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GI block > Enteric Bacteria - inflammatory diarrhea > Flashcards

Enteric Bacteria - inflammatory diarrhea Flashcards

1
Q

What are the bacteria that cause inflammatory diarrhea?

A

Shigella, EHEC, EIEC, salmonella, c. Jejuni, c. Difficile, yersinia enterocolitica.

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2
Q

Why don’t ecoli cause problems normally even though it’s in GI tract normally?

A

Don’t cause infection because they lack PAI

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3
Q

General characteristics of shigella, ecoli, and salmonella?

A

-gram neg facultative anaerobic rods! -ferment glucose with acid production -oxidase negative - reduce nitrates to nitrite (dipstick test) -motile except shigella - antigenic structures used in serotyping -h for flaggelar antigens -o antigens on o side chain of LPS- ecoli part of normal GI tract flora but don’t cause infection because they lack PAI

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4
Q

General characteristics of shigella

A
  • gram negative, non motile, nonlactose fermenting, don’t produce h2s
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5
Q

Most common cause of shigella in us?

A

S. Sonnei - 70% of cases in US esp in children

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6
Q

Most common cause of shigella worldwide?

A

S. Flexneri. 2nd most common cause in the US

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7
Q

Most common cause of shigellosis in south and Central America

A

S. Dysenteriae

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8
Q

Epidemiology of shigellosis

A

One of the mcc of BLOOdy diarrhea Highly transmissible via fecal oral route…low infectious dose needed DAYCARE centers!!! Migrant workers, travelers to developing countries, nursing homes

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9
Q

Pathogenesis of shigella?

A
  • resistant to acidic environment of stomach- gets taken up by m cells of the intestine –> proliferate intracellularly and move into lamina propria where macrophages phagocytize them causing apoptosis –> inflammation –> damage to epithelial helping shigella gain access to colonic epi cells they can no invade - shigella goes to adjacent cells via bacterium induced membrane bound protrusions from surface of host cell- these protrusions occur via formins which are cellular actin polymerization proteins - bacteria lyse surrounding membrane to go to cytoplasm of new cell
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10
Q

Clinical course of shigellosis

A

Incubation period is 1 week, Abdominal pain, diarrhea and fever x 1 week Watery diarrhea –> bloody diarrhea in half the cases

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11
Q

Complications of shigellosis

A

Reactive arthritis, urethritis, conjunctivitis, Hus can occur in some ppl after infection with S. Dysenteriae producing shiga toxin (AB toxin)

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12
Q

Tx of shigellosis

A

Ab shorten course and duration of shedding of organisms in stoolsCeftriaxone, cipro, azithromycin

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13
Q

General characteristics of enterohemorrhagic e.coli

A
  • called STEC (shiga toxin producing E.coli)
  • cant ferment sorbitol like other types of E. coli
  • categorized as 0157:h7 or non-0157:h7
  • RAW HAMBURGERS, contaminated veg and milk
  • can also be transmitted human to hum
  • need low infectious dose
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14
Q

Pathogenesis of EHEC

A
  • Locus of Enterocyte Effacement (LEE)
    • PAI
    • Type 3 secretion system- injectisome
    • deliver Ecoli R to host cell
    • pedestal formation for attachment
    • responsible for diarrhea
  • Shiga toxins - AB toxin
    • b subunit bind toxin to its receptor on cells
    • A subunit then enters the cytosol and cleaves a specific adenine residue from the 28S rRNA of teh 60S ribosomal subunit –> stop protein synthesis –> cell death
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15
Q

Clinical presentation

A
  • little fever, acute onset of cramps and watery diarrhea
  • watery diarrhea –> bloody diarrhea (hemorrhagic colitis) within 24 hours. can last about 8 days.
  • O157:H7 strains–large outbreaks, bloody diarrhea, HUS, and ischemic colitis
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16
Q

What do shiga toxins do?

A

remove adenine from large (28S ribosomal RNA) –> stopping protein synthesis.

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17
Q

What is one of the main casues of AKI in children under 3?

A

HUS- hemolytic uremic syndrome

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18
Q

Which bacteria has complications causing HUS?

A

EHEC (>90% in children) and Shigellosis (less common)

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19
Q

clinical manifestations of HUS

A
  • 5 days after onset of diarrhea
  • microangiopathic hemolytic anemia and thrombocytopenia
  • AKI w/ dialysis required in > 50% of pts (most regain kidney function)
  • neurologic symptoms like seizures and somnolence in 25%

mortality rate about 5%

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20
Q

How do shiga toxin cause damage?

A

absorbed in inflamed GI mucosa into circulation where it alters endothelial cell function –> platelet activation and aggregation somehow.

** hemolytic anemia and renal failure occur bc there are Rs for shiga toxin on surface of endothelium of small blood vessels and on the surface of kidney epithelium.

