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GI- Week 2 > Infectious Enterocolitis, Anaerobic infections, and H. pylori > Flashcards

Infectious Enterocolitis, Anaerobic infections, and H. pylori Flashcards

1
Q
A
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2
Q

90% of infectious diarrheas are caused by ______

A

viruses

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3
Q

•Persistent diarrhea (> 10-14 days) is likely from ______

A

a parasite

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4
Q

What is one thing you need to start considering with chronic diarrhea?

A

HIV status- diarrhea is a BIG problem with AIDs pts.

–Mycobacterium avium intracellulare, CMV

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5
Q

What bugs cause inflammatory diarrhea?

A
  • Shigella
  • Enterohemorrhagic E. coli
  • Enteroinvasive E. coli
  • Salmonella
  • C. jejuni
  • C. difficile
  • Yersinia enterocolitica
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6
Q

Describe Shigella, E. Coli, and Salmonella (all Enterobactereriaceae)

A

These are all gram-facultative anaerobic rods that:

are oxidase NEGATIVE (colorless on an oxidase test; i.e. cytochrome c oxidase negative)

-can reduce nitrates to nitrite (positive on a dipstick test)

All are motile except Shigella

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7
Q

What are some antigenic structures of Shigella, E. Coli, and Salmonella?

A

H (flagellar) antigens

O antigens: O-side chain (polysaccharide) of LPS

K antigen: Capsule

Shigella: O and K only, no H (not motile)

Salmonella: O, H, and Vi (capsular)

E. Coli: O, H, and K

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8
Q

E. coli are part of normal GI flora. Why dont they normally cause infection?

A

Don’t cause infection because they lack PAI

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9
Q

Describe shigella

A

Gram-negative/facultative rod

non-motile (negative on motility test),

glucose fermenting; no lactose fermentation; does not produce H2S (red slant; yellow butt on KIA Slant),

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10
Q

What are some prominent species of Shigella?

A

–S. dysenteriae: Epidemics in Central/South America

–S. sonnei: 70% of U.S. cases, mostly children

–S. flexneri: 2nd most common in US, most common worldwide

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11
Q

Is Shigella easy to get?

A

YES!! It is HIGHLY transmittable with a low infectious dose

1 of the most common causes of bloddy diarrhea (resulting in 1 million deaths/yr).

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12
Q

How is Shigella spread?

A

fecal-oral usually via contaminated water/food

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13
Q

What pts commonly get Shigella?

A

–Daycare centers, migrant workers, travelers to developing countries, nursing homes

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14
Q

What is this?

A

Shigellosis (shigella)

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15
Q

Describe the pathogenesis of Shigella

A

Shigella is taken up by GI epithelial (M) cells in the intestine and proliferate intracellularly, and then escape into the lamina propria where they are phagocytosed by macrophages. Inside macrophages, shigella induced apoptosis, producing an inflammatory response that damages epithelia and allows Shigella to gain access to colonic epithelial cells where they can invade

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16
Q

How does Shigella spread to adjacent cells once in the colonic epithelial cells?

A

Shigella spreads into adjacent cells via bacterium-induced, membrane- bound protrusions from the surface of the host cell. The formation of these protrusions depends on cellular actin polymerization proteins called formins.

The bacterium lyses the membranes that surround it, freeing itself into the cytoplasm of the new cell

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17
Q

How does Shigellosis present (give the incubation period and duration of illness)?

A

1 week incubation period following infection followed by:

  • onset of watery diarrhea (which progresses to dysentery (bloody) in 50%),
  • typically the onset of fever and abdominal pain.

All symptoms are self-limited and last about 1 week, typically

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18
Q

What are some complications of Shigellosis?

A

–reactive arthritis, urethritis, conjunctivitis (formerly known as Reiter’s syndrome)

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19
Q

What is a unique complication of S. dysenteriae and why?

A

Hemolytic uremic syndrome, if it produces Shiga (AB) toxin

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20
Q

ABX can be used to shorten the disease course of Shigellosis and reduce the duration of organism shedding in stools (ie. less likely to pass on). What are the preferred ABX options?

A

Ceftriaxone, Ciprofloxacin, Azithromycin

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21
Q

T or F. E. Coli can cause inflammatory and non-inflammatory diarrhea

A

T.

