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GI 2 Pathology--Chapt 16 and 17 > Chapter 17 part 7--small intestine organisms > Flashcards

Chapter 17 part 7--small intestine organisms Flashcards

1
Q

Yersenia

A
  • Yersinia enterocolitica and Yersenia pseudo tuberculosis
  • occurs through contaminated pork, milk, or water
  • Yersinia pestis–bubonic plague
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2
Q

Pathogenesis of Yersinia

A
  • invades M cells using bacterial adhesions to bind to host cell B1 integrins
  • Bacterial iron uptake system increases Yersinia virulence and systemic dissemination
  • Patients with hemolytic anemia or hemochromatosis are likely to become septic and die
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3
Q

Morphology of Yersenia

A

-preferentially invades the ileum, appendix, and right colon; organisms proliferate in lymph nodes resulting in regional nodal hyperplasia and overlying mucosa can become hemorrhagic and ulcerated

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4
Q

Clinical features of Yersenia

A

-Abdominal pain, fever, and diarrhea can occur (mimicking appendicitis)

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5
Q

Extra intestinal manifestations of Yersinia

A
  • common

- pharyngitis, arthralgia and erythema nodosum

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6
Q

Post-infectious complications of Yersenia

A
  • sterile arthritis
  • Reiter syndrome
  • myocarditis
  • glomerulonephritis and thyroiditis
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7
Q

Escherichia coli

A
  • gram-negative bacilli that colonize the normal GI tract
  • most are nonpathogenic but a subset (classified by morphology, in vitro characteristics and pathogenesis) cause disease:
  • ETEC, EPEC, EHEC, EIEC, EAEC
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8
Q

Enterotoxigenic E. coli (ETEC)

A
  • spread in contaminated food or water and are the chief cause of traveler’s diarrhea
  • produce heat-stable toxin that increases intracellular cyclic guanosine monophosphate (cGMP) or a heat-labile choleralike toxin that increases intracellular cAMP
  • both cause chloride and water secretion and inhibit epithelial fluid absorption leading to a noninflammatory watery diarrhea
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9
Q

Enterohemoryhagic E. coli (EHEC)

A
  • spread in contaminated meat, milk, and veggies and produce a shiva-like toxin
  • clinical symptoms and morphology resemble infections with Shigella dysenteriae
  • 2 major serotypes: O157:H7 and non-O157:H7
  • O157:H7 is more likely to cause large outbreaks, dysentery and HUS
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10
Q

Enteroinvasive E Coli (EIEC)

A
  • bacteriologically akin to Shigella

- Although not toxin producing, they invade epithelial cells and cause an acute, self-limited colitis

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11
Q

Enteroaggregative E. Coli (EAEC)

A
  • attach to epithelium by adherence fimbriae aided by a bacterial dispersion that neutralizes the negative surface charge of lipopolysaccharide
  • produce a shigalike toxin but typically cause only a non bloody diarrhea
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12
Q

Pseudomembranous colitis

A
  • formation of adherent inflammatory pseudomembranes overlying sites of mucosal injury
  • classically caused by overgrowth-and-toxin production by Clostridium Difficile after competing bowel organisms have been eliminated by antibiotics
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13
Q

Other organisms that cause PMC

A

-Salmonella, Clostridium perfringes, Staph aureus

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14
Q

Morphology of pseudomembranous colitis

A
  • epithelial denudation with plaque like adhesion of fibrinopurulent-necrotic, gray-yellow debris and mucus
  • Pseudomembrane is not specific and can form with any severe mucosal injury (e.g., ischemia or necrotizing infections)
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15
Q

Clinical features of pseudomembranous colitis

A
  • C. difficile is prevalent in hospitals

- 30% of hospitalized patients can be colonized (vs. 3% of general population)

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16
Q

PMC presentation, Dx and Tx

A
  • fever, leukocytosis, crampy abdominal pain and watery diarrhea
  • toxin detection in stool yields definitive diagnosis
  • Tx= metronidazole or vancomycin
  • 40% incidence of recurrent infection after treatment
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17
Q

Whipple Disease

A

-rare, systemic condition caused by gram-positive actinomycete Tropheryma whipplei

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18
Q

Whipple Disease presentation

A
  • diarrhea, weight loss, malabsorption
  • Extraintestinal manifestations (due to bacterial spread) include arthritis, fever, lymphadenopathy, and neurologic, cardiac, or pulmonary disease
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19
Q

Gross morphology of Whipple Disease

A

-marked villous expansion in small bowel, imparting a shaggy appearance to mucosal surface

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20
Q

Microscopic morphology of Whipple Disease

A
  • dense accumulation of distended foamy macrophages in small intestine lamina propria–these ells are stuffed with PAS-positive bacteria within lysosomes
  • Laden macrophages present in lymphatics, lymph nodes, joints and brain
  • Active inflammation is absent
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21
Q

