Download Gastointestinal Infections II

Microbiology: Intra-Abdominal Infections II (Neely)
PERITONITIS:
Basics:

Definition: inflammation of the peritoneum
Peritoneal Cavity: extends from the undersurface of the diaphragm to the floor of the pelvis
o Lined by a serous membrane
o Large surface area (about the same as the skin)
o Highly permeable
Inflammation of the Peritoneal Cavity (Peritonitis): occurs by contamination with microorganisms
o Classification:

Primary

Secondary

Post-dialysis

Symptoms:
Abdominal distention
Abdominal pain
Decreased appetite
Fever
N/V
Thirst
Absence of bowel sounds on physical exam
Signs of shock may also be present
Types of Peritonitis:

Primary (Spontaneous Bacterial) Peritonitis:
Cause: develops without an evident source (rare)
o Infection from hematogenous, lymphogenous, or transmural migration through the gut wall or via
fallopian tubes in women
o Often associated with advanced liver disease (cirrhosis with ascites)
Usually Monomicrobial:
o Gram negative rods (E.coli, Klebsiella) cause >50% of all infections
o Gram positive organisms (Streptococci) cause ~25% of infections
o 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
Usually a low concentration of bacteria (as compared to secondary)

Secondary Peritonitis:
Cause: spillage of GI or genitourinary microorganisms into the peritoneal cavity after trauma
o Examples: ruptured appendix, stomach ulcer, perforated colon, or injury
Most cases are endogenous in origin:
o Caused by the large number/variety of intestinal organisms
o Predominantly anaerobic bacteria
Mainly polymicrobial infections

Dialysis Associated Peritonisi:
Cause: complication of chronic ambulatory peritonea dialysis (CAPD); skin and oral flora frequently involved
Usually Monomicrobial:
o Common Organisms:

S.epidermis

S.aureus

E.coli

Pseudomonas aeruginosa
o Note: if bowel ruptures, will be polymicrobial
Bacteria Causing Peritonitis:

E.coli:
Virulence Factors:
o Adherence: 20 different adherence factors
o
-
-

Endotoxin: Lipid A (in LPS of outer membrane)

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)

LPS Binding:
 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)

At least 3 events triggered by interaction of LPS with patients’ cells:
 Production of cytokines
 Activation of complement cascade
 Multiple organ system failure
Etiology/Pathogenesis:
o Escapes from lumen of GI tract: leads to infections (peritonitis or abscess)
o Polymicrobial
Identification:
o Basics: Gram negative bacillus
o Lab Tests: oxidase negative, lactose positive, facultative growth
o ID of species: based on pattern of physiological reactions (phenotype)
o 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
Predominant Aerobic Bacteria in Peritonitis:
Gram negative bacilli from GI tract:
o E.coli
o Klebsiella spp.
o Enterobacter spp.
Gram positive from GI tract:
o Enterococcus faecalis
o Viridans streptococci
Predominant Anaerobic Bacteria in Peritonitis:
Gram Negative Bacilli:
o Bacteroides fragilis
o Prevotella
o Porphyrmonas
Peptostreptococcus
Clostridium spp.
-


Pseudomonas aeruginosa:
General: most frequent GNR causing CAPD peritonitis
o Causes severe infection
o Frequently associated with:

Exit site or tunnel infection

Loss of peritoneal space (peritoneal adhesions)

Abscess formation
Etiology/Pathogenesis:
o Opportunistic Pathogen: found in moist environments (water, soil, plants, fruits and vegetables)
o Nosocomial Infections: found in a variety of aqueous solutions (disinfectants, ointments, soaps, eye
drops, dialysis fluids)
o Ubiquitous: particularly in water (swimming pools, hot tubs, respiratory therapy equipment, contact
lens solution)
o Ecthyma Gangrenosum: focal skin lesions characterized by vascular invasion by the bacteria; results in
hemorrhage and necrosis
-
-
-
Resistant to many antibiotics:
o Change or loss of porins
o Beta-lactamases (including carbapenemases)
o Aminoglycoside hydrolyzing enzymes
o Efflux pumps
Identification:
o Basics: Gram negative bacillus
o Lab Tests: oxidase positive, does not ferment lactose, oxidizes carbohydrates
o Pigments (Blue-Green): pyocyanin (blue) and pyoverdin (yellow)
Yeast Causing Peritonitis:

Candida albicans:
General: causes roughly 1/3 of peritonitis in patients on CAPD; severe illness that is difficult to treat
Predisposing Conditions:
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
Etiology/Pathogenesis:
o Most infections due to host’s endogenous flora (normal flora of intestinal tract)
o Causes peritonitis due to peritoneal dialysis (CAPD)
Identification:
o Unicellular, eukaryotic, budding cells (blastospores)
o Stain Gram positive
o Multiply by the production of blastoconidia
o Germ tube positive
INTRAPERITONEAL ABSCESSES:

General:
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)
Abscesses usually occur as a complication of local or generalized peritonitis, secondary to:
o Appendicitis
o Diverticulitis
o Necrotizing enterocolitis
o Pelvic inflammatory disease
o Tubo-ovarian infection
o Surgery
o Trauma
Usually caused by anaerobic bacteria

Bacteroides fragilis:
General: anaerobic (obligate) Gram negative bacillus
o Part of normal flora of GI tract
o Causes clinical infections when it escapes GI tract following surgery, bowel perforation, or diseases like
diverticulitis

Diverticulitis: 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)
Etiology/Pathogenesis:
o Resistant to all aminoglycosides: does not have oxygen-dependent transport mechanism across cell
membrane
o 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)
Diagnosis: based on clinical features, including a foul smelling wound with the presence of gas in the tissue (CO2
and H2)
Identification:
o Basics: Gram negative, encapsulated, anaerobic bacillus
o Other: foul smelling discharge (due to anaerobic metabolism by-products)
o Broad antibiotic resistance
VISCERAL ABSCESSES:

Pancreatic Abscess: collection of pus resulting from tissue necrosis, liquefaction, and infection

Hepatic Abscess: often due to biliary tract disease

Splenic Abscess: uncommon

Appendicitis: persistent obstruction of the appendiceal lumen leads to rupture of the pus-filled appendix

Diverticulitis: herniation of mucosa and submucosa can lead to rupture and peritonitis