
- (4) esophageal features
- (5) vulvovaginal features
1- thrush 2- white plaques, detached when scraped 3- 'cotton-wool' mouth, dysphagia 4- dysphagia, retrosternal pain, AIDS-defining infection 5- itching, curd-like vaginal discharge
Candida spp. virulence factors…..
Dimorphic: yeast (organism) –> pseudohyphae (environment)
HWP1 / hyphal wall protein 1: necessary for oropharyngeal pathogenesis
(1) is the second most common cause of infectious esophagitis, described as having (2) microbial features. It will establish infections in (3) cells and mostly affects (4) patients.
1- HSV-1
2- large enveloped dsDNA
3- latent infections in neurons
4- AIDS, transplant Pts (cell-based immunity important for controlling infection)
Note- HSV-1 also causes cold sores, HSV-2 causes genital herpes
(1) is the third most common cause of infectious esophagitis, described as having (2) microbial features. It will establish infections in (3) cells and mostly affects (4) patients.
1- CMV
2- large enveloped dsDNA
3- latent infections in monocytes, granulocytes, lymphocytes [esophagitis is either primary or reactivation]
4- AIDS, transplant Pts (cell-based immunity important for controlling infection)
Note- CMV also causes retinitis
Candida spp. esophagitis:
- (1) key microbial features
- (2) endoscopy findings
1- budding yeast, germ tube (if C. albicans), pseudohyphae
2- whitish plaques, upper-mid esophagus
HSV esophagitis:
- (1) key microbial features
- (2) endoscopy findings
1- dsDNA virus
2- multiple, small, discrete superficial ulcers (punctate, linear, stellate, ‘volcano-like’)
CMV esophagitis:
- (1) key microbial features
- (2) endoscopy findings
1- dsDNA virus
2- 1 or more giant (>10cm) flat (ovoid, elongated, diamond shaped) ulcer, upper/mid-esophagus
[sometimes small satellite ulcers]
list the 3 potential outcomes from H. pylori infections
- Gastritis: stomach inflammation => epigastric pain (although has non-infectious causes)
- PUD (peptic ulcer disease) as gastric or duodenal ulcer
- Gastric cancer: usually multifactorial
list the critical microbial features of H. pylori (hint- ~7)
-Gram(-), LPS is relatively non-toxic (although helps with persistance)
- curved to spiral, 1-3 turns
- motile, 5-6 polar flagella
- microaerophilic
- catalase(+)
- urease(+)
H. pylori infections are commonly associated with ______ exposure / conditions
- poor SES status
- more likely in poor sanitary of hygienic conditions
discuss the distribution of H. pylori infections by symptoms (most to least common)
- asymptomatic
- duodenal ulcer
- gastric ulcer
- gastric cancer
- gastric lymphoma
Gastric ulcer:
- (1) pain occurs (2) hrs after food
- intolerance to (3)
- symptoms (relieved/precipitated) by food
- (5) symptoms
- (6) possible complication
1- epigastric pain 2- 1-3 hrs 3- fatty food 4- precipitated 5- fullness, bloating, belching, heartburn, nausea 6- gastric carcinoma
Duodenal ulcer:
- (1) pain occurs (2) hrs after food
- symptoms (relieved/precipitated) by food, and relieved by (4)
- (5) symptoms
1- epigastric pain 2- 2-5 hrs 3- relieved 4- antacids 5- melena / hematochezia, night awakenings (heartburn, chest discomfort less common)
H. pylori enters the stomach lumen and utilizes (1) to neutralize acidic conditions. (2) is then required from H. pylori for it to move near gastric epithelium when it will then (3). H. pylori will finally release (4) and (5) to cause host tissue damage. H. pylori and the host will then secrete CKs to activate innate immunity and neutrophils which can lead to (6) symptoms / developments.
1- urease (urea –> NH3+ to neutralize (-) gastric acid)
2- flagella mediated motility (polar, multiple)
3- attach with adhesins => colonization
4- CagA (cytotoxin associated gene A)
5- VacA (vacuolating cytotoxin A)
6- gastritis, peptic ulcer
list the 4 general steps of H. pylori pathogenesis
1) survive stomach acid via urease
2) move towards epithelium via flagella
3) attach via adhesins, LPS, outer proteins
4) tissue damage via exotoxin, enzymes, effectors
H. pylori CagA+ strains:
- inc risk for (1), (2)
- causes (3) to impact host cell physiology
- caused (4) shift in affected cells
1- ulcers
2- cancer
3- signaling alternations
4- transition from epithelial to mesenchymal cell phenotype
H. pylori VacA functions, (1)/(2)
1- forms anion selective channels in vacuole membrane => swelling
2- inserts in mitochondrial membranes => mitochondrial death
H. pylori adhesins
Baba
SabA
H. pylori Dx
Non-invasive:
- urea breath test (carbon urea C13 breath test): expensive, detects active infection
- fecal Ag test (ELISA)
- serology: cheap, widely available, but only indicates previous infection
Invasive:
- **gastric biopsy (Histo) –> culture with antimicrobial sensitivity (used in Pts who don’t respond to therapy)
- biopsy with PCR
- rapid urease test
list the common microbes involved in abdominal cavity infections
(peritonitis, appendicitis, pancreatitis, intra-abdominal abscess)
-normal flora (aerobes and anaerobes)
- Aerobic Gram(-) bacteria: E. coli, Klebsiella spp.
- Anaerobic bacilli: Bacteroides fragilis
contributing factors to abdominal cavity infections (non-microbial factors)
(peritonitis, appendicitis, pancreatitis, intra-abdominal abscess)
-reduced O2 tension / redox potential => favors anaerobic growth
- impaired blood supply –> necrosis –> favorable environment
- *primarily opportunistic infections
Bacterial Peritonitis:
- (1) main clinical association
- (2) Sxs
1- ascites via advanced cirrhosis
2- fever, diffuse continuous abdominal pain/tenderness, altered mental status (mild to delirium), diarrhea
describe primary Bacterial Periotonitis
(SBP- spontaneous bact. periot.)
- mainly alcoholic cirrhosis patients
- E. coli 43%, non-Strep. pneumonia (19%), K. pneumonia (11%)
-GIT infection transverses intestinal wall –> colonizes mesenteric lymph nodes –> travel to liver / leak into ascitic fluid or lymphatics rupture
describe secondary Bacterial Periotonitis
(less common than primary)
-usually to surgically treatable infection like duodenal ulcer
-spillage of bacteria from GIT –> peritoneal cavity
Appendicitis:
- (1) is the primary cause leading to (2) from (3) species
- (4) is a complication spreading from appendicitis
1- obstruction
2- superimposed infection
3- E. coli, B. fragilis
4- peritonitis (via perforation)
pancreatitis Sxs
- steady, ‘boring’ abdominal pain for several days
- speed of onset is variable
- n/v are common
Pancreatitis causes
- drugs: ACEIs, Sulfas
- *Infections: coxsackievirus B, CMV, mumps virus
- inherited (multiple gene mutations)
- mechnical/structural: gallstones, trauma, cancer
- toxins: ethanol
