Second part of medical micro - Sheet1.csv

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Second part of medical micro - Sheet1.csv
2012-05-07 20:30:56
Second set medical micro

From immune system
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  1. Spinal Fluid Samples (CSF)
    Located around brain and spinal cord. Used for identification of bacterial meningitis. The common form of meningitis 80 percent of infections with meningitis are life threating. Infetion can cause the tissue around the brain to swell. Obtained by a lumbar puncture. The CSF is gram stained and cultured. Cultured on blood agar. chocolate agar. and MacConkey. Looks for S.pneumonia.(most common) N. meningitis. grow on blood agar H. influenzae should grow on chocolate agar.
  2. Blood Samples
    Normally taken in 2 5ml-10ml vials. One is an anaerboic vial the other is aerobic. Can but used for culturing is taken and placed in a blodo media. Must clean site before blood is taken to minimize exposure to contaminants.
  3. Septicemia vs. Bacteremia
    Septicemia is the pressence of pathogenic organisms and/or their toxins in the blood. Can have septicemia with only toxins in blood. Bacteremia is the pressence of bacteria in the blood.
  4. Urine Samples
    Collected by clean catch method. To catch midstream in the morning . Urine should be sterile but can become easily contaminated during collection. Is a good growth media so should be used immediately. Use a quantitative Gram stain used with a calibrated loop. In addition can be cultured in special media with pH indicators to help identified. Normally a CHROagar chromagens will give a color with different organisms.
  5. Respiratory Tract Sample
    UPPER can use a pharyngeal swab. 20 percent of pharyngitis caused by bacterial infection. Group A strep. (most common in children) C. diptheriae. bodetella pertussis (usually vral self limiting). LOWER RESP. done with sputum sample. M. tuberculosis. H. influenzae. S. Pneumoniae.
  6. Stool Samples
    Need selective and differntial media. often chosen depending on expected pathogen. Should be collected before antibiotic thearpy is conducted. Can also use toxin assays (C. difficile). In addition can use enzyme immuno assay and PCR. TCBS agar used for V. cholera has bile salts. XLD agar used for shigella and salomnella.
  7. Overview of Detection Methods
    1. Microscopy (gram stain. WBC. parasites). 2. Cutlure the use of specialized media for cutlure bacteria. 3. Antigen detection. Tests for pressence of antigen (uses specific antibodies to test for pressence of antigen). 4. Serology looking for antibody response 5. Nucleic acid analysis used by PCR.
  8. Broad spectrum vs. narrow spectrum antibiotics
    Broad spectrum works against a large amount of bacteria (G+ and G-) . Narrow spectrum only works on specific bacteria
  9. Main Tests for antimicrobial resistance
    1. Kirby Bauer. 2. MIC minimum inhibitory concentration (used for dose of treatment).
  10. Bacteriostaic vs bacteriocidal
    Bacteriostatic will just inhibit growth of the bacteria. Bacteriocidal will actually destroy the bacteria.
  11. Antibiotic combinatorial therapy.
    Using combination of different antibiotics to get a synergistic effect to enchance the effectivness of the drug.
  12. Ribosome sizes in bacteria information
    ribsomes made up of ribosomal proteins. Bacterial ribosomes are made up of two subunits 50s and 30s. With a total of 70s. Eukaryotic cells 2 units of 60s and 40s with a total of 80s. S reprents the sedimentary rate called a svedburn unit.
  13. Basic mechanisms of antibiotics
    1. Inhibit cell wall synthesis. 2. DNA replication 3. RNA synthesis. 4. Protein synthesis 5. Antimetabolities (disrupt metabolic processes)
  14. Beta Lactam antibiotics
    Inhibition of Cell Wall Synthesis. TARGET. peptidoglycan cross linking enzymes. EXAMPLE. penicillins and cephalosporins. RESISTANCE MECHANISMS. 1. Prevnet interaction of antibiotic and target. 2. Modification of binding of antibiotic to target. 3. Beta lactamase. (destorys the beta lactam ring).
  15. Glycopeptides
    TARGET. is the peptide chain bridges in the cell wall. the nag nam bridge EX. vancomyocin. RESISTANCE MECHANISMS. 1. Intrinsic (D-alanine) D-lactate so wont allow binding. 2. Acquire changes on the terminus so it wont bind. ONLY WORKS ON GRAM POSITIVE.
