Infectious Enterocolitis (Bacterial and Viral) Flashcards
What are the most common causes of traveler’s diarrhea?
- ETEC
- campylobacter jejuni
- salmonella
- shigella
Where does Vibrio cholerae come from?
(endemic areas/reservoirs and transmission)
endemic to India > Gulf of Mexico
reservoirs: shellfish
fecal-oral transmission:
-contaminated drinking water (think natural disasters)
-food
How are Vibrio cholerae infections typcially described?
- comma shaped, gram-negative
- oxidase-positive
- single, polar flagella
How does Vibrio cholerae cause disease?
Cholera toxin:
- enters cell via GM1
- toxin activates Gs protien -> activates adenylate cylcase -> increased cAMP -> CFTR activation
- increased in intraluminal chloride -> secretory diarrhea
What is the presentation of cholera?
(complications?)
- diarrhea; “rice-water” stools
- “fishy” smelling stool
- fever
- vomiting
Complications:
- severe dehydration
- hypotension/shock
How is cholera treated?
fluid replacement (typically sufficient w/o abx)
Where does Campylobacter jejuni come from?
(endemic areas/reservoirs and transmission)
- livestock act as reservoir (especially chicken)
- more pervalent in developed countries
Fecal-oral transmission:
- infected animal products (especially poultry)
- contaminated water
What is Campylobacter jejuni the most common cause of?
- most common cause of bacterial enterocolitis in developed countries
- common cause of “traveler’s diarrhea”
How are Campylobacter jejuni infections typcially described?
- comma shaped, gram-negative
- oxidase-positive
- single, polar flagella
How does Campylobacter jejuni cause disease?
Specific mechanism unclear
Virulence properties:
- toxin production (certain strains)
- invasion (certain strains)
- motility
- adherence
What is the presentation of campylobacter enteritis?
(complications?)
- influenza-like prodrome
- watery diarrhea
- bloody, inflammatory diarrhea (dysentery, associated with strains capable of mucosal invasion)
Complications:
- reactive arthritis (associated with HLA-B27)
- Guillian-Barré (0.1%; ascending, demylinating neuropathy -> parasthesia and weakness)
- erythema nodosum
How is campylobacter enteritis treated?
- self-limiting, treatment typically not needed
- abx in severe cases
Where do Shigella spp. come from?
(endemic areas/reservoirs and transmission)
- humans are only reservoir
- more prevalent in underdeveloped countries
Fecal-oral transmission:
- contaminated food
- contaminated water
How are Shigella spp. infections typcially described?
- gram-negative
- unencapsulated
- nonmotile
- facultative anaerobe
- green colonies (HE agar; vs. black colonies in similar appearing Salmonella)
- preferentailly infect left colon followed by ileum
How do Shigella spp. cause disease?
Shiga toxin:
-affects 60S ribosomal subunit, inhibiting protein synthesis -> enterocyte damage
Invasion:
- tropism for M cells
- can survive intracellularly, evading immune system
What is the presentation of shigellosis?
(complications?)
- watery diarrhea -> dysentery
- fever
- abdominal pain
Atypical presentatin:
-can mimic ulcerative colits in adults as waxing and waning diarrhea
Complications:
- uncommon triad of reactive arthiritis, urethritis, and conjunctivitis (associated with HLA-B27)
- HUS (associated with shiga toxin and EHEC shiga-like toxin)
- toxic megacolon
How is shigellosis treated?
- self-limiting (2-7 days), treatment typically not needed
- abx in severe cases
**antidiarrheals contraindicated, prolong symptoms and delay clearance of Shigella**
What causes Salmonelosis and where does it come from?
(endemic areas/reservoirs and transmission)
non-typhoidal salmonella, Salmonella enteritidis
- livestock act as reservoir (particularly chicken)
- prominent worldwide
Fecal-oral transmission:
-contaminated animal products (particularly poultry)
How are Salmonella enteritidis infections typcially described?
- gram-negative, w/ multiple flagella
- obligate pathogen
- acid-labile
- do not ferment lactose
- produces hyrdogen sulfide -> black colonies (HE agar; vs. green colonies in similar appearing Shigella)
How does Salmonella enteritidis cause disease?
Invasion:
- tropism for M cells
- can survive intracellularly, evading immune system
What is the presentation of salmonellosis?
(complications?)
-severe watery diarrhea -> dysentery
-severe vomiting
- fever
- abdominal pain
Complications (related to systemic infection):
- bacteremia/sepsis
- reactive artritis
How is salmonellosis treated?
- self-limiting (3-7 days), treatment typically not needed
- abx in systemic cases only as they prolong carrier state
What causes Typhoid fever and where does it come from?
(endemic areas/reservoirs and transmission)
- Salmonella enterica* (typhi/paratyphi)
- endemic to India, Mexico, and the Phillipines
- endemic populations tend to be infected with S. typhi
- visitors to endemic regions tend to be infected with S. paratyphi
- humans are only reservoir
Fecal-oral transmission:
- contact
- contaminated water
- contaminated food
How are Salmonella typhi/paratyphi infections typcially described?
