Intra-abdominal Infections II (Dr. Neely)

Inflammation of the serous membrane lining the peritoneal cavity.

• Primary (Spontaneous)
• Develops without evident cause
• associated with adanced liver disease
• Polymicrobic 92% of the time
• Mostly Gram- rods (less common are Gram+ organisms)
• Facultative anaerobic organisms
• lower bacterial concentration than secondary peritonitis
• Secondary peritonitis
• Caused by spillage of GI or GU microorganisms into the peritoneal cavity; disease or injury to the GI or GU tract
• Most are endogenous in origin
• Mixed polymicrobial infections
• Anaerobes dominate
• Dialysis associated peritonitis
• Complication of chronic ambulatory peritoneal dialysis (CAPD)
• Skin and oral flora involved
• Polymicrobial infection
• S. epidermis, S. aureus, E. coli and P. aeruginosa are associated

Abdominal distention, pain, decreased appetite, fever, nausea, thirst, vomiting, and absence of bowel sounds. Signs of shock are less common.

• Virulence factors
• Adherence
• Endotoxin - Lipid A, leads to septic shock
• LPS - leads to production of cytokines, activation of complement cascade, and multiple organ system failure
• Etiology/Pathogenesis
• Escape the lumen of the GI tract, leads to infection of the peritoneum or a localized abscess
• Polymicrobial
• Clinical ID
• Gram- bacillus, oxidase (-), grows on MacConkey Agaer, lactose (+)
• Facultative growth
• ID of specific pattern to distinguish between species
• ID of serotypes - O, H and K antigen

• 1. B.
• 2. C.
• 3. A.

• 1. E. Coli
• 2. Klebsiella spp.
• 3. Enterobacter spp.

• 1. E. faecalis
• 2. V. strepococci

• 1. B. fragilis
• 2. Prevotella
• 3. Porphymonas

• 1. Peptostreptococcus
• 2. Clostridium spp.

• Virulence factors
• Pili
• Capsule
• Endotoxin - LPS, leads to septic shock
• Exotoxin A - inhibition of protein synthesis, similar to diptheria toxin
• Pyocyanin - oxidative tissue damage
• Etiology/Pathogenesis
• Oppurtunistic pathogen
• Nosocomial infection
• Associated with dialysis patients
• Ubiquitous
• Ecthyma gangrenosum - hemorrhage and necrosis
• Chronic ambulatory peritoneal dialysis (CAPD)
• Resistance to antibiotics - loss/change of porins
• Clinical ID
• Gram- bacillus, aerobic, oxidase growth, growth on MacConkey Agar, lactose non-fermenter, oxidizes carbohydrates
• Blue-green pigment - pyocyanin and pyoverdin

• Virulence factors
• Adherence
• Pseudohypae
• Predominance of neutrophils leads to inflammation
• Most common mycosis
• Relatively low virulence (except in immunocompromised patients)
• Etiology/Pathogenesis
• Endogenoud flora origin
• Can cause esophagitis, enteritis, peritonitis, and perianal infection
• Due to peritoneal dialysis
• Seen in patients with CAPD
• Ulcerations of the stomach, and small and large intestines
• Penetrating or perforating ulcers of bowel
• Clinical ID
• Unicellular, eukaryotic, budding cells
• Gram+
• Pseudohyphae

• 1) Skin/mucosal barriar damaged
• 2) Hormonal/nutritional imbalance
• 3) Decreased number or dysfunction of phagocytes
• 4) Cell-mediated immunity problems
• 5) CAPD
• 6) Antibiotic use

True

False, intraperitoneal abscesses infections are polymicrobial

Complication of local or generalized peritonitis; secondary to appendicitis, diverticulitis, necrotizing enterocolitis, pelvic inflammatory disease, tubo-ovarian infection, surgery or trauma.

• Virulence factors
• Capsule
• Pili
• Enzymes that destroy epithelial cells
• Superoxide dismutase
• Etiology/Pathogenesis
• Obligate anaerobe
• Normal flora
• Resistant to AMGs
• Polymicrobial infection
• Diverticulitis
• Clinical ID
• Foul smelling wound
• Gram-, encapsulated, anaerobic bacillus
• Antibiotic resistance

• 1) Pancreas
• 2) Liver
• 3) Spleen
• 4) Appendix
• 5) Diverticula

>4 weeks after intial attacks

• Virulence factors
• Fibrous wall formation around fluid collections
• Can occur from penetration of peptic ulcer
• Translocation of enteric bacterial flora
• Risk for sepsis
• Surgical intervention and drainage
• Etiology/Pathogenesis
• 30-50% polymicrobial
• Aerobic and anaerobic bacteria
• Recovery of Candida spp

• Virulence factors
• Biliary tract accounts for ~30% of liver abscess
• Associated with cholecystitic, appendicitis, diverticulitis, peritonitis, liver transplant, chronic granulomatous disease, or IBD.
• Etiology/Pathogenesis
• Polymicrobial
• Biliary duct is source of infection
• Portal
• Infection in contiguous structure
• Hepatic a. spreads infection to rest of body
• Secondary to a penetrating wound or trauma to liver
• Blood cultures - E. coli and K.pneumoniae
• Abscess cultures - Bacteroides spp. and streptococcal species
• Clinical ID
• Blood cultures 50% +
• Ultrasound

• Virulence factors
• Uncommon
• Multiple small sbscesses
• Infection from contiguous organ (urinary, abdominal, respiratory)
• Etiology/Pathogenesis
• S. aureus, K. pneumoniae and Enterococcus associated with endocarditis
• E. coli associated with UT and abdominal infection
• Bacteriodes spp. and Clostridium spp. associated with abdominal infection
• Fusobacterium spp. associated with respiratory infection (less common)
• Clinical ID
• 70% of cases splenic abscesses have + blood cultures

Appendicitis

Herniation of mucosa and submucosa that ruptures and leads to peritonitis