  16. Bacitracin
    G- are resistant. MECHANISM. Prevents the movement of the precursor peptidoglycan to the cell wall. 2. Damages cell membrane increasing permeability
  17. Polymyxin B
    Similar to Bacitracin and increases permeability of outer membrane. More effected by osmotic pressure.
  18. Aminoglycosides
    Inhibition of Protein Synthesis. TARGET: 30s ribosomal subunit (causes misread of short peptides). Examples: streptomycin. gentamicin. tobramycin. RESISTANCE MECHANISM. 1. Mutation of ribosomal binding site. 2. Decrease uptake of antibiotic into cell (pore changes). 3. Efflux of antibiotic from cell. 4. Enzymatic modification of antibiotic (destorys AB) NOT EFFECTIVE AGAINST ANAEROBES
  19. Tetracyclines
    TARGET. the 30S subunit and blocks tRNA from binding. USED MOSTLY FOR INTRACELLULAR PATHOGENS. RESISTANCE. 1. Decrese uptake of Ab into cell. 2. Efflux of Ab from cell. 3. Alter 30s target. 4. Enzymatic modification of Ab.
  20. Linezolid
    Inhibition of Protein Synthesis. Fairly new class of antibiotics. Effective against Staphylococcus. Streptococcus. Enterococcus. Usually reserved for vancomycin reistant bacterial infections. BIND 50S and prevents complex formation.
  21. Macrolides
    Inhibits protein synthesis. TARGET. 23 rRNA of 50s subunit. Ex. erythromycin. azithromycin. clarithromycin. RESISTANCE MECHANISM. Methylation of 23 rRNA so Ab cant bind. 2. Inactivation of Ab by enzymes. 3. mutations of 23 rRA and proteins Used for broad spectrum
  22. Quinolones
    Inhibition of Nucleic Acid Synthesis (made in lab). TARGET. DNA topoisomerase (DNA replication). Ex. ciprofloxacin. moxifloxacin. RESISTANCE MECHANISM. Mutation in structural DNA topoisomerase genes. 2. Effleux pump. 3. Decrease uptake Ab into cells.
  23. Rifampin
    Inhibition of Nucleic Acid Synthesis. TARGET. RNA polymerase. RESISTANCE. 1. Mutation gene codinf for RNA polymerase. G- are resistance to Ab because they cant pass through
  24. Metronidazole
    Inhibition of Nucleic Acid Syntheis. TARGET. cytotoxic to DNA. Resistance. 1. Efflux pump. 2. Decrease uptake.
  25. Sulfonamides/Trimethoprim
    "Antimetabolites TARGET. Complete with PABA so no folic acid is made. (Precursor of folic acid is PABA.) is an enzyme. Or interfere with folic acid metabolism. SULFA DRUGS ARE SIMILAR TO PABA AND WILL BIND TO THE ENZYME TO CONVERT TO FOLIC ACID AND GET STUCK. Mainly used for UTIs
  26. Major groups of pathogens
    1. Viruses. 2. Bacteria 3. Fungi 4. Parasites
  27. Immune system response to Intittial Infection 3 phases
    1. Innate immune response. 2. Early immune response. (first two are general) 3. Adaptive immune response.
  28. Innate immune response
    0-4 hours. Preformed sentinal cells that are programmed to recognize invaders. If successful will remove the invader. 1st line of defense
  29. Early induced response.
    4-96 hours. Start depends on the innate reponse. If the innate immune repsonse fails a second set of cells are used to try to remove the pathogen.
  30. Adaptive response
    Fairly specific to invading pathogen. Have effector cells called B and T cells. Parts of the cells (anitigens) are recognized by the immune system.
  31. Innate Immunity (barriers)
    Are mostly barriers used to stop infection from getting in. Basical barriers like skin. Chemical barriers like tears have lysozymes and stomach acid. Bacterial barriers like our own normal flora to outcompete invading bacteria.
  32. Innate Immunity detection of invasion
    Is recognized by PAMP. PAMP is a pathogen associated molecular pattern. Are parts of microorganisms not normally found in body. Ex. part of the bacterial cell wall (LPS. peptidoglycan. flagella). PAMP is regocongized by PRR
  33. PRR
    Pattern recognition receptors. Are used to detect PAMP and alert immune system. A normally toll-like receptors. These are located in the cell membranes and stick out to detect PAMP. Have many different kinds that detect different types of bacteria. The toll-like receptors for viruses are located inside the cell.
