Medical Micro - Sheet1(3).csv

Card Set Information

Medical Micro - Sheet1(3).csv
2012-05-07 03:31:05
so many

Holy crap
Show Answers:

  1. Animalcules
    Way back in 1674 Leeuwenhoek discovered bacteria under homemade microscopes and called them animalcules
  2. Germ theory
    "Proposed in 1840 by Friedrich Henle. Stated that an organism can cause infection in another organism. The material of
  3. contagions is not only an organic but a living one and is indeed endowed with a life of its own
    which is in relation to the diseased body
  4. Robert Koch
    former student of Henle. Isolated Bacillus anthracis. Vibrio cholera. Mycobacterium tuburculosis. Published Koch's postulate in 1890
  5. Koch Postulate
    Explained the technique to isolate and identity diseases causing pathogens. Isolate the organism out of the infected organism. Then grow it and innoculate that another host with that same bacteria and should cause the same illness.
  6. Ignaz Philipp Semmelweis
    1818-1865. Discovered the importance of handwashing but never got recognition for his attempt to apply these techniques developing medical practices.
  7. Paul Ehrlich
    1910 Discovered first medical antibiotic agent. arsinic based Salvarsan which was used to treat Syphilis
  8. Alexander Fleming
    1928 Discovered penicillin. Wasnt mass produced until WWII (1942) to prevent soliders from dying from infections. This was the start of the antibiotic era.
  9. Illnesses caused by Staphococcus aureus.
    Pneumonia. Endocartitis. Food poisoning. Wound infections
  10. Saprophyte vs commensal vs parasite
    Saprophyte lives on dead organic material. Commensal organism that lives in or on another organism with one befitting the other other having no effect.. parasite one organism benefits the other is harmed. Normally talking about Eukaryote parasites
  11. Saprophyte
    Is an organism that is growing on dead organic material
  12. True pathogen vs opportunistic pathogen
    True Pathogen is a disease causing organism. Opportunistic pathogen does not normally cause disease but under certain conditions it can cause disease.
  13. Exogenous vs endogenous infection
    Exogenous is an infection caused from an outside organism (ex. fomite. soil. etc). Endogenous infection is coming from an opportunistic infection (normal flora or latent infection).
  14. Colonization vs disease
    Colonization is an infection in which the organism is growing but does not causes symptoms. Disease is where the growth of the bacteria causes infection.
  15. MRSA
    is resistant to methicillin and all the drugs similar to this. (1960)
  16. outcomes when a microbe infects a host
    1. Transient colonization: infection comes in and tries to take hold but only lasts a short period of time. 2. Long-term symbiosis: Where the infection takes hold and stays in for a long time (ex. bacteria in gut) 3. Disease: the microbe comes in and colonizes and causes infection and harm to the host
  17. Influences on a microbe infection
    1. Number of microbes. 2. Type of organism. 3. Host 4. Health status of host. 5. Age of host. 6. Gender 7. Environment 8. Money (publich health. education. treatment).
  18. Latent vs. persistent infection
    Latent: the organism is colonized but not causing any symptoms but can flare up and cause disease again. Persistent infection is causing symptoms the whole time and is around for a long period of time
  19. Clinical vs. subclinical disease
    Subclinical disesae: mild symptoms and not openly overt. Clinical disease is very obvious and can be diagnosed.
  20. Progession of infection/disease
    Incubation (colonizes). Prodromal phase (starting to show some symptoms). Invasion phase (diagnosis most symptoms showing). Acme (the high of the infection most severe). Decline phase.
  21. Four cardinal signs of inflammation:
    1. Swelling (tumor) blood vessels dilate 2. Redness (rubor) the capillaries become leaky with more blood to the area 3. Heat: localized heat (calor) 4. Pain (dalor)
  22. Infectivity
    Colonization. Organism infecting and growing and reproducing within the host.
  23. Pathogenicity
    The ability of an organism to cause disease
  24. Virulence
    The degree of pathogenicity. How much harm can the disease cause.
  25. Measure of virulence
    Can be calculated by number of death. How many organism does it take to cause death. The LD. Lethal dose.
