Flashcards Bacteria

  1. What gram staining is streptococcus
    Gram + coccus
  2. How does growth of strep and staph differ?
    • Staph ? clusters of gram + cocci
    • Strep ? gram + cocci grow along a single axis in pairs or long chains
  3. What are group A strep
    Strep pyogenes
  4. What is the capsule of strep pyogenes made of?
    Hyaluronic acid
  5. What is special about hyaluronic acid capsule
    • Hyaluronic acid is also found in our connective tissue
    • Therefore, it is non immunogenic
  6. What kind of hemolysis does strep pyogenes have?
    Beta hemolytic
  7. What kinds of infections can strep pyogenes cause?
    • Pyogenic infections
    • Toxin mediated
  8. What pyogenic infections can strep pyogenes cause
    • Impetigo
    • Pharyngitis (strep throat)
    • Cellulitis and erysipelas
  9. What does impetigo look like?
    Skin infection that looks honey crusted
  10. What bacteria can cause impetigo
    • Staph aureus
    • Strep pyogenes
  11. What does strep throat look like?
    Red erythematous and inflamed throat
  12. What is erysipelas
    Superficial cellulitis with well demarcated borders
  13. What is the most common cause of erysipelas?
    Strep pyogenes
  14. What toxin does strep pyogenes produce
    • Streptococcal pyrogenic exotoxin (SPE)
    • Streptolysin O
    • Streptokinase
    • DNases
  15. what virulence factor mediates the beta hemolysis of strep pyogenes
    streptolysin O ? lyses red blood cells
  16. what antibodies do we create against strep pyogenes?
    ASO ? Anti Streptolysin O antibodies
  17. What does kinase mean
    To add a phosphate
  18. What does streptokinase do
    • Converts plasminogen --> plasmin
    • Plasmin is fibrinolytic (lyses clots)
  19. What can we use streptokinase for in a medical medium?
    To lyse clots in MI or ischemic strokes
  20. What do DNases / Dornases do
    Depolymerize DNA
  21. How do we differentiate group A strep form Group B strep?
    • Group A strep ? Bacitracin sensitive
    • Group B strep ? Bacitracin resistant
  22. How do we check if we have recently had a strep infection?
    ASO antibody titers
  23. What infections does streptococcal pyrogenic exotoxin cause
    • Scarlet fever
    • Toxic shock like syndrome
    • Necrotizing fasciitis
  24. What are the main symptoms of scarlet fever?
    • Strawberry tongue ? reddening and swelling of tongue
    • Pharyngitis
    • Widespread rash that spares the face
  25. What kind of toxins are pyrogenic exotoxin A and C and how does they work?
    • Super antigen
    • Causes nonspecific binding of MHC class 2 and T cell receptors --> over activation --> cytokine storm
    • Could be fatal
  26. What kind of toxin is pyrogenic exotoxin B?
  27. What types of pyrogenic exotoxin exists?
    • A ? super antigen
    • B ? protease
    • C ? super antigen
  28. Which types of pyrogenic exotoxins are responsible for toxic shock like syndrome
    A and C
  29. Which types of pyrogenic exotoxins are responsible for scarlet fever
    A and C
  30. Which types of pyrogenic exotoxin are responsible for necrotizing fasciitis
  31. What causes necrotizing fasciitis
    Toxigenic strains of strep pyogenes
  32. how does necrotizing fasciitis spread?
    • invades the fascia underlying the skin
    • spreads very rapidly
  33. how do you treat necrotizing fasciitis?
    • it is a true surgical emergency
    • it is sometimes necessary to amputate the affected region
  34. how do you treat strep infections?
  35. what are the serious complications of infections with strep pyogenes?
    • Rheumatic Fever
    • Post Streptococcal Glomerular Nephritis
  36. What is the main virulence factor responsible for rheumatic fever?
    M protein
  37. What is M protein
    Highly antigenic protein in strep pyogenes cell wall
  38. How does M protein act as a virulence factor?
    • Interferes with opsonisation ? anti-phagocytic
    • Very antigenic ? elicits strong humoral response
  39. What antigen resembles M protein
    Self-antigen ? myosin in cardiac muscle
  40. Through which process does M protein resemble myosin of the cardiac muscle
    Molecular mimicry
  41. What is the consequence of molecular mimicry in strep pyogenes infection?
    Causes our own antibodies to attack our heart
  42. Which valve is most commonly affected by rheumatic fever
    Mitral valve
  43. What problems does rheumatic fever cause for heart valves
    Mitral stenosis
  44. What disease does rheumatic fever occur after?
    • Strep pharyngitis
    • Never after skin infections
    • Does not happen if pharyngitis is promptly treated
  45. Who does rheumatic fever most commonly affect
    Children who do not have access to good medical attention (the pharyngitis is not promptly treated)
  46. What are the symptoms of rheumatic fever?
    • J ? Joint ? polyarthritis
    • <3 ? Heart ? valvular damage leading to murmurs, myocarditis, pericarditis
    • N ? Nodules ? subcutaneous nodules that appear on extensor surfaces of forearms or elbows / knees
    • E ? Erythema Marginatum ? rash with thick red borders
    • S ? Sydenham?s Chorea ? rapid involuntary movements of hands and face
  47. What are the Jones criteria?
    • J ? Joint ? polyarthritis
    • <3 ? Heart ? valvular damage leading to murmurs, myocarditis, pericarditis
    • N ? Nodules ? subcutaneous nodules that appear on extensor surfaces of forearms or elbows / knees
    • E ? Erythema Marginatum ? rash with thick red borders
    • S ? Sydenham?s Chorea ? rapid involuntary movements of hands and face
  48. What are the difference between rheumatic fever and post strep glomerulonephritis?
    • Rheumatic fever
    • type 2 hypersensitivity
    • only after pharyngitis
    • early diagnosis + treatment of pharyngitis can prevent development
    • Post strep glomerulonephritis
    • type 3 hypersensitivity
    • occurs after pharyngitis or superficial infection (e.g. impetigo)
    • early diagnosis + treatment of infection will not prevent development
  49. How does strep pyogenes cause post strep glomerular nephritis?
    • Type 3 hypersensitivity reaction
    • Damage is mediated by circulating antibody ? antigen immune complexes that eventually deposit in the glomerulus
  50. What are the main symptoms of post strep glomerular nephritis?
    • Dark brown / cola colored urine
    • Fascial swelling / puffiness from edema
  51. How long does it take to develop post strep glomerular nephritis?
    2 weeks after the initial strep infection
  52. what diseases does post strep glomerular nephritis occur after
    • pharyngitis
    • superficial infections (e.g. impetigo)
  53. how do you prevent post strep glomerular nephritis?
    you can?t ? even when strep infection is treated promptly with penicillin this complication can still occur
  54. What are the hemolytic properties of strep pneumoniae?
    Alpha hemolytic
  55. What does alpha hemolysis look like?
    Surrounding zone of hemolysis is a green hue
  56. Why is alpha hemolytic zone green
    Due to oxidation of hemoglobin
  57. What is strep pneumoniae capsule made of
  58. What are the virulence factors of strep pneumoniae?
    • Polysaccharide capsule
    • IgA protease
  59. What does IgA protease allow strep pneumoniae to do?
    Colonies and invade mucosa
  60. What does the capsule allow strep pneumoniae to do?
    Evade immune system
  61. How do you differentiate between strep pneumoniae and strep viridans?
    • Strep pneumoniae
    • optochin sensitive
    • bile soluble (can?t grow in bile)
    • encapsulated
    • Strep viridans
    • optochin resistant
    • bile insoluble (grows on bile)
    • unencapsulated
  62. What shape is strep pneumoniae under high power microscopy
    Lancet shaped gram + diplococci
  63. What gram staining does strep pneumoniae have
    Gram + coccus
  64. Why can strep pneumoniae not grow on bile
    It is bile soluble
  65. What infections do strep pneumoniae cause
    • M ? Meningitis
    • O ? Otitis Media
    • P ? Pneumonia
    • S ? Sinusitis
  66. What does MOPS stand for
    • Infections for which strep pneumoniae is the most common cause
    • M ? Meningitis
    • O ? Otitis Media
    • P ? Pneumonia
    • S ? Sinusitis
  67. What is the most common cause of community acquired pneumonia in adults?
    Strep pneumoniae
  68. What characteristic pneumonia does strep pneumoniae cause?
    • Lobar pneumonia that infiltrates the lower lobes
    • Causes rust colored sputum
  69. Which population is at higher risk of being infected by encapsulated organisms
    People who have undergone splenectomy or auto-splenectomy (e.g. in sickle cell disease)
  70. Where are encapsulated organisms removed from the body
  71. How do we treat strep pneumoniae infection?
    • Susceptible to Macrolides ? erythromycin
    • 3rd generation cephalosporin ? ceftriaxone
  72. How can we prevent strep pneumoniae infection?
    2 pneumococcal vaccines available
  73. How does the adult strep pneumoniae vaccine work?
    • 23 valent polysaccharide vaccine
    • T cell independent response generated
    • This only creates IgM
    • Not long lasting reaction
  74. How does the child strep pneumoniae vaccine work?
    • 7 valent conjugated to a protein
    • Protein means it is more antigenic
    • More robust T cell response
    • IgG production
  75. What are group B strep?
    Strep agalactiae
  76. Which group of people does strep agalactiae cause serious infections in
  77. What does hippurate in strep agalactiae do
    Hydrolysis sodium hippurate
  78. What is strep agalactiae?s capsule made of
  79. How do we distinguish strep agalactiae from all other streps?
    CAMP test
  80. What is the CAMP test?
    • When strep agalactiae is plated with staph aureus there is an increased zone of hemolysis
    • Butterfly hemolytic zone
  81. What are strep agalactiae hemolytic properties
    Beta hemolytic
  82. How do we differentiate strep pyogenes and strep agalactiae from strep pneumoniae and strep viridans?
    • Strep agalactiae + strep pyogenes ? beta hemolytic
    • Strep pneumoniae + step viridans ? alpha hemolytic
  83. How do we differentiate strep agalactiae from strep pyogenes?
    • Strep agalactiae ? bacitracin resistant
    • Strep pyogenes ? bacitracin sensitive
  84. What infections does strep agalactiae cause
    • Meningitis in neonates
    • Sepsis in neonates
    • Pneumonia
  85. What is the main cause of meningitis in neonates?
    Strep agalactiae
  86. How do neonates get strep agalactiae infections?
    When the neonate passes through the vaginal canal of the mother during delivery
  87. What prenatal care do we have to prevent neonatal strep agalactiae infections
    Swab vagina and rectum of mother at 35 weeks to see if she is colonized
  88. If mother is colonized with strep agalactiae how do we prevent strep agalactiae infection in neonate
    Prophylactic Intrapartum penicillin administered to the mother
  89. What are the hemolytic properties of strep viridans?
    Alpha hemolytic
  90. What gram staining does strep viridans have
    Gram + coccus
  91. Strep viridans capsule
  92. What bacteria are found in the strep viridans group
    • Strep mutans
    • Strep sanguinis
  93. What diseases do strep viridans cause
    • Dental carries
    • When passed into blood --> Subacute endocarditis and damaged heart valves
  94. Which heart valve is most affected by bacteremic strep viridans infection
    • Damaged heart valves ? Mitral valve
    • Mitral valve prolapses very common + rheumatic fever affects mitral valve more
  95. How do strep viridans affect heart valves?
    • Previously damaged heart valve (mitral valve prolapse)
    • Teeth cleaning --> strep viridans bacteria enter the blood stream --> transient bacteremia
    • Strep viridans able to adhere any fibrin platelet aggregates at damaged tissue via dextrans
  96. What are strep viridans virulence factors
    Dextrans ? stick to platelets
  97. How are dextrans formed
    Formed by strep viridans from glucose
  98. What does the name Enterococcus tell us?
    • Entero = inhabits intestinal tract
    • Coccus = cocci (not Enterobacter = rod)
  99. What species are in the enterococcus genus
    • E. faecalis
    • E. faecium
  100. Which species is more common in the enterococcus genus
    E. Faecalis
  101. Which species is more serious in the enterococcus genus
    E. Faecium
  102. What medium are enterococci able to grow in
    • 6.5% NaCl
    • Bile resistant so can grow on bile
  103. What infections do enterococci cause?
    • UTI
    • Endocarditis
    • Biliary tree infections
  104. E. Faecium resistance
    • To almost all antibiotics
    • Including vancomycin
  105. What kind of infection is E. Faecium?
  106. What does VRE stand for
    Vancomycin Resistant Enterococcus
  107. How do you treat VRE?
    • Linezolid ? expensive big gun antibiotic
    • Tigecycline ? expensive bug gun antibiotic
  108. What does the name staphylococcus aureus tell us?
    • Staph = grape (Latin)
    • Coccus = granule (Latin)
    • Look like bunch of grapes under microscope
    • Aureus = golden (Greek)
    • When grows on blood agar, colonies have yellow or golden appearance to them
  109. What gram staining is Staph Aureus
    Gram + coccus (take up crystal violet in thick cell wall and hold on to it even after rinse and addition of red safranin)
  110. How do you tell the difference between staph and strep?
    Catalase test ? + in staphylococci
  111. What does catalase do?
    Convert hydrogen peroxide to water
  112. How to tell the difference between staph aureus and other staph?
    • Golden color when plated
    • Coagulase test
    • Beta hemolytic
    • Grow on mannitol salt agar
  113. What is coagulase
    • An enzyme that converts fibrinogen --> fibrin
    • Present in staph aureus
  114. What does beta hemolysis look like on a petri dish?
    Glowing halo of light on a red backdrop
  115. What is special about mannitol salt agar
    • salt selects only staph species
    • see if it ferments mannitol ? positive (pink --> yellow) ? staph aureus
  116. what is the main virulence factor for staph aureus?
    Protein A
  117. How does protein A work
    • Protein A is a component of staph aureus cell wall
    • Binds the Fc portion of immunoglobulins
    • This prevents compliment from binding to the Fc region
    • Prevents opsonisation and phagocytosis
    • Allows it to better colonize its host
  118. Where does staph aureus colonize
  119. What types of diseases does staph aureus cause?
    • Infectious
    • Toxin mediated
  120. What infectious diseases does staph aureus cause?
    • Pneumonia
    • Skin infections
    • Septic arthritis
    • Endocarditis
    • Osteomyelitis
  121. What is typical of the pneumonia caused by staph aureus?
    • See patchy infiltrates on X ray
    • Usually a secondary post viral superinfection (after immune system has been weakened)
  122. What is the most common cause of septic arthritis in adults?
    Staph aureus
  123. What kinds of skin infections does staph aureus cause?
    • Cellulitis
    • Impetigo
    • Furuncles ? boils
    • Carbuncles ? slightly larger boils
    • Abscesses
  124. What kind of endocarditis does staph aureus cause?
    • Rapid onset (acute) bacterial endocarditis
    • Usually in an IV drug user ? right sided infection on tricuspid valve
  125. What is the most common cause of osteomyelitis in adults?
    Staph aureus
  126. What toxin mediated diseases does staph aureus cause?
    • Scalded skin syndrome
    • Toxic shock syndrome
    • Food poisoning
  127. What mediates scalded skin syndrome
    Exfoliative toxin ? protease
  128. What is the classic situation for someone getting toxic shock syndrome?
    Someone leaving a foreign packing in for too long (gauze after rhinoplasty / tampon)
  129. What kind of toxin is toxic shock syndrome toxin and how does it work
    • Super antigen
    • Causes nonspecific binding of MHC class 2 and T cell receptors --> over activation --> cytokine storm
    • Could be fatal
  130. What kind of food poisoning does staph aureus cause?
    • Rapid onset due to preformed toxin (1-8 hours)
    • Usually associated with vomiting more than diarrhea
    • Associated with meats and mayonnaise etc.