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22
Q

What are the 5 major strains of diarrheagenic E. Coli?

A

–Enterohemorrhagic E. coli (inflammatory)

–Enteropathogenic E. coli (non-inflammatory)

–Enterotoxigenic E. coli (non-inflammatory)

–Enteraggregative E. coli (non-inflammatory)

–Enteroinvasive E. coli (inflammatory)

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23
Q

Describe Enterohemorrhagic E. Coli (aka STEC- Shiga toxin producing E. Coli). What are the common sources?

A

This is the classic O157:H7 E.Coli caused by ingesting (foodbourne):

inadequately cooked meat (hamburgers), contaminated vegetables and milk (Or human-to-human spread- low infectious dose)

This produces Shiga-like toxins and thus presents clinically very similarly to Shigellosis (S. dysenteriae), requiring hospitalization in 25-50% of pts.

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24
Q

Enterhemorrhagic E. Coli causes ____

A

hemorrhagic colitis

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25
Q

Describe the virulence factors of EHEC

A

–Locus of Enterocyte Effacement (LEE)

  • PAI
  • Type III secretion system (Delivers E. coli receptor to host cell)
  • Pedestal formation for attachment (Responsible for the diarrhea)
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26
Q

How does EHEC present? Duration of illness?

A

Little fever,

acute onset of cramps and watery diarrhea initially. Within 24 hrs, the diarrhea becomes bloody (hemorrhagic colitis) and lasts an additional 8 days typically

-O157:H7 strains more likely to cause large outbreaks, bloody diarrhea, hemolytic uremic syndrome, and ischemic colitis

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27
Q

What toxins does EHEC use?

A

–Shiga toxins (or Shiga-like toxins), which are AB toxins encoded on a lysogenic bacteriophage

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28
Q

How do Shiga AB toxins work?

A

B subunits bind toxin to its receptor on cells and then:

the A subunit then enters the cytosol and cleaves a specific adenine residue from the 28S rRNA of the 60S ribosomal subunit, halting protein synthesis and causing death

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29
Q

Hemolytic uremic syndrome is a feared, less common complication of ____ and ______

A

EHEC and Shigellosis (less common)

NOTE: EHEC accounts for over 90% of HUS in children (but only complicates 6-9% of EHEC infections)

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30
Q

HUS caused by EHEC or Shigellosis is one of the main causes of ____ in children under 3 yo

A

AKI

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31
Q

WHEN and HOW does HUS present in EHEC and Shigellosis pts.?

A

5-10 days after the onset of diarrhea:

microangiopathic hemolytic anemia and thrombocytopenia begin, leading to dialysis requiring AKI in over 50% of pts. (most regain kidney function).

Neurologic symptoms including seizures and somnolence occur in 25%

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32
Q

How does Shiga toxin cause HUS?

A

Shiga toxin is absorbed from the inflamed gastrointestinal mucosa into the circulation, where it alters endothelial cell function in some manner that results in platelet activation and aggregation

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33
Q

Note about microangiopathic hemolytic anemia in HUS in EHEC and Shigellosis pts.

A

Microangiopathic hemolytic anemia occurs when the red cell membrane is damaged in circulation, leading to intravascular hemolysis and the appearance of schistocytes.

The hemolytic anemia and renal failure occur because there are receptors for Shiga toxin on the surface of the endothelium of small blood vessels and on the surface of kidney epithelium. Death of the endothelial cells of small blood vessels results in a microangiopathic hemolytic anemia in which the red cells passing through the damaged area become grossly distorted (schistocytes) and then lyse. Thrombocytopenia occurs because platelets adhere to the damaged endothelial surface. Death of the kidney epithelial cells leads to renal failure.

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34
Q

How is EHEC diagnosed?

A

-first a MacConkey agar to determine if it is in fact a gram negative (gram + wont grow on this), then

Sorbitol-MacConkey Agar (The 0157:H7 strain does not ferment sorbitol so colonies will be white/translucent (see arrow in picture); all other EHEC and E. Coli colonies will be red/pink

-or PCR or ELISA used to detect Shiga toxin

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35
Q

How is EHEC tx?

A

–Supportive care and monitoring for complications

–

NOTE: Avoid anti-diarrheals (increase risk of systemic complications) and ABX (not beneficial and may predispose to HUS by inducing more Shiga toxin release.)

