CLINICAL SCIENCE EXAM 1

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CLINICAL SCIENCE EXAM 1
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2013-02-11 15:17:44
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EXAM 1
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  1. Phase Microscopy
    •  Light waves pass thru cell, emerge in different phases
    •  Allows visualization of internal structures
  2. Eukaryotic cell structures includes?
    •  The Nucleus
    •  Cytoplasmic Structures
    •  Plasma membrane
    •  Motility Organelles
  3. the nucleus membrane of a eukarotic cell has what type of permeability?
    selective permeability
  4. eukaryotic cytoplasmic structure include ?
    •  Endoplasmic Reticulum (ER)
    •  Mitochondria
    •  Cytoskeleton
    •  Plasma membrane
    •  Motility Organelles
  5. what is the cell envelope in a prokaryotic cell?
    it is the layers that surround the cell. there are gram negative cell membranes and gram positive cell membranes
  6. Gram-positive cell envelopes include what structures?
    • Cytoplasmic membrane
    • Thick peptidoglycan layer (cell wall)
    • Some have outer capsule
  7. Gram-negative cell envelopes include what structures?
    • Cytoplasmic membrane
    • single sheet peptidoglycan
    • Complex outer membrane layer
    • May have outer capsule
    • Endotoxins (lipopolysaccharide)
  8. the cell wall in a prokaryotic cell function is to do what?
    • - provide osmotic protection
    • - is essential in division
  9. peptidoglycan layer function?
    • Complex polymer provides strength & shape
    • 50% of cell walls in Gram +
    • 5-10% of cell walls in Gram -
  10. what structures are found in gram positive cell walls?
    • - peptidoglycan layer
    • - polysaccarides 
    • - teichoic acids
  11. what structures are found in gram-negative cell walls?
    • - peptidoglycan layer
    • - lipoproteins
    • - an outer membrane
    • - liposaccharides (LPS)
    • - periplasmic space
  12. teichoic acid function?
    • - water soluble polymer 
    • - major surface antigen 
  13. lipoprotein function
    Most abundant protein in Gram -Stabilizes/anchors outer membrane to polysaccharides
  14. gram-negatives cell wall outer membrane purpose it to do what?
    - protect the cell from bile salts
  15. gram-negatives cell wall outer membrane has a special channel called what? what does it do?
    called porins and it allows hydrophillic compounds to pass
  16. lipopolysaccharide
    • - is an endotoxin of gram - bacteria 
    • - a major surface antigen of bacteria cell
    • - stabilizes outer membrane
    • - acts as a barrier to hydrophobic molecules 
  17. Periplasmic Space
    • - is between the inner and outer membrane
    • - makes up 20-40% of cell volume
    • - contains enzymes 
  18. capsule (polysaccharide)
    protects the cell from phagocytosis 
  19. biofilm?
  20. flagella structure and function
    • - thread-like appendages of protein (H antigen)
    • - they are organs of motility
  21. Pili structure and function
    • - it is a rigid surface of protein 
    • - its function is 
    • >> adherence to host 
    • >> attachment of donor and recipient cells in bacteria conjugation (pass DNA)
  22. endospores
    • - are resting cells but with the right conditions they swell up and start to reproduce. 
    • - can be air born to some extent
    • - highly resistant to desiccation, heat, chemical agents
    • - germination to single cell when returned to favorable nutritional conditions 
  23. spores from c. difficile can be passed from patient to patient which can cause what to happen?
    cause outbreaks in hospital patients who were not on a broad spectrum antibiotic
  24. why should we never feed babies under the age of 1 honey from the jar?
    • - it may contain botulism spores b/c pasteurization does not kill them off
    • - it can cause floppy baby syndrome
  25. most cases of botulism comes from what?
    most cases come from home caning foods that are not acidic
  26. why is leather and wool subjected to radiation?
    leather and wool commonly contain spore forming antrax
  27. look at ppt 1 slide 43
  28. what medication greatly increases the risk of C. difficile in hospital patients and pneumonia 
    PPIs
  29. what does desiccation mean?
    drying
  30. Gram Stain
    • - plays a important role in taxonomic characteristics of bacteria
    • - basis of different reaction is cell wall structure 
  31. Gram Stain procedure 
    • - application of basic dye, crystal vioelt
    • - iodine solution applied (makes it stick to bacteria); all bacteria now stained blue
    • - cell wall is treated with alcohol
  32. What occurs after cell walls are treated with alcohol?
    • Gram + cells retain crystal violet-iodine, remain blue
    • Gram - cells are completely decolorized
    • Red dye Safranin applied so Gm - cells take contrasting color
  33. why do we have to worry about the outer membrane on gram-negative organisms.
    • - b/c of it's resistance to bile
    • - also the antibiotic can penetrate the membrane wee and if it does, the outer membrane can cause a type of toxic shock
  34. name the factors that affect the growth of an organism 
    • - nutrients
    • - hydrogen ion concentration (pH)
    • - temperature
    • - aeration of atmosphere 
  35. what are the nutrients needed in the growth of an organism?
    • Carbon Source
    • Nitrogen Source
    • Sulfur Source
    • Phosphorus Source
    • Mineral sources (Mg, Fe, Ca)
    • Growth Factors (Need these, but cannot make themselves
  36. growing organisms prefer what type of pH environment?
    • - most prefer a neutral environment 
    • - few prefer low pH 
    • - fungi prefers low pH
  37. at what temperature do most organism grow at?
    37 (98 F)
  38. where in the body would you expect it to be more on the acidic side?