  131. What does MRSA stand for?
    Methicillin Resistant Staph Aureus
  132. How does MRSA become resistant?
    Altering its Penicillin Binding Proteins
  133. What does Penicillin Binding Protein do?
    Helps build the cell walls
  134. How do you treat MRSA?
  135. How do you treat staph aureus infection?
    • Determine if it is methicillin sensitive
    • If it is should use penicillin as it is more effective in killing bug
    • Nafcillin = Naf for Staph
  136. What gram staining is staph epidermidis
    Gram + coccus ? takes up a lot of crystal violet stain
  137. What does staph epidermidis often infect
    • Implanted hardware
    • Artificial joints
    • Indwelling catheters
    • Artificial heart valves (endocarditis)
  138. Why is staph epidermidis called this way
    Covers all of our skin
  139. In what situation will staph epidermidis cause infections
    When the skin is penetrated
  140. How does staph epidermidis easily infect implants etc.?
    Produces copious adherent biofilm which sticks to sleek metal and plastic surfaces
  141. What is biofilm made of
    Mesh of polysaccharides
  142. What does biofilm do
    • Helps bacteria stick to surfaces
    • Acts as a coating that protects bacteria from antibiotics and immune cells
  143. Why is staph epidermidis resistant to many antibiotics
    The biofilm provides it with a protective coating
  144. How do you treat staph epidermidis?
    • Vancomycin for endocarditis
    • Should replace any implants that are infected
  145. Why is staph epidermidis often found in blood cultures
    Part of the normal skin flora so easily contaminates cultures
  146. How can you differentiate staph epidermidis from staph saprophyticus?
    • Staph epidermidis is novobiacin sensitive
    • Staph saprophyticus is novobiacin resistant
  147. What gram staining is staph saprophyticus
    Gram + coccus ? takes up a lot of crystal violet stain
  148. What diseases does staph saprophyticus commonly cause
    UTI ? in sexually active females
  149. What features do staph epidermidis and staph saprophyticus have in common
    • Catalase positive
    • Urease positive
    • Coagulase negative
  150. how do you differentiate between staph aureus and staph saprophyticus or staph epidermidis?
    • staph aureus ? coagulase positive
    • staph epidermidis / saprophyticus ? coagulase negative
  151. What does urease do
    Converts urea into ammonia
  152. What bacteria are urease positive
    • Proteus
    • Klebsiella
    • Staph epidermidis
    • Staph saprophyticus
  153. what species are in the Neisseria genus
    • Neisseria meningitidis
    • Neisseria Gonorrhea
  154. What gram staining are Neisseria
    Gram ? diplococci
  155. What biochemical properties do Neisseria have?
    Oxidase +
  156. How do you grow Neisseria?
    • Chocolate agar
    • VPN agar = Thayer martin agar
  157. What do Neisseria species look like when grown on blood agar?
    Unable to grow on blood agar
  158. Why are Neisseria unable to grow on blood agar
    Inhibited by some of the lipids and other elements in blood agar
  159. What is chocolate agar
    Heated blood agar
  160. Why do we use chocolate agar to culture Neisseria?
    Heating inactivates the inhibitors to growth found in blood agar
  161. What is VPN agar
    Agar enriched with vancomycin + polymyxins + nyastin
  162. What is another name for VPN agar?
    Thayer martin agar
  163. Wo is more susceptible to Neisseria infections
    Compliment deficiency of C5 ? C9
  164. What does compliment deficiency of C5-C9 cause
    Unable to form Membrane Attack Complex (MAC) --> increase susceptibility to Neisseria infections
  165. What are the virulence factors of Neisseria?
    • Pilus
    • IgA protease
  166. What is the function of Neisseria pili?
    • Attachment to mucosal surfaces
    • Frequent genetic rearrangement --> antigenic variation
  167. What does the antigenic variation of Neisseria mean for our immune system?
    • Difficult to target
    • Prevents any lasting immune response
  168. How does Neisseria evade our immune system?
    Antigenic variation of pili through frequent genetic rearrangements
  169. What is IgA protease
    Protein that cleaves IgA at its hinge point
  170. What does IgA protease do?
    • Cleaves IgA at its hinge point
    • Facilitates survival along mucosal surfaces
  171. How do Neisseria survive on mucosal surfaces?
    IgA protease
  172. What gram stain is Neisseria
    Gram ? diplococci
  173. What biochemical properties does Neisseria have?
    Oxidase positive
  174. How do you grow Neisseria?
    • Chocolate agar
    • VPN agar = Thayer martin agar
  175. Who is susceptible to Neisseria infections?
    C5-C9 compliment deficient patients due to inability to form MAC complex
  176. What virulence factors does Neisseria meningitidis have
    • IgA protease
    • Pili that demonstrate antigenic variation
    • Polysaccharide capsule
  177. How is Neisseria meningitidis spread
    Respiratory droplets
  178. Where is Neisseria meningitidis spread
    Close quarters ? e.g. dorms
  179. What differentiates Neisseria meningitidis from Neisseria gonorrhea
    • Ferments glucose and maltose (Meningitidis)
    • Only ferments glucose (gonorrhea)
    • Encapsulated (meningitidis)
    • Non encapsulated (gonorrhea)
  180. How does Neisseria meningitidis infection occur
    Respiratory droplets --> colonize nasopharynx -->hematogenous spread
  181. What is the Neisseria meningitidis capsule made of?
  182. What is the function of the Neisseria meningitidis capsule?
    Inhibits phagocytosis
  183. What kind of vaccine is used for Neisseria meningitidis?
    Contain polysaccharide capsule (types A, C, D)
  184. Which polysaccharide capsules are included in the Neisseria meningitidis vaccine
    • A, C, D
    • NOT B
  185. Which strain of Neisseria meningitidis causes most infections in developed world and why
    B because it is not included in the vaccine
  186. Who is most susceptible to Neisseria meningitidis infections
    • Sickle cell anemia
    • Asplenic patients
  187. Who more susceptible to infections caused by encapsulated organisms
    • Sickle cell anemia
    • Asplenic patients
  188. Which organisms are asplenic patients more susceptible to
    • Encapsulated organisms
    • * Streptococcus pneumoniae
    • * Haemophilus influenzae
    • * Neisseria meningitidis
  189. What happens when Neisseria meningitidis enters the blood stream
    • Massive inflammatory response --> increased permeability of capillaries --> leakage of fluid into extravascular space --> hypovolemic shock --> peripheral vasoconstriction --> adrenal insufficiency --> farther exacerbation of shock
    • Thrombocytopenia --> Characteristic petechial rash
  190. What causes the massive inflammatory response to hematogenous Neisseria meningitidis?
    Lipoolygosaccharides (LOS) outgrows surface of bacteria --> blebs off
  191. What is LOS
    LipoOligoSaccharide envelope protein of Neisseria meningitidis
  192. What does petechial rash suggest in a patient?
  193. What is DIC
    Disseminated Intravascular Coagulation
  194. What are the early signs of DIC?
    Petechial rash --> purpura --> ecchymosis
  195. What would you see in a physical exam of a patient with DIC?
    • Oozing at the venipuncture sites
    • Bleeding gums
  196. What causes waterhouse frederichson syndrome
    • Neisseria meningitidis
    • Massive inflammatory response to LOS --> Hypovolemic shock --> peripheral vasoconstriction
  197. What is waterhouse Frederichson syndrome
    Adrenal infarction due to Neisseria meningitidis infection
  198. What are the general stages of Neisseria meningitidis infection?
    • Nasopharyngeal colonization
    • Hematogenous spread (meningeal symptoms)
    • Hypovolemic shock + DIC
    • Waterhouse frederichson syndrome
  199. How do you treat Neisseria meningitidis infection?
    • 3rd generation cephalosporin that can penetrate the blood brain barrier
    • Ceftriaxone
    • Prophylactic treatment of close contacts with rifampin
  200. Why do we give prophylaxis to close contacts in Neisseria meningitidis infection?
    • Spread by respiratory droplets
    • Highly contagious
  201. What is defined as a ?Close contact? in Neisseria meningitidis infection
    Someone who has spent over 8 hours with the patient during the 7 days prior to onset
  202. What is the prophylaxis for Neisseria meningitidis infection?
  203. What gram stain is Neisseria
    Gram ? diplococci
  204. What biochemical properties does Neisseria have?
    Oxidase positive
  205. How do you grow Neisseria?
    • Chocolate agar
    • VPN agar = Thayer martin agar
  206. Who is susceptible to Neisseria infections?
    C5-C9 compliment deficient patients due to inability to form MAC complex
  207. What virulence factors do Neisseria have
    • IgA protease
    • Pili that demonstrate antigenic variation
  208. What differentiates Neisseria meningitidis from Neisseria gonorrhea
    • Ferments glucose and maltose (Meningitidis)
    • Only ferments glucose (gonorrhea)
    • Encapsulated (meningitidis)
    • Non encapsulated (gonorrhea)
  209. What kind of infection is gonorrhea?
    STD ? Sexually Transmitted Disease
  210. where can Neisseria gonorrhea grow
    facultative intracellular
  211. what cells does Neisseria gonorrhea invade?
    polymorphonuclear lymphocytes (PMN)
  212. what is the area that Neisseria gonorrhea most commonly affects?
    genetelia of men and women
  213. what can Neisseria gonorrhea cause in men
    • urethritis --> prostatitis --> orchitis
    • polyarthritis
  214. what can Neisseria gonorrhea cause in women
    • urethritis --> pelvic inflammatory disease (PID) --> spread into peritoneum
    • polyarthritis
  215. what is PID
    Pelvic inflammatory disease
  216. What can PID cause
    Scarring --> infertility / atopic pregnancies
  217. What does Neisseria gonorrhea urethritis look like?
    Thick white purulent discharge
  218. What does chlamydia trachomatis urethritis look like?
    Thin watery purulent discharge
  219. What are the main causes of urethritis?
    • Chlamydia trachomatis
    • Neisseria gonorrhea
  220. What is Fitz Hugh Curtis syndrome?
    Neisseria gonorrhea infection spreading into peritoneum
  221. What can Fitz Hugh Curtis syndrome cause
    Violin string adhesions ? adhesions to the capsule of the liver (long + thin)
  222. Where does Neisseria gonorrhea polyarthritis occur
    Knee ? often asymmetric
  223. Who does Neisseria gonorrhea affect
    Young sexually active people
  224. How do you diagnose Neisseria gonorrhea polyarthritis?
    Joint tap with purulent synovial fluid that doesn?t gram stain
  225. Why is gram stain ineffective in diagnosis of Neisseria gonorrhea?
  226. How do we get congenital Neisseria gonorrhea infection?
    Expecting mother with untreated gonococcal infection passes it to child during delivery
  227. How will congenital Neisseria gonorrhea infection manifest
    Purulent conjunctivitis that occurs within first 5 days of life
  228. How will congenital chlamydia trachomatis infection manifest
    Purulent conjunctivitis that occurs a week after birth
  229. What are the main differences between Neisseria gonorrhea and chlamydia trachomatis infections?
    • Urethral discharge is thick and very purulent (gonorrhea)
    • Urethral discharge is thin and watery (chlamydia)
    • Neonatal conjunctivitis occurs within first 5 days of life (gonorrhea)
    • Neonatal conjunctivitis occurs after 1 week of life (chlamydia)
  230. How do we treat Neisseria gonorrhea infection?
    • Ceftriaxone (gonorrhea)
    • Macrolides ? azithromycin / doxycycline (chlamydia co infection)
  231. Why do we treat patients with more than one antibiotic?
    Chances of co infection with chlamydia trachomatis are very high so we should treat both in case
  232. What gram stain is Brucella
    Gram ? coccobacillus
  233. Where can we find Brucella
    Zoonotic ? associated with cattle and other farming animals
  234. What is the reservoir for Brucella?
    Farm animals ? cows / sheep / goats / pigs
  235. What species are there in Brucella genus?
    • Different species for different animals
    • Cow ? Brucella bordis
  236. Who is affected by Brucella infections
    • Direct contact with animals ? people with direct contact with animals
    • * Veterinarian
    • * Slaughter house workers
    • * Rancher
  237. How is Brucella transmitted
    • Direct contact with animals
    • Indirect contact by consumption of milk / chees products
  238. Where can Brucella grow
    • Facultative intracellular
    • Inside cells such as macrophages
  239. How do Brucella survive intracellularly in macrophages?
    Prevent phagolysosome fusion
  240. What does Brucella cause
  241. What is the clinical presentation of brucellosis?
    • Primary symptoms ? non specific
    • * Undulant fever
    • * chills
    • * anorexia
    • enlargement of reticuloendothelial organs (spleen / liver / lymph nodes)
    • osteomyelitis
  242. what is undulant fever
    • pattern of fever that rises and falls
    • can be caused by brucellosis
  243. where can Brucella spread in the body and why
    able to survive in macrophages and be carried to multiple organs in reticulo endothelial system
  244. what is the pathogenesis of brucellosis?
    • Brucella is taken up by macrophages
    • Prevents phagolysosome fusion
    • Replicates intracellularly until host cell lyses
    • Spread systemically
  245. Which organs are part of the reticulo endothelial system
    • Spleen
    • Liver
    • Lymph nodes
  246. What is a complication of chronic brucellosis?
  247. How do we treat brucellosis?
    Tetracycline (doxycycline) AND rifampin
  248. What gram stain is Francisella tularensis
    Gram ? coccobacillus
  249. What does Francisella tularensis cause
  250. Where can we find Francisella tularensis
    Zoonotic ? rabbits
  251. What is the main reservoir for Francisella tularensis?
  252. How is Francisella tularensis transmitted
    • Direct contact with rabbits ? handling rabbits / eating rabbit meat
    • Indirect contact ? tick vector
    • Aerosolized
  253. Which tick transmits Lyme disease caused by Borrelia burgdorferi
    Ixodes tick
  254. Which tick transmits Francisella tularensis
    Dermacentor tick
  255. Why is Francisella tularensis possible to use in bioterrorism
    Can be aerosolized
  256. What shape is Francisella tularensis
  257. Where can Francisella tularensis grow
    Facultative intracellular
  258. Which kind of immunity is important for recovery from Francisella tularensis infection
    Cell mediated immunity (intracellular organism)
  259. What is the pathogenesis of Francisella tularensis infection?
    • Tick bites human
    • Bacteria enters at site of bite --> painful ulcer
    • Enters macrophages
    • Travels through lymph system --> reticuloendothelial organs
  260. What is the clinical presentation of tularensis?
    • Painful ulcer at tick bite site
    • Granulomas with caseating necrosis in reticuloendothelial organs (lymph nodes)
    • Regional lymphadenopathy
    • How do we treat Francisella tularensis infection?