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36
Q

Describe EIEC (Enteroinvasive E. Coli). What toxins does it use?

A

This is similar to shigella and causes similar disease progression (no toxins however)

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37
Q

Where is EIEC most common? How does transmission occur?

A

in young children in developing countries

EIEC is transmitted via food/water or human-human and invades intestinal cells, multiples intracellularly, and then extends into adjacent intestinal cells

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38
Q

Describe Salmonella

A

Gram-negative/facultative rod (just like E. Coli and Shigella),

  • motile
  • lactose negative (like Shigella) (both are colorless/white on a regular MacConkey agar)
  • black center on SS agar due to H2S production
  • glucose fermenter; non-lactose fermentor; H2S += red slant; black butt on KIA Slant
39
Q

What are the types of Salmonella?

A
  • Salmonella enterica serotype Typhimurium (formerly S. typhi)
  • nontyphoid Salmonella (S. enteritidis) (food-poisoning)
40
Q

S. enterica is the causative agent of ________

A

Typhoid fever (S. enterica does not cause gastroenteritis)

NOTE: S. paratyphi is another species that can cause illness similar to Typhoid fever (also does not cause gastroenteritis)

41
Q

Nontyphoid Salmonella, most commonly _____ causes salmonellosis

A

S. enteritidis (Significant source of gastroenteritis from food poisoning)

42
Q

What are some sources of S. enteritidis?

A

–Dairy products

–Meat

–Poultry and eggs

–Pet turtles, lizards, other reptiles

–Human-to-human

43
Q

Describe the pathogenesis of S. enteritidis Salmonellosis

A

S. enteritidis attach to the M cells and are endocytosed through a complex pathway:

1) Virulence genes encode a type III secretion system capable of transferring bacterial proteins into M cells and enterocytes. These abcterial proteins trigger bacterial endocytosis and allow bacterial growth within endosomes.
2) Inside the endosomes, bacteria cross the basal membrane and enter the lamina propria where an inflammatory response occurs (S. enteritidis also kills macrophages)

44
Q

How does Salmonellosis present (incubation period and duration of illness too)?

A

There is a 1-3 day incubation period followed by:

N/V, diarrhea, and crampy abdominal pain (+/- fever 50%)

that all typically last around 3-4 days

45
Q

How common in invasive disease with Salmonellosis? Whos is particularly at risk?

What else can Salmonellosis cause?

A

–5% will develop invasive disease: bacteremia, endovascular infections, endocarditis, osteomyelitis.

Predilection for aortic plaques, bone prostheses

–Can also develop reactive arthritis

46
Q

How is Salmonellosis diagnosed?

A

Routine stool culture usually

other options: SS, KIA Slant, Motility test, etc.

47
Q

What Salmonellosis pts require tx?

A

Tx is NOT requires for healthy ppl between the ages of 2-50, but is indicated for those at risk of disseminated/invasive disease

48
Q

What pts with Salmonellosis are at risk for dissemination/invasive disease?

A
  • Immunocompetent patients with severe infection requiring hospitalization
  • Those with known or suspected atherosclerotic plaques and endovascular/bone prostheses
  • Immunocompromised (HIV, those who receive steroids or other immunosuppressants), sickle cell disease
49
Q

What is the tx of Salmonellosis in these pts? Should you treat right away?

A

•Flouroquinolones.

Susceptibility testing should be performed.

50
Q

What causes Typhoid (enteric) fever?

A

S. enterica serotype Typhi (S. paratyphi can cause a similar illness)

51
Q

What are the reservoirs of S. enterica?

A

ONLY humans

52
Q

How does S. enterica transmission occur?

A

•Transmission occurs person-to-person (fecal-oral, infected food handler) or via contaminated food/water

53
Q

What pts typically get Typhoid fever?

A

More common in children and young adults than in older pts.

