master Test # 2 .txt

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master Test # 2 .txt
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  1. What is staphylococcus? A family, genus or species?
    A genus
  2. Is staphylococcus gram positive cocci or gram negative cocci?
    gram positive
  3. What are the three main members of staphylococcus genus (types)?
    normal flora of the human skin, mucous membranes of the respiratory tract and GI tract
  4. What does the name "staphyl" in staphylcoccus refer to?
    Their arrangement = "clusters of cocci" "bunch of grapes"
  5. what three species are we looking at in the staphylococcus genus?
    Aureus, epidermidis, saprophyticus
  6. What species is the true pathogen of the staphylococcus genus?
    Aureus
  7. The Aureus species accounts for what percentage of bacterial infections from the staphylococus genus?
    90%
  8. What two species of the staphylocpccus genus are considered to be a part of our normal flora?
    Epidermidis and saprophyticus
  9. When can the epidermidis and saprophyticus species cause infection?
    Under opportune conditions
  10. What is a nosocomial infection?
    An infection that is hospital-acquired
  11. What species of the staphylcoccus genuc are considered to have the traits of being opportunistic or nosocomial?
    epidermidis and saprophyticus
  12. Is The staphylococcus genus gram negative or gram positive?
    Gram positive (deep blue, purple)
  13. What formation would The staphylococcus genus have?
    cluster formation
  14. Is The staphylococcus genus have spore forming species?
    no
  15. Is The staphylococcus genus motile?
    no
  16. Does The staphylococcus genus usually have a capsule?
    no (with the excetpion of staphylcoccus aureus)
  17. Which species is an exeption to the non-capsule trait of the staphylcoccus genus?
    Aureus
  18. What are the five protein toxins?
    Hemolysin, leukocidin, enterotoxin and Toxic Shock Syndrome (TSST-1)
  19. Hemolysin
    Lyses red blood cells by disrupting cell membrane
  20. Leuokcidin
    lyses white blood cells by disrupting cell membrane
  21. When leuokcidin lyses white blood cells what does it do to the Host's defense?
    Inhibits the normal host defense
  22. Enterotoxin
    toxin associated with food posioning or food infections
  23. Entero means?
    "of the butt"
  24. Toxic Shock Syndrome (TSST-1)
    Toxin that stimulates the production of interleukin (IL-1) by macrophages resulting in fever induction.
  25. Coagulase
    plasma clotting protein that converts fibrinogen to fibrin
  26. What converts fibrinogen to fibrin?
    Coagulase
  27. What are the two extra functions of coagulase?
    coast bacteria with fibrin and prevents phagocytosis, and aid in attachment
  28. Is the coagulase factor virulent? if so why?
    Yes, because it prevent phagocytosis and aids in attachment.
  29. Fibrinolysin
    digests fibrinogen (fibrin clots)
  30. Hyaluronidase "spreading factor"
    Digests hyaluronic acid around host cells
  31. Cement and brick theory for hyaluronidase?
    Hyaluronic acid is like the cement between the bricks. Hyaluronidase removes the cement and lets the infection spread.
  32. Lipase
    degrades lipids
  33. what allows bacteria to colonize oily skin?
    lipase
  34. Penicillinase
    hydrolyzes penicillin, creates drug resistance to the beta-lactan drug (dont use penicillin)
  35. Catalase
    degrades H2O2 (hydrogen peroxide), is a toxic metabolic end product
  36. Exfoliatin or epidermolytoc toxin
    protease that causes peeling of superficial skin layers by dissolving intracellular bridges
  37. Protein A
    surface component linked to peptidoglycan layer of cell wall, inhibits antibody-mediated clearance of bacteria by binding to IgG
  38. What structural surface component of staphlycoccus inhibits antibody immunity?
    Protein A
  39. Liptoteichoic acid
    binds to tissue components, aids in cell adhesion
  40. How does protein A inhibit antibody immunity?
    by going through a non competitive binding intereaction to IgG
  41. What is the major pathogen of the staphylococcus genus?
    Staphylococcus aureus
  42. Where are the carriage locations (places it lives on us)?
    anerior nares, nasopharynx and skin
  43. What is the carriage rate of staphylococcus?
    30 - 50% of healthy adults
  44. Which bacteria is the most resitant of the "non-spore formers"?
    Staph aureus (bully bacteria, very tough)
  45. Who has a high carriage rate of staph. aureus as opposed to the 3- to 50% healthy adults?
    hospital staff/personal (about 70%)
  46. What are the 5 main virulence factors of staphylococcus aureus?
    Coagulase positive, hemolysin (alpha toxin), leukocidin, protein A, capsule
  47. The toxins produced are indicative of....
    the infections they cause
  48. What are the blood cell toxins of staph Aureus?
    hemolysins, leukocidin
  49. What are the intestinal toxins of staph Aureus?
    enterotoxins
  50. What are the epithelial toxins of staph Aureus?
    exfoliatin or epidermolytic toxin
  51. What are the three main catergories of infections caused by staph Aureus?
    systemic/deeper infection, Toxigenic infections and superficial infections
  52. What is a superfical infection?
    a localized cutaneous infection
  53. What does it mean to be localized?
    It has on focal point, concentrated on a specific area
  54. Bacteremia
    bacteria that enter the blood stream
  55. Why is bacteremia dangerous?
    Because the microbes are carried to all body sites
  56. How do bacteria reach a certain site in the body once its bacteremia?
    Focus of infection, extensive surgery & traumatic injuries
  57. What two systems can bacteria travel by (two primary means)?
    Blood system or the lymphatic system
  58. What is the SSSS infection?
    Staphylococcal scalded skin syndrome
  59. What is the virulent feature of SSSS?
    exfolatin or epidermolytic toxin
  60. Which infections are the most minor?
    Superficial Cutaneous Infections
  61. How can staphylococci invade the skin?
    sebaceous gland opening (skin gland), hair follicle or wound
  62. After the Staphylocci enters the body, what does it form?
    an infection site (abscess)
  63. What is present at infetion sites (abscesses)
    bacteria, white blood cells, plasma, pus
  64. The formation of an abcess by the host is referred to as an...
    inflammatory reaction
  65. Is there a fibrin clot formation for the abcesses of the staphylcocci?
    yes
  66. What is the fibrin clot, on the abcess of a staphylcocci infection reffered to as?
    inflammatory barrier
  67. What is the purpose of the inflammatory barrier?
    to keep the infection localized and not allow it to spread
  68. Why do you have pus formation with superficial cutaneous infections?
    Because the staphylcoccus genus are pyogenic cocci, meaning they are pus producers
  69. What are pyogenic cocci
    Pus-producers
  70. What are the pyodermic infections of superfical cutaneous infections?
    pimples, boils, carbuncles and impetigo
  71. Acne is an infection caused by
    staph Aureus
  72. boils are caused by
    staph Aureus
  73. impetigo is usually found in
    young children
  74. which infection for honey crusted areas, is extremely contagious and is very itchy?
    impetigo
  75. Risk groups of superficial cutaneous infections?
    elederly and young children with poor personal hygiene.
  76. What is the mode of infection for staphylcocci in superficial cutaneous infections?
    invading skin
  77. Self resolve means..
    "you'll get over it"
  78. What are different kinds of treatment for superficial cutaneous infections?
    for minor lesions - (self resolve), surgical incision and drainage, chemotherapy-topical antibiotics
  79. Why are only topical treaments given for superficial cutaneous infections and not oral treatments?
    Because the infection site has the inflammatory barrier to keep the infection localized.An oral treatment would not be able to reach the infection site.