    • - stomach
    • - skin 
    • - vagina
  39. you run the risk of what id your stop producing acid in your stomach?
    you run the risk of getting a pathogenic bacteria and also an increased risk of c. difficile
  40. what product do most Americans used that can alter the pH balance of the skin?
    deodorant 
  41. types of media
    • Transport Media (Culturettes)
    • Basal Media 
    • Enriched Media
    • Selective Media
    • Differential Media
  42. Basal Media
    Supplies minimal (base) growth requirements
  43. Enriched Media
    Basal & additives to enhance growth. Promotes growth of most organisms. E.g.. Blood agar & Chocolate agar
  44. Selective Media
    • Allows certain bacteria to grow, inhibits others
    • Thayer Martin media: “chocolate” w/ antibiotics
  45. Differential Media
    Additives allow differentiation between organisms
  46. we are now seeing MRSA in women with bladder infections. it is treatable but what can happen if given the wrong drugs?
    it can shut down the kidneys or go into the systemic system
  47. choice of media is based off what?
    • Based on body site
    • Based on pathogens to be isolated
  48. psychrophile 
    organisms that thrive in colder temperatures 
  49. mesophile 
    organisms that thrive in warm temperatures
  50. thermophile 
    organisms that thrive in hotter temperatures 
  51. Microaerophilic bacteria 
    does not grow at normal atmospheric concentrations of oxygen but requires a small amount of it (1–15%) in metabolism. Most organisms in this category live in a habitat such as soil, water, or the human body that provides small amounts of oxygen but is not directly exposed to the atmosphere
  52. Facultative bacteria
    may or may not use oxygen
  53. types of atmosphere of incubation
    • - aerobic (most)
    • - enhanced CO2, 5-10% (haemophilus) 
    • - anaerobic 85% N2 (clostridium)
    • - Microaerophilic (campylobacter)
    • - facultative anaerobic
  54. describe a concept in virology
    a virus that has a very high vertality rate is going to dies out because its not going to be successful b/c if it kills fast it won't go anywhere else - a good example of this is 

    - but influenza is a very sucsessful virus b/c it doesnt really kill more than 10 percent of the people who contract it
  55. Sterilization
    Irreversible destruction of all organisms, including spores
  56. Decontamination
    Destruction or lowering number of microorganisms, not necessarily spores
  57. Disinfection
    Inanimate objects, but too toxic for tissues
  58. Antisepsis
    Decontamination on patient or self
  59. Bactericidal
    • Irreversibly kills bacteria
    • - the trouble is that we don't have bactericidal antibiotics for every single pathogen
  60. Bacteriostatic
    Inhibits bacteria growth, can resume if conditions are right

    ---we give you the drugs, we weaken the bacteria, and if you have a healthy immune system your immune system will kill the bacteria off
  61. Types of Physical Agents
    • Heat
    • Filtration (e.g.. Filtered water in beverages)
    • Radiation (UV, gamma): Damages DNA of bacteria
  62. physical agents: heat
    • Boiling
    • Autoclaving (Saturated steam under pressure): Most common method in hospitals
    • Pasteurization
  63. Boiling
    does not sterilize - does not kill spores
  64. Autoclaving
    can kill just about anything
  65. Pasteurization
    get rid of most pathogenic bacteria in milk - does not sterilize
  66. why irradiate meat ?
    • - ecoli
    • - salmonella
    • - bacteria
  67. Types of Chemical Agents
    • ETO (Ethylene Oxide Gas)
    • Formaldehyde Gas
    • Alcohol
    • Phenol
    • Oxidizing Agent
    • Detergents
  68. ETO (Ethylene Oxide Gas)
    Low temperatures, second most common method in hospitals
  69. Formaldehyde Gas
    Toxic, seldom used
  70. Alcohol
    Denatures protein. Used as a disinfective and antiseptic (does not sterilize)
  71. Phenol
    Inactivates enzymes systems, precipitates proteins, disrupts cell wall/membrane
  72. Oxidizing Agent
    Oxidize free sulfhydryl groups: bleach, iodine
  73. Detergents
    Disrupts cell membrane: soap, bile salt
  74. our own bile does not affect gram negative organisms. why? 
    - b/c of its tough outer membrane which makes it resistant to bile
  75. focal infection 
    just in one partex: just in the heart- or just in one lung
  76. mixed infection 
    more than one organism is contributing 
  77. primary and secondary infection 
    - primary would be the onset of a an illness 

    - secondary infection is cause by the treatment of the primary infection 
  78. nosocomial infections
    infections the patient gets when they come under long term institution care
  79. endemic occurrence 
    disease that is prevalent in the country or the world
  80. epidemic occurrence 
    spreading across to different regions
  81. sporadic occerrence 
    you have little hot spots of certain outbreaks
  82. pandemic occurrence 
    occurs all over the world 
  83. two things have to happen in order to contract an infection or disease
    • - you have to have enough viral particles or bacterial organism
    • - it depends on your immunal competence
  84. Direct ways of transmission
    • - contact (kissing, sex [gonorrhea])
    • - droplets (colds, chickenpox)
    • - vertical (HIV, syphilis)
    • - biological vector (west Nile virus, malaria)
  85. indirect ways of transmission
    • - fomite (staphylococcus aureus)
    • - ingestion (food, water, biological products (salmonella, E.coli ))
    • - inhalation (air (terberculosis, influenza virus))
  86. koch's postulates
    • - organisms found in all cases of the disease
    • - organism should be cultured 
    • - organism should cause same distress if introduced into another host (mouse)
    • - organism can be cultured from the new host
  87. PANDAS
    post streptococcal syndrome that causes or exacerbates OCD = koch's postulates cannot be applied to PANDAS
  88. pathogen
    organism capable of causing disease
  89. non-pathogen
    organism that does not cause
  90. opportunist
    organism only causes disease when host defenses are impaired
  91. direct contact e.g.?
    anthrax, staph aureus on hands of health care workers
  92. sexual contact e.g.?
    syphilis, gonorrhea 
  93. vector borne contact
    • - caused by insects, rodents, etc. 
