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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