  80. what does SSSS look like?
    "like somebody has bad skinburn" blistering and peeling of the skin which exposes the red underlayer
  81. What is the mode of infection of SSSS
    The syndrome usually begins as an erythema around the mouth and nose, only to then spread rapidly to infect the skin of the neck, trunk and extremities.
  82. What are the risk groups of SSSS?
    Infants and young children under the age of 4.
  83. Which infection is primarily a neonatal one?
    SSSS
  84. What are the primary infected sites of SSSS
    umbilical cord and eyes
  85. does SSSS have a high mortality rate?
    no
  86. If SSSS has a low mortality rate, how can SSSS result in death?
    by a secondary infection of the denuded skin by other bacterial patohgens (peeling away the host defense, imunity decreased)
  87. What kind of treatment is given for SSSS
    Topical antibiotic (mupirocin)
  88. What is the incidence of infection for Toxic Shock Syndrome, TSS?
    Usage of super absorbent vaginal tampons
  89. Explain how the tampons were killin' errbody? (immunological breakdown)
    Superabsorbent tampons were cellulose based and could bind mg from the moisture. a low level of mg then triggers the growth of the TSST-1 toxin. The TSST-1 Toxin then stimulates the T lymphocytes, which create cytokines which create endothelial cell damage, which causes shock and multisystem organ failure.
  90. What are the inital symptoms of TSS?
    high fever, vomiting, diarrhea and muscle cramps (myalgia)
  91. What are the symptoms of TSS ten days later?
    hands and soles of feet develop a sunburn-like rash which results in a peeling of the skin.
  92. What are the severe symptoms of TSS?
    shock and mutli organ failure.
  93. What is the death of TSS due to?
    2-5% respiratory failure
  94. what are the high risk groups for TSS?
    menstruating women (using high absobancy tampons), non-menustrating groups like postpartum womean with surgical wound infections (hysterectomies) nasal surgery and packaging
  95. How can TSS be prevented or controlled?
    Removal of cellulose based superabsorbent tampons from market in 1980. CDC reccomends that tampons are not used continuosly during a memstrual cycle.
  96. What is the treatment of TSS?
    Fluid replacement and chemotherapy.
  97. What are the five kinds of sytemic infections?
    osteomyelitis, pneumonia, endocarditis, meningitis, pyoarthritis
  98. osteomyelitis
    inflammation of the bone
  99. Endocarditis
    infflammation of endocardium (heart)
  100. Meningitis
    inflammation of the membrane surrounding the brain and spinal column (brain)
  101. Pyoarthritis
    inflammation of the joints
  102. Who is at risk for getting a systemic infection?
    Anyone who has pre-condtions. (diabetes, burn wounds, extensive surgery, cystic fibrosis, cirrhosis of the liver or those immunosuppressed or immunodefective in phagocytic properties)
  103. What is the treatment for systemic infections?
    prolonged combination of antibiotic therapy
  104. What is Toxigenic Gastrointestinal Disease?
    Food Poisioning (food intoxication)
  105. What is the source of contamination of food posioning?
    Food handler
  106. What is the immunological path of how food poisoning is produced?
    Staphylococcal lesions of skin (hands and nose carriers) contaminate the food, the food is left unrefrigerated, room temperature causes the growth of staph Aureus, staph Aureus produces enterotoxin (exotoxin)
  107. Why is there a higher risk of getting food posioning during the summer months?
    Picnics, leaving the food out.
  108. What is the virulent feature of food posioning?
    Enterotxin(exotoxin) is heat stable, no inactivated by stomach acid (digestive enzymes), and the production of toxins do not alter food tast or smell.
  109. What is the action of enterotoxins in food poisioning?
    disrupts gastrointestinal lining
  110. What are the symptoms of food poisioning?
    starts in 4-6 hours - vomiting, cramps, diarrhea and nausea
  111. What is the recovery time of food poisioning?
    Self limited, 24-48 hours
  112. What are coagulase negative staphylococci?
    Staphylococcus epidermidis and Staphylococcus saprophyticus
  113. Staphylococcus saprophyticus is in the normal flora of...
    vaginal and intestinal tract
  114. Staphylococcus epidermidis is in the normal flora of...
    the skin
  115. What is the route of infection for Staphylococcus epidermidis?
    artificial heart alves, prosthetic hips and atrioentricular shunts (surgical related things conttaminated by nurse, health personel, staph epi stays on materials then grows inside body.)
  116. What kind of infection is staph epi?
    opportunistic infection
  117. What is the mode of a staph epi infection?
    attachment of bacteria to foreign body, multiplication/colonization
  118. What kinds of infection are cause bey Staphylococcus epidermidis?
    endocarditis (heart valve), urinary tract infections (catherers), and wound infections
  119. What are the common inhabitants of the Staphylococcus saprophyticus?
    lower intestinal tract and vaginal
  120. What is the primary infection caused by Staphylococcus saprophyticus?
    Urinary tract infections (UTI), dysuria (pain during urination), pyuria (pus in urine) and high numbers of the bacteria in the urine
  121. What is the highest risk group for the UTI by Staphylococcus saprophyticus?
    Aldolescent, young women
  122. How can you differentitate between the two coagulase negative stapyhlcocci?
    Bacterial sensitivity or resistance to the antibiotic novobiocin
  123. What is staphylococcus epidermidis' bacterial reaction to the antibiotic novobiocin?
    sensitive to it
  124. What is staphylococcus saphrophyticus' bacterial reaction to the antibiotic novobiocin?
    resistant to it
  125. Is there a vaccine available for staphycoccal infections?
    no.
  126. How can you prevent staphylococcal infections?
    minimizing opportunity for infection
  127. how can you minimize opportunity for staphylococcal infection?
    Hygiene (hand washing), adequate cleansing of wounds; changes bandages frequently, attention to indwelling devices (needles and catheters), treat surfaces with disinfectants.
  128. How are staphylococcal infections ID in the lab? (3 ways)
    Clinical presentation of the patient, isolation and demonstration of the bacterium from clinical specimens (skin scrapings, blood, pus) and biochemical tests
  129. how can we use isolationa and demonstration of the bacteria to id an infection?
    Gram stain, inoculation of media, blood agar (enriched medium) by hemolytic pattern or colony color, mannitol salt agar (selective medium) additivve 7.5 naCl is a differential medium where the fermentation of mannitol can monitor the change in pH.
  130. What two types of biochemical tests are available to ID a staphylococcus infection?
    catalase test and coagulase test
  131. Who are at risk for nosocomial infections?
    neonates (babies) and surgical patients
  132. What is the carrier rate of Staphylococcus aureus in hospital personnel?
    70-80%
  133. What is the carrier rate of Staphylococcus aureus in the general population?
    30-50%
  134. What is the imporatant emerging Staphylococcus aureus superbug?
    MRSA
  135. What does MRSA stand for?
    Methicillin (or multiple) resitant Staphylococcus aureus
  136. What are the two kinds of MRSA?
    Health care associated MRSA and Community associated MRSA
  137. What is HA-MRSA?
    Health Care Associated MRSA
  138. What is CA-MRSA?
    Community Associated MRSA
  139. What are increased risk factors for HA-MRSA?
    older adults, weakened immune system, burns, surgical wounds, hospital stays of 10 days, invasive devices – dialysis (catherterized) or feeding tubes, living in a long-term facility, recent antibiotic use
  140. What are increased risk factors for CA-MRSA?
    daycare settings, NFL/NBA players, dorm residents, prisons, military training camps, gay men
  141. What are the five C's that make it easier for MRSA to spread?
    CROWDING, frequent skin-to-skin CONTACT, COMPROMISED skin, CONTAMINATED items, lack of CLEANLINESS
  142. Most Staphylococcus aureus infections are resistant to _________ and need ________ to be eliminated.
    Penicillin....Vancomyocin
  143. What family is the Staphylococcus genus in?
    Micrococcaceae
  144. "strepto" is a greek word that means...?
    twisted
  145. "Cocci" means?