  26. Growth characteristics
    How the bacteria grow on the agar. Colony formation. Form: the shape of the colony. Elevation. Margins.
  27. Cell morphology and arrangement
    Cocci. Bacillus. Rod shaped. Coccobacillus (ecoli). Fusiform bacillus. Vibrio. Sprillum. Spirochete.
  28. Gam postive cell wall info
    Contains peptidoglycan. Lipoteichoic acid bound to the cytoplasmic membrane forms a matrix structure with teichoic acid.
  29. Gram negative cell wall info
    Very small peptidoglycan layer. Has an outer membrane with lipopolysaccharides (LPS can be used for identification) attached to it. Contains pores (porins). Has a periplasmic space. Direct linking between animo acids in cell wall.
  30. Metabolic signature
    What enzymes do they produce. Ex. manitol fermination (MSA). Catalase positive. Aerobic glucose metabolism. fermination. anarobic respiration is not fermination.
  31. Serotyping
    What surface antigens the microbe displays . Can be used to classify
  32. Genetic analysis
    Used to classify to subspecies level. Use DNA hybridization. PCR. rRNA. whole genome sequencing
  33. Horizontal Gene transfer types
    Transfromation: uptake of genetic material by competent cell. Conjugation uptake of foreign DNA by pilus. Transduction: use of a transducing phage. Can take place between species
  34. Antibotic resistance are located
    Located on plasmid of bacteria. Can be passed via transformation or conjugation.
  35. Colonization of sterile sites in the healthy individuals
    Colonization of one these sites generally involves a defect or breach in the natural defenses that creates a portal of entry
  36. Resident Biota
    The human as a habitat. Cell for cell microbes on the human body outnumber human cells at least ten to tone. Normal (resident) biota. Metagenoic being used to identify the microbial profile inside and on humans. Human microbiome project.
  37. Acquring Resident Biota
    The body provies a wide range of habitats and supports a wide range of microbes
  38. HMP
    Human microbiome project. 1. Determine whether individual share a core human microbiome. 2. Understanding whether change in the human microbiome can be correlated with changes in human health.
  39. Habitat of microbes
    Habitat (location) Is the main driving force differences of bacteria in different regions.
  40. Different habitats for microbes
    Upper respiratory tract. Lower respir. tract. GI tract (stomach/small intestine/large intestine). Gentiourinary Tract.
  41. GI tract large intestine (colon) most abundant microbe
    Bacteroides more prevalent than E. coli.
  42. Gut microbiome affects
    "1. Vitamin production (K).2. Development of innate and adaptive immunity. (outcompete foreign microbe 3.Turnover of gut epithelial cells. 4. Metabolism of drugs. 5. Harvest of nutreints/energy. 6. Propensity to develop obesity. 7. Organ size (heart
  43. Microbe habitat vagina
    Diverse population of microbes. Varies due to hormone levels. The vaginal microbiota affects the health of women and impacts the success of pregnancy. Vagina hosts unique consortia of microbes suggesting selection for these key organisms
  44. Bacterial Vaginosis
    BV. Is a condition linked to numerous health including. The most prevalent cause of vaginal symptoms among women of childbearing age. About 4 million visits in US. High rate of relapse cause is unknown. Normally contains few types lactobacillus. During BV contains a greater diversity of morphotypes and clue cells. INCREASES RICHNESS AND DIVERSITY OF MICROBES. Treatment with antibiotics result in a rapid decline of anaerobic bacteria.
  45. Skin microbes and habitat
    Is transiently colonized. Mostly gram positive bacteria.
  46. Virulence
    The degree of pathnogenicty. Determined by its ability to establish itself in the host and cause damage. Different healthy individual share widely varying responses to the same microorganism. host evolve.
  47. Virulence factors (ones that aid in virulence)
    Any characteristic or structure of the microbe that contributes to its virulence. Adhesins. 1.Invasins. 2. Toxins. 3. Byproduct of growth. 4. Mechanisms to evade immune response. 5. Ability to grow intracellularly.