    • Aminoglycosides ? streptomycin
  261. What does Bordetella pertussis infection cause?
    Whooping cough
  262. What gram stain is Bordetella pertussis
    Gram ? coccobacillus
  263. How is Bordetella pertussis transmitted?
    Respiratory droplets
  264. How does Bordetella pertussis cause infection?
    • Attaches to respiratory epithelium using pili
    • Releases toxins to cause systemic effects
  265. What are virulence factors of Bordetella pertussis?
    • Pilli ? filamentous hemagglutinin
    • Toxins
    • * Pertussis toxin
    • * Adenylate cyclase toxin
    • * Tracheal toxin
  266. What does Bordetella pertussis use filamentous hemagglutinin for?
    Attaching to respiratory epithelium
  267. What is the name of Bordetella pertussis pili?
    Filamentous hemagglutinin
  268. How does Bordetella pertussis cause systemic effects?
    Releasing toxins after attaching to respiratory epithelium
  269. What do antibodies target in Bordetella pertussis?
    Filamentous hemagglutinin pili
  270. Which toxins does Bordetella pertussis have
    • Pertussis toxin
    • Adenylate cyclase toxin
    • Tracheal toxin
  271. How does Bordetella pertussis work?
    • ADP ribosylation of Gi (inhibitory G) protein --> Gi is inhibition --> rise in cAMP
    • Also disables chemokine receptors for lymphocytes --> Lymphocytes unable to enter lymphoid tissue --> stuck in blood stream --> massive lymphocytosis
  272. What is the function of Gi protein?
    • Inhibitory G protein
    • Inhibits cAMP formation
  273. What causes massive lymphocytosis in Bordetella pertussis
    Pertussis toxin disables chemokine receptors for lymphocytes
  274. How does
    Acts as an adenylate cyclase --> Increases cAMP levels
  275. What do Bordetella pertussis and Bacillus anthracis have in common?
    • Adenylate cyclase toxin (Bordetella pertussis)
    • Edema factor (Bacillus anthracis)
  276. How does tracheal toxin work?
    • Damages ciliated cells in respiratory epithelium
    • Cleaves cilia
  277. Where do we find tracheal toxin?
    Part of peptidoglycan wall of Bordetella pertussis
  278. What is the target for tracheal toxin?
    Ciliated cells in respiratory epithelium
  279. Who is most affected by Bordetella pertussis infection
  280. What is the clinical presentation of Bordetella pertussis infection?
    • Catarrhal phase ? Initially nonspecific symptoms (1-2 weeks)
    • Paroxysmal phase ? whooping cough (2 weeks ? 2 months)
    • Convalescent phase ? gradual reduction in symptoms (up to 3 months)
  281. How long does the catarrhal phase of Bordetella pertussis infection last?
    1-2 weeks
  282. What is the clinical presentation of the catarrhal phase of Bordetella pertussis infection?
    • Nonspecific symptoms
    • * Conjunctival injection
    • * Lacrimation
    • Lasts 1-2 weeks
  283. How long does the paroxysmal phase of Bordetella pertussis infection last?
    2 weeks ? 2 months
  284. What is the clinical presentation of the paroxysmal phase of Bordetella pertussis infection?
    Intense bouts of coughing that get children so out of breath that when eventually breath in it makes characteristic whooping sound on inspiration
  285. How long does the convalescent phase of Bordetella pertussis infection last?
    Up to 3 months
  286. What is the clinical presentation of convalescent phase of Bordetella pertussis infection?
    Gradual reduction in symptoms
  287. What is another way to call whooping cough and why?
    • 100-day cough
    • Lasts for a very long time with phases going on for months
  288. How do we treat Bordetella pertussis infection?
    • Macrolides ? remove bacteria in the respiratory tract
    • Vaccination
  289. Why is it important to start treatment early in Bordetella pertussis infection?
    • Macrolides can remove the bacteria but do not affect the toxins already circulating in the body
    • So macrolides are ineffective in symptom improvement
  290. What kind of vaccines do we have for Bordetella pertussis?
    • Killed vaccine ? no longer in use
    • Acellular vaccine
  291. What is the acellular vaccine for Bordetella pertussis made of?
    Purified antigens
  292. What is DPT
    • Vaccine given to children
    • Diphtheria toxoid
    • Pertussis antigens
    • Tetanus toxoid
  293. What gram stain is Haemophilus influenzae
    Gram ? coccobacillus
  294. What shape does Haemophilus influenzae have
  295. How do we grow Haemophilus influenzae?
    Chocolate agar with Factor 5 (NAD) and Factor 10 (hematin)
  296. What is factor 5
  297. What is factor 10
    Hematin (hema-ten)
  298. Which bacteria required factor 5 + 10 to grow
    Haemophilus influenzae
  299. How is Haemophilus influenzae transmitted
    Aerosol transmission
  300. What does Haemophilus influenzae infection cause
    • Pneumonia
    • Epiglottitis
    • Otitis media
    • Meningitis
    • Sepsis
    • Septic arthritis
  301. What is a common causes epiglottitis?
    Haemophilus influenzae
  302. What is the clinical presentation of epiglottis caused by Haemophilus influenzae?
    • Inflamed epiglottis ? cherry red epiglottis
    • Inspiratory stridor
    • Drooling
  303. Who is most affected by epiglottitis caused by Haemophilus influenzae
  304. What is otitis media
    Inflammation of the middle ear
  305. Which form of Haemophilus influenzae causes meningitis
    Type B capsular strain
  306. Who is most affected by septic Haemophilus influenzae infections
    • Asplenic patients
    • Sickle cell patients
  307. What is the function of the spleen in relation to bacteria?
    Remove encapsulated organisms
  308. Why is Haemophilus influenzae meningitis rare in the USA
    Successful vaccination efforts
  309. What kind of vaccine is vaccine for Haemophilus influenzae?
    Polysaccharide capsular antigen (type B) conjugated to the diphtheria toxoid
  310. Why do we have conjugated vaccines?
    • Proteins increase antigenicity of capsular polysaccharide
    • Body produces strong IgG response
  311. When do we vaccinate for Haemophilus influenzae?
    2-18 months
  312. How do you treat Haemophilus influenzae?
    • Beta lactams
    • Meningitis / systemic disease ? ceftriaxone
    • Prophylaxis for meningitis ? rifampin
  313. How do we treat Haemophilus influenzae meningitis?
  314. what do you use for prophylaxis of Haemophilus influenzae in close contacts?
  315. What gram stain is Listeria monocytogenes
    Gram + bacillus
  316. What is Listeria monocytogenes most associated with?
    Infections in pregnant women
  317. What are listerias hemolytic properties
    Beta hemolytic with narrow zone of hemolysis
  318. Where can Listeria grow
    Facultative intracellular organism
  319. What does listeria use its flagella for?
    Tumbling motility when it is extracellular
  320. How does listeria move intracellularly?
    • Actin rockets ? rapidly polymerizes actin against the bacteria wall so that it is propelled along in opposite direction
    • Can be from cell to cell
  321. How does listeria move from cell to cell?
    Through actin rocket propulsion across cell membranes
  322. What biochemical markers does listeria have?
    Catalase + (like staph)
  323. Why are listeria able to contaminate food items
    Able to survive and multiply in near freezing temperatures ? contaminates refrigerated items
  324. What kind of food does listeria contaminate?
    • Unpasteurized milk
    • Packages meat
    • Soft cheeses
  325. Who does listeriosis affect most
    Pregnant women ? 20x more likely
  326. What does listeriosis during pregnancy cause
    • Early in pregnancy ? termination
    • Later in pregnancy ? diseases in the newborn
  327. How do we decrease likelihood of getting listeriosis in pregnant women?
    Discouraged from eating unpasteurized products and soft cheeses
  328. What diseases does listeria monocytogenes cause?
    Meningitis in newborns and adults over 60
  329. What are the 3 most common causes of meningitis in newborns
    • Group B strep
    • E. coli
    • Listeria Monocytogenes
  330. What is the standard empirical treatment for meningitis in adults?
    • Vancomycin (gram +)
    • AND Ceftriaxone (gram -)

    • What is the treatment for meningitis in adults over 60?
    • Vancomycin (gram +)
    • AND Ceftriaxone (gram -)
    • And Ampicillin (listeria)
  331. How do we treat listeriosis?
  332. What are the gram staining properties of Corynebacterium?
    Gram + rod (club shaped)
  333. What does Corynebacterium diphtheriae cause
  334. What does Corynebacterium diphtheria look like?
    • Club shaped ? Y or V formation
    • Contains metachromatic granules
  335. How do you stain metachromatic granules?
    Aniline dyes
  336. What toxin does Corynebacterium diphtheria produce?
    Diphtheria Exotoxin
  337. What is the structure of Corynebacterium diphtheria exotoxin?
    • 2 subunits A and B
    • A ? Active
    • B ? Binding
  338. What does Corynebacterium diphtheria exotoxin do?
    Causes ADP ribosylation of elongation factor 2 --> inhibits ribosome function --> inhibits protein synthesis cell death
  339. What is a pseudomembrane of the oropharynx
    Thick greyish exudate over the mucosal surface
  340. What bacteria causes a pseudomembrane in the oropharynx
    Corynebacterium diphtheriae
  341. What bacteria cause pseudomembrane formation
    • Corynebacterium diphtheriae
    • Clostridium difficile
  342. Where are Corynebacterium diphtheriae psuedomembranes formed
    Throat and tonsils (oropharynx) --> larynx --> trachea
  343. How is Corynebacterium diphtheriae infection transmitted
    Respiratory droplets
  344. What symptoms does Corynebacterium diphtheriae cause?
    • Airway obstruction (when spread to larynx and trachea)
    • Bulls neck ? severe lymphadenopathy with characteristic thickening of the neck
  345. What causes bulls neck
    Corynebacterium diphtheriae lymphadenopathy --> thickening of the neck
  346. When causes systemic effects of Corynebacterium diphtheriae infection
    Exotoxin going into bloodstream
  347. What systemic effects can Corynebacterium diphtheriae infection cause
    • Cardiotoxic effects
    • * Life threatening myocarditis
    • * Arrhythmias
    • * Heart block
    • Neurotoxic effects
    • * Local paralysis that begin in the posterior pharynx --> other cranial nerve deficits
  348. What life threatening effects does Corynebacterium diphtheriae have
    Life threatening myocarditis
  349. How does diphtheria exotoxin cause neurogenic effects?
    Damages myelin of nerve fibers
  350. How do you definitively diagnose Corynebacterium diphtheriae infection?
    • Good clinical history + physical exam ? gives a good idea but not definitive
    • Culturing
    • Toxin assay
  351. how do you grow Corynebacterium diphtheriae?
    • Tellurite media
    • Loeffler?s media
  352. How do you differentiate between toxic and nontoxic strains of Corynebacterium diphtheriae?
    ELEKs test
  353. How does ELEKs test work
    • In vitro assay on filter paper that has antitoxin on it
    • If toxin binds on it there is a reaction --> strain is toxic
  354. What is ELEKs test used for
    Differentiating between toxic and nontoxic strains of Corynebacterium diphtheriae
  355. Which population is at greater risk of getting diphtheria
    Unvaccinated (immigrant) children
  356. What kind of vaccine is Corynebacterium diphtheriae vaccine?
    Toxoid vaccine
  357. What is a toxoid vaccine?
    Consists of inactivated exotoxin bound to protein
  358. What kind of immune response do we get from toxoid vaccines
    Powerful IgG response
  359. What is DPT vaccine
    • Diphtheria ? toxoid vaccine (Corynebacterium diphtheriae)
    • Pertussis ? acellular vaccine (Bordetella pertussis)
    • Tetanus ? toxoid vaccine (Clostridium tetani)
  360. How do you treat diphtheria?
    • Preventative vaccination
    • Passive immunization
  361. What is passive immunization
    Administering antitoxoid
  362. What gram stain is Escherichia coli
    Gram ? rod (enterobactericiae)
  363. What bacteria are part of the Escherichia coli group
    • EHEC ? Entero Hemorrhagic
    • ETEC ? Entero Toxigenic
    • EPEC ? Entero Pathogenic
    • EIEC ? Entero Invasive
  364. What biochemical properties do Escherichia coli have?
    • Ferment lactose
    • Catalase +
  365. How do you test for lactose fermentation?
    Grow pink on MacConkey agar
  366. Which bacteria are lactose fermenters
    • Klebsiella
    • Enterobacter
    • Serratia
    • Escherichia coli
  367. What are Escherichia coli virulence factors?
    • Capsule
    • Fimbriae
    • LipoPolySaccharide (LPS) endotoxin
  368. What is Escherichia coli capsule made of?
    K antigen
  369. What do we use to serotype Escherichia coli?
    K antigen of the capsule
  370. What is EMB agar
    Eosin Methylene blue agar
  371. how does Escherichia coli look on EMB agar?
    metallic green sheen
  372. what is necessary for Escherichia to cause urinary tract infection
  373. what does Escherichia coli infection cause?
    • urinary tract infection (UTI)
    • sepsis
    • meningitis in neonates
  374. what is the number one cause of urinary tract infection?
    Escherichia coli
  375. What is the number one cause of gram ? sepsis
    Escherichia coli
  376. What is the virulence factor important for causing Escherichia coli sepsis?
    Lipopolysaccharide (LPS) endotoxin
  377. What does Escherichia coli endotoxin cause?
  378. Where is Escherichia coli endotoxin located
    Outer cell membrane

    • What is a common virulence factor for all gram ? bacteria
    • Lipopolysaccharide (LPS) endotoxin
  379. What virulence factor must be present for Escherichia coli to cause meningitis in neonates
    K capsular antigen
  380. How is Enterohemorrhagic Escherichia coli most commonly transmitted
    Undercooked meat (e.g. hamburgers)
  381. What does Enterohemorrhagic Escherichia coli infection cause
    • Bloody diarrhea
    • Hemolytic uremic syndrome (HUS)
  382. How can you differentiate Enterohemorrhagic Escherichia coli from other E. coli?
    Does not ferment sorbitol
  383. What are Enterohemorrhagic Escherichia coli virulence factors
    • Capsule
    • LPS endotoxin
    • Fimbriae
    • Shiga like toxin
  384. What toxin does Enterohemorrhagic Escherichia coli secrete
    Shiga like toxin
  385. How does shiga like toxin cause damage
    Inhibits ribosomes at the 60S position
  386. What can shiga like toxin cause
    • Tissue damage
    • Hemolytic Uremic Syndrome (HUS) in children under 10
  387. What is the pathogenesis of hemolytic uremic syndrome?
    • Shiga (like) toxin damages endothelial cells of the capillaries in the glomerulus
    • Damaged endothelial lining becomes thrombogenic --> platelets adhere
    • Clumps of platelets lyse red blood cells as they pass through capillaries
  388. Which Enterohemorrhagic Escherichia coli serotype causes massive outbreaks
    O157 H7
  389. What is O157 H7
    Enterohemorrhagic Escherichia coli strain known to cause massive outbreaks
  390. What does Enterotoxigenic Escherichia coli infection cause
    Travelers diarrhea
  391. How is Enterotoxigenic Escherichia coli transmitted
    Water sources
  392. Where is Enterotoxigenic Escherichia coli commonly found
    Mexico in the water
  393. What virulence factors does Enterotoxigenic Escherichia coli have
    • Capsule
    • Fimbriae
    • LPS endotoxin
    • Heat labile toxin
    • Heat stable toxin
  394. Which toxins does Enterotoxigenic Escherichia coli secrete
    • Heat labile toxin
    • Heat stable toxin
  395. How does Enterotoxigenic Escherichia coli heat labile toxin work
    Increases cAMP
  396. How does Enterotoxigenic Escherichia coli heat stable toxin work
    Increase cGMP
  397. Which Enterotoxigenic Escherichia coli and Vibrio cholerae toxins are similar
    • Heat labile toxin (Enterotoxigenic Escherichia coli)
    • Cholera toxin (Vibrio cholerae)
    • Both increase cAMP
  398. What is the clinical presentation of Enterotoxigenic Escherichia coli infection?
    Watery diarrhea
  399. What gram stain is salmonella
    Gram ? rod (Enterobacteriaceae)
  400. What virulence factors does salmonella have
    • Motile
    • Encapsulated
    • Facultative intracellular (macrophages)
  401. What is a common feature of all motile Enterobacteriaceae?
    H2S +
  402. How do we test for H2S positivity?
    Black colonies on Hektoen enteric agar
  403. What biochemical properties do salmonella have?
    • Acid labile
    • H2S +
  404. Why are do you need a high dose of salmonella to cause infection
    Acid labile ? easily degraded in the stomach
  405. Which Enterobacteriaceae requires high doses to cause infection
    Salmonella (1,000 organisms to cause infection)
  406. Which Enterobacteriaceae requires very low dose to cause infection
    Shigella (10-100 organisms to cause infection)
  407. Who is more susceptible to salmonella infection
    • Patients with lowered stomach acidity
    • * Omeprazole (treatment for reflux)
    • * Pernicious anemia
  408. How do salmonella infections progress?
    Ingested --> stomach --> small intestine --> colon --> lymphatics --> taken up by macrophages --> blood
  409. What is the reservoir for salmonella typhi?
    • Gallbladders of chronic carriers
    • What does salmonella typhi infection cause
    • Enteric fever ? typhoid fever
    • Osteomyelitis in patients with sickle cell disease
  410. What is the clinical presentation of enteric fever?
    • Rose colored macules on abdomen (25% of patients)
    • Usually constipation
    • Can be diarrhea ? pea soup colored
  411. What is the number one cause of osteomyelitis in patients with sickle cell disease?
    Salmonella typhi
  412. How do we treat salmonella typhi infection?
    • Fluoroquinolones
    • Vaccination
  413. What kind of vaccine do we have for salmonella typhi?
    Live attenuated
  414. What bacteria can cause paratyphoid fever
    • Salmonella enterica?subsp.?Enterica
    • * Salmonella enteritidis
    • * Salmonella Typhimurium
    • * Salmonella infantis
    • * Salmonella Hadar
    • * Salmonella Heidelberg
    • * Salmonella paratyphi
    • * Salmonella Typhi
  415. how do we get salmonella enteritidis infection?
    uncooked chicken
  416. what is the main reservoir of salmonella enteritidis?