    Round berry
  146. Streptocicci stain well and have a large cell wall, this means they are gram ______.
    positive
  147. What are the two tyoes of cocci streptococci can be?
    Spherical or ovoid in pairs and chains
  148. How can you differentiate streptococci from staphylcocci?
    Whether it is catalse negative of positive, strepto is catalse negative.
  149. What does it mean that streptococci are facultative anaerobes?
    It means that they are primarily fermenters that can tolerate oxygen
  150. What pathway do streptococci usually use to obtain energy?
    Lactic acid fermentation - anaerobic pathway
  151. Homolactic fermenters
    bacteria that produce only lactic acid
  152. heterolactic fermenters
    bacteria that produce other products along with lactc acid (ethanol, acetate, fomate and butanediol
  153. What are the three hemolytic patterns used to classify streptococci?
    Beta B-hemolytic, Alpha A-hemolytic, and Gamma Y-hemolytic
  154. What color is alpha-hemolysis?
    green
  155. What color is gamma-hemolysis?
    n/a - no hemolysis
  156. What color is Beta-hemolysis?
    Clear
  157. what kind of hemolysis is the beta hemolysis?
    Complete hemolysis
  158. What kind of hemolysis is the alpha hemolysis?
    partial hemolysis
  159. What kind of hemolysis the gamma hemolysis?
    N/A no hemolyosis takes place here
  160. What is alpha hemolysis really?
    oxidation of hemogloubin
  161. Why is alpha-hemolytic organisms not considered to perform a complete hemolysis?
    because they just form hydrogen peroxide and oxidize hemogloubin which makes "Billy Verdin" which makes it green.
  162. What is the process of the beta hemolytic pattern?
    toxins make holes in the red blood cell to lyse them completely
  163. What is streptococcus group a?
    pyogenes
  164. What is streptococcus group b?
    agalactiae
  165. is pyogenes bacitracin resistant or sensitive?'
    sensitive
  166. is agalactiae bacitracin resistant or sensitive?
    resistant
  167. what is pyogenes hemolytic pattern?
    beta hemolytic
  168. what is agalactiae's hemolytic pattern?
    beta hemolytic
  169. what is pneumoniae's hemolytic pattern
    alpha hemolytic
  170. What is the representative species of lancefield group A?
    S. pyogenes
  171. What is the representative species of lancefield group B?
    S. agalactiae
  172. What is the representative species of lancefield group C?
    S. equi, equisimilis
  173. What is the representative species of lancefield group D?
    Enterococcus faecalis, faecium, S. bovis, equinus
  174. What is the representative species of lancefield group F?
    S. anginosus
  175. What is the representative species of lancefield group G?
    S. canis
  176. What is the representative species of lancefield group, Viridans group (no antigen)?
    S. mutans, mitis, salivarius, thermophilus, sanguinis
  177. What is the representative species of lancefield group that has no antigen at all?
    S. pneumoniae
  178. What infection can come from lancefield group A?
    Pharyngitis and skin/soft tissue infection
  179. What infection can come from lancefield group B?
    Neonatal pneumonia, sepsis
  180. What infection can come from lancefield group C?
    URI
  181. What infection can come from lancefield group D?
    UTI and endocarditis
  182. What infection can come from lancefield group F?
    Abscesses
  183. What infection can come from lancefield group G?
    Cellulitis
  184. What infection can come from lancefield group (viridans group)?
    Caries, Endocarditis
  185. What infection can come from lancefield group with no antigens?
    pneumonia, meningitis, Otitis media, sepsis
  186. what is viridan's hemolytic pattern?
    alpha hemolytic
  187. what is enterococcus' hemolytic pattern?
    gamma hemolytic
  188. What is used for phylogenetic analysis?
    16S RNA
  189. How does the phylogenetic analysis work?
    It works by, when you treat everything with 16S RNA and set up a tree phylumm, you get a cluster of the different organisms that are similare to each other, creating different characteristical groups and making for easier ID.
  190. A,B,C is which group in phylogenetic analysis?
    pyogenic group
  191. D is which group in phylogenetic analysis?
    Bovis group
  192. Viridans is which group in phylogenetic analysis?
    mutans, salivarius and mitis groups
  193. F is which group in phylogenetic analysis?
    anginosus group
  194. What is the group A streptococcus (gram, hemoly, shape and form?)
    Gram positive, beta-hemolytic coccus that grows in chains.
  195. What expresses that group A carbohydrate?
    Group A streptococcus
  196. What is the group A carbohydrate?
    N-acetyl-B-D-glucosamine linked to poly-rhamnose
  197. What is the group A carbohydrate linked to?
    poly-rhamnose
  198. Why was streptococcus pyogenes named that way?
    It was based on its purulent infection in 1884 by Dr. rosenbach
  199. What kind of colonization is common in streptococcus?
    Asymptomatic colonization
  200. What is asymptomatic colonization?
    When infections can colonize and form without having the host display any symptoms
  201. Where is colonization for streptococci most common?
    oropharynx, respiratory tract and skin
  202. Streptococcus mostly affects children ages ___ to ____.
    1-15
  203. What is the mode of transportation for streptococcus?
    via droplets, facilitated by many people in a shared environment
  204. What streptococcal infection can reoccur even after antibiotic treatment?
    "strept throat"
  205. What are some clinical manifestations of streptococcus?
    asymptomatic carriage, colonization, localized infection, invasive infection and post-infectous sequalae
  206. what are the 4 examples of localized streptococcal infections?
    pharyngitis (strept throat), scarlet fever (rash), impetigo (superficial skin infection), Cellulitis/erysipelas (deeper skin infection)
  207. what are the 3 examples of streptococcal invasive infections?
    bacteremia, streptooccal toxic shock syndrome (rash, fever, edema), necrotizing fasciltis (flesh-eating infections)
  208. what are the 2 examples of post-infectous sequalae?
    acute rheumatic fever (arithis and endocarditis) and glomerulonephritis
  209. How are post-infection sequalae possible?
    the orignal streptococcal that causes the original infection has antigen on their surface that a similar to the antigens in our body. that makes it easter for them to sneak around and wait to attack or be accepted again, after the initial infection
  210. What is glomerulonephritis?
    inflammation in the kidneys
  211. what is the most common cause of pharyngitis in children 1-15?
    GAS (Group A streptococcus)
  212. Strains that cause pharyngitis tend not to cause...
    skin infection and vice versa
  213. What is the important sqequelae of pharyngitis that 3% of patients get?
    rheumatic fever
  214. What are the sequlae associated with pharygitis?
    arthritis, endocarditis, CNS symptoms, skin lesions and subcutaneous nodules seen
  215. what are the symptoms of pharygitis?
    chills, fever, headache, red pharynx with exudate, anterior cervical lymphadenitis?