Recap–Causes of infectious enterocolitis

A
  • Cholera
  • Campylobacter
  • Shigella
  • Salmonella
  • Typhoid fever
  • Yersenia
  • E. Coli
  • PMC
  • Whipple Disease
  • Viral Gastroenteritis
  • Parasitic Enterocolitis
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22
Q

Re-cap–causes of malabsorption and Diarrhea

A
  • CF
  • Celiac Disease
  • Environmental Enteropathy
  • Autoimmune Enteropathy
  • Lactase Deficiency
  • Abetalipoproteinemia
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23
Q

Causes of Viral Gastroenteritis

A
  • Norovirus
  • Rotavirus
  • Adenovirus
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24
Q

Norovirus

A
  • Norwalklike virus
  • single stranded RNA virus
  • accounts for half of all gastroenteritis outbreaks in world
  • Local outbreaks due to contaminated food or water but person-person transmission underlies most sporadic cases
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25
Q

Symptoms of Norovirus

A
  • Immunocompetent patients=self-limited watery diarrhea, often with abdominal pain, nausea and vomiting
  • Biopsy morphology non-specific
26
Q

Rotavirus

A
  • Encapsulated segmented double stranded RNA virus
  • most common cause of severe childhood diarrhea
  • readily spread bw people
  • minimal infective inoculum is 10 particles
27
Q

Rotavirus infects what cells?

A
  • selectively infects and destroys mature small intestine enterocytes and epithelium is repopulated with immature secretory cells
  • net secretion of water and electrolytes is compounded by malabsorption and osmotic diarrhea
28
Q

Adenovirus

A
  • second most common cause of pediatric diarrhea
  • present with self-limited diarrhea, vomiting and abdominal pain
  • histo=non-specific
29
Q

Parasitic Enterocolitis

A
  • common organisms:
  • Ascaris lumbricoides
  • Strogyloides
  • Necator duodenal and Ancylostoma duodenale
  • Enterobious vermicularis (pinworms)
  • Trichuris trichina (whipworms)
  • Schistosoma
  • Intestinal cestodes (tapeworms)
  • Diphyllobothrium datum
  • Entamoeba histolytica
  • Giardia lambda
  • Cryptosporidium
30
Q

Ascaris lumbricoides

A
  • infects over billion ppl worldwide
  • fecal-oral transmission followed by intestine-liver-lung-intestine life cycle
  • Systemically disseminated larvae can cause hepatic abscesses or pneumonitis
  • adult from masses induce an eosinophil-rich inflammation that can physically obstruct the intestine or biliary tract
  • Dx by detecting eggs in stool
31
Q

Stronyloides

A
  • larvae in focally contaminated soil penetrate unbroken skin, migrate to lungs (where they cause inflammation) and then mature into adult worms in GI tract
  • Eggs hatch in intestine and luminal larvae can penetrate mucosa causing auto infection
  • induces strong eosinophil responses!
32
Q

Nectar duodenale and Ancylostoma duodenale (hookworms)

A
  • billions of ppl infected
  • life-cycle begins with larval penetration through skin and subsequent maturation in lung
  • after migration to trachea, they are swallowed
  • worms then attach to duodenal mucosa and extract blood causing mucosal damage and iron-deficiency anemia
33
Q

Enterobius vermicularis (pinworms)

A
  • fecal-oral transmission
  • do not invade host tissue and entire life cycle transpires in intestinal lumen, they rarely cause serious illness
  • Adult worms migrate at night to anal orifice where eggs are deposited causing intense irritation and pruritis
34
Q

Trichuris triciuria (whipworms)

A
  • primarily infect children

- no tissue invasion but heavy manifestations can cause bloody diarrhea and rectal prolapse

35
Q

Schistosoma

A
  • adult worms reside within mesenteric veins

- trapped eggs in mucosa and submucosa induce a granulomatous response with bleeding and obstruction

36
Q

Intestinal cestodes (tapeworms)

A
  • infections occur by ingesting raw or undercooked fish, pork, or other contaminated meats
  • Parasites reside within lumen without tissue invasion
  • a codex attaches to mucosa, and proglottids contain eggs that shed in feces
37
Q

D. latum

A
  • fish tapeworm

- compete for host dietary vitamin B12 and cause B12 deficiency with megaloblastic anemia

38
Q

Entamoeba histolytica

A
  • fecal-oral transmission
  • Infection occurs by ingesting acid-resistant cysts
  • released trophozoites colonize colonic epithelium and reproduce under anaerobic conditions
  • Dysentery results when amoebae induce colonic epithelial apoptosis, invade into lamina propria, and attract neutrophils
  • Subsequent damage yields classic flask-shaped ulcer with narrow neck and broad base
39
Q

Entamoeba histolytica–amoeba can also embolize to? Tx?