  • Worldwide, most prevalent in impoverished, overcrowded areas with poor access to sanitation
  • 200-300 cases reported in the U.S. each year, 80% occurring among travelers to countries where typhoid fever is endemic (South-central Asia common). Outbreaks in the U.S. most often foodborne
54
Q

Describe the pathogenesis options of Typhoid fever

A

In the small intestine S. enterica is taken up by M cells. Bacteria are then engulfed by macrophages in the underlying lymphoid tissue, where they are then free to disseminate to lymph nodes and RES, with subsequent bacteremia and possible sepsis OR

Organisms proliferate in the submucosa and lead to hypertrophy of Peyer’s patches due to influx of inflammatory cells. Hypertrophy and subsequent necrosis of submucosal tissues can cause GI tract perforation OR

-Chronic carriage can occur in the biliary tract

55
Q

T or F. Patients with typhoid fever may develop “secondary” bacteremia with other organisms due to microscopic or macroscopic breaches in the intestinal mucosal barrier

A

T. This is important to understand!!

56
Q
A
57
Q

How does Typhoid fever present (incubation period too)?

A

There is an incudbation period of 5-21 days followed by distinct periods of disease marked by weeks from day 21 incubation

58
Q

What are the symptoms of the 1st week of Typhoid fever following incubation?

A

–rising fever/chills develop; patients are bacteremic

•Relative bradycardia can be observed

59
Q

What are the symptoms of the 2nd week of Typhoid fever following incubation?

A

–adominal pain and “rose spots” (faint salmon-colored macules on trunk/abdomen) may appear (see picture)

60
Q

What are the symptoms of the 3rd week of typhoid fever? What is the outcome of most infections?

A

–hepatosplenomegaly, GI bleeding, perforation, secondary bacteremia

•Septic shock may develop as well as AMS

–In the absence of death or severe complications, symptoms resolve over weeks to months

61
Q

How is Typhoid fever diagnosed?

A

Blood cultures positive in 50-80% of patients. May require several days of incubation

62
Q

How is Typhoid fever tx?

A

Ceftriaxone, Azithromycin, or Ciprofloxacin (unless patient has been in an area with high rates of flouroquinolone resistance such as South Asia)

63
Q

T or F. There is a preventative Typhoid fever vaccine

A

T.

64
Q

Describe Campylobacter jejuni

A

Thin, spiral shaped gram negative rods

MOST common bacterial enteric pathogen in developed countries and are an important cause of traveler’s diarrhea

65
Q

How do most Camp jej. infections occur?

A

Most infections due to eating improperly cooked chicken;

other sources include unpasteurized milk or contaminated water.

66
Q

What are some reservoirs for Campylobacter jejuni?

A

sheep, cattle, chickens, wild birds, dogs

(HIGHLY transmisible-very low infectious dose)

67
Q

How does Campylobacter jejuni infection present (inucbation period)?

A

There is a 1 week incubation period followed by:

onset of watery diarrhea (10+ BM/day) which bccomes bloody in 15% of adults and 50+% of children, along with fever, crampy and periumbilical abdominal pain

that are ALL self-limited over the coruse of 3-7 days

68
Q

How is Camp jej infection diagnosed?

A

stool culture

69
Q

How is Camp jej infection tx? For everyone?

A

–Azithromycin or Cipro are DOC, however resistance rates to flouroquinolones are rising

Only warranted for those with severe disease or at risk of severe disease (bloody stools, high fever, worsening symptoms)

70
Q

What are some complications of Campylobacter jejuni infection?

A
  • Guiilain Barre Syndrome (note that camp jej is the most common cause of GBS BUT this complication only occurs in 0.1% of infections)
  • Erythema nodosum
  • Reactive arthritis and manifestations such as urethritis, conjunctivits (Reiter’s Syndrome) (can also be seen with Salmonella, Shigella, and Yersinia)
71
Q

Reiter’s Syndrome as a complication fo Camp jej infection is mroe common with which pts?

A

Those with HLAB27 haplotypes

72
Q

Describe Guillian Barre Syndrome. When does this occur in relation to C. jejuni infection if its going to happen?

A
  • Molecular mimicry caused by serum antibodies to C. jejuni LPS cross-reacting with peripheral and central nervous system gangliosides resulting in Ascending paralysis
  • Symptoms start one to two weeks after GI infection
73
Q

Describe Yersinia enterocolitica

A

A gram neg coccobacilli with bipolar (safety pin) staining

74
Q

What are some sources of Yersinia entero.

A

pork, raw milk, contaiminated water, pet feces

75
Q

What parts of the GI are most commonly infected by Yersinia entero.?

A

•Infection preferentially involves ileum, appendix, right/ascending colon (RLQ)

76
Q

How does Yersinia entero infection present?