  34. Inflammation
    Another part of the innate immune response. Signs of inflammation tumor. rubor. palor. dalor. Swelling. reddness. pain. and heat. Immune cells are signaled by other cells to where the bacteria are. Capillaries in this area dilate to allow more blood flow to the area to bring more immune cells. And fluid moving into the surrounding area this causes swelling. This is a very effective way to remove a pathogen.
  35. Innate cell mechanism
    Use phagocytosis by recognizing components on pathogen. They are broken down by chemicals in the lysozymes.
  36. Innate vs Adaptive response
    Innate response time hours. Adaptive days. Innate specificity is limited and fixed. Specificity of adaptive is very diverse improves during the course of immune response. Response to repeat infection similar time with innate. ADAPTIVE RESPONSE DURING SECOND RESPONSE IS FASTER AND A STRONGER RESPONSE. Major component of innate are barriers. phagocytosis. inflammation. and PRR. Major components of the adaptive response are lymphocyctes. antigen specific receptors. antibodies
  37. Organs of the immune system
    Primary organs are the bone marrow and thymus. Where the cells are produced and mature. Secondary organs is where the mature T and B cells are exposed to bacteria and pathogens. Spleen and lymphnodes are where the majority of the organs where immune response begin. Also have peyer patches in lungs as well.
  38. Blood and lymph
    Is the location of immune cells are ciruclating. The lymph goes through lymphnodes. Infection in the tissues are normally detected by the lymphnodes. The blood goes through your spleen. So a blood infection would be recognized by a spleen.
  39. Cells of the immune system
    Come from progenetor cells in the bone marrow. Myloid line are blood cells and platelets and white blood cells . Lymphoid line are B and T cells.
  40. Important myloid cells (granulocytes)
    Neutrophils (toxic compound in granuoles. IMPORTANT PHAGOCYTES) Basophil (histamine) and Eosinophil (parasites). Have large granuoles inside the cells which contain toxic compounds. Basophils have histamine in them. When they are activated they release contents of their granuoles.
  41. Macrophages and dendrict cells
    Main function is ANTIGEN PRESENTATION. Are of vial importance to activate B and T cells. These cells will take up bacteria and present it on the surface present the antigen to stimulate immune response.
  42. B cells
    Have anitgen bind receptor (antibody). Are very specific for specific antigen. Once they recognize an anitgen with a receptor they will become active. Will begin to produce soluble antibodies. Antibodies have many difference functions to help remove pathogen. ARE HUMORAL RESPONSE INVOLVES ANTIBODIES.
  43. Antibody classes
    IgG most common during an infection in blood. First antibody made is IgM forms a pentamer which gives it 10 antigen binding site good at clumping. IgA is at the mucosal surfaces and forms a dimer. IgE involved in allergic responses.
  44. Cell mediated immune response
    This involves T cells. The T helper cells and the Tc cells. Have to recognize antigen that is presented to them
  45. TH cells (helper)
    Have a coreceotor is **CD4** Help activate B cells. Have their own receptor for binding to antigen. Also have a coreceptor CD4. Have to recognize antigen that is presented to them by APC by macrophages. The MHC class II will present the antigen to the T helper cell.
  46. T cytotoxic cells
    Have a coreceptor CD8. Have to recognize antigen that is presented to them by a MHC class I which is located on every cell in your body
  47. Rule of 8
    MHC class I must be used with CD8. 1 x 8 = 8. Where MHC class II must be used with CD4 2 x 4 = 8.
  48. MHC class I info
    Present antibody on all cells. This shows that the cell is infected with a pathogen and T cytotoxic cells kill it. ANTIGEN PRESENTED FROM OUTSIDE THE CELL.
  49. MHC class II info
    Presents antigens that come from outside the cell. The macrophages are presenting to the T helper and they will activate other cells in the immune response. ANTIGENS PRESENTED FROM OUTSIDE THE CELL.
  50. Cytokines
    Are chemcial messengers. Can cause a bunch of different responses in cell. Are used to help fine tune and activate the immune response.