A
  • liver–producing abscesses in over 40% of infected individuals
  • Metronidazole targets organism-specific enzyme pyruvate oxidoreductase
40
Q

Giardia Lamblia

A
  • Flagellated protozoan and most common pathogenic parasitic infection in humans
  • cysts are ingested from focally contaminated water or food
  • duodenal trophozoites exhibit characteristic morphology (pear-shaped and binucleate!!!)
41
Q

Giardia invasion? How does it cause damage?

A
  • does not invade tissue but secrete products that damage the microvillus brush border and cause malabsorption
  • Secretory IgA and mucosal IL-6 needed for clearance so immunocompromised severely affected
42
Q

How do Giardia persist for prolonged duration in Immunocompromised hosts?

A

-through continuous modification of their major surface Ag

43
Q

Cryptosporidium

A
  • cause self-limited diarrhea in immunocompetent hosts but can cause chronic diarrhea in IC
  • contaminated drinking water=transmission
  • as few as 10 oocytes can cause Dz
  • Stomach acid activates proteases that release motile sporozoites which are subsequently internalized by absorptive enterocytes
44
Q

What causes the watery diarrhea seen in cryptosporidium infection

A

-Sodium malabsorption, chloride secretion and increased epithelial permeability responsible for ensuing watery diarrhea

45
Q

Irritable Bowel Syndrome

A
  • chronic, relapsing abdominal pain, bloating, and changes in stool frequency or form
  • most common in females aged 20-40
  • results from interplay of psychologic stressors, diet, and abnormal GI motility, perhaps via disruption of signaling in brain-gut axis
46
Q

Inflammatory Bowel Disease

A
  • results from inappropriate mucosal immune responses to normal gut flora; comprises two disorders:
  • Ulcerative colitis
  • CD (regional enteritis)
47
Q

Ulcerative colitis

A
  • severe ulcerating inflammation extend into mucosa and submucosa
  • limited to colon and rectum
48
Q

CD (also called regional enteritis)

A

-typically transmural inflammation, occurring anywhere in GI tract

49
Q

Epidemiology of IBD

A
  • more common in women–in teens/20s

- more common in developed countries leading to hygiene hypothesis

50
Q

Hygiene hypothesis

A

-reduced frequency of enteric infections results in inadequate development of mucosal immune regulation

51
Q

Pathogenesis of IBD

A

-results from combo of defects in host interactions with GI flora, intestinal epithelial dysfunction and aberrant mucosal immunity!!

52
Q

Current model of pathogenesis of IBD

A
  • transepithelial flux of microbes activates innate and adaptive immune responses
  • In susceptible host, subsequent TNF release and other inflammatory signals increase tight junction permeability
  • establish a self-amplyfing cycle of microbial influx and host immune responses that ultimately culminate in IBD
53
Q

Genetics of IBD

A
  • most genes are shared bw UC and CD

- familial clustering and concordance of monozygotic twins is 50% for CD and 50% for UC

54
Q

What gene polymorphisms is associated with CD? What does it encode?

A
  • NOD2 (nucleotide oligomerization binding domain 2)
  • encodes a protein that binds to intracellular bacterial peptidoglycan and subsequently activates NF-kB
  • Disease associated NOD2 variants are less effective are recognizing and combating microbes which enter lamina propria and trigger greater inflammatory responses
  • Other genes also related to microbial recognition and regulate immune responses
55
Q

Mucosal immune responses

A
  • In CD, helper T cells are polarized to produce TH1 cytokines
  • TH17 cells may also be contributory and polymorphisms in the IL-23 receptor (regulating TH17 cell development) may be protective
56
Q

What cytokines are associated with IBD pathogenesis

A

-TNF, IFN-y, and IL-13 and immunoregulatoriy molecules like IL-10 and TGF-B also contribute to IBD pathogenesis

57
Q

Mutations in what are linked to severe, early onset IBD?

A

-Autosomal recessive mutations of IL-10 and IL-10 receptor

58
Q

Epithelial cell defects in IBD

A

-Barrier dysfunction, including defects in epithelial tight junctions, transporter genes, and polymorphisms in extracellular matrix proteins or metalloproteinases are associated with IBD

59
Q

Microbiota

A

-Composition of the GI flora, and in particular those organisms that populate the intestinal mucus layer may influence pathogenesis by affecting innate and adaptive immune responses

60
Q

Treatment of IBD

A

-Antibiotics can be helpful in managing IBD

GI 2 Pathology--Chapt 16 and 17 (14 decks)

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