  • death of endothelial cells of small blood vessels result in microangiopathic hemolytic anemia –> schistocytes and then lysis or RBC.
  • Thrombocytopenia occur bc platelets adhere to the damaged endothelial surface . Death of kidney epithelial cells lead to renal failure.
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21
Q

how do you diagnose EHEC

A
  • use sorbitol macconkey agar- the 0157:h7 strain doesnt ferment sorbitol so will be white but other ecoli and EHEC will be red/pink
  • PCR or ELISA to detect Shiga toxin
22
Q

Tx for EHEC?

A

- supportive care and monitoring for complications

  • Avoid anti-diarrheals as they can risk systemic complications
  • Antibiotics not helpful and may predispose HUS by inducing more shiga toxin release!
23
Q
A
24
Q

General characteristics of EIEC (enteroinvasive E. Coli)

A
  • similar to shigella and causes similar disease but no toxins produced

**- **food/water transmission

  • person to person contact
  • most commonly seen in YOUNG CHILDREN IN DEVELOPING COUNTRIES.
25
Q

pathogenesis of EIEC

A
  • bacteria invades intestinal cell–> multiplies intracellularly and extends into adjacent intestinal cells
26
Q

General characteristics of Salmonella

A

gram negative bacilli

  • non lactose fermenting

produces H2S

  • Salmonella Enterica- typhoid fever. does NOT cause gastroenteritis
  • S. Paratyphi-like typhoid fever also and does NOT cause gastroenteritis
  • Nontyphoid salmonella aka S. enteritidis- DOES cause gastroenteritis from food poisoning.
27
Q

Salmonella enteritidis source of infection?

A
  • dairy products, meat, poultry and eggs

- pet turtles, lizards and other reptiles

  • human to human
28
Q

pathogensis of salmonellosis

A
  • attach to M cells and endocytosed through complex pathway
  • type 3 syringe secretion system capable of tranferring bacterial proteins into M cells and enterocytes
  • bacterial proteins trigger endocytosis and allow bacterial growth within endosomes
  • bacteria cross basal membrane to enter the lamina propria
  • inflammatory response occurs: s. enteritidis also kills macrophages
29
Q

clinical presentation of salmonellosis

A
  • incubation period 1-3 days
  • Nausea, vomiting, diarrhea (can be bloody), crampy abd pain
  • fever in 50%

illness lasts about 3-4 days

  • 5% will develop invasive disease like bacteremia, endovascular infections, endocarditis, osteomyelitis
  • predilection for aortic plaques, and bone prosthesis.
  • can also develop reactive arthritis
30
Q

how do you diagnose salmonellosis?

A

routine stool culture

31
Q

Tx of salmonellosis?

A
  • not required for healthy ppl btwn ages of 2 and 50
  • tx indiciated for those at risk of disseminated/invasive disease:
    • like immunicompetent patients with severe infection requiring hospitaliztion,
    • suspected atherosclerotic plaques and endovasuclar/bone prostheses
    • immunocompromised ppl like HIV, those receiving steroids, sickle cell disease
  • Tx : Flouroquinolones- susceptibility testing should be performed
32
Q

general characteristics of typhoid fever

A
  • caused by s enterica. s. paratyphi can cause a similar illness
  • humans are sole reservoir
  • transmission person to person (fecal-oral, infected food handler) or via contaminated food/water

children and young adults > older pts

  • worldwide, impoverished, overcrowded area with poor access to sanitation
  • travelers to south central asia

outbreaks in US most often foodborne

33
Q

pathogenesis of typhoid fever

A
  • in small intestine, organisms are taken up by and invade M cells
  • bacteria engulved by macrophages in the lyphoid tissue
  • organisms disseminate to lymph nodes and RES –> spread to blood (sepsis)
  • organism can proliferate in submucosa leading to hypertrophy of peyer’s patch d/t influx of inflammatory cells
  • chronic carriage can occur in biliary tract
  • hypertrophy and subsequent necrosis of submucosal tissue can cause GI tract perforation.
34
Q

clinical presentation of typhoid fever

A
  • incubation period 5-21 days
  • 1st week of illness: rising fever/ chills develop. pts are bacteremic. relative brady can be observed
  • 2nd week: abd pain and rose spots on turnk/abd
  • 3rd week: hepatosplenomegaly, GI bleed, perforation, secondary bacteremia (septic shock and AMS can occur)
  • in absence of death or severe complications, symptoms resolve over weeks to months
35
Q

Diagnosis of typhoid fever

A
  • blood cultures positive in 50-80% of pts. May require several days of incubation
36
Q

Tx of typhoid fever

A
  • Ceftriaxone, azithro, cipro (unless pt has been in an area with high rates of flouroquinolone resistance such as south asia)

**prevention with vaccine

37
Q

general characteristics of Campylobacter jejuni?