  48. Microbes cause disease by
    1. Gaining access to the host.(routes of transmission) 2. Adhering to and colonizing cell surfaces. 3. Invading tissues. 4. Producing toxins and other harmful metabolic substances.
  49. Pathogenesis of Bacterial Disease
    Maintain a reservior. Initial transport to /entry into host. Adhere to colonize or invade host cells. Evade host defenses. Multiply (damage to host). Return to environment (shedding).
  50. Pedestals
    E. coli remain extracellular and induce the formation of pedestals on the host cell surface. Help them to stick on hold onto the cell.
  51. Surface cell adhesion
    Salmonella typhirum. Have surface cell adhesions. Enter the epithelia cells and can be taken up by macrophages. Inside the phage can live and grow within the vacuole. Allows transport and a growth environment of the microbe.
  52. Hyaluronidase
    Digests hyaluronic acid that holds cells together. S. pyogenes
  53. Coagulase
    Contributes to clotting of blood. Wall of protection form immune defesnes. S. aureus
  54. Streptokinase
    Disssolve blood clooting. Free themselves from blood clots so they can spread.
  55. Macrophage survival
    Some organsims survive within host phagocytic cells (escape destruction and obtain free transportaion to deeper body tissue). Mycobacterium tuberculosis and Neiseria gonorrhoeae
  56. Endotoxins
    Part of the bacterial cell. A componenet of the outher membrane of Gram negative bacteria. Ex. LPS (lipopolysaccharides) . Also known as lipid A. Heat stable. Relatively less toxic. Not convertible to toxoids. Poor neutralized by antibodies. Siilar toxicites for most tissues and cells low blood pressure and raised temperature. may cause endotoxic shock. generalized organ failure. intravascular coagulation and death.
  57. Toxin
    Any substance that is poisonous to other organism. According to hwo the toxins are released from the bacterial cells endo/exo toxins.
  58. Exotoxins
    Specific to a particular bacterial species that produces the disease associated with the toxin. Clostridium tetani produces tetanus toxin. Viruulent strains produce toxins while avirulent strains do not. Toxin is the major determination of virulence. Produced by both Gram positive and Gram negative bacteria. Usually secreted and are proteins. Highly toxic in very low concentrations
  59. Info on exotoxin proteins
    Protein toxins resemble enzymes. Denatured by heat. Acid and proteolyic enzymes. High a high biological activity (most act catalytically). Strongly antigenic and can be readily neutralized by antibodies. Unstable lost toxicity (retain antigenicity) toxoid. immunizing capacity.
  60. Toxoid
    "Loses toxicity
  61. Diphtheria toxin
    Produced by Corynebacterium diptheriae. Very potent in its action. AB toxin. B is binding part of toxin. A subunit is lethal single diphteria bacillus can produce 5000 molecules per hour. INTERRUPTS PEPTIDE FORMATION AT THE RIBOSOMAL LEVEL.
  62. Hemolysins
    Alpha: hemolyze blood cells partially breakdown hemoglobin produce greenish ring around colonies. Beta hemolysins hemolyze blood cells.
  63. Leukocidins
    Exotoxins produced by many bacteria like Streptococci or Staphylococci. Destroy neutrophils and macrophages. More effective when released by microbes engulfed by neutrophil. Count of WBC decrease
  64. Leukostatin
    Exotoxins interferes with teh ability of leukocytes to engulf microrganisms that secrete the exotoxin.
  65. Toxemia
    The spreading of exotoxins by blood from the site of infection. Some diseases caused due to ingestion of preformed toxins. Called intoxications. Foodborne botulism. Neurotoxin that causes a flaccid paralyis where muscles go limp.
  66. Botulism
    Clostridum botulinum. Gram-positive endospore forming anaerobe ubiquitous in soil in water. Exotoxins A. B. E cause most human illness. Mechanism of action. Irreversible inhibition of ACh release from motor neuron. Can be treated antibiotics. Prevention proper canning. Nitrites prevent endospre germination in sausages.
  67. Vibrio cholerae
    GI toxin (enterotoxin). Causes diarrhea due to loss of cell nutrients. Caused by increased cAMP activity.
