Neely: Intra-Abdominal Infections II Flashcards

1
Q

PERITONITIS

Definition:

A

Inflammation of the peritoneum

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2
Q

Peritoneal Cavity extends from where to where?
Lined by what?
Surface area is similar to:
Permeable?

A

Peritoneal Cavity: extends from the undersurface of the diaphragm to the floor of the pelvis

Lined by a serous membrane

Large surface area (about the same as the skin)

Highly permeable

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3
Q

Peritonitis classifications (3):

A

Primary
Secondary
Post-dialysis

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4
Q

Peritonitis
Symptoms: (8)

Bowel sounds on exam:

A
  • Abdominal distention
  • Abdominal pain
  • Decreased appetite
  • N/V
  • Thirst
  • Fever
  • Absence of bowel sounds on physical exam
  • Signs of shock may also be present
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5
Q

Primary Peritonitis

aka:
Cause:
Infection is from:
Associated with:

A

Primary (Spontaneous Bacterial) Peritonitis:

Cause: develops without an evident source (rare)

Infection from hematogenous, lymphogenous, or transmural migration through the gut wall or via fallopian tubes in women

Often associated with advanced liver disease (cirrhosis with ascites)

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6
Q

Primary Peritonitis

Polymicrobial?
G+/-

A

Usually Monomicrobial:

Gram negative rods (E.coli, Klebsiella) cause >50% of all infections

Gram positive organisms (Streptococci) cause ~25% of infections

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7
Q

Primary Peritonitis can only be caused by:

What is the accumulation of fluid in peritoneal cavity? O2 Content:

Obligate anaerobes:

A

Can only be caused by facultative anaerobes

Ascitic fluid (accumulation of fluid in peritoneal cavity) has a high oxygen content

Obligate anaerobes (ie. Bacteroides spp.) cannot proliferate

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8
Q

Primary Peritonitis

Bacterial concentration compared to secondary:

A

Usually a low concentration of bacteria (as compared to secondary)

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9
Q

Secondary Peritonitis

Cause:
Examples:

A

Cause: spillage of GI or genitourinary microorganisms into the peritoneal cavity after trauma

Examples: ruptured appendix, stomach ulcer, perforated colon, or injury

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10
Q

Secondary Peritonitis

What is the origin of most cases?

Caused by what?
Predominately what type of bacteria?

A

Most cases are endogenous in origin:

Caused by the large number/variety of intestinal organisms

Predominantly anaerobic bacteria

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11
Q

Secondary Peritonitis

Polymicrobial?

A

Mainly polymicrobial infections

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12
Q

Dialysis Associated Peritonitis

Cause:

A

Cause: complication of chronic ambulatory peritoneal dialysis (CAPD); skin and oral flora frequently involved

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13
Q

Dialysis Associated Peritonitis

Polymicrobial?
Common organisms:
What happens if bowel ruptures?

A

Usually Monomicrobial

Common Organisms:

  • S.epidermis
  • S.aureus
  • E.coli
  • Pseudomonas aeruginosa

Note: if bowel ruptures, will be polymicrobial

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14
Q

E.coli

Virulence Factors:

A

Adherence

Endotoxin: Lipid A (in LPS of outer membrane)

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15
Q

E.coli

How many different adherence factors are there?

A

Adherence: 20 different adherence factors

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16
Q

E.coli
Endotoxin: Lipid A (in LPS of outer membrane)

Lipid A Toxicity activates what?
What causes inflammation?
What causes septic shock?

A

Lipid A Toxicity: activates complement and stimulates the release of cytokines, which can become toxic to the patient in high concentrations

Activation of Complement: inflammation

Release of Cytokines: septic shock (collapse of circulatory system, multiple organ system failure)

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17
Q

E.coli
Endotoxin: Lipid A (in LPS of outer membrane)

What does LPS bind?
Where are CD14 receptors found? What do they bind?

A

Binds to LPS-binding protein

LPS + LPS binding protein binds to CD14 receptors on monocytes and macrophages, as well as other receptors on other cells (ie. endothelia cells)

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18
Q

E.coli
Endotoxin: Lipid A (in LPS of outer membrane)

At least 3 events triggered by interaction of LPS with patients’ cells:

A

Production of cytokines
Activation of complement cascade
Multiple organ system failure

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19
Q

E.coli
Etiology/Pathogenesis

What does it do in the lumen of the GI tract?
Polymicrobial?