  417. what does salmonella enteritidis cause
    inflammatory diarrhea
  418. what is type 3 secretion system
    protein that detects eukaryotic cells and secretes protein that helps with infectivity
  419. which bacteria have type 3 secretion system
    • salmonella enteritidis
    • shigella
    • Yersinia pestis
  420. What virulence factors does salmonella enteritidis have
    • Capsule
    • Motile
    • Facultative intracellular (macrophages)
    • Type 3 secretion system
  421. What gram stain is shigella
    Gram ? rod (Enterobacteriaceae)
  422. What do shigella infections cause
    Gastroenteritis with blood diarrhea
  423. What is the clinical presentation of shigella gastroenteritis?
    Bloody diarrhea
  424. What species are in the shigella genus
    • Shigella sonnei
    • Shigella dysenteriae
  425. How does shigella look when cultured on hektoin agar?
    Green colonies
  426. How do you differentiate shigella from salmonella?
    • Green colonies on hektoin agar (shigella)
    • Black colonies on hektoin agar (salmonella)
    • Immotile (shigella)
    • Motile (salmonella)
    • Acid stabile (shigella)
    • Acid labile (salmonella)
  427. Which Enterobacteriaceae requires very low dose to cause infection
    Shigella (10-100 organisms to cause infection)
  428. Why are only small doses of shigella needed to cause infection
    Acid stabile
  429. How do shigella infections progress
    Ingested --> intestinal lumen --> M cells --> lymphoid tissue + enterocytes
  430. What cells are found in peyers patches
    M cells
  431. What is the function of M cells?
    Sample things in the lumen and bring back antigens to the immune cells on other side of intestinal lumen
  432. How does shigella get out of the intestinal lumen?
    • Induces M cells to phagocytose them
    • Escape from phagolysosome before they get degraded
    • Use M cell?s actin to make a tail that it uses to propel itself from one cell to another
  433. How does shigella move from one cell to another?
    Use host cells actin cytoskeleton to create a tail that it can use to propel itself from one cell to another
  434. What is a similarity between shigella and listeria?
    • Actin rockets (listeria)
    • Use actin tails created from M cell actin to propel itself (shigella)
  435. What are virulence factors of shigella?
    • Facultative intracellular
    • Shiga toxin (salmonella dysinteriae)
    • Type 3 secretion system
  436. Which enterobactericiae are facultative intracellular
    • Shigella
    • Salmonella
  437. What does shigella do once it has invaded lymphoid tissue + enterocytes surrounding M cells
    Damages tissues + releases cytokines --> large immune response
  438. What triggers the large immune response in shigella infection?
    Release of cytokines
  439. What does the large immune response in shigella infections cause?
    • Inflammatory diarrhea
    • Fecal blood and leukocytes
  440. What can shigella dysinteriae cause
    • Gastroenteritis with blood diarrhea
    • Hemolytic Uremic Syndrome (HUS)
  441. What is hemolytic uremic syndrome
    • Hemolytic uremic syndrome
    • Presents as acute renal failure
  442. What causes hemolytic uremic syndrome
    • E.coli (more common)
    • Shigella dysinteriae
  443. What causes Hemolytic uremic syndrome
    Shiga toxin
  444. How does shiga toxin cause hemolytic uremic syndrome
    • Once in the blood stream it can induce endothelial damage including in the endothelium of the kidney --> activates platelets --> aggregation of platelets --> drop in platelet count
    • Platelet clots lyse red blood cells as they pass by
  445. What is a schistocytes
    Helmet shaped red blood cell caused by hemolysis as red blood cells pass through platelet aggregates
  446. Who is affected by hemolytic uremic syndrome
    Patients under 10 years of age (shigella)
  447. How does shiga toxin cause tissue damage
    Binds to 60S subunit of ribosomes --> inhibits translation
  448. What does shigella use type 3 secretion system for
    Secrete inflammatory cytokines
  449. What species are in the yersiniae genus
    • Yersinia enterocolitica
    • Yersinia pestis
  450. Who discovered Yersinia pestis
    Alexander yersin ? Swiss French
  451. What is the cause of the black plague?
    Yersinia pestis
  452. What gram stain are yersiniae
    • Gram ? rod (enterobactericiae)
    • Bipolar staining
  453. How is Yersinia enterocolitica transmitted
    • Primarily through dog feces
    • Contaminated milk products
  454. Who is commonly affected by Yersinia enterocolitica
  455. Which bacteria contaminate milk
    • Listeria
    • Yersinia enterocolitica
  456. Why are Yersinia enterocolitica and listeria able to infect milk
    Resistant to cold temperatures
  457. What is bipolar staining
    • Stains more heavily on ends and lighter in middle
    • Looks like a safety pin
  458. Which bacteria has bipolar staining
    • Yersinia enterocolitica
    • Pasteurella multocida
  459. What virulence factors does Yersinia have
  460. What does Yersinia enterocolitica infection cause
    • Diarrhea
    • Invasive --> bloody diarrhea + systemic effects
  461. What is the clinical presentation of systemic Yersinia enterocolitica?
    • Fever
    • leukocytosis
    • abscesses
    • intestinal perforation
    • intussusception
    • paralytic ilius
    • many other GI tract effects
    • can mimic appendicitis
  462. what kind of pain can Yersinia enterocolitica cause when in abdomen?
    • mimic appendicitis
    • right lower quadrant pain
  463. what causes the black death / bubonic plague?
    Yersinia pestis
  464. what does Yersinia pestis infection cause
    bubonic plague / black death
  465. when did the black death pandemic occur
    14th century
  466. What is the main reservoir of Yersinia pestis?
    • Rodents (e.g. rats)
    • Prairie dogs
  467. How is Yersinia pestis transmitted
    Fleas bite the rodents and then bite the human
  468. What is the clinical presentation of bubonic plague?
    • Buboes ? swollen tender lymph nodes
    • Abscesses in organs
    • DIC
    • Cutaneous hemorrhage
  469. How does Yersinia pestis infection progress
    Once infection established bacteria rise to higher and higher concentrations --> blood stream
  470. What causes disseminated intracellular coagulation in Yersinia pestis infection
    LPS endotoxin
  471. What is the clinical presentation of disseminated intracellular coagulation due to Yersinia pestis?
    • Necrosis of digits and other appendages
    • (blackening of fingers)
  472. What virulence factors does Yersinia pestis have
    • LPS endotoxin
    • Exotoxins
    • Yersinia associated Outer Proteins (YOPs)
    • Type 3 secretion system
  473. What is the function Yersinia associated outer proteins
    • Macrophage and neutrophil dysfunction by inhibiting phagocytosis and cytokine production
    • Allows Yersinia to replicate rapidly and spread
  474. What is the function of type 3 secretion system in Yersinia pestis?
    Secrete Yersinia associated outer proteins
  475. How do you treat Yersinia pestis infection?
    • Aminoglycosides (streptomycin) + tetracycline
    • Vaccine
  476. What kind of vaccine is Yersinia pestis vaccine?
    Killed vaccine
  477. What species are in the vibrio genus
    • Vibrio cholera
    • Vibrio parahaemolyticus
    • Vibrio vulnificus
  478. Where is cholera endemic
    Developing countries
  479. What is the gram stain of vibrio?
    • Gram ? curved rod (enterobactericiae)
    • Coma shaped
  480. What shape are vibrio
    Coma shaped
  481. What does vibrio cholera infection cause?
    Cholera ? perfuse watery diarrhea (10-20L a day)
  482. What is the clinical presentation of cholera?
    • Perfuse (10-20L/day) watery diarrhea
    • Rice water stool
  483. How is vibrio cholerae transmitted
    Fecal oral root by poor sanitation --> contamination of food and water sources by human feces
  484. What is the pathogenesis of cholera?
    Cholera toxin secreted by vibrio cholerae
  485. What are the virulence factors of vibrio cholerae?
    • Fimbriae
    • Cholera toxin
  486. What is the function of fimbriae in vibrio cholerae infection?
    Attach the ganglioside receptors in intestinal wall
  487. How does cholera toxin work?
    • Binds to and constitutively activates adenylate cyclase of the GS pathway
    • Increases cAMP
    • Secretion of water into intestinal lumen
  488. How do we treat vibrio cholerae infection?
    • Oral rehydration therapy with electrolytes
    • Antibiotics ? reduce duration of symptoms
  489. How do we grow vibrio cholerae?
    Alkaline media
  490. Why is it difficult for vibrio cholerae to survive in the stomach?
    Acid labile
  491. What biochemical properties does vibrio cholerae have?
    • Oxidase +
    • Acid labile
  492. Where can we find vibrio parahemolyticus and vibrio vulnificus
    Contaminate sea food
  493. What gram stain is campylobacter
    • Gram ? curved rod (enterobactericiae)
    • Coma shaped
  494. What does campylobacter jejuni cause
    Enterocolitis and diarrhea
  495. How do we culture campylobacter?
    Thermophilic ? likes warmth (42oC)
  496. What is the main reservoir of campylobacter jejuni?
    Intestinal tract of other animals (e.g. poultry)
  497. How is campylobacter jejuni transmitted
    • Fecal oral transmission
    • During slaughtering process gut is perforated and intestinal contents can leak out and infect the meat
  498. What does campylobacter jejuni infection causes
    • A lot of watery diarrhea
    • Invasive ? bloody diarrhea + bacteremia
    • Reiter?s syndrome ? reactive arthritis
  499. What shape is campylobacter jejuni
    Coma shaped
  500. What biochemical properties does campylobacter jejuni have?
    Oxidase positive
  501. Which bacteria are curved gram ? rods
    • Campylobacter jejuni
    • Helicobacter
    • Vibrio
  502. What is a common feature for all curved gram ? rods
    Oxidase positive
  503. How does campylobacter jejuni disease progress
    Enters gut --> penetrates mucosa --> enters the blood stream
  504. What is Reiter?s syndrome
    • Reactive arthritis
    • Seronegative spondyloarthropathies that can be precipitated by campylobacter jejuni infection
  505. What can cause Reiter?s syndrome
    Campylobacter jejuni infection
  506. What is the most classic causes guillain-barr? syndrome?
    Complications of Campylobacter jejuni infection
  507. How does guillain-barr? syndrome occur
    Body has autoimmune response that causes demyelination of peripheral nerves
  508. What is the clinical presentation of guillain-barr? syndrome?
    Ascending paralysis
  509. What is the clinical presentation of botulism?
    Descending paralysis
  510. What is the difference between guillain-barr? syndrome and botulism?
    • Ascending paralysis (guillain-barr? syndrome)
    • Descending paralysis (botulism)
  511. What does the name helicobacter pylori tell us?
    • Helicon ? helical shape
    • Pylori ? infects pylorus in the antrum of our stomach
  512. What gram stain is helicobacter pylori
    Gram ? curved rod (enterobactericiae)
  513. What shape does helicobacter pylori have
    Helical shape
  514. Who is affected by helicobacter pylori
    • 80% adults in developing countries
    • 50% adults in USA
  515. What virulence factors does helicobacter pylori have
    Flagella ? motile
  516. What does helicobacter pylori use its flagella for
    Spins and whips flagella around to propel it around the stomach
  517. What kind of motility does helicobacter pylori have?
  518. What biochemical properties does helicobacter pylori have?
    • Urease +
    • Oxidase +
  519. What is the function of urease?
    • Splits urea into ammonia and CO2
    • helps reduce the acidity of the environment
  520. why does helicobacter pylori need to invade the stomach and why
    urease ? to negate the acidity of the stomach
  521. how do we screen for helicobacter pylori infection?
    • urea breath test
    • biopsy during endoscopy
  522. how do we perform the urea breath test?
    • patient swallow urea labelled with radioactive carbon
    • this is split into CO2 and ammonia
    • CO2 labelled with radioactive carbon is exhaled
    • Detect radioisotopes on exhalation
  523. What do we detect in urea breath test?
    CO2 labelled with radioisotopes
  524. How do we detect helicobacter pylori using biopsy?
    Directly check for urease with rapid test
  525. What does helicobacter pylori infection cause
  526. What is the most common cause of duodenal ulcers?
    Helicobacter pylori
  527. How does helicobacter pylori cause ulcers
    Chronic infections --> reducing somatostatin / increasing gastrin production --> increased acid production
  528. What is the risk associated with untreated duodenal ulcers?
    • Adenocarcinoma of the stomach
    • Lymphoma of the mucous associated lymphoid tissue (MALToma)
  529. What bacteria is linked to almost half of gastric carcinomas
    Helicobacter pylori
  530. What is a possible treatment for MALToma?
    Treatment of helicobacter pylori
  531. How do we treat helicobacter pylori infection?
    • At least triple therapy
    • Proton pump inhibiter (PPI)
    • Amoxicillin
    • Macrolide ? clarithromycin
  532. Why do we use a proton pump inhibiter in treatment of helicobacter pylori infections?
    Counter increased acid production caused by chronic helicobacter pylori infections
  533. What gram stain are pseudomonas
    Gram ? rod (enterobactericiae)
  534. Where do we find pseudomonas?
    Aquatic environments
  535. Why do pseudomonas cause hot tub folliculitis
    Thrive in aquatic environments
  536. What biochemical properties do pseudomonas have?
    • Oxidase +
    • Catalase +
  537. What organisms are chronic granulomatous disease patients at high risk for
    Catalase + organisms
  538. Which patients are most susceptible to catalase positive organisms
    Patients with Chronic Granulomatous Disease
  539. Which bacteria are patients with CGD most susceptible to
    • Chronic Granulomatous Disease ? catalase + organisms
    • * SPACE, nous voyons notre chat, gros petit tresor, houra!
    • * Staphylococci
    • * Pseudomonas aeruginosa
    • * Aspergillus fumigatus
    • * Candida
    • * Enterobacteriaceae
    • * Neisseria
    • * Vibrio
    • * Nocardiae
    • * Campylobacter
    • * Helicobacter
    • * Gardnerella vaginalis
    • * Pseudomonas cepacia
    • * Mycobacterium Tuberculosis
  540. What does pseudomonas look like when plated
    • Blue green pigment
    • Fruity grape like odor
  541. What produces the blue green pigment in pseudomonas?
    • Pyocyanin
    • Pyoverdin
  542. Which bacteria can cause wounds to turn blue
    • Pseudomonas
    • Blue green pigments ? pyocyanin + pyoverdin
  543. How do you grow pseudomonas?
    • Obligate aerobe
    • Thrives in aquatic environments
  544. How do you distinguish pseudomonas from the rest of the Enterobacteriaceae family?
    • Obligate aerobe (pseudomonas)
    • Facultative anaerobe (others)
  545. What can pseudomonas infection cause
    • Gram ? nosocomial pneumonia
    • Pulmonary infection in cystic fibrosis patients
    • Osteomyelitis
    • Infection of burn wounds
    • Urinary Tract Infection (UTI)
    • Skin lesions
    • Otitis externa
  546. What is the number one cause of gram ? nosocomial pneumonia
  547. Who is most affected by pulmonary infections of pseudomonas
    • Nosocomial pneumonia ? patients in hospital
    • Pulmonary infections ? cystic fibrosis patients
  548. What is the most common cause of respiratory failure in cystic fibrosis patients?
  549. What is the pathogenesis of cystic fibrosis?
    • Mutation in CFTR gene
    • Nonfunctional transporter that regulates chloride ions
    • Unable to actively pump chloride ions
  550. Who is most affected by pseudomonal osteomyelitis
    • IV drug users ? directly introduce microbe into blood stream when using needles
    • Diabetics ? traumatic injury of foot due to diabetic neuropathy
  551. What are the virulence factors of pseudomonas?
    • Encapsulated
    • Exotoxin A
  552. What is a serious complication of burn injuries?
  553. Why is pseudomonas a feared complication of burn injuries
    • Often fatal
    • Unresponsive to antibiotics
  554. What is often colonized by nosocomial bacteria
    Indwelling catheters
  555. What is common clinical presentation of nosocomial pseudomonas infection
    Urinary Tract Infection (UTI)
  556. What skin lesions can pseudomonas cause
    • Pruritic papular pustular folliculitis = hot tub folliculitis
    • Ecthyma gangrenosum = toxin mediated cutaneous necrosis
  557. Who is at risk of developing pseudomonal folliculitis
    People using underchlorinated hot tubs
  558. How does pseudomonas cause ecthyma gangrenosum
    Exotoxin A
  559. What does pseudomonal ecthyma gangrenosum look like
    Black necrotic lesions of the skin
  560. What is swimmers ear
    Pseudomonal otitis externa ? infection of the outer ear
  561. What do pseudomonas and Corynebacterium have in common
    • Exotoxin A (pseudomonas)
    • Diphtheria exotoxin (Corynebacterium diphtheriae)
  562. How does pseudomonas exotoxin A work
    • Ribosylates elongation factor 2
    • Causes inhibition of protein synthesis and cell death
  563. How do you treat pseudomonas infection?
    • Antipseudomonal penicillin ? piperacillin + tazobactam
    • Aminoglycosides (in combination with beta lactams)
    • Fluoroquinolones ? UTI
  564. What gram stain is Mycobacterium tuberculosis
    Does not stain with gram stain
  565. How do we visualize Mycobacterium tuberculosis?
    Acid fast stain
  566. What is acid fast stain
  567. Which bacteria are acid fast
    • Nocordiae ? partially
    • Mycobacterium
  568. What does carbolfuschin stain in acid fast bacteria
    High concentration of mycolic acids in cell wall
  569. What are mycolic acids
    Waxy fatty acids with 2 side chains
  570. How do we grow Mycobacterium tuberculosis?
    • Cultures very slowly (2-6 weeks)
    • Lowenstein Jensen media
    • obligate aerobe
  571. what is Lowenstein Jensen media?