  51. Cytokine storm
    Super antigens induce an overactive response of immune system. Is abundant release of cytokines activating T cells.
  52. TH1 vs TH2 repsonse (different types T helper cells)
    TH1 goes more towards inflammation. Activates macrophages and inflammation. Is really good at intracellular pathogens. TH2 response is more towards an antibody response.
  53. Resisting phagocytosis
    1. Capsules make bacteria slippery and cant bind to bacteria. 2. Produce leukocidins that destroy phagocytes.
  54. Evading specific immune response
    Genetic variation of surface proteins. N. gonorrhease will bury and change the surface pili and now one immune response antibodies will not work. Also can use proteases that destroy antibodies.
  55. Defense against viruses
    1. Cytotoxic T cells 2. Interferon (a cytokine) makes other cells go into a antiviral state.
  56. Hypersensitivity Type III
    Brough on by immune complexs. Is where there is a antigen and antibody complexes floating in blood and gets stuck or is sticking in the capillary. When neutrophil cant engulf this complex will release the chemicals from the granuoles onto the tissue.
  57. Type IV hypersensitivity
    Delayed type hypersensitivity. The first exposure nothing happnes. During second exposure is must more severe. Inflammation.
  58. Vaccine
    Stimulate the immune system to create a response and induce memory of a pathogen. First vaccine was small pox created by Edward Jenner.
  59. Passive immunity
    Where you given preformed immuno molecules. Preformed antibodies. Used if you have been exposed to diease to stop the disease to taking hold. PREFORMED MOLECULES ANTIBODIES (artificial). Natural from breast feeding from mom.
  60. Active immunity
    Part of a piece of a pathogen. bacteria. toxoid. That small piece of the bacteria induces a immune respone and doesn't trigger an infection. Can be inactive like tetanus which is an inactive toxoid. Atenuated bacteria are genentically manipulated bacteria to trigger disease which will give a stronger immune response. (ARTIFICAL). Getting disease gives natural active immunity.
  61. Louis Pasteur vaccines
    Chicken cholera. Antrhax. Rabies.
  62. Pyogenic Cocci
    Pus forming. Are staphlococcus and micrococcus. Are infections that cause pus. Pus is dead white blood cells.
  63. General characteristics of staph/micrrococcus
    1. Facultative anaerobes. 2. Halotolerant (ability to live on skin) 3. CATALASE POSITIVE. 4Present on skin an dmucous membranes of human
  64. S. aureus
    Colonies turn a gold color as the stay longer on the media. Called old gold. Also Beta hemolytic.
  65. 3 Major Pathogenic Staphylococcus
    1. S. aureus (found in nasal passages). 2. S. epidermis (on skin). 3. S. saprophyticus (can be normal flora of genitourinary tract in women).
  66. M lutues colony color
    Has a bright yellow pigmented colony. Often confused with S. aureus but NO HEMOLYTIC.
  67. Staphylococcus aureus biochemical results
    Positive on MSA plate. Coagulase positive. Staph latex kit postive clumping. Baird parker reduces tellurite and breaks down egg yolk by proteolysis.
  68. Staphlyococcus Epidemiolgoy
    Can survive on surfaces for a long time. Person to person spread by direct contact or fomite. Opportunistic pathogen.
  69. Cytotoxins
    Produced by S. aureus. Kill other cells (white and red blood cells). Alpha toxins. Beta toxins used for beta hemolysis. Delta toxins. P-V leukocidin. Kills white blood cells. (not produced by all S. aureus and found in MRSA strains)
  70. Exfollative toxins
    ETA and ETB. Are proteases that destroy the ECM and skin peels off. 5-10% strains. Cause Staphylococcal scalded skin syndrome (SSSS).
  71. Enterotoxins
    Intestine (gut) target causes food poisoning. Exterotoxin A is the most common. Heat satble (100 degrees) acid resistant can pass through gut.. 30-50% of S. aureus. Fast onset and quick recovery. Ingestion of prefromed toxins FOOD BORN INTOXICATION. Quick onset usually preformed toxins.
  72. Toxic shock syntrop toxin 1
    TSST-1. Exotoxin excreted outside of the cell. A superantigen by some S. aureus. Activates T cells without an antigen. A nonspecific manner. The result is that you get a huge immune response.