  216. What is scarlet fever caused by?
    Group A streptococcus exotoxoj
  217. What are the symptoms of scarlet fever?
    sore throat, fever, diffuse rash, strawberry tongue
  218. impetigo is a _______skin infection
    superficial
  219. what is the histological evidence of impetigo
    1-2mm vesicles that evolve tno pustules which eventually crust (typically bellow nares or under lip)
  220. Impetigo usually has regional _________ without systemic symptoms.
    adenopathy
  221. what is adenopathy?
    Swelling or abnormal enlargement of the lymph nodes
  222. What can untreated impetigo lead to?
    glomerunlonephritis as well as sepsi
  223. What is sepsis?
    When the bloodstream is overwhelmed by bacteria
  224. What are the symptoms of most people who have cellulitis?
    Feel mildly ill, fever, chills, rapid hear rate, local lymphadenitis
  225. Can cellulitis lead to sepsis?
    yes
  226. What are the symptoms of Streptococcal toxic shock sydrome?
    rash, fever, edema, shock (hypotension), multiple ogran failure
  227. What can the skin rash of streptococaal toxic shock syndrome be confused for?
    the skin rash of scarlet fever.
  228. What is the approx. death rate of steptococcal toxics shock syndrome?
    30%
  229. what is streptoccoccal toxic shock induced by? (the steps involved)
    streptococcal superantigens which activates non-specific T cell receptors which causes polyclonal activation of T cells which causes a cytokine storm
  230. what can streptoccoccal toxic shock cause?
    necrotizing faciitis
  231. What kind of infections are necrotizing faciitis?
    "flesh-eating" infections
  232. What are the side effects of necrotizing fasciitis?
    Hypotension, shock, multiple organ failure, rapid necrosis of fascia and skin, gangrene
  233. when you have Necrotizing fasciitis you have an infection around a cut or bruise that is much more painful than expected with ________.
    high fever.
  234. How fast can necrotizing fasciitis spread through the affected body part?
    1 inch per hour
  235. Does necrotizing fasciitis have a high mortality rate?
    yes
  236. What are the virulence factors for streptococcal?
    hyaluronic acid capsule, pyrogenic exotoxins, protease, steptokinase, C5a-peptidase, strepdornase(DNAses)
  237. what is the mortality rate for necrotizing fasciitis?
    Over 50%
  238. What is Acute rheumatic fever?
    arthritis and endocarditis
  239. acute rhemumatic fever is the sequalae after __________.
    pharyngitis
  240. What is the risk of developing rheumatic fever following untreated tonsillopharyngitis?
    1-3%
  241. What does a casual strain of acute rheumatic fever do?
    It adheres to the oral and pharyngeal cells and then releases its degradation products which cross-react with certain human tissues particularly in cardiac valve and myocardium tissue.
  242. What are the symptoms of acute rheumatic fever?
    Fever, painful joints, chest pain, fatigue and rapid fluttering heartbeats
  243. What is the sequalae after skin infections and sometimes pharyngitis?
    glomerulonephritis
  244. How long after pharyngitis can glomerulonephritis develop?
    10 days
  245. how long after impetigo w/ a nephritogenic strain of GAS can glomerulonephritis develop?
    2 weeks
  246. what are the symptoms of glomerulonephritis?
    gross hematuria (red urine), headache, and generalized symptoms like anorexia, nausea, vomiting and malaise.
  247. What does a physical examination with someone with glomerulonephritis reveal?
    hypervolemia, edema and hypertension.
  248. What does hyaluronic acid make up in our bodies?
    our eyes
  249. M protein has more than _______ serotypes
    100
  250. Serotype
    distinct variations within a subspecies of bacteria or viruses
  251. M proteins block the white blood cells from doing what to them?
    phagocyting them
  252. M protein's two main virulent factors is that is is...
    anti-phagocytic and that it can bind to things
  253. what inhibitor can the m protein use specifically for adherence?
    CD46
  254. What are all the inhibitors the M protein can bind to?
    Factor H, Factor H-like protein, fibrinogen, C4BP, CD46
  255. What protein binds to the IgA inhibitor?
    Arp4
  256. What protein binds to IgG and albumin?
    Protein H
  257. Why is the hyaluronic acid capsule an important virulence factor of streptococcal?
    Without it, it cannot cause invasive disease
  258. Why does streptococcal appear slimy when it has a capsule?
    Because the capsule produces a mucoid phenotype
  259. What are the two main important virulence factors of hyaluronic acid?
    protects against complement-mediated phagocytic killing and binds to surface receptor CD44 and causes cell disruption leading to invasion of the bacteria through mucoas.
  260. What happens when Streptolysin O is released?
    lyses whole cells
  261. How does streptolysin O lyse whole cells?
    Makes a pore in the membrane, can aslo "juice" that pore to get NADase to go into the cell and cleave NAD from cyclice ADP-ribose that can activate calcium-channels in the enoplasmic reticulum causing the cell to die.
  262. What is a member of a large, growing family of cholesterol-dependent pore-forming toxins?
    streptolysin O
  263. Is steptolysin O oxygen-labile?
    yes
  264. Steptolysin and NADase are both ________.
    immunogenic
  265. What is responsible for beta-hemolysis?
    Streptolysin S
  266. What kind of hemolysin is Streptolysin S?
    oxygen-stable
  267. what is streptolysin S encoded by?
    sag operon
  268. is streptolysin S immunogenic?
    no
  269. What's required for lyses of the red blood cell?
    streptolysin s
  270. What kind of antigens are the pyrogenic exotoxins?
    Superantigens
  271. What are the two pyrogenic exotoxins that are involved in scarlet fever?
    SpeA and SpeC
  272. Which exotoxin plays a role in streptococcal toxic shock syndrome?
    SpeA
  273. what's another term for pyrogenic exotoxins?
    eryhrogenic toxins
  274. How do we diagnose streptococci?
    Rapid strept antigen detection test that detects group A carb (only 75% sensitive), culture on a blood agar for bets-hemolytic colonies, catalse negative to differentitate from staphylococci and sequelae detected based on serology (anti SLO or DNAse antibodies)
  275. What is the treatment for streptococci?
    Penicillin and erythromycin still effective
  276. what is the prevention for streptococci?
    no prevention available
  277. Does streptococcus pneumoniae have streptococcal antigen?
    no
  278. What is the form of streptococcus pneumoniae
    diplococcus
  279. Is streptococcus pneumoniae gram positive or gram negative?
    Gram positive
  280. What kind of hemolysis does streptococcus pneumoniae do?
    alpha-hemolytic
  281. What are streptococcus pneumoniae's two major sensitvities?
    bile and optochin
  282. how many capsular serotypes does streptococcus pneumoniae have?
    92
  283. what are the bile and optochin sensitivities of streptococcus pneumoniae help differentiate it from?
    viridans group
  284. why cant we use optochin anymore?
    extremely toxic
  285. What are the four major historical points in streptococcus pneumoniae's history?
    1881-isolated by george sternberg and louis pasteur, 1884-ID facilitated by Hans Christian gram's stain, 1928- Frederick Griffith-capsule transformation in vivo, 1944-avery,mcleod, mccarty-dna carries genetic info
  286. Is streptococci an exclusively human pathogen?
    yes
  287. what form does streptococci transmit in?
    droplet transmission
  288. what kind of infections are streptococci associated?
    virus infections (influenza)
  289. What are streptococci diseases mostly related to in the host immunity?
    "defects"
  290. Who are most infected by streptococci?
    Children and the elderly
  291. What is the socioeconomic cost of AOM?
    4 billion
  292. What does AOM stand for?
    Acute Otitis Media
  293. how many cases of acute otitis media are there per year?