    • - can cause malaria (tick); rocky mountain spotted fever (tick)
  94. zoonosis
    contact with animals/animal products, e.g... hantavirus, brucella, helicobacter pylori
  95. vertical transmission 
    infection from mother to child or father to child 
  96. endogenous transmission 
    • normal flora an advantage over other flora
    • - clotridium difficile 
    • - viridans streptococci following tooth surgery 
  97. Virulence Factor 
    things bacteria do to cause infection 
  98. virulence factors of pathogens
    • - adherence to host cell
    • - invasion of host cell and tissue 
    • - toxin production 
    • - enzymes 
    • - antiphagocytosis 
    • - intracellular pathogenicity 
  99. ways pathogens adhere to cells 
    • - pili
    • - fimbriae 
  100. ways pathogens invade a host cell and tissue
    • - some induce host to engulf them
    • - some enter via junctions in host cells
  101. toxins pathogens produce 
    • - exotoxins
    • - endotoxins
  102. endotoxin
    • - primarily in gram - pathogens 
    • - attach to cell wall, release if cell is lysed. 
    • - cannot be made into a vaccine
    • - causes (fever, leukopina, hypotension, disseminated intravascular coagulation (DIC)
  103. exotoxin target organs
    • - heart
    • - muscles
    • - blood cells
    • - intestinal tract show dysfunction 
  104. endotoxin general physiological effects
    • - fever
    • - malaise
    • - aches
    • - shock
  105. pathogen enzymes
    • - are tissue degrading enzymes (...ases)that enable organism to spread
    • - IgA proteases breaks down IgA antibody (important antibody on mucosal surfaces, first line of defense)
  106. antiphagocytic factors
    some bacteria evade phagocytosis by WBCs 
  107. intracellular pathogenicity 
    some bacteria capable of livinf inside cells (hide from immune system) e.g. TB and legionella
  108. host defenses consists of what two categories 
    • - natural immunity 
    • - acquired immunity 
  109. natural immunity physiologic barriers 
    • - skin 
    • - mucous membrane
    • - GI tract
    • - genital/ urinary tract
  110. natural immunity: how does skin act as a host defense
    few bacteria can penetrate. sweat (pH) helps kill some
  111. natural immunity: how does mucous membrane act as a host defense 
    mucous collect, cilia beat or move bacteria up and out, noise hairs, coughing, IgA antibodies
  112. natural immunity: how does the genital/ urinary tract act as a host defense
    acid pH of the vagina, cervical secretions w/ lysozome, urine flushing thru urethra  
  113. natural immunity: how does the GI act as a host defense
    saliva enzymes, pH of stomach (2), normal flora
  114. factors that weaken host defenses and increase susceptibility to infection are what?
    • - old age and extreme youth
    • - genetic defects in immunity and acquired defects in immunity 
    • - surgery and organ transplant
    • - organic disease: cancer, liver malfunction, diabetes
    • - chemotherapy/immunosuppressive drugs
    • - physical and mental stress
    • - other infections
  115. why are older adults and infants more susceptible to infections?
    because they do not have a functioning hypothalamus 
  116. Reticuloendothelial System
    • is a filtering system 
    • - lymph nodes
    • - spleen
    • - liver 
  117. acquired immunity includes what two categories 
    • - passive
    • - active
  118. acquired immunity: passive
    Transmitted by antibody or lymphocytes preformed in another host, e.g.. Hepatitis B, Tetanus at time of contact
  119. acquired immunity: active 
    produce antibody after exposure to antigen, e.g.. Vaccines, having measles as child
  120. Humoral immunity
    antibody mediated: On first exposure body develops antibodies, next exposure body rapidly produces higher amounts of antibodies
  121. Cell-Mediated immunity
    Mediated by WBCs. Biggest defense against parasites & intracellular organisms
  122. normal flora
    organism that inhibit the skin and mucous 
  123. resident 
    regularly found at site
  124. transient
    non or potentially pathogenic organisms only temporarily on skin or mucous 
  125. what are the sterile anatomical sites and fluids in the human body
    all internal organs and fluids
  126. sites that harbor a normal flora
    • - skin and its contiguous mucous membranes
    • - upper respiratory tract
    • - gastrointestinal tract (various parts)
    • - outer opening of urethra 
    • - external genitalia
    • - vagina
    • - external ear and canal
    • - external eye (lids, lash follicles)
  127. advantages of normal flora?
    • - in GI tract synthesize vitamin K and aid in absorption of nutrients
    • - NF on skin and mucous hinder colonization by completeing for space and nutrients  suppression creates a void that can be occupied by pathogens
  128. Normal flora disadvantages 
    NF may produce disease such as accessing the blood stream/ tissues after flossing or tooth extraction; IV catherters
  129. normal flora of mouth and upper respiratory tract habitat 
    - sterile at birth but contaminated in birth canal 

    - 4-12 hours later strep is established
  130. normal flora of GI tract habitat
    sterile at birth, organisms induced by food 
  131. normal flora of vagina habitat
    NF changes with maturity; newborn, infant, puberty, menopause 
  132. why do we care about normal flora?
    b/c they outwit and ou tcompete the pathogenic flore
  133. specimen quality
    screen specimen for squamous epithelial cells and neutrophils 
  134. squamous cells found in a specimen is considered what?
    a lousy specimen 
  135. neutrophils found in a specimen in considered what?
    a good specimen 
  136. impact of anti-microbial agent on normal flora
    • excessive antibiotics can cause a shift in flora
    • - instead you want to have a narrow spectrum antibiotic that only works on that organism 
  137. reasons for wound culture?
    • - identify infectious agents and determine appropriate antibiotic therapy
    • - especially important in immunocompromised (AIDS, CA) who lack normal clinical signs of inflammation  infection
    • - document presence of specific organisms e.g.. MRSA that could be transmitted to other patients
    • - document absence of above 
    •  
  138. when to culture wounds?
