Bacterial GI infections Flashcards
1
Q
Major causal species of bacterial gastroenteritis
A
- GN bacilli: E coli (commensal, C), vibrio (not C), salmonella (not C), shigella (not C), campylobacter jejuni (not C), yersinia enterocolitica (not C)
- GP cocci: Staph (C)
- GP bacilli: bacillus anthracis and bacillus cereus (not C), clostridium (C)
- Campylobacter and salmonella are most common cause in US (both associated w/ poultry)
2
Q
Diarrhea
A
- Due to increased secretion or reduced absorption of fluids
- Inflammatory: large number of WBCs (PMNs and mononuclear)
- Non-inflammatory: absence of large amounts of WBCs
- RBCs may be incidental, except hemorrhagic E coli (EHEC) infections
3
Q
Types of E Coli GI infections 1
A
- ETEC: enterotoxigenic E Coli, cause of 1/3 of bacterial-induced traveler’s diarrhea (most common for traveler’s)
- Does this by enterotoxin production in SI (either heat stable or heat labile)
- Heat labile enterotoxin activates AC (like cholera) and stimulates fluid secretion
- Heat stable enterotoxin activates GC and inhibits fluid absorption
- Non-inflammatory diarrhea, (-RBCs)
4
Q
Types of E Coli GI infections 2
A
- EPEC: enteropathogenic E Coli adhere to epithelial cells in SI and prevent fluid absorption
- Risk higher for non-breast fed infants (epidemic infantile diarrhea)
- Causes inflammatory diarrhea but few WBCs (-RBCs)
- EAEC: enteroaggregative E Coli aggregate and adhere to epithelial lining in SI and prevent fluid absorption
- Causes inflammatory diarrhea but few WBCs (-RBCs)
- EPEC and EAEC both cause production of IL8
5
Q
Types of E Coli GI infections 3
A
- EIEC: enteroinvasive E Coli invades and destroys the epithelial lining of the colon
- Destruction of epithelial cells causes inhibition of fluid absorption
- Causes inflammatory diarrhea w/ lots of WBCs (+ RBCs)
- EHEC: enterohemorrhagic E Coli: produces a shigella-like toxin that destroys (but doesn’t invade) the epithelial lining of the colon
- Destruction of epithelial cells causes inhibition of fluid absorption
- Can cause hemolytic uremic syndrome
- Causes inflammatory diarrhea w/ no WBCs but lots of RBCs
- DAEC: diffusely adherent E Coli, affects SI
6
Q
Overview of E Coli pathogenesis mechanisms
A
- EPEC and EAEC prevent fluid absorption by destroying epithelial cells via adherence (SI)
- EIEC prevent fluid absorption by destroying epithelial cells via invasion (LI)
- EHEC prevent fluid absorption by destroying epithelial cells via shiva-like toxin (LI)
- ETEC can prevent fluid absorption by destroying epithelial cells via heat stable toxin that activates GC (SI)
- ETEC can also cause increased fluid secretion by heat labile toxin that activates AC (SI)
7
Q
Other GN bacterial gastrointestinal infection etiologies 1
A
- Vibrio cholera: binary toxin that increases fluid secretion via AC stimulation
- Found in shell fish, causes rice water diarrhea
- 3 types of vaccines: killed, live attenuated, toxoid
- Salmonella typhi: can cause typhoid fever (systemic, characterized by rash)
- Survives phagocytosis and can replicate intracellularly
- Shigella: F-O, produces shiga toxin, can replicate intracellularly
- Characteristic bloody, mucoid stools
8
Q
Other GN bacterial gastrointestinal infection etiologies 2
A
- Campylobacter: associated w/ undercooked poultry, causes bloody (inflammatory) diarrhea
- Complication: guillan-barre (Th1 and Th2) syndrome due to cross reaction of Abs to bacterial wall and nerve myelin
- Yersinia enterocolitica: inflammatory diarrhea, can cause pseudo appendicitis syndrome
9
Q
Food poisoning causes
A
- Can be due to Staph aureus, B cereus, clostridium botulinum
- Food poisoning due to preformed toxins, leading to early illness (1-6 hr) that is often emetic (+/- ab pain, diarrhea)
10
Q
Staph aureus and B cereus
A
- Staph aureus: from improper food handling, expresses several enterotoxins and a heat stable toxin (responsible for food poisoning)
- B cereus: spore forming, emetic illness associated w/ recooked rice, diarrheal illness associated w/ undercooked foods
- Food poisoning (emetic form) due to preformed heat stable toxin, live cells not required (YES vomiting, +/- diarrhea)
- Also has diarrheal form (1-24hr incubation): due to overgrowth of cells in intestine that produce enterotoxin (NO vomiting, YES diarrhea)
11
Q
Clostridium sp
A
- Clostridium difficile: spore former, can be commensal but overgrows w/ ANTIBIO Rx (nosocomial)
- Produces enterotoxin and cytotoxin (both increase inflammatory response
- Overgrowth of C Dif due to antibio Rx can lead to diarrhea, pseudomembranous colitis
- Clostridium perfringens: produces many toxins that can cause food poisoning (diarrhea, no N/V)
- Cooking kills bacteria but not spores, spores germinate in cooled foods and when ingested produce enterotoxins
- Associated w/ smoked/cured meats (sausage, dear)
- Commensal, but can lead to food poisoning, soft tissue infections (gas gangrene), septicemia
12
Q
Clostridium botulinum 1
A
- Spores and preformed toxins are transmitted into improperly prepared foods
- Foodborne botulism: inadequately preserved canned goods allow botulinum spores to germinate, bacteria multiply and produce toxin under anaerobic conditions
- Bacteria cannot multiply in healthy adult GI tract, toxin is what causes food poisoning and Sx
- Toxin inhibits ACh release at NMJs leading to flaccid paralysis, blurred vision
- Also causes diarrhea, N/V
13
Q
Clostridium botulinum 2
A
- Infant botulism: HONEY contaminated w/ botulinum spores is ingested by baby
- Bacteria multiple (less competing microflora) and toxin is produced in vivo
- Sx: constipation, poor breast feeding, lethargy, floppy baby
14
Q
Helicobacter Pylori
A
- Established infections in pyloric region of stomach cause gastritis, gastric and duodenal ulcers
- Gastric ulcers may lead to gastric CA due to chronic inflammation
- May be a cause of MALT B cell lymphoma
- cagA gene is correlated w/ gastric CA, possibly inactivates tumor suppressor proteins (p53 and RUNX3)
- Is commensal but virulence factors can make it pathogenic
15
Q
H Pylori virulence factors
A
- Heat shock protein: induces expression of urease
- Urease: neutralizes gastric acidity by producing ammonia, breaks down unstirred layer
- Mucinase and phospholipase: disrupts gastric mucus
- Acid inhibitory protein: prevents production of stomach acid
- Catalase and superoxide dismutase: prevents phagocytosis
- VacA: helps w/ intracellular replication
- Overall there is an increased amount of gastric acid secretion, since the inflammatory response leads to hyper secretion of acid
- There is also increased gastrin