2.2_Microbio

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sirchubbsalot13
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2.2_Microbio
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2010-03-31 16:58:33
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Microbiology
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  1. Q: Group A Strep?
    A: G+ and Catalase - and B-hemolytic and Lancefield A.
  2. Q: Group B Strep?
    A: G+ and Catalase - and B-hemolytic.
  3. Q: 3 organisms that cause neonatal meningitis?
    A: Strep B and Listeria monocytogenes and E Coli.
  4. Q: Streptolysin O?
    A: Oxygen labile enzyme, which is inactivated by oxygen, of Strep A that destroys RBCs and WBCs.
  5. Q: Streptolysin S?
    A: Oxygen stable enzyme of Strep A that destroys RBCs and WBCs.
  6. Q: M protein?
    A: Major virulence factor for Strep A.
  7. Q: Scarlet Fever?
    A: caused by pyrogenic exotoxin from Strep A - Scarlet red rash. strawberry tongue. Pharyngitis.
  8. Q: Rheumatic fever?
    A: Follows Strep pharyngitis - Antibody mediated. Fever. Myocarditis -valve damage years later-. Joint swelling. Chorea. Subcutaneous Nodules. Erythema marginatum (rash).
  9. Q: Glomerulonephritis?
    A: Inflammatory disease of the kidney following Strep pharyngitis or skin infection. Due to deposition of antigen-antibody complexes: Puffy face. Dark urine (hematuria and proteinuria)'. Hypervolumia which can cause high BP.
  10. Q: Viridans Group Strep?
    A: G+ and Catalase - and a-hemolytic -green-. Dental Infections -caries-. Endocarditis -subacute-. Abscesses.
  11. Q: Strep Intermedius?
    A: Subgroup of Viridans Strep that causes abscesses.
  12. Q: Enterococci?
    A: G+ and catalase - and a-hemolytic. Normal bowel flora. Common in UTIs. Biliary infections. Subacute endocarditis. Not as virulent as Strep A. Opportunistic. Common cause of nosocomial infections. Resistant to many antibiotics, some even vancomycin.
  13. Q: Streptococcus pneumoniae?
    A: G+ and catalase - and a-hemolytic -. Lancet-shaped Diplococci. Pneumonia. Meningitis in adults. Otitis media in kids.
  14. Q: Pneumococcal pneumonia?
    A: high fever. Rigors. cp with respirations. sob. In lungs - pus and bacteria and exudates.
  15. Q: Staphylococcus Aureus?
    A: G+ and catalase + and B-hemolytic. gold pigment. In clusters. coagulase +. Scalded skin syndrome. Toxic shock syndrome. Gastroenteritis. Pneumonia. Meningitis and Brain abscess. Osteomyelitis. Acute endocarditis. Septic arthritis. Skin infections. Wound infections.
  16. Q: Staph enzymes that disable our immune defenses?
    A: Protein A: Binds the Fc part of IgG. Coagulase leads to fibrin clot around bacteria, protecting it. Hemolysins destroy RBCs, neutrophils, macrophages, and platelets. Leukocidins destroy WBCs. Penicillinase inactivates penicillin.
  17. Q: Staph proteins that help it tunnel through tissue?
    A: Hyalurodinase: Breaks down proteoglycans in CT. Staphylokinase: Lyses fibrin clots. Lipase: Degrades fats.
  18. Q: Staph exotoxins?
    A: Exfoliatin: Scalded skin syndrome. Enterotoxins: Food poisoning gastroenteritis. Toxic shock syndrome toxin (TSST-1).
  19. Q: Toxic Shock Syndrome?
    A: Staph and Strep A. Shock. Renal failure. Rash. Respiratory Failure.
  20. Q: Group C-G Strep?
    A: G+ and Catalase - and B-hemolytic. Can cause purulent infections like Strep A but no Rheumatic Fever or glomerulonephritis.
  21. Q: Bacterimia of which critter is associated with colon cancer?
    A: Strep D.
  22. Q: Which Streps are associated with abscesses?
    A: Group F Strep milleri and Viridans group Strep intermedias.
  23. Q: 5 bacteria associated with food poisoning?
    A: Staph Aureus and Listeria monocytogenes and Clostridium botulinum and Clostridium perfringens and Bacillus cereus.
  24. Q: Listeria monocytogenes?
    A: G+ and Catalase + and B-hemolytic. Rods in pairs. Aerobic. Transmission from meat product. Bacterimia and meningitis in newborns. Likely to have obtained from birth canal. Common cause of food borne outbreaks and meat recalls.
  25. Q: How do you diagnose Listeria in the lab?
    A: Culture blood or CSF and B-hemolytic then not cornebacteria and Catalase + then not Strep B.