    • - when amount, consistency, odor of wound drainage changes
    • - when patient is about to be dischared
    • - when newly transferred patient wound is draining 
  139. excessive wound draining 
    pronounced inflammatory response (soft-tissue infection, abscess or osteomyelitis)
  140. exudate on surface of wound contains what?
    skin flora, white cells, proteins
  141. when culturing a wound, we should irrigate it with what?
    irrigate wound with normal saline (NOT antiseptic solution) and absorb excess saline with sterile gauze to remove exudate and topical antiseptics 
  142. you should culture wounds on which part?
    the part that is highly vascular and has granulation tissue 
  143. cultures on pressure wounds 
    • - Organisms vary as lesion heals
    • - best to do with needle aspiration or deep tissue biopsy 
  144. types of wound cultures?
    • - swab culture
    • - aspiration culture
    • - tissue biopsy 
  145. swab culture
    • - if eschar present, need to debride 
    • - avoid touching swab to intact skin at wound edges
    • - send to lab within 1-2 hours max
  146. eschar
    hardened necrotic tissue esp. burns
  147. aspiration culture 
    • - prep with alcohol
    • - use 3ml syringe, 22 gauge needle, take 1 ml fluid 
  148. tissue biopsy
    • in wounds of surgery, or burns 
    • - can damage tissue so its not a good idea
  149. information lab needs when culturing a wound
    • Date, time specimen collected
    • Anatomical site, source
    • Type of specimen
    • Pharmocotherapy
    • Exam requested (e.g.. Gm stain, culture)
    • Diagnosis
  150. staphylococcus epidermidis
    (nosocomial esp. from shunts, catheters), causes endocarditis, UTIs
  151. Staphylococcus saprophyticus 
    (2nd most common cause of UTI in sexually active young women)
  152. Staphylococcus aureus virulence factors
    • - catalase
    • - coagulase
    • - hyaluronidase
    • - exfoliative toxin (produced by S. sureus)
    • - Toxic Shock Toxin
    • - Enterotoxins
    • - Penicillinase
  153. Catalase
    • (produced by all staph)
    • - Enzyme breaks down H2O2 to H2O, O2 (bubbles)
    • - not found in strep or necro
  154. Coagulase
    • (produced by S. Aureus)
    • - causes fibrin to deposit around staph cells, prevents phagocytosis?
  155. Hyaluronidase
    • produced but both staph and strep
    • - digests intercellular “glue” (hyaluronic acid) of connective tissue - “spreading factor”
    • - allows cellulitis to be sucessful. cellulitis
  156. cellulitis
    a small pustule in the skin and then it starts going under and deeper
  157. Exfoliative Toxin
    • (produced by S. Sureus)
    • - Causes desquamation of skin in staph scalded skin syndrome (SSSS)
    • - is an exotoxin 
    • - can also cause impetigo
  158. Toxic Shock Toxin
    • (produced by S. Aureus)
    • - Causes symptoms of toxic shock syndrome
  159. toxic shock syndrome symptoms 
    • symptoms common in young teens
    • - hand/skin starts peeling
    • - high fever
    • - liver involvement
    • - cardio involvement
    • - can be fatal
    • (is cause by staph then it usually refers to using tampons for too long)
  160. Enterotoxins
    • Exotoxins that act on gut (food poisoning)
    • Not destroyed by heat or gut enzymes  

    • (stap organism can die but the toxin does not)
    • Induce nausea, vomiting, and diarrhea
  161. Staph Aureus Food Poisoning
    • Food preparer touches face, then food
    • With time, temp., S. aureus grows, releases toxin (has to have a non acidic pH)
    • Eg. egg salad, cream fillings, lime pie
  162. staph: localized infections 
    • - pimple, folliculitis (most common result)
    • - suppuration (pus formation)
    • - may lead to abescess 
  163. the spreach of staph from its localized site can cause what?
    • - pneumonia 
    • - osteomyelitis 
    • - endocarditis (IV drug users)
  164. staph onset takes how long?
    1--6 hours
  165. Staph food poisoning 
    • due to action of ecterotoxins
    • - S. aureus grows in food, toxin ingested. 1-6 hours later VOMITING , nausea  diarrhea (short incubation food poisoning)
  166. Staph - toxic shock syndrome 
    • Most common in young women using tampons, others with S. aureus wound infections
    • Abrupt fever, hypotension, multiple system failure, desquamation of hands and feet
  167. Coagulase - Negative Staph
    • Infections associated with implants, catheters
    • UTI S. Saprophyticus
  168. Diagnostic Lab Tests for Staph: specimen
    swabs of pus, blood, respiratory secretions, sterile body fluids
  169. Diagnostic Lab Tests for Staph: gram stain
    gram + (blue/purple) cocci in clusters (“grapes”)
  170. Diagnostic Lab Tests for Staph: identification 
    • Catalase test
    • Coagulase test
  171. Coagulase test
    • organism added to rabbit plasma
    • Clot - positive - S. Aureus
    • No clot - negative - S. not Aureus
  172. Catalase test
    • place organism in drop of H2O2
    • Bubbles - positive - staph
    • No bubbles - negative - strep
  173. staph treatment/ prevention 
    • Local antisepsis & abscess drainage
    • Antibiotic therapy of clinically important isolates
    • Vancomycin, cefazolin, nafcillin
    • Prevent by hand washing!
  174. MULTIPLE RESTISTANT STAPH. AUREUS - (MRSA) Risks
    • Multiple antibiotic treatment
    • Broad-spectrum agents
    • Prolonged antibiotic therapy
    • Poor nutrition status
    • 50% of colonized pts develop infection
    • Trauma, burns, aged, immunocompromised
    • Now can be community acquired!