  73. Toxic shock syndrome
    Result from antigen independent. Activation of many T cells induce a cytokine storm. Is systemic. Symptoms includes fever. rash. hyoptension (increase size of capillaries). desquamation of skin. vomiting. Death form massive organ failure.
  74. Localized Cutaneous infections Staphylococcus
    Impetigo a pustual rash on face. Pyogenic co infection with strep. Folliculitis. Stye (S. aureus). Furuncle (boil inflammation and deeper skin infection). Carbuncle accompanied by fever and chills systemic effect.
  75. Systemic infections caused by S. aureus
    1. Bacteremia (blood infection). 2. Pneumonia. 3. Osteomyelitis (bone infection). 4 Septic arthritis. 5. ACUTE ENDOCARDITIS. (destruction and inflammation of heart valves)
  76. Staphylococcus epidermidis
    Frequent contaminant of blood cultures. Causes of nosocomial infections. Causes biofilm on catheters which are very antibiotic resistant.
  77. Staphylococcus saprophyticus
    2nd most common cuase of UTI. RESISTANT TO NOVOBIOCIN. Distinguishes from S. aureus and S. epi
  78. Diagnosis of Staphylococcus infection
    1. Clincal presentation of patient. 2. Gram stain of specimen can be confirmatory. 3. Culture on primary media. MSA. Baird Parker. BA (from sterile sites).
  79. S aureus is identified by
    1. Yellow colonies on MSA. 2. Coagulase positive. 3. Staph latex agglutination test.
  80. Treatment of S. aureus
    Less than 10 percent susceptible to penicillin lots of reistance to synthetic penicillins and beta lactams. Methicillin and oxacillin are resistant to hydrolysis by Beta lactamase.
  81. MRSA
    Majority of nosocomial and community acquired infections. Treat wtih intravenous vancomycin ororal antibitoics clindamycin. sulfa drugs. doxycycline. VISA and VRSA.
  82. Streptococcus/Enterococcus
    Usually form chains or pairs. Facultative anaeroves. capnophilic (grow best in increased CO2). Fastidious (very picky nutrionally) CATALASE NEGATIVE. Normal flora of respiratory tract. GI. and genitourinary tract. Opportunitic pathogens
  83. Differenttiation of species of Strep/Entero
    1. Lancefield groupsn (carbohydrates on cell wall). 2. Hemolytic patterns on BA. 3. Biochemical properties.
  84. Group A strep
    Streptococcus pyogenes. Most poteint pathogen. Rarely normal flora. ONLY HUMAN organism. Reseviors are humans who carry the bacteria. Beta Hemolytic
  85. Toxins produced by S. pyogenes
    1. Steptococcal pyrogenic exotoxins (SpeA. B. C. and F). Fever inducing. 2. Superantigens (over stimulation of immune system). 3 Streptolysin S (beta hemolysis). 4. Steptolysin O. 5. Streptokinase. hyaluronidase. DNase. Spreading factors.
  86. Suppurative diseases caused by S. pyogenes
    Pus forming. Pharyngitis (strep throat). Rash from scarlet fever. (rash spreads from torso non fatal) Folliculitis. Impetigo. Cellulitis (inflammed swollen of deeper tissue). Erysipelas ( another version of cellulits)
  87. Necrotizing fasciitis
    Very rare disease caused by S. pyogene. Super antigen exotoxins. begin like cellulits but does massive tissue damge. Needs debreedment to remove.
  88. Streptococcal toxic shock syndrome
    Soft tissue infection that progess to shock and organ failure due to superantigen. ACCOMPANIED BY BACTEREMIA. Often necrotizing faciitis. At risk populations HIV positive. cancer. diabetes. heart disease. IV drug users.
  89. Delayed aintibody Mediated disease
    Caused by S. pyogenese. and a untreated strep throat (pharyngititis). Rheumatic Fever. associated with paryngitis only. Is caused by the immune system making antibodies and the antibodies react with different parts of the body. Specifcally in Rheumatic fever it is the heart valves. Glomerulonephritis. associated with both pharyngitis and skin infections. Kidney become inflammed similar to hypersensitivity III.
  90. S. pyogenes laboratory tests
    Rapid Strep A swab. Not very accurate. PYR test. Bacitracin resistant.