  26. Q: Corynebacterium?
    A: Also called diptheroids. G+ and rods forming Chinese character clusters. Large numbers on normal skin flora. Most often contaminants in culture. Assumed to be cause of the disease only if in 2 samples. Endocarditis in prosthetic heart valves.
  27. Q: Corynebacteria jeikeium?
    A: opportunistic. Lymphadenitis. Abscesses. Meningitis. skin infections. bacterimia.
  28. Q: Corynebacteria diphtheria?
    A: Pharyngitis with thick membrane and edema. May have cutaneous ulcers. When contains a bacteriophage produces exotoxin that effect myocardium and peripheral nervous system. Death by asphyxiation or myocarditis.
  29. Q: Aerobic Gram + Bacilli?
    A: Listeria monocytogenes and Corynebacterium and Erysipelothrix rhusiopathiae and Bacillus and Lactobacillus.
  30. Q: Erysipelothrix rhusiopathiae?
    A: G+ and rods that form long filaments and a-hemolytic. Produces hydrogen sulfide gas (unique among aerobic G+). Colonizes animals and causes infections in fisherman, butchers, and veterinarians. erysipeloid: ulcerating, erythematous skin infections.
  31. Q: Bacillus species?
    A: G+ and large rods. Form spores (unique among aerobic G+). Bacterimia and endocarditis in drug abusers and immune compromised. B. anthracis and B. cereus.
  32. Q: Bacillus anthracis?
    A: Large G+ rods. Rare in US but common elsewhere else. 3 forms: 1) cutaneous: painless ulcer with black eschar 2) inhalation: spore forming, severe SOB, appearance of extreme toxicity, and widened medistinum 3) GI form - deadly.
  33. Q: Bacillus cereus?
    A: Commonly causes food poisoning. Associated with under cooked rice. Toxin mediated.
  34. Q: Lactobacillus?
    A: G+ and catalase - and a-hemolytic and small long slender rods. Major normal flora of GI tract and genital tract. Found in yogurt. Virtually always protective against infection.
  35. Q: Anaerobic Gram + Bacilli?
    A: Clostridium perfringes and Clostridium botulinum and Clostridium tetani and Clostridium difficiles and Propionibacterium and acnes.
  36. Q: Clostridium perfringens?
    A: G+ and large rods and spore forming. Gas gangrene. Necrotizing Fasciitis. Cellulitis. Puerperal sepsis. Food poisoning.
  37. Q: Gas gangrene?
    A: Clostidium perfringens. Rare. Rapidly progressing. Traumatic and surgical wounds. Destruction of muscle. Gas in tissue. Hemorrhagic bullae. Foul watery discharge. Liver and Renal failure. Shock and Death.
  38. Q: Necrotizing fasciitis?
    A: Clostridium perfringens. Strep A. Mixed aerobic and anaerobic. Doesn't involve muscle, more local, less lethal than gas gangrene.
  39. Q: Clostridium tetani?
    A: G+ and large rods and spore forming. In soil, Common component of GI flora. Tetanospasmin toxin. Causes paralysis that is spastic. Fever. Difficulty swallowing.
  40. Q: Closridium botulinum?
    A: G+ and large rods and spore forming. Common in soil. 8 toxins so no vaccine (bacteriophage required for production). Food poisoning. Wounds. Infections. Infant botulism.
  41. Q: Clinical manifestations of food-borne botulism?
    A: generalized weakness, dry mouth, constipation, and urinary retention. Followed by descending paralysis, blurred vision, photophobia, dilated unreactive pupils.
  42. Q: Wound botulism?
    A: Lesions appear 4 to 14 days after injury. similar clinical manifestations as food-bourn disease.
  43. Q: Infant botulism?
    A: 3 to 20 week old infants. Constipation, weak suck, feeble cry, descending flaccidity, ptosis, absent gag reflex. seen in adults.
  44. Q: Clostridium difficile?
    A: G+ and large rods and spore forming. GI flora, under antibiotic pressure makes toxins. psuedomembranous colitis. Fever. Diarrhea. ABD pain. Exudate and ulcer formation in large intestine. Failure to recognize and treat may lead to bowel perforation and peritonitis.
  45. Q: Propionibacterium acne?
    A: Prominent normal skin flora. Common contaminant. Infections in prosthetic devices (CNS shunts). Acne.
  46. Q: Characteristics of Enterobacteriacea?
    A: Gram - Large bacilli. aerobic or anaerobic. do NOT form spores. produce endotoxins. live in lower GI tract.
  47. Q: Antigen structure of Enterobacteriacea?
    A: Cell wall lipopolysaccharide (heat stable). capsule polysacharide (heat labile). flagellar proteins.
  48. Q: All Enterobacteriacea share the following characteristics?
    A: 1) Gram - bacilli 2) ferment glucose 3) reduce nitrates to nitrites 4) oxidase.