A

thin, spiral shaped gram neg rods (C.coli) is another species that can cause enterocolitis

  • most common bacterial enteric pathogen in developed countries
  • important bc of TRAVELER’S DIARRHEA
  • most infections d/t eating improperly cooked chicken, unpasterized milk or contaminated water
  • low infectious dose needed
    reservoirs: sheep, cattle, chicken, dog, wild birds
38
Q

clinical presentation of c. jejuni

A
  • incubation period 1 week
  • watery diarrhea (10+ bm/day) –> bloody diarrhea in 15% of adults and > 50% of children

fever, crampy periumbilical abd pain

  • self limited over 3-7 days
39
Q

diagnosis of C. jejuni?

A

stool culture

40
Q

Tx of C. Jejuni?

A
  • Only warranted for those with severe disease or at risk of severe disease (bloody stools, high fever, worsening symptoms)
  • azithromycin, cipro are DOC, resistance to fluoroquinolores are rising though
41
Q

Complications of C. Jejuni?

A

Guillain barre syndrome- develops in only 0.1% or less

  • molecular mimicry implicated in pathogenesis: serum ab to c. jejuni LPS cross-react with peripheral and central nervous system gangliosides
  • erethyma nodosum
  • reactive arthritis- more commonw ith HLAB27 phenotype—can also be seen with salmonella shigella and yersinia
42
Q

reactive arthritis can be a complication of disease caused by which bacteria?

A
  • salmonella, shigella, and yersinia
43
Q

general characterisitics of yersinia enterocolitica

A
  • gram - coccobacilli with bipolar staining
  • more common in eurpoe
  • sources: pork, raw milk, contaminated water, pet feces
  • infection prefers ileum, appendix, and right colon (organisms multiply in lymphoid tissue resulting in regional lymph node and peyer patch hyperplasia)
44
Q

clinical presentation of yersinia enterocolitica?

A
  • abd pain- main feature (peyer patch and mesenteric lymph node hyperplasia can mimic appendicitis in teens and young adults)
  • nausea/vom
  • fever/diarrhea
  • extraintestinal symptoms like pharyngitis, arthralgia, erythema nodusm
45
Q

diagnosis of yersinia enterocolitica?

A

stool culture

46
Q

tx of yersinia enterocolitica

A

most cases dont warrant tx

47
Q

general characteristics about C. diff

A

anaerobic, spore forming gram positive rod

  • fecal oral transmission
  • hands of hospital personal
  • most common NOSOCOMIAL CUASE OF DIARRHEA and MOST COMMON cause of antibiotic associated diarrhea
48
Q

pathogenesis of c diff?

A
  • ab suppress normal flora allowing c diff to multiply and produce exotoxins A and B
  • Exotoxins A and B cause glucosylation of small GTPases such as Rho which are involved in cytoskeleton structure and signal transduction
  • toxin A (enterotoxin) - disrupt colonic mucosal cell adherence to colonic basement membrane and damage villous tips. inflammation –> fluid secretion
  • toxin B (cytotoxin)- cause depolymerization of actin causing loss of cytoskeletal integrity –> apoptosis and death of enterocytes
  • both toxins (A > B) stimulate monocytes and macrophages, which release IL8 resulting in tissue infiltration with neutrophils; both cause disruption of epithelial tight junction
49
Q

Clinical presentation of C diff?

A
  • watery diarrhea!
  • cdiff associated diarrhea with colitis (CDAD)- watery diarrhea (10-15 bm/day), mild lower abd pain/cramping, low grade fever, leukocytosis

** CDAD occur in setting o ab. Symps begin during ab therapy or 5-10 days following ab administration

  • pseudomembranous colitis- similar presentaiton but in sigmoidoscopy it shows pseudomembranes (Adherent layer of inflammatory cells and debris at sites of colonic muscle injury)
  • Fulminant colitis- severe disease (severe abd pain, abd distention, fever, hypovolemia)
  • toxic megaoclon: colonic dilatation > 7cm with severe systemic toxicity
  • hypervirulent strains are emerging with more severe disease, lower clinical cure rates and high relapse rate.
50
Q

Risk factors for C diff infection?

A

advanced age, hospitalization, antibiotic tx

51
Q

diagnosis of c DIFF?

A
  • PCR detect toxins A and B
  • EIA for tonxis A B but there’shigh false negative rate
  • cell culture cytotoxicity assay- gold standard. stool sample added to monolayer of cultured cells. if c diff toxin present, it exerts cytopathic effect in tissue culture. labor intensive.
52
Q

c diff tx?

A
  • flagyl 1st line. if severe, PO vanc as first line
  • 1st recurrence: flagyl,

2nd recurrence: vanc extended course

  • fidaxomycin- new. superior clinical response and less recurrences when compared with vanc
  • fecal transplants

GI block (12 decks)

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