  175. multiple anitbiotic treatments can cause what in a patient with MRSA
    can end up with their normal flora becoming resistant and if it gets rich in B, you've got a problem
  176. MULTIPLE RESTISTANT STAPH. AUREUS - (MRSA) Prevention and Control
    • Prevention and Control
    • Eradication infeasible
    • Hand washing, universal precautions as effective as isolation
    • Treat colonized pts
    • ?Treat colonized carriers??
  177. Community Acquired MRSA UTIs
    • From “empiric” treatment with broad spectrum quinolone - not based on anything
    • Susceptible to “old fashioned” antibiotics for UTIs: Bactrim (sulfa), nitrofurantoin
    • Need to culture urine specimens
  178. Essential Characteristics of STREPTOCOCCI
    • Cocci in chains
    • Gram + (Stain blue or purple)
    • Catalase negative (don’t bubble in H2O2)
  179. STREPTOCOCCI Antigenic Structure
    • Group specific cell wall structure
    • M protein
    • Hemolysis (lysis of RBCs)
    • Group specific Antigen (Lancefield Group)
  180. STREPTOCOCCI - Group specific cell wall structure
    • Carbohydrate
    • Basis of serologic grouping - Lancefield Grouping
  181. STREPTOCOCCI - M protein
    • Major virulence factor of group A strep
    • Helps organism resist phagocytosis
    • May play role in the pathogenesis of rheumatic fever, cross-reactive antigens w/ cardiac tissue
  182. GASP
    Group A Streptococcus pyogenes
  183. M PROTEIN RANDOM FACT
    they think it has a way of working with out own immune system post-strep p. causing antibodies to form which causes the body to get confused they made antibodies to the M proteins but the antigens on the heart, kidneys, and other parts of the body look similar to these antibodies so the antibodies start attacking the normal tissues in the body - also called cross-reactive antigens
  184. Hemolysis (lysis of RBCs) consists of what?
    • - alpha: partial hemolysis (green)
    • - beta: complete hemolysis (clear)
    • - gamma: no hemolysis
  185. STREPTOCOCCI - Group specific Antigen (Lancefield Group)
    • Typing generally done for only groups A-D which cause disease in humans
    • Capsular Polysaccharides (sugars)
    • Biochemical Tests
  186. Streptococcus pyogenes
    • Beta - hemolytic (large zone)
    • Group A antigen
    • Streptokinase
    • Streptococcal deoxyribonuclease
    • Hyaluronidase
    • Erythrogenic toxin
    • Streptolysin O
  187. Streptokinase
    • activates a pathway leading to the digestion of blood clots and may play a role in invasion, dissolving fibrin clots and expediting the invasion of damaged tissues
    • Used to treat pulmonary emboli and coronary thrombosis
  188. Streptococcal deoxyribonuclease (DNA)
    Depolymerizes DNA
  189. Streptococcus pyogenes - Hyaluronidase
    • Breaks down hyaluronic acid, an important component of connective tissue
    • Allows organism to spread
  190. Erythrogenic toxin
    contribute to increased tissue injury by acting as superantigens, produces fever and the bright red rash. An exotoxin produced by lysogenized group A strains of b-hemolytic streptococci that is responsible for the severe fever and rash of scarlet fever in the nonimmune individual.
  191. Streptolysin O
    • Hemolysin that is antigenic
    • Antistreptolysin O can be measured to determine a recent infection or persistent high levels
  192. Streptococcus pyogenes local infection 
    • Streptococcal sore throat (pharyngitis)
    • Streptococcal pyoderma
  193. Streptococcal sore throat (pharyngitis)
    • Purulent exudate, enlarged nodes, high fever
    • Scarlet fever rash can occur if the strep produces erythrogenic toxin & patient has no antitoxin immunity
  194. Streptococcal pyoderma
    • Impetigo: local infection of superficial skin layers, highly communicable
    • Wounded skins/ burns result in widespread infection that may progress to cellulitis
  195. Streptococcus pyogenes systemic infection 
    • Erysipelas
    • Sepsis
    • Endocarditis
  196. Erysipelas
    • most common cause is strep throatbut can also come in the form of a skin infection
    • Portal of entry is skin
    • Massive edema & rapidly advancing margins
  197. why would we worry if the pain is way out of proportion to how the wound looks?
    it could be narcotizing fasciitis
  198. Streptococcus pyogenes - Fulminate infections with streptococcal toxic shock
    • Shock, bacteremia, respiratory failure, & multi-organ failure
    • Death in 30% of patients
  199. streptococcal toxic shock tends to happen to who?
    to people who haven't had the scarlatina os strep throat - scarlet fever 
  200. what can happen if people are not treated for poststreptococcal
    • Acute Glomerulonephritis
    • Rheumatic Fever
  201. Rheumatic Fever
    • Develops 1-4 weeks after untreated strep throat
    • Damages heart muscle & valves
  202. Acute Glomerulonephritis
    Can develop 3 weeks after untreated infection
  203. Streptococcus pyogenes Diagnostic Lab Tests include?
    • - specimens 
    • - gram stains
    • - rapid antigen detection tests
    • - antistreptolysin O titer
  204. Streptococcus pyogenes Streptococcus pyogenes: Specimens
    Depend on type of infection, I.e. throat swab, pus, blood
  205. Streptococcus pyogenes Streptococcus pyogenes: Gram stain
    • Gram + (blue or purple) cocci in chains
    • Do not take swabs from throat
  206. gram stain of the throat is not really productive. why?