  49. Q: 3 major genus of Enterobacteriacea that ferment lactose?
    A: 1) E. coli 2) Klebsiella 3) Enterobacter.
  50. Q: 3 major genus of Enterobacteriacea that do not ferment lactose?
    A: 1) Salmonella 2) Shigella 3) Yersinia.
  51. Q: Enterobacteriacea that cause non-diarrhea diseases?
    A: 1) E. coli 2) Klebsiella 3) Enterobacter 4) Serratia 5) Citrobacter.
  52. Q: Non-diarrheal E. coli diseases?
    A: UTI. meningitis (most commonly in neonates). Nosocomial - wounds and bacterimia and pneumonia.
  53. Q: Klebsiella diseases?
    A: UTIs. Pneumonia. nosocomial infections.
  54. Q: Enterobacter?
    A: nosocomial infections.
  55. Q: Serratia?
    A: opportunistic. red pigment. blood of Christ dripping in church paintings.
  56. Q: Citrobacter?
    A: neonatal meningitis and bacterimia. swarms.
  57. Q: Proteus?
    A: swarms. UTI. wound infections. bacterimia.
  58. Q: Provinca, Morganella?
    A: nosocomial infections in pts with catheters.
  59. Q: ETEC epidemiology?
    A: Traveler’s diarrhea. Childhood diarrhea. Contaminated food and water.
  60. Q: ETEC pathology?
    A: Adhere to small intestinal wall. Enterotoxin - LT: heat labile toxin and ST: heat stable toxin.
  61. Q: ETEC clinical manifestations?
    A: Stools - copious and watery and no blood or RBCs. no fever.
  62. Q: EHEC epidemiology?
    A: Contaminated food - beef, unpasteurized milk, apple cider, fast food. Contaminated water. Person to person (daycares).
  63. Q: EHEC pathology?
    A: Adhere to large intestine wall. Shiga-like toxin 1 and 2. Damage endothelial cells in GI tract and renal glomeruli. Hemorrhagic colitis. Hemolytic uremic syndrome.
  64. Q: EHEC clinical manifestations?
    A: Stools - copious and bloody and no WBCs. No Fever.
  65. Q: How do you treat EHEC?
    A: No antibiotics, aggravate HUS. supportive care and dialysis. Prevention.
  66. Q: EIEC epidemiology?
    A: sporadic and uncommon.
  67. Q: EIEC pathology?
    A: Invades large intestine enterocytes. Necrosis. Ulceration. Inflammation.
  68. Q: EIEC clinical manifestations?
    A: Stools - scant and blood and WBCs and purulent. Fever.
  69. Q: EPEC epidemiology?
    A: infantile and childhood diarrhea.
  70. Q: EPEC pathology?
    A: Adhere to small intestine enterocytes. efface microvilli.
  71. Q: EPEC clinical manifestations?
    A: Stool - copious and watery and no blood and few WBCs. Fever.
  72. Q: EAEC pathology?
    A: Adhere to enterocytes.
  73. Q: EAEC clinical manifestations?
    A: Stools - watery and no blood and no WBCs. Fever occasionally.
  74. Q: Shigella epidemiology?
    A: Strictly human disease. Needs very low inoculum. Fecal-oral transmission. Contaminated food or water.
  75. Q: Shigella pathology?
    A: Invades colonic mucosa - but no further. Makes Shiga toxin. causes HUS. - S. dysentery and S. sonnei.
  76. Q: S. dysentery?
    A: Abd cramps. Tenesmus - painful straining to poo. Fever. Stools - bloody and mucoid and large # of fecal leucocytes.
  77. Q: S. sonnei?
    A: fever. systemic symptoms. watery diarrhea.
  78. Q: Treatment for Shigella?
    A: none, it will go away on its own. Antibiotics prevent transmission and shorten clinical course.
  79. Q: Salmonella epidemiology?
    A: improper food handling. poultry (eggs) most common. exotic pet turtles. Affects mostly the very old and the young.
  80. Q: Salmonella gastroenteritis?
    A: Adhere to brush border of intestinal cells. Ruffles in intestinal wall. Invade enterocytes.
  81. Q: Clinical manifestations of Salmonella gastroenteritis?
    A: onset 24-48 hrs. duration 3-4 days. Nausea. Vomiting. Cramping. Diarrhea. Fever (50 percent). Bacterimia (old and young).
  82. Q: Treatment of Salmonella gastroenteritis?
    A: Resolves spontaneously. fluids and electrolytes. Antibiotics only for those at risk for bacterimia (very old and young).
  83. Q: Typhoid fever pathology?
    A: Salmonella typhi. Enter and kill M cells. Invade macrophages and multiply. Bacterimia. rose spots.