    • starch + egg
    • things that inhibit growth of other bacteria that may be present in patient?s sputum
  572. how is Mycobacterium tuberculosis transmitted?
    respiratory droplets
  573. where can Mycobacterium tuberculosis grow
    facultative intracellular ? in macrophages
  574. what is the pathogenesis of Mycobacterium tuberculosis infection?
    • infects someone via respiratory droplets
    • fails to be cleared immediately by immune system
    • primarily resides and proliferates in macrophages
  575. what are Mycobacterium tuberculosis virulence factors?
    • mycolic acids in cell wall
    • chord factor = glycolipids in cell wall
    • sulfatides
  576. what is the function of the chord factor in Mycobacterium tuberculosis?
    protects bacteria from being destroyed by causing granuloma formation
  577. what is essential for virulence of Mycobacterium tuberculosis
    Chord factor (glycolipids) to allow formation of serpentine like clumps of bacteria
  578. What is chord factor of Mycobacterium tuberculosis
    Glycolipids found in the cell wall that are involved in clumping of the bacteria into serpentine like formation
  579. How does chord factor of Mycobacterium tuberculosis work?
    • Increases Tissue Necrosis Factor alpha and other inflammatory cytokines
    • This activates other macrophages
    • Newly activated macrophages form granuloma
    • Bacteria is walled off
  580. What is the function of sulfatides in Mycobacterium tuberculosis?
    Allows survival of the bacteria inside macrophages
  581. How do sulfatides of Mycobacterium tuberculosis work
    • Prevent phagolysosome fusion
    • Sparing bacteria from exposure to lysosomal hydrolases
    • Accumulate in phagosomes and create incompetent secondary lysosomes which are unable to fuse
  582. How does Mycobacterium tuberculosis infection progress?
    • Primary infection
    • 3 different outcomes
    • * Healed latent infection
    • * Systemic infection = military TB
    • * Reactivation of latent TB later in life
  583. What does primary Mycobacterium tuberculosis infection cause?
    • Affects lower / middle lobe of lung
    • Nearby hilar lymph nodes also affected
    • After primary lesion heals --> fibrotic --> calcified
  584. What is the Ghon complex
    Visible calcifications of lung parenchyma + hilar lymph nodes affected by Mycobacterium tuberculosis
  585. How can we visualize primary Mycobacterium tuberculosis infection?
    Chest x-ray to see Ghon complex
  586. What kind of granulomas does Mycobacterium tuberculosis cause?
    Caseating granuloma = tubercle
  587. Why are granulomas formed
    Attempt to wall off infection
  588. What do granulomas look like?
    Collection of activated macrophages = Langerhans giant cells
  589. What are Langerhans giant cells
    Activated macrophages found in granulomas
  590. What do tubercles of Mycobacterium tuberculosis infection look like
    • Langerhans giant cells surrounding a central area of caseating necrosis (caseating granuloma)
    • Often developing fibrosis and scarring surrounding granuloma
  591. What is the clinical presentation of Mycobacterium tuberculosis primary infection?
    Prolonged fever
  592. Who is most affected by Mycobacterium tuberculosis primary infection
    Children in area endemic to tuberculosis
  593. What is the most common path of Mycobacterium tuberculosis infection after primary infection?
    Resolves heals by fibrosis and calcification and becomes latent
  594. Who has a positive Mantoux test
    • Someone after primary infection of Mycobacterium tuberculosis
    • Someone with an active infection
    • Someone with a latent infection
    • Someone who has been vaccinated against Mycobacterium tuberculosis
  595. What is PPD
    Purified Protein Derivative (PPD)
  596. What is the mantoux test
    Tuberculin skin test using Purified Protein Derivative (PPD)
  597. What does a positive mantoux test look like?
    Wheel on skin where TB particles are injected
  598. why is there a lump in positive mantoux test?
    type 4 (delayed type) hypersentivity reaction to TB particles
  599. what is the BCG vaccine?
    developed from attenuated Mycobacterium bovis
  600. how effective is BCG vaccine in protecting against Mycobacterium tuberculosis?
    variable ranging from 0-80% effective
  601. what happens in military TB?
    • bacteremia --> Mycobacterium tuberculosis can seed in almost any organ of the body
    • Acute very dangerous process that can quickly progress to death
  602. What organs are most affected in military TB?
    • Bone
    • Liver
    • Lymphatics
  603. What is military TB
    Systemic spread of Mycobacterium tuberculosis
  604. What is the clinical presentation of military TB?
    • Depends on the organ affected
    • Fulminant multi-organ failure
    • Potentially lethal
  605. Who is most affected by military TB
    Immigrant from Mycobacterium tuberculosis endemic area
  606. Who is affected by reactivation of latent TB
    • Only in 5 ? 10% people
    • Associated with state of immunosuppression ? HIV / old age / cancer
  607. How does latent TB become reactivated?
    Downregulation of Tissue Necrosis Factor alpha release
  608. What is Tissue Necrosis Factor alpha?
    Pro inflammatory cytokine that causes Mycobacterium tuberculosis infection to be contained
  609. What happens in Mycobacterium tuberculosis infection if TNF alpha is inhibited?
    Immune system is defenseless --> uncontained infection
  610. What must you do before giving a TNF inhibitor
    Screen using mantoux test (PPD) to check for Mycobacterium tuberculosis latent infection
  611. What does reactivated Mycobacterium tuberculosis infection affect most commonly
    • Upper lobes of lung
    • Skeletal system
    • CNS
  612. What is the clinical presentation of reactivation of TB?
    • Cough
    • Night sweats
    • Hemoptysis = coughing up of blood
    • Cachexia = wasting and weight loss
  613. Where does reactivation of TB originate from
    Within macrophages
  614. Why do patients experience cachexia in reactivation of TB?
    TNF alpha produced in reaction to chord factor promotes wasting
  615. What is Pott?s disease
    • Reactivated Mycobacterium tuberculosis infects the spinal column
    • Usually multiple vertebrae are affected
  616. What is the clinical presentation of Pott?s disease?
    • Demineralization of bone with soft tissue swelling
    • Pain
    • Abscess formation
    • Spinal deformities
    • Weakness due to loss of support
  617. How does CNS involvement of reactivated Mycobacterium tuberculosis manifest?
    • Meningitis
    • Tuberculoma
  618. What is a tuberculoma
    Cavitary lesion in the brain
  619. How do we treat Mycobacterium tuberculosis?
  620. Why does Mycobacterium tuberculosis form resistance to drugs easily?
    • Treatment period is very long
    • RIPE combination therapy
    • * R ? Rifampin
    • * I ? Isoniazid
    • * P ? Pyrazinamide
    • * E ? Ethambutol
    • Vaccination
  621. Why do we use combination therapy to treat Mycobacterium tuberculosis infection?
    Prevent drug resistance during long course of treatment form developing
  622. What is the treatment as prophylaxis of latent TB?
    Rifampin + Isoniazid for 9 months
  623. What gram stain is Mycobacterium tuberculosis
    • Does not stain with gram stain
    • Acid fast
  624. How do we visualize mycobacterium leprae?
    Acid fast stain ? carbolfuchsin
  625. What does carbolfuchsin stain
    Mycolic acid ? made of 2 waxy chains
  626. How do we grow mycobacterium leprae?
    Thrives in cold temperatures
  627. Why does mycobacterium leprae infection affect the extremities
    Prefers cooler temperatures
  628. What is the reservoir for mycobacterium leprae?
  629. What does mycobacterium leprae cause
    • Leprosy = Hansen?s disease
    • Tuberculoid leprosy
    • Lepromatous leprosy
  630. What is Hansen?s disease
    Leprosy caused by mycobacterium leprae
  631. What is the clinical presentation of tuberculoid leprosy caused by mycobacterium leprae?
    • Relatively mild symptoms
    • Well demarcated hairless hypo esthetic skin plaque anywhere on the body
  632. What is the helper T cell immune response to tuberculoid leprosy caused by mycobacterium leprae?
    • TH1 cells ? promotes cell mediated immunity
    • Macrophages engulf the bacteria
  633. What is the TH1 immune response
    • Promotes cell mediated immunity
    • Contains bacteria within macrophages
  634. How do we diagnose tuberculoid leprosy caused by mycobacterium leprae?
    Lepromin skin test
  635. What is a lepromin skin test?
    Intradermal injection of mycobacterium leprae antigens to test for presence of immune reaction
  636. What is the helper T cell immune response to lepromatous leprosy caused by mycobacterium leprae?
    TH2 cells ? promotes humoral response
  637. What is the TH2 immune response
    Promotes humoral response
  638. When does lepromatous leprosy caused by mycobacterium leprae occur
    • When body is unable to mount an appropriate cell mediated response
    • Unable to contain the mycobacterium leprae in the macrophages
  639. How is lepromatous leprosy caused by mycobacterium leprae transmitted?
    • Unknown mode of transmission between humans
    • Maybe via respiratory droplets
  640. What is the clinical presentation of lepromatous leprosy caused by mycobacterium leprae?
    • Symmetric neuropathy with glove and stocking pattern
    • Numerous poorly demarcated raised lesion often on the extensor surfaces
    • Profound fascial deformity ? Leonine facies
  641. What is leonine facies
    • Profound fascial deformities caused by lepromatous leprosy
    • thickening of skin, loss of eyebrows and eyelashes, collapse of nose and formation of nodular ear lobes
  642. What would you see on biopsy of lepromatous leprosy skin lesions?
    Large amounts of mycobacterium leprae bacteria
  643. What would you see on biopsy of tuberculoid skin lesions?
    Small amounts of mycobacterium leprae bacteria
  644. What is the difference between lepromatous and tuberculoid leprosy caused by mycobacterium leprae?
    • 2 opposite ends of a spectrum
    • Tuberculoid ? cell mediated immune response
    • Lepromatous ? humoral immune response
    • Tuberculoid skin lesions ? well demarcated and contain few bacteria
    • Lepromatous skin lesions ? poorly demarcated and contain many bacteria
  645. How do we treat mycobacterium leprae infection?
    Long term multidrug therapy
  646. How do we treat tuberculoid leprosy caused by mycobacterium leprae?
    Dapsone + Rifampin for 6 months
  647. Who do we treat lepromatous leprosy caused by mycobacterium leprae?
    • Dapsone + Rifampin + Clofazimine for 2-5 years
    • Deformities and neuropathies may not be reversible
  648. What gram stain are actinomycetes
    Gram + branching rod (filamentous)
  649. What species are in actinomyces genus
    Actinomyces Israeli
  650. What conditions do we grow actinomyces Israeli in?
    Obligate Anaerobic
  651. Where is actinomyces found
    Normal flora of the oral cavity
  652. In what situation do actinomyces infections occur
    After jaw trauma (dental procedures)
  653. Where does actinomyces infection spread
    From oral cavity --> head and neck
  654. What infections are caused by actinomyces
    Cervical facial actinomyces infection
  655. What does cervical fascial actinomyces infection look like
    • Begins with non-tender lump in jaw --> abscess --> sinus tracks that drain infection site through the skin
    • Thick yellow pus
  656. Why is pus from actinomyces infection yellow
    Characteristic yellow sulfur granules
  657. How do you treat actinomyces infection?
    • Penicillin G
    • Surgical drainage of complicated infections
  658. What gram stain is Nocardiae
    • Gram + filamentous branching rods
    • Weak acid fast
  659. What species are in the Nocardiae genus
    Nocardiae asteroids
  660. What conditions do we grow Nocardiae in?
    Obligate aerobe
  661. How do we tell the difference between actinomyces and nocardiae?
    • Obligate anaerobe (actinomyces)
    • Obligate aerobe (Nocardiae)
    • Weak acid fast (Nocardiae)
  662. what are the gram + filamentous branching rods?
    • actinomyces
    • nocardiae
  663. where can nocardiae be found
    in the soil
  664. what bacteria can be found in the soil
    • clostridium tetani (spore)
    • clostridium perfringens (spore)
    • nocardiae (gram + rod)
  665. what is the acid fast technique of staining?
    carbolfuchsin stain taken up when bacteria have mycolic acids in their cell walls
  666. what are mycolic acids
    long chained fatty acids with 2 tails
  667. why are nocardiae weakly acid fast
    contain mycolic acid in their cell walls
  668. What biochemical markers do nocardiae have?
    • Catalase +
    • Urease +
  669. Which patients are most susceptible to catalase positive organisms
    Patients with Chronic Granulomatous Disease
  670. Which bacteria are patients with CGD most susceptible to
    • Chronic Granulomatous Disease ? catalase + organisms
    • * SPACE, nous voyons notre chat, gros petit tresor, houra!
    • * Staphylococci
    • * Pseudomonas aeruginosa
    • * Aspergillus fumigatus
    • * Candida
    • * Enterobacteriaceae
    • * Neisseria
    • * Vibrio
    • * Nocardiae
    • * Campylobacter
    • * Helicobacter
    • * Gardnerella vaginalis
    • * Pseudomonas cepacia
    • * Mycobacterium Tuberculosis
  671. what infections does nocardiae cause
    • pulmonary ? pneumonia with lung abscess formation
    • CNS ? brain abscesses
    • Cutaneous
  672. Who is most affected by nocardiae infections
    • Immunocompromised Men with impaired cell mediated immunity
    • * HIV
    • * Transplant
    • * Glucocorticoids
    • More common in men than women
  673. How does pulmonary nocardiosis manifest
    Pneumonia with lung abscess formation (cavitary lesions)
  674. Where does nocardiae spread after infecting lungs
    • CNS
    • Can go anywhere in body
  675. Why does nocardiae cause CNS infections
    Nocardiae has affinity for neural tissue
  676. How does CNS nocardiosis manifest
    Brain abscesses
  677. How is cutaneous nocardiosis transmitted
    Open wounds exposed to dirt
  678. How does cutaneous nocardiosis manifest
    Pyogenic (inflammatory) response with production of indurated lesions
  679. How do you treat nocardiosis?
  680. What does clostridium tetani cause
  681. What gram stain is clostridium
    Gram + rod
  682. What conditions do clostridia need to grow?
    Obligate anaerobes ? cannot survive in presence of oxygen
  683. Which bacteria are spore forming
    • Clostridia genus
    • Bacillus genus
  684. Where is clostridium tetani spores often found
  685. How can clostridium tetani cause infection
    • Must get under the skin into an anaerobic environment
    • e.g. under a puncture wound closed off to air
  686. what kind of wounds are classically associated with clostridium tetani infection?