    6-10 million cases
  294. how many hospitalizations occur per year for pneumonia?
    175,000
  295. what percentage of pneumonia hospitalizations are community acquired?
    36%
  296. what percentage of pneumonia hospitalizations are hospital acquired?
    50%
  297. how many cases of bacteremia are there per year?
    50,000
  298. how many cases of meningitis are there per year?
    3,000-6,000
  299. How many cases of death are there per year for streptococci related illnesses?
    10,000-20,000
  300. Why can't streptococci survive on surfaces?
    needs human contact to transmit
  301. what is AOM?
    middle ear infection
  302. What kind of carriage/colonization does streptococcus pneumoniae have?
    asymptomatic carriage/colonization
  303. What percentage of childrem will have been colonized with streptococcus pneumoniae by age 1?
    100% all children
  304. What are the two localized infections of streptococcus pneumoniae?
    pneumonia and otitis media.
  305. Who mostly gets pneumonia?
    The elderly
  306. Who mostly gets otitis media?
    The children
  307. What percentage of children have had one episode of otitis media by age 3?
    75%
  308. what are the invasive infections of streptococcus pneumoniae?
    bacteremia/sepsis, meningitis
  309. what are the symptoms of AOM?
    redness, edema and bulgining of the pairs flaccida
  310. How many people die worldwide from pneumonia each year?
    more than 1.6 million
  311. how many cases per 100,000 are invaseive pneumococcal disease?
    15 cases
  312. What is the leading vaccine-preventable killer of children?
    pneumococcal disease
  313. how many children die from pneumococcal disease?
    1 million
  314. From 11% of all children that die, what percentage is from the developing world?
    90%
  315. What are the 8 steps in patogenesis?
    colonization and fitness, invasion, apoptosis, immune evasion, clearance, intracellular kill, signaling, and immune activation.
  316. what decides colonizaton or infection in pathogenesis?
    the balance between bacterial factors and host factors
  317. in pathogenesis, what happens in colonization and fitness?
    adherernece to mucosa and acquistion of nutriets
  318. in pathogenesis, what happens in invasion?
    bacteria can get into cells and go through cells
  319. in pathogenesis, what happens in apoptosis?
    bacteria kill cells and invade between cells
  320. in pathogenesis, what happens in immune evasion?
    bacteria inactivate components of the immune system
  321. in pathogenesis, what happens in clearance?
    mucus clears bacteria and mucose produce antimicrobial factors
  322. in pathogenesis, what happens in intracellular kill?
    epitheleial cells kill bacteria in vesicles
  323. in pathogenesis, what happens in signaling?
    infected cells signal for help to the immune system
  324. in pathogenesis, what happens in immune activation?
    immune cells and proteins fight off infection
  325. in pathogenesis what steps are the bacteria factors?
    colonization and fitness, invasion, apoptosis and immune evasion
  326. in pathogenesis what steps are the host factors?
    clearance, intracellular kill, signaling and immune activation
  327. What are the pneumococcal virulence factors?
    adherence, nutrient acquisition, immune evasion and spread
  328. What does penumococci use to adhere to things?
    PspC (CbpA), PsaA, PC, PavA
  329. what percentage of adults are colonized by pnemococci at any time?
    5-70%
  330. how does pneumococci grow?
    ABC transporters (Zn, Fe, CSP, etc.), PTS systems, Porins and mineral acquistion systems
  331. What helps pneumococci evade the immune system?
    pneumolysin (LytA) H2O2 (hydro. perox), capsules, PspA, PspC, IgA protease
  332. how is pneumococci diagnosed?
    physical exam and chest x-ray (pneumonia), microscopy from source (gram + cocci), culture on blood agar, bile and optochin sensitivty(diff. from viridans group), serology (anti-pneumococcal antibodies)
  333. What is used for treatment for pnemococci?
    penicillin mostly useful
  334. some places in the world have over ___% penicillin resistance
    60%
  335. in a recent study in 2008, ____% penicillin, ____% macrolides and ____% multidrug resistant when dealing with pneumococci.
    22%, 30% and 30%
  336. what are ways to prevent pneumococcal disease?
    breast-feeding, pneumovax, prevnar
  337. How many serotypes are in pneumovax?
    23
  338. How many serotypes are in prevnar?
    7-13
  339. which pneumococcal vaccine is poorly immunogenic and is not used in young children?
    pneumovax
  340. is pneumovax effective in high risk adults?
    no
  341. how effective is penumovax against invasive disease in the elderly?
    21%
  342. what kind of vaccine is pneumovax?
    polysaccharide vaccine.
  343. what kind of vaccine is prevnar?
    polysaccharide conjugate vaccine
  344. when was pneumovax made?
    1977
  345. when was prevnar made?
    2000
  346. is prevnar protective against invasive disease in children?
    yes
  347. which pneumococcal vaccine is not protective against otitis media?
    prevnar
  348. which pneumococcal vaccine is expensive and was developed based on the epidemiology in the US and Europe?
    prevnar
  349. What is the major example bacteria from the group B streptococcus?
    streptococcus agalactiae
  350. Where is group B streptococcus found on the body?
    Normal flora in intestinal and genital tract of healthy people and in the vagina of 2-40% of pregnant women.
  351. What can group b streptococcus cause?
    urinary, ear and wound infections in adults and neonatal sepsis in infants w. a high mortality rate (55%)
  352. What are the virulence factors of group B streptococcus?
    Capsule, beta-hemolysin, C5a peptidase, adhesins
  353. How can group B streptococcus be diagnosed?
    secretes CAMP factor- beta hemolysis in the presence of S. aureus
  354. What is the treatment of group B streptococcus?
    penicllin
  355. is there a vaccine for group b streptocccus?
    no
  356. What kind of strep is enterococcus?
    group D
  357. What are the three examples of how enterococci are able to survive harsh environmental conditions
    tolerate a wide range of temperatures (-10C to 45C), tolerate hypotoniic, hypertonic acidic or alkaline environments, tolerate sodium azide and concentrated bile salts (which inhibt or kill most other bacteria)
  358. Is enterococci resistant to many antibiotics?
    yes
  359. what is the intrinsic resistance of enterococci based on?
    chromosomal genes
  360. how can enteroccci acquire antibiotic resistance?
    through the exchange of resistance-encoding genes carried on transposons and plasmids
  361. Which antibiotics show inhibitory activity against enterococci?
    penicillin, ampicillin, piperacillin a vancomyocin
  362. How do you diagnose enterococci?
    identify the substance by the culture
  363. how can you treat enterococci?
    usually ampicillin or vancomyocin, sometimes combined with gentamicin
  364. what are promising new treatments for enterococci?
    linezolid, daptomycin and tigecycline
  365. is there a vaccine available for enterococci?
    no
  366. How many species of viridans streptococcus is identified?
    19
  367. what are the 4 characteristics that viridans strep. have that differs it from S. pneumoniae?
    optochin-resistant, bile-resistant, cannot have ferment inulin, has no capsule
  368. what makes up 70% of viridans Streptococcus?
    bacterial endocarditis
  369. what treats viridans s.?
    penicillin
  370. is there a vaccine for virdans S.?
    no
  371. which normal flora does virdans S. dominate?
    normal flora of the mouth and pharynx
  372. what does viridans S. do to hard tooth surfaces?
    predominately colonize them
  373. what are viridans s.' three virulence factors?
    galactosyl transferases, sugar metabolism genes and adhesins
  374. what forms complex oral bacterial communities? (or biofilms)
    viridan S.