  91. Test for antibodies against streptolysin O
    ASO KIT is a titer for antibodies. Confirmatory for rhematic fever or glomerulonephritis. ASO antiboddies appear 3-4 weeks affter intial infection and titer remains high.
  92. Group B strep
    Stptococcus agalactiae. Weakly beta hemolytic.
  93. Diseases casued by GBS
    Puerperal sepsis (childbed fever). Neonatal disease bacteremia. meningitis. pneumonia. Women would carry GBS in vagina. Early on set vs. late onset (after birth). Infections in pregenant women postpartum endometritis. would infection. UTI.
  94. Laboratory diagnosis of S. agalactiae
    Hippurate hydrolysis. Reaction in carrot broth. Positive CAMP test. S. agalactiae will have it hemolysis enhanced in the presence of S. aureus.
  95. Strep viridians
    Are all alpha hemolytic. Are normal body flora. Cause a subacute bacterial endocarditits. Normally in long chains. Are only pathogenic if they get into blood
  96. S. Pneumonia
    Part of the viridians group. Will not give lancefield typing. Is an opportunistic pathogen casues inflammation. Makes diplococci. Look lancet shaped not exactly round. Produce no toxins and form a capsule. CAPSULE IS MAIN VIRULENCE FACTOR.
  97. Dieaseas caused by S. pneumoniae
    1. Pneumonia. Normally in elder patients normally casued aspiration pneumonia. Usually a complication of flu 2. Sinus infections and otitis media (Middle ear infection). Meningitis in children and adults.
  98. S. agalactiae and menigitis
    Causes meningitis in newborns
  99. Laboratory Diagnosis of S. pneumonia
    Alpha hemolytic. Forms viscous gooey colonies. OPTOCHIN SENSITIVE. Very fragile in lab and doesn't survive very long. Will being to AUTOLYSE after a few days. Lives better in broth. BILE SOLUBLE ADDITION OF BILE SALTS DESTROY COLONIES AND THEY SINK IN.
  100. Quellung reaction.
    Special stain that loos for capsule. Take the bacteria and add an antibody to the capsule. If they react with the capsule it begins to swell and becomes more visible. Look for visible clearing.
  101. Treatment and Prevention of S. pneumoniae
    Penicillin. fluroquinolones. vancomycin and ceftiaxone. Very little resistance in S. pneumoniae. PNEUMONOCCOCAL polysaccharide vaccine. The vaccine is a subunit of the capsule it is a polysaccharide and conjugated to a protein. toxoid.
  102. Enterococcus species
    Known as group D Strep. E. faecalis. E. faecium. Are normal flora in small intestine. Form short chains and diplo. Gamma hemolytic. No toxins produced lack of well defined virulence factors. MAJOR CAUSES OF NOSOCOMIAL INFECTIONS.
  103. Diseases caused by Enterococcus
    UTI. endocarditis from bacteremia. Polymicrobial wound and abdominal infections. Cause a lot of post infections. IS A POLYMICROBIAL INFECTION.
  104. Laboratory diagnosis of Enterococci
    GROWTH ON BILE. HYDROLYSIS OF ESCULIN AND BILE SLANT. PYR POSITIVE. GROWTH IN 6.5 NaCl. Broad temperature range 1--45 can grow in wide temp.
  105. Enterococcus and antibiotic resistance
    25 percent of enterococci resistant to aminoglycosides. Majority of E. faecium isolates are resistant to ampicllin and vancoycin (VRE). Linezolid is used to treat VRE infections. Believe S. aureus got its resistane from E. faecium
  106. General characteritics of coynebacterium. listeria. erysipelothrix
    Gram positive bacilli. Aerobic or faculatavie. NON-SPROREFORMING. INclude outright pathogens. opportunists. and zoonotic pathogens.
  107. Listeria monocytogenes
    FACULTATIVE ANAEROBE. Grows in a wide range of temperatures. Halotolerant. Short rods that occur in pairs or short chains. almost look like cocci. FACULTATIVE INTRACELLULAR PATHOGEN. Can get to grow well under colder temperatures.
  108. Literia moncytogenes chemical results
    CATALASE POSITIVE. Weakly beta hemolytic normally under colony. Small bacillus. coccobacillus. look similar to S. pneumonia. CAMP POSITIVE. MOTILITY POSITIVE. ESCULINE HYDROLYSIS. TSI REACTION A/A-. Sulfide negative. Inodole negative. Gelative negative.