    • puncture wound closed off to air
    • e.g. by rusty nails or barbed wire
  687. what are the symptoms of tetanus?
    • spastic paralysis
    • risus sardonicus
    • lockjaw
    • opisthotonus
  688. what does spastic paralysis look like?
    patients experience relentless muscle contractions leading to rigidity
  689. what are the symptoms of botulism?
    flaccid paralysis
  690. what does risus sardonicus mean
    evil smile
  691. what is lockjaw
    tense masseters prevent the jaw from opening
  692. what is opisthotonus
    characteristic extension and arching of the back due to powerful spasms of the back muscles
  693. what is the pathogenesis of clostridium tetani?
    puncture wound with foreign object with tetani spores on it --> spores are embedded in flesh --> organism vegetates and stays at wound site --> organism releases tetanus toxin --> symptoms occur
  694. what toxins does clostridium tetani produce?
  695. what causes the symptoms of tetanus
    tetanospasmin released by the clostridium tetani
  696. how does tetanospasmin travel in the body
    • retrograde through motor axons --> spinal cord
    • i.e. from the periphery --> spinal cord
  697. how does tetanospasmin work
    • acts as a protease
    • cleaves SNARE proteins --> inhibits exocytosis of neurotransmitter into synapse --> neurotransmitters remain in vesicles
  698. what kinds of neurons release gabba and glycine?
    • inhibitory
    • e.g. Renshaw cells
  699. which types of neurotransmitters does tetanospasmin affect
    inhibits released of gabba and glycine (inhibitory neurotransmitters) --> decreased inhibition
  700. what do Renshaw cells do?
    sense over activity of nearby motor neurons (tetanus) --> fire --> inhibit overactive neuron
  701. what neurons are inhibited by tetanospasmin
    Renshaw cells
  702. What kind of vaccine is tetanus vaccine?
    Toxoid vaccine
  703. What is a toxoid vaccine?
    Toxin conjugated to a protein to increase immunogenicity
  704. What is the antibody response created by the tetanus vaccine?
    • Antibody response to the toxin
    • NOT to the organism
  705. What does clostridium botulinum cause?
  706. What gram stain is clostridium botulinum
    Gram + rod
  707. Where is clostridium botulinum commonly found?
    • Improper canning of foods ? flourish of bacteria
    • Honey ? spores
  708. Why is clostridium botulinum able to grow in canned foods?
    Improper or insufficient heating cycles when canning food --> survival of spores --> spores germinate + flourish in anaerobic environment --> toxin is produced (heat stable)
  709. What toxin does clostridium botulinum produce?
    Relatively heat stable botulinotoxin
  710. why is it important to cook canned food thoroughly?
    denatures the relatively heat stable botulinotoxin produced in canned foods
  711. what are the symptoms of botulism?
    • descending flaccid paralysis ? absence of muscle contraction
    • diplopia / ptosis of eyes in eyes
    • floppy baby syndrome in babies
  712. what is flaccid paralysis
    absence of muscle contraction
  713. How do you tell the difference between flaccid paralysis in botulism and Guillain-Barre syndrome?
    • Botulism
    • Descending paralysis (i.e. starts superiorly --> inferiorly)
    • Affects multiple family members who have all eaten the same canned food
    • Guillain-Barre syndrome
    • ascending paralysis (i.e. starts inferiorly --> superiorly)
    • very unusual for multiple people to present with the same symptoms
  714. transmission of botulism in adults
    bacteria grow and reproduces in anaerobic conditions of canned foods --> toxin is formed in food --> preformed toxin absorbed into the gut --> blood --> peripheral nervous system
  715. which nervous system does botulinotoxin affect and why
    • peripheral nervous system
    • toxin is unable to cross the blood brain barrier
  716. how does botulinotoxin work
    protease that cleaves the SNARE protein --> prevents fusion of vesicles with presynaptic nerve terminal
  717. what is the difference between tetanospasmin and botulinotoxin?
    • tetanospasmin ? inhibitory Renshaw cells
    • botulinotoxin ? motor neurons
  718. which types of neurotransmitters does botulinotoxin affect
    inhibits released of acetylcholine (excitatory neurotransmitters) --> decreased excitation
  719. what kind of neurons release acetylcholine?
    excitatory neurons
  720. what kind of neurons are inhibited by botulinotoxin?
    motor neurons
  721. transmission of botulism in babies
    honey contains many spores of clostridium botulinum which can flourish in the babies? gut
  722. what is floppy baby syndrome
    flaccid paralysis caused by botulinotoxin in newborn
  723. what is the differences between adult and baby botulism?
    • adult ? toxin is pre-formed in canned food anaerobic environment
    • baby ? toxin is formed by bacteria in the gut releasing toxin in the gut
  724. why is ingestion of clostridium botulinum spores not a risk for adults
    normal gut flora outcompete it so there is no germination of spores
  725. why is ingestion of clostridium botulinum spores dangerous to babies?
    • GIT of babies is a perfect anaerobic environment
    • No gut flora to compete with it
    • Spores germinate + produce toxin in the gut
  726. What is the most common form of botulism and why?
    • Floppy baby syndrome
    • Honey contains many spores (canned foods are less commonly infected for adults)
  727. What gram staining is Clostridium difficile
    Gram + rods
  728. What does Clostridium difficile cause
    Nosocomial diarrhea (pseudomembranous colitis)
  729. What does nosocomial mean
    People are affected while hospitalized
  730. Why is clostridium difficile a nosocomial infection
    Spores are easily transferred from patient to patient
  731. How can you prevent passing clostridium difficile spores from patient to patient?
    • Quick wipe-down with alcohol will not work
    • MUST thoroughly wash with soap and water
  732. Why Is clostridium difficile unable to infect normal individuals
    Clostridium difficile is not good at competing with normal gut flora
  733. Why is clostridium difficile able to infect hospitalized patients
    • Hospitalized patients often take antibiotics which can wipe-out the normal gut flora
    • This means spores are able to germinate and grow in the cleared gut
  734. Which antibiotics are most associated with clostridium difficile infections
  735. What causes the symptoms of clostridium difficile infection
  736. How is clostridium difficile commonly transmitted
    Improper handwashing by healthcare providers
  737. What toxins does clostridium difficile produce?
    • Exotoxin A
    • Exotoxin B
  738. What does exotoxin A do
    Binds to the brush border of intestine
  739. What does exotoxin A cause
    • Inflammation
    • Cell death
    • Watery diarrhea
  740. What does exotoxin B do?
    Disrupts cytoskeleton integrity by depolymerizing actin
  741. What does exotoxin B cause?
    • Enterocyte death
    • Necrosis
    • Yellowish grey exudate --> pseudo membrane covering colonic mucosa
  742. Why do we call Clostridium difficile infection pseudomembranous colitis?
    Pseudo membrane covering the colonic mucosa is formed by exotoxin B action
  743. How do you diagnose clostridium difficile infection?
    • Visualize pseudo membrane directly either histologically or endoscopically
    • Look for toxins in the stool using various assays (usually PCR)
    • Do NOT look for organism
  744. Why is detecting clostridium difficile in the stool not a good method of diagnosis for infection
    Almost 1/3 patients are colonized by the bacteria without any toxins being released to cause infection
  745. Why do we diagnose clostridium difficile using toxins?
    Only toxin producing strains cause infections
  746. How do we treat clostridium difficile infection?
    • Oral vancomycin
    • Metronidazole
  747. Why do we treat clostridium difficile with oral vancomycin (and not IV)?
    • Clostridium difficile bacteria are in the gut so it is better to deliver the drug to the site directly
    • Vancomycin has poor absorption so there will be fewer side effects
  748. What gram staining is clostridium perfringens
    Gram + rod
  749. In what situations do we see clostridium perfringens infections
    • Motorcycle accidents
    • deep penetrating wounds from military combat
    • i.e. when a large amount of flesh is exposed to dirt or dust
  750. where are clostridium perfringens spores commonly found
    dirt and soil
  751. what conditions does clostridium perfringens need to grow?
    obligate anaerobe
  752. what does clostridium perfringens cause?
    • gas gangrene ? soft tissue infection (clostridial myonecrosis)
    • food poisoning
  753. what is the other name for clostridial myonecrosis and why?
    Gas gangrene ? in the disease process gas is produced under the infected tissue
  754. in what situation does clostridial myonecrosis occur
    when clostridium perfringens enters a wound and causes infection
  755. what are the clinical presentations of gas gangrene?
    crepitus / crackling sound on palpation
  756. why is gas produced in clostridial myonecrosis?
    clostridium perfringens consumes carbohydrates and releases gas
  757. what toxins does clostridium perfringens produce?
    alpha toxin
  758. what does alpha toxin cause?
  759. how does the alpha toxin of clostridium perfringens work?
    • it is a lecithinase
    • cleaves lecithin phospholipase --> damage lipoproteins --> damage of cell membranes --> hemolysis of RBC
  760. what are the hemolytic properties of clostridium perfringens?
    forms a double zone of hemolysis on blood agar
  761. why is clostridium perfringens hemolytic?
    alpha toxin
  762. how do you differentiate clostridium perfringens from other hemolytic bacteria?
    MUST be cultured anaerobically so would not grow anaerobically
  763. How do you treat clostridium perfringens gas gangrene?
    IV penicillin G
  764. What are the symptoms of food poisoning caused by clostridium perfringens?
    Late onset diarrhea
  765. Why is clostridium perfringens diarrhea late onset?
    Caused by ingestion of many spores which must germinate in the gut THEN produce toxin whilst in the gut
  766. how does clostridium perfringens cause food poisoning?
    ingestion of spores --> germination in gut --> bacteria flourish --> toxin is produced
  767. how do you treat clostridium perfringens diarrhea?
    usually transient so does not require antibiotic treatment
  768. What Gram stain and shape are Bacilli
    Gram + Rods
  769. What species are in the Bacillus genus
    • Bacillus anthracis
    • Bacillus Cereus
  770. What does a black eschar look like?
    Black necrotic cutaneous lesion with surrounding erythematous ring
  771. What does Bacillus anthracis usually look like under microscope?
    Large gram + rods in chains
  772. What is the capsule of bacilli made of?
    Protein ? poly D glutamate
  773. What conditions do bacillus anthracis need to survive?
    Obligate aerobe ? only survive in the presence of oxygen
  774. Why is bacillus anthracis able to be weaponized?
    Forms spores
  775. What does a spore allow the bacteria to do?
    • hibernate in a state without any significant metabolic activity
    • sturdy protective covering means it is highly resistant to temperature and chemicals
    • able to survive an extremely long time in almost any external environment
    • small and durable
    • grow back into metabolically active state when the environmental conditions are favorable
  776. which bacteria produce spores
    • bacillus genus
    • clostridium genus
  777. what do spores do when they are in environmentally favorable conditions
    revert back to a metabolically active state
  778. what toxins does bacillus anthracis produce?
    • lethal factor
    • edema factor
  779. which toxin must be present to cause symptoms in bacillus anthracis infection
    both lethal factor and edema factor
  780. how does edema factor of bacillus anthracis work?
    acts as an adenylate cyclase --> increases cAMP intracellularly --> fluid goes into intracellular space --> edema
  781. how does edema benefit the bacillus anthracis bacteria?
    • inhibits host defenses
    • indirectly prevents phagocytosis
  782. how does lethal factor of bacillus anthracis work?
    exotoxin that acts as a protease --> cleaves MAP kinase (signal transduction protein)
  783. what is MAP kinase
    • signal transduction protein
    • involved in control of cell growth
    • ultimately is responsible for tissue necrosis
  784. what does lethal factor of bacillus anthracis cause?
    tissue necrosis --> black escar
  785. what diseases does bacillus anthracis cause?
    • black escars
    • pulmonary anthrax = wool sorter?s disease
  786. where are the spores of bacillus anthracis often found and why?
    • soil --> wool /hide of animals
    • can survive for long periods of time
  787. how do people get pulmonary anthrax?
    inhale anthrax spores (e.g. when handling wool of sheep) --> spores germinate in lungs
  788. what are the symptoms of pulmonary anthrax?
    • starts as nonspecific pulmonary symptoms (dry cough)
    • progresses to hemorrhagic mediastinitis
  789. why is it important to catch and treat anthrax early?
    bacillus anthracis can rapidly move to mediastinal lymph nodes --> hemorrhagic mediastinitis
  790. what are the symptoms of hemorrhagic mediastinitis?
    • pulmonary hemorrhage
    • widened mediastinum on chest X ray
  791. what is the mortality rate once anthrax pulmonary hemorrhage has developed?
    almost 100%
  792. how do we treat bacillus anthracis?
    • drug of choice: fluoroquinolones
    • secondary treatment: doxycycline
  793. what conditions does bacillus cereus need to grow?
  794. what diseases does bacillus cereus cause?
    food poisoning
  795. how do we get bacillus cereus food poisoning?
    eating reheated fried rice
  796. what are the symptoms of bacillus cereus food poisoning?
    vomiting and maybe diarrhea
  797. What gram stain is Leptospira interrogans
    Doesn?t stain with gram stain (spirochete)
  798. How do we visualize Leptospira interrogans?
    You can?t with a light microscope
  799. What does Leptospira interrogans infection cause
  800. Where is Leptospira interrogans infection endemic
    Tropical regions
  801. What is Leptospira interrogans shape
    • Spirochete
    • Question mark shaped
  802. Where can we find Leptospira interrogans
    Rodents / dogs
  803. How is Leptospira interrogans transmitted
    • Excreted in animal?s urine
    • Transmitted to humans when they swim in contaminated water
  804. Who is most affected by Leptospira interrogans infection
    People who take part in water sports
  805. What is the clinical presentation of Leptospira interrogans infection?
    • Flu like symptoms ? fever + intense headaches
    • Conjunctival suffusion ? diffuse reddening of the eyes with no inflammatory exudate
    • Weil?s disease ? renal dysfunction and jaundice
  806. What is the difference between conjunctivitis and conjunctival suffusion?
    No inflammatory exudate in conjunctival suffusion
  807. What is Weil?s disease
    • Caused by Leptospira interrogans
    • Renal dysfunction
    • Jaundice from liver damage
  808. What is the pathogenesis of Leptospira interrogans infection?
    • Travels through bloodstream
    • Multiplies in various organs ? kidneys / liver
  809. Which organs does Leptospira interrogans affect most commonly
    • Kidney
    • Liver
  810. How do we test for renal dysfunction?
    • High creatinine levels
    • Azotemia
  811. What gram stain is Treponema pallidum
    Doesn?t stain with gram stain (spirochete)
  812. How do we visualize Treponema pallidum?
    Can?t be visualized using light microscopy
  813. What does Treponema pallidum cause?
    Syphilis (STD)
  814. How is Treponema pallidum transmitted?
    Sexually transmitted disease
  815. What causes syphilis
    Treponema pallidum
  816. Why is syphilis called ?the great imitatorjQuery110104336385577609254_1485168348375
    Many of the symptoms look like many other diseases
  817. What are the most common sexually transmitted diseases?
    • Chlamydia (Chlamydia trachomatis)
    • Gonorrhea (Neisseria Gonorrheae)
  818. How is Treponema pallidum visualized?
    Dark field microscopy
  819. How do we collect a sample for Treponema pallidum visualization?
    Direct sample from a lesion on a patient
  820. Why is direct visualization of Treponema pallidum not commonly used?
    Dark field microscopy is time consuming and not all labs are equipped to use it
  821. How do we diagnose syphilis caused by Treponema pallidum?
    • Dark field microscopy
    • Blood tests
    • * VDRL ? screening
    • * RPR ? screening
    • * FTA-Ab ? confirmatory
  822. What is the mean screening test for Treponema pallidum?
    • Venereal Disease Research Laboratory (VDRL)
    • Rapid Plasmin Reagent Test (RPR)
  823. What is the VDRL
    • Venereal Disease Research Laboratory
    • Non Treponema test (for syphilis)
    • Tests for antibody reactivity in patient?s serum to a cardiolipin cholesterol lecithin antigen