  84. Q: Clinical manifestations of Typhoid fever?
    A: Fever. Headache. Constipation more than diarrhea. may have intestinal perforations.
  85. Q: Treatment of typhoid fever?
    A: Antimicrobics. Vaccine.
  86. Q: Typhoid Carrier state?
    A: asymptomatic. Salmonella in stools or urine for years. reservoir for epidemics.
  87. Q: Yersinia pathology?
    A: Invade M cells of peyer's patches. Proliferation in lymph nodes. Small intestinal inflammations and ulceration.
  88. Q: Clinical manifestations of Yersinia?
    A: Fever. Diarrhea. Abd PN (like appendicitis).
  89. Q: Vibrios?
    A: Comma shaped Gram - rod.
  90. Q: Vibrio epidemiology?
    A: Unsanitary water systems leading to Traveler's diarrhea. Imported seafood (raw oysters). Requires huge inoculation.
  91. Q: Vibrio cholera pathology?
    A: non-invasive. Attach to intestinal wall and produce toxin. Inhibits cAMP and water reabsorbtion. 15 L absorbed by gut a day is lost.
  92. Q: Clinical manifestations of Vibrio cholera?
    A: Incubation is from hours to 5 days. Onset is sudden. Stools - rice water stools and no tenesmus and vomiting common and volume shock.
  93. Q: Treatment of Vibrio cholera?
    A: Fluids (water, electrolytes, glucose). Self limited. Tetracyclin or other antibiotics reduce duration of illness. Prevention includes vaccine and sanitation.
  94. Q: Vibrio parahemolyticus?
    A: acute gastroenteritis after eating seafood. self limited. Iron loving - grow more and more virulent and dangerous to people with liver disease.
  95. Q: Vibrio vulnificus?
    A: Wound infections (unique among vibrios). Fishermen. iron loving. dangerous to people with liver disease.
  96. Q: Campylobacter characteristic?
    A: Gram - comma shaped or spiral rods. requires special conditions for isolation.
  97. Q: Campylobacter epidemiology?
    A: Most common cause of bacterial gastroenteritis in US. 5-12 percent of diarrheal stool samples. Food and water contamination. Animal reservoirs - Fowl, cattle, swine, pets. Fecal oral spread.
  98. Q: Campylobacter pathology?
    A: Invades intestinal mucosa.
  99. Q: Clinical manifestations of Campylobacter infections?
    A: Incubation 1-7 days. Rapid onset. Fever. Abd PN. Stools - copious and watery and mucoid and bile stained and WBCs and blood. May relapse.
  100. Q: Treatment of Campylobacter?
    A: Spontaneous clearance. IgG and IgM produced. Often antibiotics not used but can decrease chance of bacterimia. Treat early with quinolones.
  101. Q: Helobacter pylori epidemiology?
    A: 60 percent of adults exposed by age 50.
  102. Q: Helicobacter pylori?
    A: Limited to stomach mucosa. High urease activity - cleaves urea to ammonia and protects from stomach acid.
  103. Q: Clinical manifestations of Helicobacter pylori?
    A: Gastritis - Gastric ulcer (50-70 percent of them) and Duodenal ulcer (90 percent of them) and Possible role in gastric carcinoma.
  104. Q: Gastroenteritis via preformed toxins?
    A: Staph aureus and Bacillus cereus and Clostridium perfringes and Clostridium botulinum.
  105. Q: Characteristics of preformed toxin gastroenteritis?
    A: upper level disease. Nauseaandvomiting. Abd PN. onset within hours.
  106. Q: Toxin mediated gastroenteritis?
    A: Vibrios and V. cholera and V. parahemolyticus and E. coli and ETEC and EHEC and EPEC and EAEC.
  107. Q: Characteristics of toxin mediated gastroenteritis?
    A: Block water reabsorbtion. Copious, watery stools. Vomiting. little PN or toxicity. generally self limiting. 2-3 day onset.
  108. Q: Invasive Gastroenteritis?
    A: Salmonella and Shigella (low inoculum) and Yersinia and Campylobacter (most common) and Helicobacter pylori and EIEC and Listeria monocytogenes.
  109. Q: Characteristics of invasive gastroenteritis?
    A: Toxic, Fever, Abd PN, Stools - small volume and blood and WBCs and purulent. 2-5 day onset.
  110. Q: Neiserria?
    A: Gram - cocci. usually kidney bean shaped and diplococci like a donut. N. meningitides and N. gonorrhea.
  111. Q: Virulence factors of N. meningitidis?
    A: 1) Capsule 2) Endotoxin (LPS): causes blood vessel destruction and petechiae 3) IgA protease.
  112. Q: Do you get a fever with tetanus?
    A: Yes.

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