  109. Epidemiology of Listeria
    Common in soil. water. and vegetation. Saphrophyte. (ubituitis found everywhere). Also carried by animals and birds from animals. Usually transmitted via contaminated food. Normally ready to eat cooked foods like deli meats. hot dogs. soft cheeses. CAN CROSS THE PLACENTA FROM MOTHER TO FETUS.
  110. Listeria monocytogenes entry into cells
    Wants to be engulfed by phagocyte/macrophage. Once inside the lysosome it breaks out and replicates in cytoplasm. Spreads cell to cell without leaving the cell. For movement it polymerises actin.
  111. Listeriosis
    Infection with listeria. 1. Neonatal in the womb early onset causes spontanous abortion. Can have late onest after birth and cause meningitis. Also infects pregnant women and immunocompromised patients and the elderly. Primary bacteria. Strapholoccocus alagalactiae cause neonatal menigits.
  112. Treatment and prevention of Listeriosis.
    Gentamycin and ampicillin and penicillin. Since it is inside cells. At risk populations should avoid certain foods. No vaccine available.
  113. Erysipelothrix rhusiopathiae
    Slender rods that form long threads. Microaerophiles. Commonly colonizes swine and turkeys. Causes ZOONOTIC DISEASE IN HUMANS. Occupational disease of butchers meat processors farmers vets. Negative motility. Positive hydrogen sulfide. Catalase Negative.
  114. Erysipeloid
    Localized skin infections. NO PUS PRODUCTION. When compared to teh one caused by Strep does produce pus
  115. Corynbacterium general info
    Coryneform irregular shaped rods club shaped. (chinese lettering) Aerobic or facultative. Nonmotile. Catalse positive. many species are diphteroids. C. diptheriae is the main human pathogen.
  116. C. diphtheriae
    Gamma hemolytic. Grow on lofters media. Will grow metachromatic granuoles that store phosphate. PRODUCE DIPTHERIA TOXIN. Is an AB toxin
  117. Diphtheria toxin
    Is an AB toxin. A subunit inhibit protein synthesis; leading to cell death. Gets this toxicity from bacteriophage.
  118. Epidemiology of C. diptheriae
    Humans are the ONLY known reservoir. Spread by respiratory droplets or skin contact. Vaccination has decreased incidences worldwide.
  119. Respiratory diptheria
    Exudative (dead cells) pharyngitis. development of pseudomembrane. This is a yellowing at the back of the throat due to cell death. Can not remove will cause bleeding. Sign would be a bowl neck.
  120. Complication of respiratory diphteria
    Myocarditis. Heart inflammation due to the toxin moving to the heart. Neurotoxicity. spreading of bacteria to the brain.
  121. Cutaneous Diphteria
    Chronic non healing ulcer. Diptheriae into open wound or break in skin. Skin to skin contact.
  122. Diagnosis of C. diptheriae
    Swab from nasopharynx or throat. Is a plated on Tinsdale medium (fance cystine-tellurite). Hydrolyzes cystine and gives a brown halo around colony. Helps to differeniate between C. xerosis.
  123. Elek Test
    Test for Toxigneic C. diptheriae An immunodiffusion test. A strip of filter paper is soaked with an antibody is placed in the middle of the media. The toxin and the antibody will bind and will aglutinate and and can see it on the media.
  124. Laboratory Diagnosis of C. diphteriae
    Pyrazinamidase test. Pathogens tend to be negative. Diptheroids are positive.
  125. Treatment and Prevention o Diphtheria
    Administration of antitoxin (neutral toxin). Maintain open airway (intubation). Antibiotics. penicllin erythromycin. For prevention you give the DTaP vaccine. Diptheria. tetanus. Perusus.
  126. Corynebacterium ulcerans
    Can cause clinical diphteria. Is positive for Reverse CAMP. This tests for phospholipase (inhibits CAMP action)
  127. Corynbacterium urealyticum
    Imporant urinary tract pathogen. Strongly urease positive. Associated with renal stones. Resistant to many antibiotics.
  128. Corynbacterium jeikeium
    Opportunistic in immunocompromised patients. Very resistant to antibiotics. Treat with vancomycin is necessary.