  824. What does VDRL test for
    Antibody reactivity to cardiolipin cholesterol lecithin
  825. Who do we screen for syphilis?
    • Patients with symptoms
    • Patients at high risk
  826. Why do we get false positives in VDRL and RPR?
    • Cross reactivity with other antigens
    • * Mononucleosis (Epstein Barr Virus)
    • * Rheumatoid factor (autoimmune)
    • * Systemic Lupus Erythematosis (autoimmune)
    • * Leprosy (Mycobacterium leprae)
    • * IV drug users
  827. What is the confirmation test for Treponema pallidum infection?
    • FTA Antibody test (FTA-Ab)
    • Treponemal test
    • Tests for antibodies directly against Treponema pallidum
  828. What does FTA-Ab test for
    Tests for antibodies directly against Treponema pallidum
  829. When do we perform FTA-Ab test?
    Used after non-treponemal tests show reactivity
  830. What are the stages of syphilis caused by Treponema pallidum?
    • Early stage ? first year
    • * Primary
    • * Secondary
    • * Early latent
    • Late stage
    • * Tertiary
    • * Late latent
  831. What is the clinical presentation of primary syphilis caused by Treponema pallidum?
    Painless genital chancre that appears a few weeks after inoculation and heals in 3-6 weeks
  832. How does Treponema pallidum cause genital chancres?
    • Locally invading small blood vessels and damaging them
    • Causes small areas of ischemic necrosis --> chancre
    • Also ischemic nerve damage
  833. When does syphilis progress to the secondary stage
    When chancre is left untreated (because it is painless)
  834. What is the clinical presentation of secondary syphilis caused by Treponema pallidum?
    • Systemic disease
    • Maculopapular rash everywhere including palms of hands and soles of feet that occurs weeks to months after infection
    • Condyloma lata
  835. Which STD causes rash to appear on the hands and soles of feet
    Syphilis ? Treponema pallidum
  836. What causes condyloma lata and what does it look like
    • Treponema pallidum
    • Flat topped bumps on mucous membranes
  837. What causes condyloma acuminata and what does it look like
    • Human Papilloma Virus
    • Wart like
  838. How can you visualize the pathogen in condyloma lata?
    Dark field microscopy to see spirochete Treponema pallidum
  839. What is the clinical presentation of tertiary syphilis caused by Treponema pallidum?
    • Gomas = soft growths with firm necrotic center
    • Aortitis (of ascending thoracic aorta) --> ascending thoracic aneurysm
    • Tabes dorsalis = demyelination of nerves in posterior column
    • argyll robertson pupil = accommodate but do not react to light
  840. What are gomas and what causes them
    • Treponema pallidum in tertiary syphilis
    • Soft growths with firm necrotic center that can occur anywhere
  841. What are the complications of aortitis caused by tertiary syphilis?
    • Aneurysm
    • Aorta demonstrates tree barking (thick + wrinkled)
  842. How does syphilis cause aortic aneurysm?
    • Targets vasa vasorum which supply wall of aorta --> weakening of aortic wall --> aneurysm formation
    • Similar to small vessel damage --> chancre in primary syphilis
  843. What is tabes dorsalis and what causes it
    • Treponema pallidum in tertiary syphilis
    • Demyelination of nerves in the dorsal / posterior columns of the spinal cord
  844. What is the clinical presentation of tabes dorsalis in tertiary syphilis?
    • Loss of vibration sense
    • Propriosense --> off gait
    • Discriminative touch
    • lancinating pain ? piercing / stabbing pain
  845. what is argyll robertson pupil and what causes it
    • Treponema pallidum in tertiary syphilis
    • Accommodate but do not react to light
  846. Why is congenital syphilis not as common nowadays?
    Standard screening of pregnant women
  847. What is the clinical presentation of congenital syphilis?
    • Constellation of symptoms in children
    • Saber shins = anterior bowing of tibia
    • Saddle shaped nose
  848. What are saber shins and what infection can cause them?
    • Congenital syphilis
    • Anterior bowing of the tibia
    • Hutchinson?s teeth ? notched incisors
    • Mulberry molars ? molars with several enamel outgrowths
    • Congenital deafness
  849. How do we treat syphilis caused by Treponema pallidum?
    • Penicillin in every stage and in everyone
    • Should desensitize allergic patients and still use penicillin
  850. Why can?t we use tetracycline in pregnancy?
    Affects teeth and bond growth
  851. What is the Jarisch Herxheimer reaction
    Fever / chills / headache that occurs within hours of starting penicillin treatment against Treponema pallidum in syphilis
  852. What causes the Jarisch Herxheimer reaction
    • Treatment of patient with syphilis using penicillin causes huge spirochete death
    • Dyeing spirochetes release a bunch of Lipopolysaccharide --> increase in cytokines
  853. What is a good indicator that penicillin treatment is working in syphilis?
    Fever / chills / headache of Jarisch Herxheimer reaction
  854. What gram stain is Legionella pneumophila
    • Gram ? thin pleomorphic
    • Does not take up gram stain very well
  855. How do we visuals Legionella pneumophila
    Silver stain
  856. How do we grow Legionella pneumophila?
    • Buffered charcoal yeast extract
    • In the presence of cysteine and iron
  857. What does Legionella pneumophila infection cause
    • Legionnaire?s disease ? very serious + potentially fatal
    • Pontiac fever ? less serious
  858. What is the clinical presentation of Pontiac fever caused by Legionella pneumophila?
    • Fever
    • Malaise
    • Self-limited
  859. Who is most affected by legionnaire?s disease caused by Legionella pneumophila
  860. What bacteria cause atypical pneumonia
    • Legionella pneumophila
    • Mycoplasma pneumoniae
    • Chlamydophila pneumoniae
  861. What does atypical pneumonia caused by Legionella pneumophila look like on chest X-ray
    • Patchy infiltrate with consolidation of one lobe
    • Highly variable and can easily be mistaken for another type of pneumonia
  862. What is the clinical presentation of legionnaire?s diseases caused by Legionella pneumophila?
    • Atypical pneumonia
    • Hyponatremia (<130mmol/L)
    • Neurologic symptoms ? headache with confusion
    • Diarrhea
    • High fever (>40oC)
  863. Which bacteria causes pneumonia with diarrhea and hyponatremia
    Legionella pneumophila
  864. How do we diagnose legionnaire?s disease caused by Legionella pneumophila?
    • Culture respiratory sputum ? 3-5 days
    • Rapid urine antigen test
  865. How do we treat legionnaire?s disease caused by Legionella pneumophila?
    • Macrolides
    • Fluoroquinolones ? have fewer complications than macrolides
  866. How do we treat atypical pneumonia?
  867. How do we treat Pontiac diseases caused by Legionella pneumophila?
    We don?t ? it is self-limited
  868. What biochemical properties does Legionella pneumophila have?
    Oxidase +
  869. What gram stain are Borreliae
    Don?t gram stain (spirochete)
  870. What are spirochetes
    Bacteria that are spiral shaped
  871. Which bacteria are spirochetes
    • Borrelia
    • Leptospira
    • Treponema
  872. What does Borrelia burgdorferi cause
    Lyme disease
  873. Where do we commonly find Borrelia burgdorferi
    Northeastern united states
  874. Who is affected by Borrelia burgdorferi
    • People who were on hiking or camping trips
    • Hunters
  875. How is Borrelia burgdorferi transmitted
    • Tick born disease
    • ixodes scapularis tick
  876. what diseases does the ixodes scapularis tick transmit?
    • Lyme disease (Borrelia burgdorferi)
    • Ehrlichiosis (ehrlichiae genus / Anaplasma genus)
    • Babesiosis (Protozoa Babesia)
  877. Where can we find Ixodes scapularis larvae
    White footed mouse
  878. Where can we find adult Ixodes scapularis
    White tailed deer
  879. What is the main reservoir for Ixodes scapularis?
    White footed mouse
  880. What is an obligatory host for Ixodes scapularis?
    White tailed deer
  881. What is the vector for Borrelia burgdorferi infection?
    Ixodes scapularis tick
  882. What are humans in the life cycle of the Ixodes scapularis tick
    Incidental dead end host
  883. Why don?t spirochetes gram stain
    Have very thin walls
  884. How do we visualize Borrelia burgdorferi?
    • Wright stain
    • Giemsa stain
  885. Which spirochete are we able to visualize under light microscope
    Borrelia burgdorferi
  886. What is the clinical presentation of Borrelia burgdorferi infection?
    • 3 stages
    • 1. Erythema chronica migrans
    • 2. Heart block caused by myocarditis + bilateral fascial nerve palsy
    • 3. Migratory polyarthritis + Encephalopathic effects
  887. What does erythema chronica migrans in Borrelia burgdorferi infection look like
    • Bulls eye rash
    • Not painful
    • Not puritis
    • Flu like symptoms
  888. What is the name for the bull?s eye rash you get in Borrelia burgdorferi infection?
    Erythema chronica migrans
  889. When do we see erythema chronica migrans?
    One month after tick bite infected with Borrelia burgdorferi
  890. What is bell?s palsy
    Idiopathic fascial nerve palsy
  891. What is the second stage of Borrelia burgdorferi infection?
    • Heart block caused by myocarditis
    • Bilateral fascial nerve palsy
  892. What is the clinical presentation of migratory polyarthritis caused by Borrelia burgdorferi infection?
    • Arthritis of large joints (e.g. knee)
    • Many joints can be affected
    • Can move from joint to joint
  893. What are the CNS effects of Borrelia burgdorferi infection?
    • Subtle Encephalopathy
    • Memory difficulty
    • Cognitive slowing
    • Lymphocytic meningitis
  894. How do we treat Borrelia burgdorferi infection?
    • As early as possible
    • Doxycycline ? in stage 1
    • Ceftriaxone ? later presentation
  895. Which species are in the Rickettsiae genus
    • Rickettsia prowazekii
    • Rickettsia rickettsii
  896. Where can Rickettsiae grow
    Obligate intracellular ? unable to produce NAD+ and CoA
  897. What gram stain are Rickettsiae
    • Does not take up gram stain very well
    • Gram ? coccobacillus
  898. How do we visualize Rickettsia?
    Giemsa stain
  899. Why are Rickettsiae obligate intracellular
    • Unable to produce NAD+ and CoA
    • Both are needed for bacterial growth and replication
    • Get them form eukaryotic cells instead
  900. What is the Weil Felix test?
    • Agglutination test to diagnose Rickettsial infections
    • Tests for cross reactivity between Rickettsia species and Proteus Vulgaris
    • Not very sensitive or specific
  901. What are the general prodromal symptoms of a Rickettsial infection?
    • Headache
    • Fever
    • Vasculitis
  902. Which vessels are affected by vasculitis in Rickettsial infection
    Thin blood vessels of capillary beds

    • What is the clinical presentation of vasculitis caused by Rickettsial infections?
    • Granular bumpy rash
  903. How do we treat Rickettsiae infections?
    Tetracycline ? doxycycline
  904. What is the clinical presentation of epidemic typhus caused by Rickettsia prowazekii?
    • Rash that starts at trunk and spreads to extremities
    • Rash spares hands, feet and head
    • Myalgia + arthralgia
    • Pneumonia
    • Encephalitis with dizziness and confusion
    • Coma
  905. Who is most affected by Rickettsia prowazekii
    • Anyone living in close quarters (e.g. military or prisoners)
    • Poor hygiene
  906. How is Rickettsia prowazekii transmitted
    Arthropod vectors ? lice
  907. Why are lice a good vector for spreading of Rickettsia prowazekii
    • Feed on human blood
    • Defecates near feeding site
    • Scratching --> introduction of bacteria into blood stream
  908. What does Rickettsia prowazekii infection cause
    Epidemic typhus
  909. What is the difference between Rickettsia prowazekii and Rickettsia typhi?
    • Epidemic typhus (prowazekii)
    • Endemic typhus (typhi)
  910. What does endemic mean
    disease localized to a region that doesn?t necessarily comment on magnitude of population getting illness
  911. what does epidemic mean
    wide spread rampant outbreak
  912. what does Rickettsia rickettsii cause
    rocky mountain spotted fever
  913. how is Rickettsia rickettsii transmitted
    arthropod vectors ? dermacentor tick
  914. how do dermacentor ticks transmit Rickettsia rickettsii infection
    direct biting
  915. what is the clinical presentation of rocky mountain spotted fever caused by Rickettsia rickettsii?
    • incubation period ranging from 2-14 days
    • rash starts at ankles and wrists --> central
    • rash covers hands and feet in later stages of disease
    • headache
    • fever
    • myalgia ? sever muscle pain
  916. What does Coxiella burnetii infection cause
    Q fever
  917. What gram stain is Coxiella
    Gram ? coccobacillus
  918. What is the clinical presentation of Q fever caused by Coxiella burnetii?
    No rash
  919. Where can we fine Coxiella burnetii
    Obligate intracellular
  920. How is Coxiella burnetii able to survive digestive tracts of animals
    Forms a sturdy spore like structure
  921. Where can we find Coxiella burnetii ?spores?
    In animal droppings in dirt
  922. How is Coxiella burnetii transmitted
    Aerosol transmission
  923. What is a major reservoir for Coxiella burnetii?
    Farm animals
  924. Who is most affected by Coxiella burnetii
    • Farmers
    • Veterinarian that has just delivered a baby animal and was exposed to placental excretions
  925. What is the clinical presentation of Q fever caused by Coxiella burnetii?
    • Pneumonia
    • Headache
    • Fever
    • Hepatitis
  926. How do you tell the difference between Q fever (Coxiella burnetii) and Brucellosis?
    • Brucellosis ? undulating fever
    • Both have pneumonia and hepatitis symptoms
  927. How do you treat Q fever caused by Coxiella burnetii?
    • Usually self-limiting ? goes away within 2 weeks
    • Pasteurizing milk kills most organisms
    • Vaccine
  928. Who can get chronic Q fever caused by Coxiella burnetii
    • Immunocompromised patients
    • Patients with previous valvular damage
  929. What is the clinical presentation of chronic Q fever caused by Coxiella burnetii?
  930. What kind of vaccine is Coxiella burnetii vaccine?
  931. Who gets the Coxiella burnetii vaccine
    • Veterinarians
    • Other high risk people ? farmers
  932. What species are in the Bartonella genus
    Bartonella henselae
  933. What does Bartonella henselae cause
    • Cat scratch fever
    • Bacillary angiomatsosis
  934. What gram stain are Bartonella
    Gram ? rod
  935. How do we visualize Bartonella henselae?
    Warthin starry stain ? type of silver stain
  936. What is the Warthin starry stain?
    Type of silver stain used to stain Bartonella henselae
  937. What is the clinical presentation of cat scratch disease caused by Bartonella henselae?
    • Fever
    • Painful large lymph nodes in axilla ? lymphadenitis
  938. How is Bartonella henselae transmitted
    Cat scratches or bites
  939. Who is affected by cat scratch disease caused by Bartonella henselae
    Immunocompetent healthy people
  940. Who is affected by bacillary angiomatosis caused by Bartonella henselae
    • Immunocompromised people
    • HIV infected patients
  941. What is the clinical presentation of bacillary angiomatosis caused by Bartonella henselae?
    • Fever chills headaches
    • Raised red vascular legions all over skin
  942. What is similar between Kaposi sarcoma and bacillary angiomatosis
    • Immunocompromised patients ? HIV
    • Red vascular lesions on skin
  943. How do you differentiate between Kaposi sarcoma and bacillary angiomatosis caused by Bartonella henselae?
    Skin biopsy stained with Warthin starry silver stain
  944. How do you treat bacillary angiomatosis caused by Bartonella henselae?
    • Doxycycline
    • Macrolides ? azithromycin
  945. How do you treat cat scratch disease caused by Bartonella henselae?
    • Usually self-limited so don?t treat
    • Azithromycin ? if swelling and pain from lymph nodes too severe
  946. What species are in the chlamydia genus
    • Chlamydia trachomatis
    • Chlamydophila pneumoniae
    • Chlamydophila psittaci
  947. How is chlamydia transmitted
    Sexually transmitted disease
  948. Where can chlamydia grow
    Obligate intracellular bacteria
  949. What gram stain are chlamydia
    No staining with gram stain
  950. What do chlamydiae and rickettsia have in common
    • Both obligate intracellular organisms ? can?t create their own ATP
    • Both stain poorly with gram stain
  951. Why are chlamydia obligate intracellular organisms?
    Cant create own ATP
  952. What is special about chlamydia cell wall
    Does not have muramic acid
  953. What is muramic acid
    Part of peptidoglycans that make up the cell wall
  954. What is the life cycle of chlamydia?
    • Elementary bodies
    • Reticular bodies
  955. What is the elementary body of chlamydia?
    • 1st stage of life cycle
    • Found outside of cell
  956. What is the reticular body of chlamydia?
    • 2nd stage of life cycle
    • Found inside the cell
  957. Where and how do chlamydia multiply
    • Inside cells
    • By binary fission
  958. Which form of chlamydia is the active form
    • Reticular body
    • Able to multiply
  959. How are newly formed chlamydia released from cells
    In their elementary form
  960. Which form of chlamydia is the infectious form
    Elementary body
  961. How do we visualize chlamydia?
    • Giemsa stain
    • See inclusion bodies in cells infected with chlamydia under the microscope
  962. What are chlamydia inclusion bodies?
    • Bunches of reticular cells dividing inside the cell
    • What do we use Giemsa stain to visualize?