A

–Abdominal pain is the main feature located in the RLQ

•***Peyer patch and mesenteric lymph node hyperplasia can mimic acute appendicitis in teenagers and young adults***

–Nausea/vomiting common

–Fever/diarrhea can also occur

77
Q

What extraintestinal symptoms are common with Yersinia entero?

A

Reiter’s syndrome

erythema nodosum

78
Q

How is Yersinia entero diagnosed and tx?

A

Diag: stool culture

Tx: most cases not warranted

79
Q

Describe Clostridium difficile

A

This is an anaerobic, spore-forming gram-positive rod

•Organism is carried in the GI tract in 3% of the population and 30% of hospitalized patients (NOT really commensal!)

80
Q

How is C. diff transmitted?

A

fecal-oral (Hands of hospital personnel are important intermediaries)

81
Q

_____ is the most common nosocomial cause of diarrhea and most common cause of antibiotic-associated diarrhea

A

C. diff

82
Q

Describe the pathogenesis of C. diff. What toxins does it use?

A

Typically infection occurs in nosocomial settings when ABX use suppresses the normal flora allowing for C. diff to multiply and produce its major toxins, A and B, which cause glucosylation of small GTPases such as Rho which are involved in cytoskeleton structure and signal transduction

83
Q

Describe Toxin A (enterotoxin) of C. diff

A

This toxin disrupts colonic mucosal cell adherence to colonic basement membrane and damages villous tips; the subsequent inflammation leads to fluid secretion

84
Q

Describe Toxin B (cytotoxin) of C. diff

A

•Toxin B (cytotoxin) causes depolymerization of actin, resulting in loss of cytoskeletal integrity, apoptosis and death of enterocytes

NOTE: Both toxins (A>B) stimulate monocytes and macrophages, which release IL-8 resulting in tissue infiltration with neutrophils; both cause disruption of epithelial tight junctions

85
Q

How does C. diff infection present? What are the variants?

A

Watery diarrhea is the cardinal and most consistent symptom but the spectrum of manifestations include asymptomatic carrier states to fulminant disease with toxic megacolon. The main clinical variants include:

  • C. diff associated diarrhea (CDAD) with colitis
  • Pseudomembranous colitis
  • Fulminant colitis
  • Toxic megacolon
86
Q

Describe the presentation of C. diff associated diarrhea (CDAD) with colitis variant

A

–watery diarrhea (10-15 BM/day), leukocytosis, mild lower abdominal pain/cramping, low grade fever,

CDAD occur in the setting of an antibiotic; symptoms may begin during antibiotic therapy or 5-10 days following antibiotic administration

87
Q

Describe the Pseudomembranous colitis variant of C. diff infection

A

–Present similarly to CDAD. In addition, sigmoidoscopy shows pseudomembranes, which are adherent layers of inflammatory cells and debris at sites of colonic muscle injury

88
Q

Describe the Fulminant colitis variant of C. diff infection.

Toxic megacolon variant?

A

–severe disease (severe abdominal pain, abdominal distention, fever, hypovolemia)

–Toxic megacolon variant: Colonic dilatation >7 cm with severe systemic toxicity

89
Q

Note about C. diff

A

–Hypervirulent strains are emerging: more severe disease, lower clinical cure rates, higher relapse rates (NAP-1/027)

90
Q

C. diff

A
91
Q

What are the risk factors for C. diff infection?

A

Age, hospitalization, ABX tx

PPI use is NOT a risk factor!!

92
Q

How is C. diff infection diagnosed?

A

–Cell culture cytotoxicity assay: “gold standard”. Stool sample is added to a monolayer of cultured cells. If C diff toxin is present, it exerts a cytopathic effect in tissue culture. Labor intensive, takes 2 days.

–PCR detecting toxins A and B: highly sensitive and specific

–EIA for toxins A and B: high false negative rate (sensitivity 75%)

93
Q

How is C. diff tx today?

A

–Flagyl (metronidazole) 1st line usually. If C. diff is severe, PO Vancomycin is indicated as 1st line.

1st recurrence: Flagyl.

2nd recurrence: PO Vancomycin extended course

94
Q

What are some other options for C. diff tx?

A

Fidaxomycin relatively new, superior clinical response and less recurrences when compared head-to-head with Vanc

–Fecal transplants hot new thing

GI- Week 2 (27 decks)

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