- gram-negative, w/ multiple flagella
- obligate pathogen
- produces hyrdogen sulfide
- do not ferment lactose
- enlarged Peyer patches in distal ileum
-typhoid nodules in the liver (macrophage aggregates)
How do Salmonella typhi/paratyphi cause disease?
Invasion:
- tropism for M cells
- can survive intracellularly, evading immune system
- capable of disseminateing via lymph and blood vessels (unlike non-typhoidal salmonella)
What is the presentation of Typoid fever?
(complications?)
Initial infection:
- bloody diarrhea (“pea soup” green)
- N/V
- abdominal pain/bloating
Febrile phase (preceeded by brief asymptomatic period):
- fever
- “rose spots” on chest and abdomen
Complications:
- cholecystitis (chronic carriers)
- encephoapathy
- myocarditis
How is typhoid fever treated?
antibiotics in all causes unlike non-typhoidal salmonella
What causes Yersiniosis and where does it come from?
(endemic areas/reservoirs and transmission)
Yersinia enterocolitica and Yersinia pseudotuberculosis (not Y. pestis)
- domestic animals (dogs/cats)
- cows/pigs
- endemic in northern and central Europe
Fecal-oral transmission:
- dog/cat feces
- consumption of raw pork or unpasturized milk
- contaminated water
How are Yersinia spp. infections typcially described?
- gram-negative, rod-shaped
- obligate pathogen
- bipolar staining -> “safety pin” appearance
- preferentially affects right side -> ileum, appendix, and right colon (mimics Crohn disease and appendicitis)
How do Yersinia spp. cause disease?
Invasion:
-tropism for M cells
What factor increases the virulence of Yersinia spp.?
-increased non-heme iron
What is the presentation of yersiniosis?
(complications?)
-abdominal pain (can mimic appendicitis)
-N/V
- fever
- diarrhea (can be bloody)
Complications:
- sepsis (associated with high non-heme iron)
- reactive arthritis (associated with HLA-B27)
- erythema nodosum
How are E. coli infections typcially described?
- gram-negative, baccili
- flagellated
What causes EHEC and how does it cause disease?
E. coli O157:H7
- produces Shiga-like toxin -> HUS
- widespread with many reservoirs; cattle are most notable
What is the presentation of EHEC infection?
(complications?)
- watery diarrhea -> bloody/dysentery
- fever
- abdominal pain
Complications:
-HUS (due to to Shiga-like toxin)
How are EHEC infections treated?
antibiotic are contraindicated; increase release of shiga-like toxin increasing risk of HUS
What causes pseudomembranous colitis and where does it come from?
(endemic areas/reservoirs and transmission)
Clostridioides difficile
-hospitals act as reservoirs
not so much transmitted as allowed to grow
many people are colonized but asymptomatic, antibiotic use/immune suppression allow for overgrowth
How is pseudomembranous colitis typically described?
(bacteria and pseudomembrane)
- gram-positive, bacillus
- spore forming
- toxin A/B (diagnostic)
- obligate anaerobe
- formation of pseudomembranes (not specific)
- exudate eruption from crypts (pathognomonic)
How does C. difficile cause disease?
Toxin A (enterotoxin):
-damages brush borders
Toxin B (cytotoxin):
- disruption of cytoskeleton
- loss of tight junctions
- apoptosis
What is the presentation of pseudomembranous colitis?
(complications?)
- watery diarrhea (occsionally with leukocytes and blood)
- fever
- abdominal pain
- leukocytosis
Complicaitons:
- dehydration
- protein loss -> hypoalbunemia
- toxic megacolon
How is pseudomembranous colitis treated?
metronidazole and vancomycin
What causes Whipple disease and how does it cause disease?
Tropheryma whippelii
bacteria grow in macrophages which then accumulate in the lamina propria and LNs of the bowel -> obstruction of lymph flow -> fat malabsorption
How is Whipple disease typically described?
-intracellular, gram-positive
PAS-positive foamy macrophages in the lamina propria (DDx intestinal tuberculosis; acid-fast stain differentiates, negative in T. whippelii)
What is the presentation of Whipple disease?
Triad:
- diarrhea (malabsorptive)
- weight loss
- arthralgia
What are the viral causes of diarrhea?
- norovirus
- rotavirus
- adenovirus
What are important notes about norovirus?
(description, population, transmission)
-icosahedral, ssRNA virus
causes self-limited diarrhea in both adults and children
- outbreaks associated with water contamination
- sporadic cases associated with person-to-person transmission
What are important notes about rotavirus?
(description, population)
encapsulated, segemented, dsRNA virus
- severe diarrhea in children
- significant cause of mortality in chidlren
What are bacterial causes of secretory diarrhea?