    • Chlamydia
    • Borrelia
  963. How do we diagnose chlamydia infection?
    Nucleic Acid Amplification test (NAAT)
  964. What is NAAT
    • Nucleic Acid Amplification Test
    • Basically PCR
  965. What serovars are there in chlamydia trachomatis species
    • A-C
    • D-K ? STD
    • L1-L3
  966. what is the most common bacterial STD in USA?
    chlamydia trachomatis D-K infection
  967. what does chlamydia trachomatis D-K cause?
    sexually transmitted disease
  968. what is the clinical presentation of chlamydia trachomatis D-K infection?
    • symptoms vary / remain asymptomatic
    • watery discharge
    • can progress ? Pelvic inflammatory disease
  969. what is the difference between chlamydia and gonorrhea?
    • Chlamydia ? watery discharge (chlamydia trachomatis D-K)
    • Gonorrhea ? mucopurulent white discharge (Neisseria gonorrhea)
    • Chlamydia ? congenital conjunctivitis after 1st week of life
    • Gonorrhea ? congenital conjunctivitis within first 2-4 days of life
  970. What is pelvic inflammatory disease
    Ascending infection that can lead to cervicitis, salpingitis, pelvic pain, abscess formation, scarring of the tubes that can lead to infertility / atopic pregnancies later in life
  971. Why is it important to treat STDs as soon as possible ]
    To avoid progression to pelvic inflammatory disease and its complications (including infertility / atopic pregnancies)
  972. What do congenital chlamydia trachomatis D-K infection cause
    • Neonatal conjunctivitis
    • Neonatal pneumonia
  973. How does congenital chlamydia D-K occur
    When mother gives birth whilst with an active infection
  974. What is the clinical presentation of chlamydia trachomatis D-K congenital conjunctivitis
    Conjunctivitis occurs after first week of life
  975. What is the clinical presentation of chlamydia trachomatis D-K pneumonia
    Staccato cough ? cough with short sudden bursts
  976. What is the most common serovar to cause chlamydia STD?
  977. What do chlamydia trachomatis L1-L3 cause?
    Lympho Granuloma Venereum (LGV)
  978. What is LGV caused by chlamydia trachomatis L1-L3
    • Lymphogranuloma venereum
    • Infection of the inguinal lymph nodes
  979. What is the clinical presentation of chlamydia trachomatis L1-L3 lymphogranuloma venereum?
    • Starts as painless genital ulcer (like syphilis)
    • Tender lymphadenopathy with draining lymph nodes weeks-months later
  980. What do chlamydia trachomatis A-C cause?
  981. What is the leading cause of blindness in the world?
    Trachoma caused by chlamydia trachomatis serovars A-C
  982. How are chlamydia trachomatis A-C transmitted?
    • Hand to eye contact
    • Fomites
  983. What are long term complications of chlamydia trachomatis infection
    • Pelvic Inflammatory disease in women --> infertility / atopic pregnancies
    • Reactive arthritis = Reiter?s syndrome
  984. What is the pathogenesis of Reiter?s syndrome?
    • Maladaptive autoimmune response
    • Antibodies against bacteria cross react and attack the body
  985. What is the clinical presentation of Reiter?s syndrome?
    • Can?t see, can?t pee, can?t climb a tree
    • Reactive arthritis often in sacro-iliac joint / knee
    • Uveitis = infection of the eyes
    • Urethritis
  986. What could cause Reiter?s syndrome
    • Campylobacter
    • Chlamydia
  987. How do we treat chlamydia infection?
    • Treatment is very effective
    • Macrolides ? azithromycin
    • Tetracycline ? Doxycycline
  988. Why can?t we use penicillins to treat chlamydia infections?
    Do muramic acid in their cell wall so antibiotics that target cell wall?s cannot be used
  989. How do we treat neonatal conjunctivitis caused by chlamydia trachomatis D-K?
    • Topical macrolides are not effective for conjunctivitis in the newborn
    • Oral Macrolides must be given
  990. Why do we use combination therapy to treat chlamydia trachomatis D-K STD?
    • Treat for gonorrhea too
    • Often have a coinfection with Neisseria gonorrhea
    • Often hard to tell them apart as they present almost identically
  991. How do we treat chlamydia trachomatis D-K STD?
    • Combination therapy
    • Macrolides ? azithromycin (chlamydia trachomatis D-K)
    • Ceftriaxone (Neisseria gonorrhea)
  992. What does chlamydophila pneumoniae infection cause
    Atypical pneumonia in adults
  993. What is walking pneumonia
    Atypical pneumonia
  994. What bacteria cause atypical pneumonia
    • Legionella pneumophila
    • Mycoplasma pneumoniae
    • Chlamydophila pneumoniae
  995. Which bacteria more commonly causes atypical pneumonia in the elderly
    Chlamydophila pneumoniae
  996. How do we treat chlamydophila pneumoniae atypical pneumonia?
    • Tetracycline ? doxycycline
    • Macrolides ? azithromycin
  997. What does Mycoplasma pneumoniae cause
    Walking pneumonia = atypical pneumonia
  998. What gram stain is mycoplasma
    No gram stain
  999. Why doesn?t mycoplasma stain with gram stain
    No cell wall
  1000. What do mycoplasma have instead of a cell wall
    Special cell membrane with cholesterol in it
  1001. What is the function of cholesterol in mycoplasma cell membrane?
    • Stabilize membrane
    • Allow membrane to be more flexible
  1002. What is the only bacteria with cholesterol in their cell membrane?
  1003. What is the molecular structure of a sterol?
    4 ringed structure made of benzene rings
  1004. What bacteria cause atypical pneumonia
    • Legionella pneumophila
    • Mycoplasma pneumoniae
    • Chlamydophila pneumoniae
  1005. Why do we call atypical pneumonia this way?
    Can?t easily culture or isolate the microbes causing it
  1006. Why do we call atypical pneumonia caused by Mycoplasma pneumoniae a walking pneumonia?
    Severe pneumonia seen on X-ray but not too many clinical symptoms
  1007. What is the clinical presentation of walking pneumonia caused by Mycoplasma pneumoniae?
    • Few clinical symptoms
    • X-ray appears much worse than patients do clinically
  1008. What does an X-ray for Mycoplasma pneumoniae atypical pneumonia look like?
    Reticulo nodular / patchy infiltrate
  1009. Who is most affected by Mycoplasma pneumoniae infection
    Young adults in areas of close contact (e.g. Military)
  1010. How do you diagnose Mycoplasma pneumoniae infection?
    Cold agglutinins found in 50-70% patients
  1011. How do we grow Mycoplasma pneumoniae?
    • Takes a week
    • Eaton?s agar
  1012. What are cold agglutinins
    • 1-2 weeks into Mycoplasma infection people develop IgM molecules that agglutinate erythrocytes in cold temperatures
    • Can lead to lysis of red blood cells
  1013. What is the molecular structure of IgM?
    Pentamere circles
  1014. How do we treat Mycoplasma pneumoniae infection?
    Macrolides ? erythromycin
  1015. Why can?t we use penicillins to treat mycoplasma pneumoniae infection?
    No cell wall so cannot use antibiotics that target cell wall

    • What does Enterobacter cloacae infection cause?
    • Pneumonia
    • Urinary Tract Infection (UTI)
  1016. Where do we find Enterobacter cloacae?
    In hospitals ? nosocomial infections
  1017. Why is Enterobacter cloacae a nosocomial infection?
    Multidrug resistance
  1018. How do we treat Enterobacter cloacae infection?
    Carbopenems ? no resistance
  1019. why are there nosocomial infections
    multidrug resistance
  1020. how do we treat nosocomial infections?
    Carbopenems ? no resistance
  1021. what are Enterobacter cloacae biochemical properties?
    ferment lactose
  1022. which Enterobacteriaceae ferment lactose
    • Enterobacter
    • Serratia
    • Klebsiella
    • E. coli
  1023. How do we detect lactose fermenters?
    Form pink colonies on MacConkey agar
  1024. What gram stain is Enterobacter cloacae
    Gram ? rod (Enterobacteriaceae)
  1025. What are Enterobacter cloacae virulence factors?
  1026. What does serratia marcescens infection cause
    • Pneumonia
    • Urinary Tract Infection (UTI)
  1027. Where do we find serratia marcescens?
    In hospitals ? nosocomial infections
  1028. Why is serratia marcescens a nosocomial infection
    Multidrug resistance
  1029. How do we treat serratia marcescens infection?
    Carbopenems ? no resistance
  1030. what are serratia marcescens biochemical properties
    ferment lactose (very slowly)
  1031. what gram stain is serratia marcescens
    gram ? rod (Enterobacteriaceae)
  1032. what are serratia marcescens virulence factors
  1033. how do we differentiate serratia from other Enterobacteriaceae?
    produces red pigment when cultured
  1034. where can you find serratia bacteria
    anywhere ? e.g. pink ring when don?t clean shower is serratia
  1035. What does klebsiella pneumoniae infection cause
    • Pneumonia
    • Urinary Tract Infection (UTI)
  1036. Where do we find klebsiella pneumoniae?
    In hospitals ? nosocomial infections
  1037. Why is klebsiella pneumoniae a nosocomial infection
    Multidrug resistance
  1038. How do we treat klebsiella pneumoniae infection?
    Carbopenems ? no resistance
  1039. what are klebsiella pneumoniae biochemical properties
    • ferment lactose
    • urease positive
  1040. what gram stain is klebsiella pneumoniae
    gram ? rod (Enterobacteriaceae)
  1041. who does klebsiella pneumoniae affect
    alcoholics ? due to aspiration
  1042. how do klebsiella pneumoniae pass into the lungs
  1043. how does klebsiella pneumoniae infection present
    • abscesses ? cavitary lesions that resemble TB
    • current jelly sputum
  1044. what are the virulence factors of klebsiella pneumoniae?
    • polysaccharide capsule
    • NON motile
  1045. what is the capsule of klebsiella pneumoniae mad of?

    • What species are in the proteus genus
    • Proteus mirabilis
  1046. What gram stain are proteus
    Gram ? rod (enterobactericiae)
  1047. What does proteus look like when plated
    • Demonstrates swarming motility
    • Fishy odor
  1048. What are virulence factors of proteus?
  1049. What kind of motility does proteus have?
    Swarming motility when plated
  1050. What shape do kidney stones formed in the renal pelvis due to proteus have?
    Stag horn calculi
  1051. What do proteus infections cause
    • Stag horn calculi of the renal pelvis
    • Urinary Tract Infections (UTI)
  1052. What are biochemical properties of proteus
    Urease +
  1053. What is important for proteus to be able to form stag horn calculi
  1054. What is the function of urease?
    • Produces ammonia and CO2 rom urea
    • Creates alkaline environment
  1055. How does proteus cause stag horn calculi
    • Creates alkaline environment (urease)
    • Perfect environment for precipitation of struvite stones
  1056. What are struvite stones made of?
    • Ammonia
    • Magnesium
    • Phosphate
  1057. What is the complication of struvite kidney stones?
    • Pain
    • Kidney damage
    • Nidus for proteus --> recurrent infections
  1058. How do you treat proteus infection?
  1059. Who is the founding father of microbiology?
    Louis Pasteur
  1060. Where can we find Pasteurella multocida
    Respiratory tract of small mammals ? cats / dogs
  1061. How is Pasteurella multocida transmitted to humans
    Dogs and cat bites
  1062. What does Pasteurella multocida infection cause
    • Soft tissue infections --> Cellulitis in first 24 hours --> necrotizing fasciitis / osteomyelitis
    • Lymphadenopathy
    • Systemic infection
  1063. What is the clinical presentation of Pasteurella multocida infection?
    Erythematous area of skin where bite is
  1064. How long after initial exposure does Pasteurella multocida cause infection
    Within first 24 hours
  1065. Who is at most risk for systemic spread of Pasteurella multocida
    • Liver disease patients
    • COPD patients
  1066. What biochemical properties does Pasteurella multocida have?
    • Catalase +
    • Oxidase +
  1067. What are Pasteurella multocida virulence factors
  1068. How do we grow Pasteurella multocida?
    5% sheep?s blood agar
  1069. What gram stain is Pasteurella multocida
    • Gram ? coccobacillus
    • Bipolar staining = safety pin staining
  1070. What is bipolar staining
    • Bacteria takes up stain most readily at its 2 ends
    • Looks like safety pin
  1071. Which bacteria demonstrate bipolar staining
    • Pasteurella multocida
    • Yersinia enterocolitica
  1072. How do we treat Pasteurella multocida infection?
    • Penicillin ? amoxicillin
    • AND Beta lactamase inhibitor (prevent resistance) ? clavulanic acid
  1073. Why do we use combination of penicillin and beta lactamase inhibitor in treatment of Pasteurella multocida?
    To prevent development of resistance
  1074. What does chlamydophila psittaci cause
  1075. How is chlamydophila psittaci transmitted
    Birds ? often parrots
  1076. What does Gardnerella vaginalis cause
    bacterial vaginosis
  1077. what is the clinical presentation of bacterial vaginosis caused by Gardnerella vaginalis?
    thin greyish white malodorous (fishy) discharge from vagina
  1078. what gram stain is Gardnerella vaginalis
    • Gram variable rod
    • Stains as either gram + or gram -
  1079. How does Gardnerella vaginalis cause infection
    • Increase in anaerobic flora of the vagina --> overgrowth --> decreased amount of lactobacilli
    • Creates environment more suitable for Gardnerella vaginalis
  1080. What is the normal vaginal flora?
    • Mainly Lactobacilli
    • Minority of anaerobic gram ?
  1081. How do we diagnose vaginosis caused by Gardnerella vaginalis?
    • Discharge should have a pH above 4.5 (usually between 5 ? 6.5)
    • Whiff test
    • Microscopic exam ? with wet mount
  1082. What is the whiff test?
    • Prep vaginosis discharge with 10% KOH and smell pungent fishy odor
    • Diagnosis for Gardnerella vaginalis vaginosis
  1083. How do we do a microscopic exam of Gardnerella vaginalis
    • Wet mount preparation of bacterial vaginosis discharge
    • Clue cells
  1084. What are clue cells
    Epithelial cells diffusely coated with Gardnerella vaginalis bacteria
  1085. How do we treat bacterial vaginosis caused by Gardnerella vaginalis?
  1086. Which bacteria do we treat using metronidazole
    • Clostridium difficile
    • Gardnerella vaginalis
Card Set
Flashcards Bacteria
Bacteriology missing: Bordetella parapertussis other haemophilus species Corynebacterium other potentially pathogenic corynebacterium Arcanobacterium Haemolyticum Characterisation fo Enterbacteriaceae family Non typhoidal salmonella spp Other clinically non-significant non fermenters (Acinetobacter, Burkholderia, Stenotrophomonas) Atypical mycobacteria Non spore forming anaerobes Borrelia recurentis other mycoplasma