A

Escapes from lumen of GI tract: leads to infections (peritonitis or abscess)

Polymicrobial

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20
Q

E.coli

G +/-?
Shape
Ox +/-?
Lac +/-?
ID of species is based on:
A

Gram negative bacillus

Lab Tests: oxidase negative, lactose positive, facultative growth

ID of species: based on pattern of physiological reactions (phenotype)

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21
Q

E.coli

ID of serotypes is based on:
O antigen: what does region 1 of LPS contain?
H antigen: protein antigens of what?
K antigen:

A

ID of serotypes: based on antigen classification

O antigen: region 1 of LPS contains polysaccharide antigens

H antigen: protein antigens of flagella

K antigen: extracellular polysaccharide antigens

22
Q

Predominant Aerobic Bacteria in Peritonitis

Gram negative bacilli from GI tract: (3)

A

Gram negative bacilli from GI tract:
o E.coli
o Klebsiella spp.
o Enterobacter spp.

23
Q

Predominant Anaerobic Bacteria in Peritonitis: (5)

A

Anaerobic Gram Negative Bacilli (AGNB):
o Bacteroides fragilis
o Prevotella
o Porphyrmonas

  • Peptostreptococcus
  • Clostridium spp.
24
Q

Predominant Aerobic Bacteria in Peritonitis

Gram positive from GI tract: (2)

A

Gram positive from GI tract:
o Enterococcus faecalis
o Viridans streptococci

25
Q

What is the most frequent gram (-) rod causing CAPD peritonitis?

A

Pseudomonas aeruginosa

26
Q

Pseudomonas aeruginosa

Causes:
Frequently associated with: (3)

A

Causes severe infection

Frequently associated with:

  • Exit site or tunnel infection
  • Loss of peritoneal space (peritoneal adhesions)
  • Abscess formation
27
Q

Pseudomonas aeruginosa

Opportunistic Pathogen:
Nosocomial Infections:

A

Opportunistic Pathogen: found in moist environments (water, soil, plants, fruits and vegetables)

Nosocomial Infections: found in a variety of aqueous solutions (disinfectants, ointments, soaps, eye drops, dialysis fluids)

28
Q

Pseudomonas aeruginosa

Ubiquitous:
Ecthyma Gangrenosum:

A

Ubiquitous: particularly in water (swimming pools, hot tubs, respiratory therapy equipment, contact lens solution)

Ecthyma Gangrenosum: focal skin lesions characterized by vascular invasion by the bacteria; results in hemorrhage and necrosis

29
Q

Pseudomonas aeruginosa

Resistant to many antibiotics: (4)

A

o Change or loss of porins
o Beta-lactamases (including carbapenemases)
o Aminoglycoside hydrolyzing enzymes
o Efflux pumps

30
Q

Pseudomonas aeruginosa
Identification

G +/-?
Shape
Ox +/-?
Lac +/-?
Oxidize carbohydrates?
Pigments:
A

Basics: Gram negative bacillus

Lab Tests: oxidase positive, does not ferment lactose, oxidizes carbohydrates

Pigments (Blue-Green): pyocyanin (blue) and pyoverdin (yellow)

31
Q

Pseudomonas aeruginosa

Virulence factors

A
Pili
Capsule
Endotoxin
Exotoxin A
Multiply extracellular enzymes, including Pyocyanin - Blue pigment
32
Q

Pseudomonas aeruginosa
Virulence factors

What is antiphagocytic and promotes adherence to tracheal epithelium?

Does the pili do?

What causes septic shock?

A

Capsule – antiphagocytic and promotes adherence to tracheal epithelium

Pili - Enhances adherence to host epithelial cells

Endotoxin - LPS; may cause septic shock

33
Q

Pseudomonas aeruginosa
Virulence factors

What causes oxidative tissue damage and suppresses other bacteria?

What does exotoxin A do?