  68. Evasion of Host Defenses
    Resistance to phagocytosis by macrophages and neutrophils. Survival inside phagocytic cells. Antigenic variation. Destruction of antibodies complement.
  69. Anitphagocytic factors
    Used to avoid phagocytosis. Leukocidins. Extracellular surface layer makes it difficult to engulf them (Strep. Neisseria) . Can survive within phagocytes after ingestion. (Mycobacterium). Change surface antigen (neisseria gonorrhoeae).
  70. Capsule
    Made of chemicals normally found in host. Prevents phagocytosis. S. pneumoniae. B. anthracis. Haemophilus influenzae
  71. Antigenic variation and antigenic variety
    Antigenic variation will change the antigenic composition. Antigenic variety numerous serological types among strains in the world (each strain is antigencally stable. large amount of different antigens ex. S. pneumoniae 84 serotypes is a vaccine). Degrades antibodies another mechanism.
  72. M-protein
    Protein produced on its cell wall. Reisits phagocytosis. Also Opa protein inhibits T helper cells.
  73. Evasion of Host Defenses Compliment system
    "1. Prevent binding of antigen (capsule) 2. inhibition of activation and amplification
  74. cascade system (compliment). 3. activation away from cell membrane 4. Secrete proteases destroy compliment system proteins."
  75. Compliment system
    "opsonization - C3b (increased phagocytosis). ysis of gram-negatives - C5-9 (Membrane Attack
  76. Complex [MAC]). inflammation"
  77. Portals of Exit
    Respiratory tract (exhalation). GI tract (siliva fecal oral route). Genitourinary tract . Skin. Blood (vector/needles)
  78. Reservoir
    anything that is the source of infectious agent. Does not have to be susceptible to bacteria (soil/water)
  79. Carrier
    host that is infected may or may not show symptoms
  80. Zoonosis
    transmitted between animal to human (direct transmission)
  81. Communicable vs non-communicable
    Communicable infectious disease passed form resevior to a host or carrier to host. Non-communicable can not be passed usually genetic or environmental
  82. Types of Disease Transmission
    1. Biological (direct contact) kissing. touching. etc. 2. Vector biological (important part of the life cycle in the vector) or mechanical carrying from on agent to the other (does not reproduce in the vector) 3. Vehicle the way the infectious agent enters the body (food. air. etc)
  83. Common Routes of Transmission
    Entry of pathogen into body by penetrating the skin or mucous membranes. sexual transmission. ingestion with food/water. inhaled with aerosols. transmission on a fomite (inanimate object)
  84. BSL
    Biological safety level. Different levels. Level 1 not considered highly pathogenic or non-aerosal. Level 2 now risk probably not transmitted by aerosol. If immuno compromised can cause illness but can be treated. Level 3. Can cause diseased via aerosol highly transmittable but do have treatment for these agents. (another level of protection needed). Level 4 easily via aerosol do not have treatment for them will cause death. Only at certain facilities in the US.
  85. Prevention of Infection Disease
    1. natural reistance (immune system. skin) 2. Block transmission (oral fecal route clean water) 3. normal flora (out competes any pathogens) 4. Immunizations. 5. Chemoprophylaxis (treatment with antibiotics). Eradication of disease agent (complete removal of disease).
  86. Epidemiology
    The study of the DISTRIBUTION and DETERMINANTS of disease (health-event) frequency in a human population. Scientific discipline wiht roots in biology. logic. and philosophy of science. Stats are an important tool but not foundation for epidemiology. Primarily a method of reasoning. Uses a set of ideas to make sense of events that occurred in a population.
  87. Fundamental assumptions of Epidemiology
    Diseases do not occur by chance. Diseases are not randomly distributed. Disease distribution indicates sometimes. identifying the something causes and factors through systematic investigation
  88. Three key components of Epidemiology
    Frequency. a prerequisite for any systematic investigation of pattern of disease (how often it occurs). Distribution. who where and when to describe the pattern. Determinants. uses the first two to test epidemiological hypothesis. (what different factors are playing a role in the frequency and distribution)
  89. Use of Epidemiology
    Establish causation of a disease. Study the natural history of a disease (changes). Assess the health status of a population. Evaluate the impact of intervention.