  375. What forms plaque and cavities through fermentation of carbs with acid producation?
    viridans s.
  376. What is needed for strep. endocarditis to be formed?
    transient bacteremia from skin or mucosa needed
  377. what kind of formation does strep. endoccarditis must have?
    propagation-vegatation (low blood supply)
  378. what are the sytemic effects of strep.endocarditis?
    vegetation is the source of persistant bacteremia, chronic infection leads to immuine response and immune complex related disease, risk of embolic phenomenon to ther organs (brain, spleen, liver, kidney ,skin, lungs (right sided lesions)
  379. what are the symptoms of strept. endocarditis?
    fever of unkown origin, possibly heart murmur, and embolism
  380. Is Clostridium a genus, family or species?
    genus
  381. What are the four species we are looking at in the Clostridium genus?
    • Clostridium perfringens
    • Clostridium difficile
    • Clostridium tetani
    • Clostridium botulinum
  382. Is Clostridium gram positive or gram negative?
    gram positive
  383. is Clostridium cocci , bacilli or spirillium?
    bacilli
  384. Does the Clostridium genus contain spore formers?
    yes
  385. Most of the Clostridium genus are obligate __________.
    anaerobes
  386. Are most Clostridium species motile?
    yes
  387. What growth condition is needed for anaerobic growth of Clostridium?
    thioglycollate broth
  388. What growth condition is needed for "stromy fermementation" growth of Clostridium?
    Litmus Milk (b/c a lot of gas is produced)
  389. What growth condition is needed for double zone hemolysis of Clostridium?
    Blood Agar
  390. What growth condition is needed for β-lecithinase of Clostridium?
    Egg Yolk Agar
  391. what happens to β-lecithinase on egg yolk agar?
    it degrades lecithinase and produces a white opaque zone (α-toxin)
  392. Is Clostridium invasive?
    no, its non-invasive
  393. If Clostridium is non-invasive, how does it perform pathogenesis?
    Produces enzyme and toxins that aid in pathogenesis
  394. Are Clostridium infections communicable?
    no
  395. in the Clostridium infections, can spores contaminate or be ingested?
    both
  396. What are the four kinds of Pathogenic Clostridia?
    • Histotoxic Clostridia
    • Enterotoxigenic Clostridia
    • Clostridium tetani
    • Clostridium botulinum
  397. Which clostridia is c. perfringens in?
    • Hisotoxic Clostridia
    • Enterotoxigenic Clostridia
  398. Which clostridia is c. difficile in.?
    Enterotoxigenic Clostridia
  399. What is histotoxic clostridia?
    gas gangrene
  400. What is the causative agent of histotoxic clostridia?
    C. Perfringes type A
  401. When is C. perfrienges most likely to cause an infection?
    When the opportunity presents itself (non-invasive)
  402. What are the four environmental factors that assiste in the growth of C. perfringens?
    • traumatized tissue
    • vascular damage
    • necrotic tissue
    • decreased oxygen
  403. C. perfringens produces a large number of exotoxins and extracellular enzymes that do what?
    break down muscle and connective tissue
  404. What are the main five enzymes produced by C. perfringens?
    • collagenase
    • proteinase
    • deoxyribonuclease
    • Alpha-toxin-(phospholipase C) –
    • Beta-toxin- hemolysin
  405. What is the most important enzyme that C perfringes produces?
    Alpha-toxin
  406. Why is the alpha-toxin the most important enzyme that C perfringes produces?
    lecithinase disrupts cell membrane of hosts rbc, leukocytes and muscle cells
  407. What is the beta-toxin that C. perfringes produces?
    hemolysin
  408. what are the two Clostridial wound infections that C. perfringens causes?
    • Anaerobic myonecrosis (gas gangrene)
    • anaerobic cellulitis
  409. What is Anaerobic myonecrosis?
    Ever widening expansion of necrotic lesion to adjacent healthy muscle tissues.
  410. What are the five symptoms of anaerobic myonecrosis?
    • local edema (swelling)
    • gas production - H2 and CO2 (bubbles in skin) (fermentation of necrotic tissue)
    • change of skin color to black (b/c of poor vascular supply)
    • generalized fever
    • pain in infected tissue
  411. Who is at risk for anaerobic myonecrosis?
    • traumatic injuries
    • surgical procedures in close proximity to intestinal microflora - bowel surgery, abortions
    • elderly
  412. What is the immunity of anaerobic myonecrosis?
    • NO host defense
    • Phagocytic cells useless
    • Repeated infections do not produce immunity
  413. What is the treatment for anaerobic myonecrosis?
    • removal of dead tissue (debridement)
    • application of antiserum (polyvalent antitoxin)
    • broad spectrum antibiotic - penicillin or tetracycline
    • being put in a hyperbaric O2 chamber (increase amount of Oxygen present at the site to decrease the growth of the organism)
  414. What is anaerobic cellulitis?
    Localized infection of necrotic muscle tissue only
  415. What are the symptoms of anaerobic cellulitis?
    • similar to anaerobic myonecrosis but of a lesser severity
    • local edema (swelling)
    • gas production - H2 and CO2 (bubbles in skin) (fermentation of necrotic tissue)
    • change of skin color to black (b/c of poor vascular supply)
    • generalized fever
    • pain in infected tissue
  416. What is Enterotoxigenic Clostridia w/ C. perfringens ?
    Food Poisoning
  417. What is the 2nd most common form of food poisioning?
    entertoxigenic clostridia
  418. What is the causative agent of enterotoxigenic clostridia(FP)?
    C. perfringens type A
  419. enterotoxigenic clostridia(FP) has high associations with what foods?
    beef and stews
  420. When dealing with enterotoxigenic clostridia(FP), where are the spores originally?
    in the food
  421. What is the temperature to kill spores?
    121 C
  422. What is the temp. to kill bacteria?
    100 C
  423. What is the temp to kill toxins?
    80 C
  424. What is the spore's path in food poisioning? (mode of infection)
    • Spores develop in room temp. germination,
    • cells are ingested,
    • enterotoxin produced in small intestine,
    • enterotoxin breaks down intestinal mucosa
    • plasma membrane leakage
    • enterotoxin disrupts osmotic equilibrium (diareahea)
  425. Why do we get diarrhaea in food poisioning?
    osmosis not in equilibrium (electrolyte imbalance)