A

Multiply extracellular enzymes, including Pyocyanin - Blue pigment-Causes oxidative tissue damage, suppresses other bacteria, impairs the normal function of human nasal cilia

Exotoxin A- Increases tissue destruction by inhibition of protein synthesis (similar to diptheria toxin)

34
Q

Candida albicans

General:

A

General: causes roughly 1/3 of peritonitis in patients on CAPD; severe illness that is difficult to treat

35
Q

Candida albicans

Predisposing Conditions:

A

o Skin or mucosal barrier damaged
o Hormonal or nutritional imbalance
o Decreased numbers of phagocytic cells
o Intrinsic defects in function of phagocytic cells
o Cell-mediated immunity problems
o CAPD
o Use of antibiotics can deplete normal flora, allowing overgrowth of yeast

36
Q

Candida albicans

Most infections are due to what?
Causes peritonitis due to:

A

Most infections due to host’s endogenous flora (normal flora of intestinal tract)

Causes peritonitis due to peritoneal dialysis (CAPD)

37
Q

Candida albicans
Identification

Cellularity:
G +/-?
Multiply by producing:
Germ tube +/-?

A

Unicellular, eukaryotic, budding cells (blastospores)

Stain Gram positive

Multiply by the production of blastoconidia

Germ tube positive

38
Q

Candida albicans

Types of infection:
Candida ulceration –
What may bowel involvement be characterized by?

A

Esophagitis, enteritis, peritonitis and perianal infection

Candida ulceration – gastric, small or large bowel

Bowel involvement may be characterized by ulceration, superficial erosions, pseudomembrane formation, penetrating ulcers and perforation.

39
Q

INTRAPERITONEAL ABSCESSES

What are most cases in origin?
Monomicrobial or polymicrobial?

A

Most cases are endogenous in origin (organisms from normal flora of mucous membranes lining the viscera of the abdominal cavity; intact mucosa blocks invasion of organisms)

Infection is usually polymicrobial (4 organisms on average)

40
Q

INTRAPERITONEAL ABSCESSES

Abscesses usually occur as a complication of local or generalized peritonitis, secondary to: (7)

A
o	Appendicitis
o	Diverticulitis
o	Necrotizing enterocolitis
o	Pelvic inflammatory disease
o	Tubo-ovarian infection
o	Surgery
o	Trauma
41
Q

Intraperitoneal Abscesses are usually caused by:

A

Usually caused by anaerobic bacteria

42
Q

Bacteroides fragilis

Aerobic or Anaerobic?
G +/-?
Found where?
When does it cause infection?

A

Anaerobic (obligate) Gram negative bacillus

Part of normal flora of GI tract

Causes clinical infections when it escapes GI tract following surgery, bowel perforation, or diseases like diverticulitis

43
Q

Diverticulitis:

A

Inflammation of a small bulging sac (food or particle collecting) in the colon wall (can lead to colonic rupture that allows GI bacteria to enter the peritoneal cavity)

44
Q

What is Bacteroides fragilis resistant to? Why?

A

Resistant to all aminoglycosides: does not have oxygen-dependent transport mechanism across cell membrane.

45
Q

What cause the initial infection and consume oxygen after B. fragilis escapes from the intestine?
What happens afterwards?

A

Escapes from the intestine to cause polymicrobic infection:

Facultative organisms cause the initial infection and consume oxygen, allowing anaerobes like B.fragilis to grow

B.fragilis (and other anaerobes) can then cause the intra-abdominal abscess (synergistic pathogenicity)

46
Q

Bacteroides fragilis

Diagnosis:

A

Based on clinical features, including a foul smelling wound with the presence of gas in the tissue (CO2 and H2)

47
Q

Bacteroides fragilis
Identification

G +/-?
Encapulated?
Aerobic or Anaerobic?
What else is notable?
Antibiotics resistance:
A

Basics: Gram negative, encapsulated, anaerobic bacillus

Other: foul smelling discharge (due to anaerobic metabolism by-products)

Broad antibiotic resistance

48
Q

VISCERAL ABSCESSES

Pancreatic Abscess:

A

Pancreatic Abscess: collection of pus resulting from tissue necrosis, liquefaction, and infection

49
Q

VISCERAL ABSCESSES

Hepatic Abscess is often due to:

A

Hepatic Abscess: often due to biliary tract disease

50
Q

VISCERAL ABSCESSES

Splenic Abscess:
Appendicitis:

A

Splenic Abscess: uncommon

Appendicitis: persistent obstruction of the appendiceal lumen leads to rupture of the pus-filled appendix

51
Q

VISCERAL ABSCESSES

Diverticulitis:

A

Diverticulitis: herniation of mucosa and submucosa can lead to rupture and peritonitis