    - there are many strept variants so you cant identify one from another
  207. Streptococcus pyogenes Streptococcus pyogenes: Rapid Antigen Detection Tests
    • Throat swab (fast but not 100% reliable)
    • 60 - 90% sensitive; if negative confirm with more reliable, but time consuming tests
  208. Streptococcus pyogenes Streptococcus pyogenes: Antistreptolysin O titer (ASO titer)
    primarily used with some one who has a post strep syndrome like rheumatic fever - it tells us that they've has a recent strep infection
  209. Streptococcus pyogenes Treatment
    • Penicillin (DOC)
    • 1st generation cephalosporin
    • 2nd generation cephalosporin (e.g. cefaclor) less effective
  210. Streptococcus agalacitae
    • Most are beta-hemolytic (small zone)
    • Normal flora of the female genital tract - as many as 40% of women have this organism in their normal flora 
  211. Streptococcus agalacitae - Infections
    • Most common cause of neonatal sepsis & meningitis (few hours after birth to several months after birth)
    • Opportunistic infections; esp. in elderly UTIs
  212. Streptococcus agalacitae Prevention / Therapy
    • Late PG vaginal, rectal swab/culture (35-37 wks)
    • Ampicillin (give IV during labor, PO ineffective!) - tp preven colonization of the infant and to treat an infection 
  213. Can Streptococcus agalacitaebe made into a vaccine?
    no,b/c there are too many strains
  214. Streptococcus pneumoniae
    • Gram + (blue/purple) lancet shaped diplococci
    • Readily undergoes autolysis (bile souble)
    • Alpha-hemolytic colonies
    • Polysaccharide capsule
    • No toxins
    • Normal Flora in many people
  215. Virulence of Streptococcus pneumoniae
    Virulence of the organism is a function of its capsule, prevents / delays phagocytosis
  216. Streptococcus pneumoniae: Predisposing factors to infection
    • Compromised respiratory tract; i.e. other infections, excess mucus (allergies), obstruction, smoking
    • Alcohol / drug intoxication
    • Abnormal circulatory dynamics; i.e. pulmonary congestion, heart failure
    • Malnutrition, general debility, hyposplenism
    • - also people who take PPIs
  217. The onset of pneumococcal pneumonia?
    • is usually sudden w/ fever, chills, & sharp pleural pain
    • Bloody or rust colored sputum
    • Can result in meningitis, endocarditis, septic arthritis
    • Also causes otitis & sinusitis
  218. Streptococcus pneumoniae Diagnostic Lab Tests include what?
    • Specimens
    • Gram Stain
    • Quelling Reaction
  219. Streptococcus pneumoniae Diagnostic Lab Tests: Specimens
    Blood, sputum, CSF
  220. Streptococcus pneumoniae Diagnostic Lab Tests: Gram Stain
    useful for sputum & CSF
  221. Streptococcus pneumoniae Diagnostic Lab Tests: Quelling Reaction
    • Capsule swelling test
    • Capsule swells when the pneumococcus is mixed w/ antibodies specific for its type of polysaccharide
    • A rapid history test, rarely used today
  222. Streptococcus pneumoniae Treatment / Prevention
    • Antibiotics - Penicillin: Rx of choice but some strains can be a problem in meningitis
    • Vaccine
    • - contains type-specific polysaccharides 
    • - appropriate for day care kids, those with sickle cell, age >60, debilitated, immunosuppressed 
  223. Viridans Streptococci
    is a group of organisms, no single disease

    • Primarily alpha-hemolytic (also some non-hemolytic)
    • Prevalent normal flora in upper respiratory tract
  224. Viridans Streptococci Infections
    Principal cause of endocarditis on abnormal heart valves (eg. Rheumatic heart disease, mitral valve prolapse) following dental work (including cleaning)
  225. Viridans Streptococci Treatment / Prevention
    • Prophylaxis of certain patients with abnormal heart valves (not MVP)
    • Treat endocarditis w/ penicillin & aminoglycoside
  226. Enterococci
    • Primarily non-hemolytic (some alpha-hemolytic)
    • React w/ group D antisera
    • More resistant to penicillin G than strep
    • Part of enteric NF
  227. important species of Enterococci include?
    • Enterococcus faecalis (85-90% of infections)
    • Enterococcus faecium (5-10% of infections) - VRE ( resistant to the antibiotic vancomycin)
  228. Enterococci Infections
    • Frequent cause of nosocomial infections
    • Selected by therapy w/ cephalosporins
    • Transmitted between patients / staff via hands
  229. Enterococci: Common site of infection
    • Urinary tract
    • Wounds
    • Biliary tract
    • Blood
    • Endocarditis (subacute usually)
  230. Enterococci Treatment
    • Can be complicated because of resistance to cephalosporins, penicillins, & aminoglycosides
    • Must treat severe infections w/ vancomycin plus an aminoglycoside
  231. Neisseria Essential Characteristics
    • Cocci in pairs (diplococci)
    • Gram -
  232. Neisseria Culture & Identification
    • Require enriched medium (“chocolate” agar)
    • Identify species by carbohydrate usage
  233. Neisseria Pathogenic Species
    • Neisseria gonorhoeae
    • Neisseria meningitidis
  234. Neisseria gonorrhoeae
    • Ferments only glucose (N.G. - Glucose)
    • Evades host immune system by switching from one antigenic form to another
  235. Neisseria gonorrhoeae Infections
    • Gonococci attack mucous membranes of GI tract, eye, rectum, throat
    • Almost exclusively by sexual contact
    • Gonococcal bacteremia
  236. Neisseria gonorrhoeae in females
    Primary infection in endocervix, urethra, vagina w/ mucopurulent discharge. May progress to salpingitis (inflammation fallopian tubes) 20% infertility. Chronic cervicitis can be asymptomatic
  237. Neisseria gonorrhoeae in males
    develop urethritis w/ pus & painful urination, may expend to epididymitis, fibrosis urethral strictures. Urethral infections may be asymptomatic.