  426. What are the symptoms of enterotoxigenic clostridia(FP)?
    • watery diarrhea
    • abdominal cramps
  427. What is the immunity of enterotoxigenic clostridia(FP)?
    No natural immunity, can have repeat attacks
  428. How can you control and prevent food posioning (What are the ways and what do they do specifically?)?
    • cook food thoroughly initially - destroys spores
    • food refrigeration after preparation - prevents enterotoxin production
    • reheating food - destroys toxin
  429. What is Enterotoxigenic Clostridia w/ C. difficile?
    antibiotic-associated colitis
  430. What is the causative agent for antibiotic-associated colitis?
    C. difficile
  431. How does antibiotic-associated colitis come about?
    disrupts normal flora of intestine allowing a superinfection or secondary infection with C. difficile
  432. What is the mode of infection for pseudomembranous colitis (antibiotic-associated colitis)?
    • 1.Antibiotic therapy
    • 2.Colonization of intestine by C. difficile
    • 3.Toxins produced - injure intestinal lining by inhibiting protein synthesis; produces hemorrhagic necrosis
    • 4.Leukocyte infiltration into colon due to toxin production
    • 5.Pseudomembrane - (white patch on colon) - mixture of fibrin, mucus, leukocytes and necrotic epithelial cells
  433. What are the symptoms antibiotic-associated colitis?
    abdominal pain, watery diarrhea, nausea
  434. Who are at risk for antibiotic-associated colitis?
    • patients receiving antibiotic therapy - primarily a disease of antibiotic induced colitis
    • hospitalized patients
  435. What is the treatment for antibiotic-associated colitis?
    • discontinue antibiotics
    • maintain fluid/electrolyte balance
    • administer vancomycin (inhibitis c.difficile Growth)
  436. What are the two types of tetanus under Clostridium tetani?
    • generalized tetanus
    • neonatal tetanus
  437. is Clostridium tetani invasive or non-invasive?
    non-invasive
  438. What is generalized tetanus?
    initial involvement of neck and jaw muscles with progression to large muscle groups
  439. What is neonatal tetanus?
    initial infection of umbilical stump; can progress to generalized tetanus
  440. What are the condition for infection for Clostridium tetani?
    • 1.small puncture wounds mode of entry
    • 2.necrotic tissue at wound site
    • 3.decreased oxygen
  441. What is the important toxin produced by Clostridium tetani?
    A nuerotoxin called tetanospasmin (spasmogenic toxin)
  442. Why is tetanospasmin (spasmogenic toxin) in Clostridium tetani the primary toxin of importance?
    Accounts for classic symptoms (completes with glycine)
  443. Where is the site of action for tetanospasmin (spasmogenic toxin)?
    target neurons in the spinal column
  444. What is the function of tetanospasmin (spasmogenic toxin) w/ the neural tissue?
    • Toxin binds to gangliosides in neural tissue
    • blocks release of neuroinhibitor glycine
    • leading to continual contraction of muscles (tetany)
  445. What is the function of the neural tissue when working properly?
    • Neural Tissue + neuroinhibitor glycine
    • prevents muscle contraction
  446. What is tetany?
    continual contraction of muscles
  447. What are the inital symptoms of tetanus?
    Cramping and twitching of muscle around wound
  448. What does it mean that tetanus is a polymicrobic infection?
    (needs a buddy) needs an anearobic environment, grows w. facultatvive anaerobe, use up oxygen and make clostridia Tetani grow.
  449. What are the later symptoms of tetanus?
    • sweating
    • pain around wound area
    • lockjaw or trismus - clenching of the jaw, muscle stiffness neck and jaw muscles
    • risus sardonicus - sarcastic grin
    • opithotonos – arching of the back
  450. What are the extreme symptoms of tetanus?
    • Progression to other muscle groups
    • Violent spasms trunk and back leading to bone fractures
  451. Who is at risk for getting tetanus?
    • elderly
    • intravenous drug abusers
    • infants - neonatal tetanus (tetanus neonatorum)
  452. How can you die from tetanus?
    paralysis of respiratory muscles
  453. What is the immunity of tetanus?
    • No innate immunity
    • Repeated infections do not produce immunity
    • small amount of toxin in the circulation
    • toxins strong affinity for neural tissue
  454. What is the convalescence of tetanus?
    no permanent damage to muscles
  455. What is convalescence?
    Recovery
  456. How do you treat teatnus?
    • debridement of necrotic tissue
    • anti-toxin
    • unimmunized - human tetanus immune globulin (TIGH) - passive immunization
    • immunized - received DPT series, may require a booster shot of tetanus toxoid
    • Antibiotics - metronidazole or penicillin
    • Anti-spasmatic drugs or muscle relaxants - phenobarbital or chlorpromazine
  457. How can teatnus be controlled/prevented?
    Active immunization – Diphtheria-Pertussis-Tetanus (DPT) series (tetanus toxoid)
  458. Teatnus is the Most easily preventable disease because…
    Active immunization – Diphtheria-Pertussis-Tetanus (DPT) series (tetanus toxoid)
  459. What is Clostridium botulinum?
    botulism - food posioning
  460. In Clostridium botulinum, Neurotoxins A, B,E and F are attributable to what kind of disease?
    Human disease
  461. What is another name for Neurotoxin A in Clostridium botulinum?
    Neurotoxin - hemagglutinin
  462. What is the Function of hemagglutinin?
    prevents deactivation of neurotoxin by gastric enzymes and loweres pH of stomach
  463. What are the three types of botulism?
    • Food-borne botulism
    • Infant botulism
    • Wound botulism
  464. The neurotoxin botulium (or botulin) is congujated with what?
    a hemoglutmin
  465. Why is botulin and hemoglutmin congujated?
    Because it protects botulin from being deactivated by the low pH and enzymes of stomach
  466. What is food-borne botulism?
    food poisoning or food intoxication
  467. What are the modes of infection for food-borne botulism?
    ingestion and Gastrointestinal tract toxin absorption
  468. what is the mode of infection of "ingestion" for food borne botulism (7)
    • Ingestion of poorly preserved food containing Botulin (Botulinum toxin)
    • Spores not killed
    • Improper(home canned) food preservation created ideal environment for spores to germinate.
    • anaerobic environment
    • storage - room temperature
    • alkaline foods (beans), low associated with tomato (acid based)
    • Botulin (Botulinum toxin) product of metabolism
  469. what is the mode of infection of "Gastrointestinal tract toxin absorption"
    • Gastrointestinal tract toxin absorption
    • lymphatics and circulation
    • neuromuscular junction of skeletal muscle (site of toxin action)
  470. what is the action of the toxin in the Gastrointestinal tract toxin absorption of food borne botulism?
    • Toxin binds to receptor sites at neuromuscular junction
    • blocks release acetyl-choline (transmitter)
    • prevents muscle contraction (flaccid paralysis)
  471. ACH tells the muscles to ______.
    retract
  472. What are the early symptoms of food borne boutlism?
    gastrointestinal disturbance
  473. What are the neuromuscular symptoms of food borne botulism?
    • first affect the muscles of the head
    • blurred or double vision (diplopia)
    • slurred speech (dipphonia)
    • difficulty swallowing (dysphagia)
  474. What are the critical symptoms of food borne botulism?
    descending paralysis with involvement of respiratory system
  475. What is the convalescence/immunity of food borne botulism?
    • Repeated infections do not produce immunity;
    • small amount toxin in the circulation
    • toxins strong affinity for neural tissue
  476. Why is there no immunity againt food borne botulism?
    Strong binding neurotransmitter
  477. What is the treatment for food-borne botulism?
    • Polyvalent antitoxin therapy
    • Stomach lavage and enemas
  478. How can food borne botulism be controlled/preventer?
    • Adequate food preservation - kill spores
    • Heat all canned food - toxin inactivated at 80oC for 20 minutes
  479. Why does Alaska have the most case of botulisms?
    Because they eat fermented fish products and dont reheat them
  480. What is infant botulism?
    (flaccid paralysis or "floppy head baby syndrome")
  481. How does infant botulism occur?
    • Ingestion of spores - dietary supplement honey
    • Multiplies in colon due to the immature state of neonatal intestine and flora
  482. In infant botulism, how can the baby get sick but not the mother?
    Different state of bacterial colonization within the intestinal tract
  483. Kids who ingest honey that are 2 weeks-6 months have a high associaton with what?
    SIDS
  484. Kids less than _________ should not have honey
    1 year
  485. what are the symptoms of infant botulism?
