Intra-abdominal Infections II (Dr. Neely)

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davis.tiff
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Intra-abdominal Infections II (Dr. Neely)
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2012-09-02 10:59:10
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MICROBIOLOGY INFECTIOUS DISEASES
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Micro/ID Exam III
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  1. What is peritonitis and what are the 3 different types?
    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
  2. What are the most common symptoms of peritonitis?
    Abdominal distention, pain, decreased appetite, fever, nausea, thirst, vomiting, and absence of bowel sounds. Signs of shock are less common.
  3. E. coli
    Virulence factors? Etiology/Pathogenesis? Clinical ID?
    • 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
  4. Match the following.

    1. O antigen
    2. H antigen
    3. K antigen

    A. Extracellular polysaccharide antigen
    B. Region 1 of LPS
    C. Protein antigens of flagella
    • 1. B.
    • 2. C.
    • 3. A.
  5. What are the 3 predominant aerobic Gram- bacilli involved in peritonitis?
    • 1. E. Coli
    • 2. Klebsiella spp.
    • 3. Enterobacter spp.
  6. What are the 2 predominant Gram+ cocci involved in peritonitis?
    • 1. E. faecalis
    • 2. V. strepococci
  7. What are the 3 predominant anaerobic Gram- bacilli involved in peritonitis?
    • 1. B. fragilis
    • 2. Prevotella
    • 3. Porphymonas
  8. What are the 2 predominant anaerobic Gram+ bacteria involved in peritonitis?
    • 1. Peptostreptococcus
    • 2. Clostridium spp.
  9. Pseudomonas aeruginosa
    Virulence factors? Etiology/Pathogenesis? Clinical ID?
    • 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
  10. Candida albicans
    Virulence factors? Etiology/Pathogenesis? Clinical ID?
    • 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
  11. What 6 conditions predispose someone to becoming infected by Candida albicans and developing peritonitis?
    • 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
  12. True or false. Most cases of intraperitoneal abscesses are endogenous in origin.
    True
  13. True or false. Intraperitoneal abscesses infections are usually monomicrobial.
    False, intraperitoneal abscesses infections are polymicrobial
  14. How do intraperitoneal abscesses infections usually occur?
    Complication of local or generalized peritonitis; secondary to appendicitis, diverticulitis, necrotizing enterocolitis, pelvic inflammatory disease, tubo-ovarian infection, surgery or trauma.
  15. Bacteroides fragilis
    Virulence factors? Etiology/Pathogenesis? Clinical ID?
    • 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
  16. What are the 5 main organs involved in visceral abscess formation?
    • 1) Pancreas
    • 2) Liver
    • 3) Spleen
    • 4) Appendix
    • 5) Diverticula
  17. When does a pancreatic abscess usually form?
    >4 weeks after intial attacks
  18. Pancreatic abscess
    Virulence factors? Etiology/Pathogenesis?
    • 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
  19. Hepatic abscess
    Virulence factors? Etiology/Pathogenesis? Clinical ID?
    • 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
  20. Splenic abscess
    Virulence factors? Etiology/Pathogenesis? Clinical ID?
    • 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
  21. A patient who has lower right quadrant abdominal pain and are positive for anaerobic bacteria and Enterobacteriaceae, would most likely be diagnosed with what?
    Appendicitis
  22. What is diverticulitis?
    Herniation of mucosa and submucosa that ruptures and leads to peritonitis

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