  238. Gonococcal bacteremia leads to
    • Hemorrhagic skin lesions
    • Suppurative arthritis
  239. Gonococcal ophthalmia neonatorum
    (during birth). Progresses rapidly, blindness if untreated
  240. Neisseria gonorrhoeae Diagnostic Lab Tests include
    • - specimens
    • - submit for culture and smear
    • - gram stain
  241. Neisseria gonorrhoeae Diagnostic Lab Tests: Specimens
    urethra, cervix, rectum, conjunctiva, throat, synovial fluid, blood
  242. Neisseria gonorrhoeae Diagnostic Lab Tests: Gram stain
    • Smears of urethral / endocervical exudate w/ many Gonococcal diplococci within neutrophils - presumptive diagnosis
    • Urethral smears from men are 90% sensitive, 99% specific. If smear is positive, culture is not necessary
    • Endocervical smears 50% sensitive, 95% specific. Culture is necessary
    • Smears from conjunctiva can also be diagnostic
  243. Neisseria gonorrhoeae Diagnostic Lab Tests: Culture
    • Must be processed ASAP (specimen dies quickly)
    • Organisms identified by gram stain, oxidase positivity, & carbohydrate usage
  244. Neisseria gonorrhoeae Prevention / Treatment
    • Many now resistant to penicillin. Rx - ceftriaxone (3rd gen. cephalosporin)
    • Prevent ophthalmia neonatum by applying erythromycin or tetracycline ointment to newborn’s conjunctiva
  245. Neisseria meningitidis
    • Ferments glucose and maltose (N.M. - g&m)
    • Most important serogroups associated w/ human disease are A, B, C, Y, & W-135
  246. Neisseria meningitidis Infections cause 
    • Nasopharynx blood
    • Blood 
    • Loss of limbs
  247. Neisseria meningitidis: Blood CSF
    • Meningitis is the most common result of bacteremia
    • Meningitis occurs in epidemic waves, i.e. military camps, universities (UConn 1990), etc.
    • age >40 have high resistance to infection!
  248. Neisseria meningitidis symptoms
    • - severe headache
    • - high fever
    • - photo phobia
    • - stiff neck
  249. Neisseria meningitidis Diagnostic Lab Tests Include
    • Specimens: blood, CSF, hemorrhagic rash
    • Gram stain
    • Culture
  250. Neisseria meningitidis Prevention / Treatment
    • Infections treated with penicillin G, ceftriaxone
    • Rifampin - prophylaxis of close contacts
    • Vaccine - capsular antigens
  251. Bacillis anthracis Pathogenesis
    • Primarily disease of animals, humans rarely affected
    • Spores enter via injured skin or mucosa
    • Necrotic ulcer with edema
    • Inhalation: woolsorters disease hemorrhagic pneumonia
    • Anthrax toxin
    • Agent of biological warfare
  252. Bacillis anthracis Diagnostic Lab Tests: Specimens
    fluids, pus from lesions, sputum, blood
  253. Bacillis anthracis Treatment / Control
    • Treat with penicillin, tetracycline, ciprofloxacin - give early
    • Prevent by vaccinating, dispose of animal carcass properly
    •  Gas hides, hair, bone products with ETO to kill SPORES
  254. Clostridium perfringens Toxins
    • Toxins that help spread infection - gas gangrene
    • Exotoxins produce food poisoning
  255. Clostridium perfringens Clinical Disease
    • Gas gangrene
    • Food poisoning
  256. Gas gangrene
    • Organism enters wound, grows and produces gas
    • Crepitation (crepitus): gas in tissue
    • Foul-smelling discharge, blackened necrotic tissue
  257. name the two types of gas gangrene
    • Anaerobic cellulitis
    • Myonecrosis
  258. Anaerobic cellulitis
    infections remain localized in damaged necrotic tissue
  259. Myonecrosis
    toxins diffuse into nearby necrotic tissue and breaks it down
  260. what predisposes a person a gangrene
    The conditions that predispose a person to gangrene are surgical incisions, compound fractures, diabetic ulcers,septic abortions, puncture and gunshot wounds, and crushing injuriescontaminated by spores from the body or the environment
  261. Clostridium perfringens Food poisoning
    • Enterotoxin (meat)
    • Incubation 6-18 hours
    • Diarrhea - usually self-limiting, death extremely rare
  262. Clostridium perfringens
  263. Diagnostic Lab Tests: Specimens
    pus, tissue from wounds
  264. Clostridium perfringens Treatment / Prevention
    • Debridement (dih-breed’-ment)
    • Penicillin or cephalosporin
    • Maggots
    • Hyperbaric oxygen
  265. Clostridium difficile (antibiotic associated diarrhea)
    • Use of antibiotics decreases gut NF C. difficile gains advantage
    • Produces toxin that causes diarrhea or pseudomembranouscolitis
  266. Clostridium difficile Diagnosis
    detect toxin in stool
  267. Clostridium difficile Treatment
    stop antibiotics, give metronidazole (Flagyl). (Vancomycin is now second choice in order to avoid VRE)
  268. VRE
    Vancoymicin Resistant Enterococci (VRE)
  269. Clostridium tetani toxins
    Toxin Tetanospasmin
  270. Toxin Tetanospasmin
    Inhibits post synaptic spinal neurons, blocks release of inhibitory mediator of muscle spasms
  271. Clostridium tetani Clinical Disease
    Wound (puncture, burns) infected with spores, organism makes toxin that permanently binds to neurons

    • Most cases are elderly or IV drug abusers
    • Lesser developed nations - 200,000 infants die/yr from infected umbilicus stump or circumcision
  272. Clostridium tetani Symptoms
    • Incubation 4-5 days to many weeks
    • Convulsive contractions of voluntary muscles
    • Jaw muscles (lock jaw)
    • Tetonic seizure
    • Facial expression (looks like the Joker) risus sardonicus
    • Paralysis respiratory muscles
  273. Clostridium tetani Treatment / Prevention
    • Give antitoxin - can neutralize toxin ONLY before it binds to neurons
    • Penicillin - stops toxin production
    • Tetanus vaccination (DTaP)
    • Booster every 10 years
  274. Clostridium botulinum toxin
    • Botulin toxin
    • Binds to presynaptic membrane, prevents ACh release
    • Most potent microbial toxin known
    • Heat labile (breaks down in heat)
    • blocks release of acetylcholine causing flacid paralysis.