    Suck and gag reflexes decrease, drooling, head control lost
  486. What is the treatment of infant boutlism?
    antibbiotic therapy
  487. how can infant botulism be controlled/prevented?
    Vaccinate pregnant females
  488. What kind of disease is wound botulism?
    rare neuroparalytic disease
  489. How does a wound botulism occur?
    • spores enter a puncture wound
    • in vitro toxin produced
  490. What are the symptoms of wound botulism?
    similar to food-borne botulism
  491. Who is at risk for wound botulism?
    intravenous drug abusers
  492. `What kind of bacteria is Listeria monocytogenes?
    Gram positive rods (bacilli)
  493. Listeria monocytogenes is more frequently seen in what kind of patients?
    immunocompromised patients
  494. Who can typically get Listeria monocytogenes?
    neonates, the elderly, and the immunocompromised
  495. Listeria monocytogenes frequently causes an infection in...
    the central nervous system
  496. What kind of motility does Listeria monocytogenes have?
    Tumbling
  497. Why does Listeria monocytogenes have tumbling motility?
    because of flagella
  498. How can Listeria monocytogenes be mistaken for a gram negative rod?
    over-decolorization
  499. Which bacteria requires through pasteurization?
    Listeria monocytogenes
  500. Listeria monocytogenes can multiply at the low temperature of _____.
    4C
  501. What bacteria can survive frozen?
    Listeria monocytogenes
  502. Why are pregnant people at risk for Listeria monocytogenes?
    Because they can have the infection or they can pass it on to the neonate
  503. What infection is zoonotic(comes from animals and needs pasteurization)?
    Listeria monocytogenes
  504. Listeria monocytogenes is associated with what food products?
    milk and milk products, particularly soft cheese
  505. How many cases of Listeria monocytogenes are there per year?
    2000 cases
  506. How many deaths occur from Listeria monocytogenes per year?
    400
  507. Who are those that are at risk of injury and death from Listeria monocytogenes?
    • infants younger than 1 month
    • adults older that 60 years old
    • pregnant women
    • those with altered cell mediated immunity.
  508. how does Listeria monocytogenes replicate?
    intracellularly (inside the cells)
  509. What must be ingested to get Listeria monocytogenes? (cells, spores, etc.?)
    the organisms
  510. How does Listeria monocytogenes perform pathogenisis?
    • Attaches to intestinal epithelial cell and macrophages
    • Once in phagolysosome secretes a hemolysin (listeriolysin) which allows escape from the phagosome and replication in the cytoplasm
    • Alteration of cell shape and actin extruded processes allow for cell to cell spread
  511. Where in the body does Listeria monocytogenes prefer to spread to in the body?
    placenta and CNS
  512. Who has a lowered immunity towards Listeria monocytogenes?
    • Those who are Pregnant and neonate
    • Lymphoma, transplant patients on immunosuppressive, AIDS patients, patients on steroids, other cell mediated immune defects
    • Patients receiving TNF blocking agents
    • Elderly
  513. What are the major clinical syndromes of Listeria monocytogenes?
    • Meningitis Encephalitis (brain)
    • Bacteremia (bloodstream)
    • Placenta and Fetus (uterus)
  514. What is the treatment for Listeria monocytogenes?
    • Ampicillin
    • Trimethorim-sulfamethoxasole
  515. Diptheria is the greek word for?
    leather
  516. what kind of bacteria is Corynebcterium diptheriae (C. diptheriae)?
    Gram positive bacillus
  517. What is C. diptheriae known to look like under the microscope?
    "chinese letters"
  518. What kind of agar is used to improve the identification and recovery of C. diptheriae?
    Tellurite agar
  519. C. diptheriae "Disease-producing" strains carry a ..
    b-phage encoding a gene for toxin production (tox+)
  520. What are the only reservoir for C. diptheriae?
    Humans
  521. How does C. diptheriae spread?
    By droplet or airborne
  522. is C. diptheriae non-invasive or invasive?
    Non-invasive
  523. What are the two segments of the C. diptheriae exotoxins and what are their function?
    • B = binds to specifice receptors on susceptible cells
    • A= the active segment
  524. How does C. diptheriae stop protein synthesis?
    Toxin ADP-ribosylates Elongation Factor-2 (EF2)which is responsible for tRNA translocase acivity (causing the protein synthesis to stop)
  525. ADP-ribosylation is seen in c. diptheriae, but is also seen with..
    cholera and pertussis toxin
  526. What does the exotoxin of C. diptheriae target in the body and what is the name of the associated infection (toxin-mediated disease)?
    • Targets heart (myocarditis)
    • nerves (demyelination)
    • kidneys (tubular necrosis).
  527. Pharyngeal infection causes what in C. diptheriae?
    causes local necrosis and formation of a “pseudomembrane” which can extend down the respiratory tract and lead to suffocation from aspiration of the cast.
  528. What is Bull Neck
    A symptom of C. diptheriae that is associated with massive lymphadenopathy
  529. Is there a natural immunity for C. diptheriae?
    no
  530. Is there a vaccine for C. diptheriae?
    yes
  531. What is the toxoid vaccine used for C. diptheriae?
    Formalin-inactivated toxin used as vaccine
  532. What is the treatment for C. diptheriae?
    • Pencillin and erythromycin should be active
    • May need antitoxin in severe disease
  533. Bacillus anthracis = ?
    anthrax
  534. What kind of bacteria is anthrax?
    Gram-positive bacilli
  535. What kind of hemolytic growth does anthrax do on a blood agar plate?
    non-hemolytic growth
  536. Where is the PGA Capsule encoded on in the anthrax?
    pX02 plasmid
  537. What are the three components that pX01 plasmid encodes?
    protective antigen (PA), edema factor (EF), and lethal factor (LF)
  538. What is the edema toxin composed of?
    composed of PA combined with EF
  539. what does the edema toxin produce?
    local skin edema
  540. What is the lethal toxin composed of?
    PA and LF (highly lethal for experimental animals)
  541. The combination of pX01 plasmid, edema toxin, lethal toxin was the most lethal and produced many characteristics of what kind of infection?
    anthrax infection
  542. What is PA?
    An Antigen that produces protective antibody
  543. What is cleaved by cellular protesases to form a heptamer?
    PA
  544. What is EF?
    a calmodulin-dependent, adenylate cyclase that increases intracellular cyclic AMP concentrations and interferes with cell function
  545. what is LF?
    LF is a zinc metalloprotease that cleaves and inactivates multiple mitogen-activated protein kinases (MAP Kinase) and interferes with signal transduction
  546. Where are anthrax toxins taken to mediate cellular damage?
    cytosol
  547. What form of anthrax has no purulence, is painless and develops classic black eschar?
    cutaneous anthrax
  548. What is woolsorter's disease?
    inhalational anthrax
  549. which form of anthrax contains Pleural fluid and widened mediastinum w/ Enlarging and hemorrhagic medistinal node?
    inhalational anthrax
  550. How do you treat anthrax?
    • Ciprofloxacin
    • Penicillin
    • Tetracycline

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