  275. Clostridium botulinum Clinical Disease
    flaccid paralysis
  276. flaccid paralysis
    • caused by Clostridium botulinum when 
    • Ingest food containing toxin (canned foods with high pH)
    • Most cases from home cooked green beans, corn, meat, fish (spores highly heat resistant)
    • Common cause of death in livestock, aquatic birds (esp. mallards)
  277. Clostridium botulinum Symptoms
    • Begin 12-72 hours
    • Double vision
    • Can’t swallow, dry mouth, can’t talk
    • Respiratory paralysis, death (10%)
  278. Botulism:Wound
    organism from soil gets into wound, makes toxin (esp. IV drug abusers)
  279. Botulism: Infant
    ingestion of spores in food (esp. raw honey) higher pH of neonatal stomach allows germination, production of toxin
  280. Clostridium botulinum Treatment / Prevention
    • Give botulism antitoxin immediately
    • Biggest threat is home canned food
    • Avoid cans with bulges, leaks!
    • Toxin is heat labile at 100 C (boiling for 15 min)
  281. NEW USES BOTULINUM
    • Botox
    • Spasmodic toricollis (cervical dystonia)
    • Hyperhidrosis (XS sweating)Spastic muscle pain
    • Masseter muscle to dec. size lower jaw
    • Other
  282. Spasmodic toricollis (cervical dystonia)
    bad spasms in the neck - is extremely painful
  283. Hyperhidrosis (XS sweating)
    excess palm sweating 
  284. Blood agar
    made by adding sterile animal blood from sheep to a sterile agar base, used to grow fastidious streptococci and other pathogens
  285. Chocolate agar
    made by heating blood, used for the pathogenic Neisseria (one kind causes Gonorrhea), a physical medium to put the colonies on
  286. Which type of infectious diseases are now killing the most people worldwide?
    • - AIDS
    • - Respiratory tract infection
    • - Diarrhea 
  287. Glycocalyx
    Function:attatchment for other cells, sites for receptors 
  288. Lag phase
    an early “flat” period on the graph when the population appears not to be growing or is growing at less than the exponential rate 
  289. Exponential phase
    where the cells reach the maximum rate of cell division, the curve increases geometrically. Will continue as long as cells have adequate nutrients and the environment is favorable. During this phase the population fulfills its potential generation time, and growth is balanced and genetically coordinated 
  290. Stationary phaseStationary phase
    population enters a survival mode in which the cells stop growing or grow slowly. The curve levels off. 
  291. Decline/Death phase
    when cells begin to die at an exponential rate the curve dips downward. Speed of death depends on resistance and how toxic the conditions are
  292. binary fission consists of which phases 
    • • Lag phase
    • • Exponential phase
    • • Stationary phase
    • • Decline/Death phase
  293. Symbiont
    two organisms live together in a close partnership
  294. Mutualist
    organisms live in an obligatory but mutually beneficial relationship
  295. What is the most likely cause (organism) of diarrhea in a patient who has been on long-term (1 month) antibiotic therapy? Give examples of antibiotics that can cause this
    • Clostridium difficile Also known as antibiotic-associated colitis. This bacterium is able to infect the large intestine when the antibiotics have disrupted the normal flora. • Antibiotics: amoxicillin, clindamycin, cephalosporins
  296. List 3 organisms that can cause nosocomial infections in hospitalized patients.  Explain how each is acquired.  If transmission is possible, how can transmission be prevented?
    • 1) Staphylococcus Epidermidis (from shuts & catheters- STERILIZE)
    • 2) Enterococci (spread b/t patients via staff hands- WASH HANDS)
    • 3) Strep pneumoniae (communicable,vaccines)
  297. What would you expect to see in a urethral smear that is positive for Neisseria gonorrhea?
    • Endocervical exudate with many Gonococcal diplococci within neutrophils (gram negative diplococci in neutrophils)
  298. Who should be given a Streptococcus pneumoniae vaccine?
    o day care kids, those with sickle cell anemia, older than 60 (revaccination at 65), debilitated, immunosuppressed, hospitalized patients, chronic drinkers/smokers, those with heart disorders, malnutrition, hyposplenism (removal of spleen), chronic diseases
  299. Why are people over age 55 less susceptible to streptococcal toxic shock syndrome?
    o It is related to strain of strep pyogenes that causes scarlet fever and most people over 55 have had scarlet fever which helps body to become immune/quickly fight strep TSS.
  300. What factors increase the risk of developing bacterial meningitis?
    o Age, pregnancy, living in a community setting, working with animals, compromised immune system, those not immunized/immunization wore off, heavy drinks/smokers, going to bars, sharing drinks, possibly head trauma?
  301. What are the early symptoms of necrotizing fasciitis arising from a wound infected with Streptococcus pyogenes?
    • • pain out of proportion to wound
    • • first sign usually is a painful small, red bump or spot on the skin.
    • • Bacteria releases the toxin, S. pyogenes, that kills the tissue, streptococcal toxin shock syndrome is associated with this disease.
  302. The CDC estimates that 65% of chronic infections are due to biofilms. Where do biofilms occur and how do biofilms contribute to chronic wound infections in older adults? 
    • - Acting as an impenetrableshield, they hide the infectious agent and make it inaccessibleto the host defenses.
    • - They can also block the effects ofantimicrobic drugs by slowing passage into the embedded microbes.

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