  90. Descriptive Epidemiology
    Person. who is getting disease? Time. when does disease occur? Common or rarely? Place. Where are the rate of disease highest and lowest?
  91. Types of Epidemiological studies
    Observational studies (descriptive and analytic studies) or Experimental Studies which runs trials.
  92. Ability of different studies to prove causation
    Clinical trial (experimental). Community trial (in the community sampling). Cohort study (group of individual if they get infected) Case-control study (comparing history of different groups). Cross-sectional study (going into the population and collecting information). Correlation study (taking a number of population and pooling the results).
  93. Public health
    "Organized community efforts aimed at the prevention of disease and promotion of health. Views a whole population. Interdisciplinary effort that addresses the physical
  94. How are epideomiology and public health linked
    Epidemiology is core science of public health. Public heath information is collect during epidemiology and then public health uses that information to educate/empower COMMUNITY and to organized community efftorts aimed at the prevention of disease and promotion of health.
  95. John Snow
    A medical doctor in London in the 19th century. During a cholera outbreak John Snow investigated the outbreak. Used a systematic approach to find cause of outbreak. Went door to door and interviewed people to gather information. Looked for a pattern and cause of outbreak. Used time and place.
  96. Public health model vs. Medical Model
    Public focus on population. public service ethnic concerns for the individual. Empahsis on prevetion and health promotion for the whole community. Intervention target the environment/behavior/lifestyles. Medical model focus on individual. conditioned by awareness of social responsibilities. emphasis on diagnosis treatment and care. places emphasis on medical care
  97. Ten essential Public health servies
    Provide a common ground for professionals trained in either public health or the medical model so they can work collaboratively towards fulfilling the public health mission.
  98. Definitions of 10 essential public health services
    "1. Monitor health status to identify community health problems. (over time) 2. Diagnose and investigate health problems and health hazards in the community. 3. Inform
  99. Public Health and disease
    Public health basically tries to prevent disease at a community level. Disease is due to an infectious agent and is waht may heppen while youre immune response tries to control an infection.
  100. Asymptoatic
    Infected and showing no clinical symptoms but can transmit the illness. Important can be a potential carrier
  101. Morbidity/Motaliity
    Number of people contracting the disease is morbiidty. Number of people dying is mortality
  102. Types of serious/scary infectious Threats
    1. Mass casualty events. Can be bioterroism. Pandemics (worldwide epidemic). 2. Antimicrobial resistance 3. New infectious agents.
  103. Mass Casualty events
    Can be intentional (bioterroism). Unintentional (Pandemics like flu. the plague).
  104. Antimicrobial Resistance
    Came around because of slection pressures to prescribe medications. Solution: Reduce infection by hygene. Judicious use of antibiotics (selective use). Limit human antibiotic use in animals. Combintaiton therapy. Targe virulence factors. Competive exclusion.
  105. Incidence of infection
    Rate of infections. Number of new cases each year. The when the where and the who
  106. Prevalence of infection
    Proportion of population infected. How much of popluation is infected
  107. Intesnity of infection
    Level of infection. Number of bacteria. Severity of infection (morbidity/mortality). Is a percent
  108. Infectious disease Surveillance
    Systematic collection. anaylsis and use of data on given infectious disesase.
  109. Major types of public health activities
    Surveillance. Outbreak investigation. Reference diagnosis and consultation. Research (bench to field to prevention). Technical assistance adn training (lab). Initiate and support implementation of projects. Health policy and health communcation
  110. 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.
  111. 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.
  112. 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.
  113. 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.
  114. 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.
  115. 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.
  116. 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.
  117. 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
  118. Main Tests for antimicrobial resistance
    1. Kirby Bauer. 2. MIC minimum inhibitory concentration (used for dose of treatment).
  119. Bacteriostaic vs bacteriocidal
    Bacteriostatic will just inhibit growth of the bacteria. Bacteriocidal will actually destroy the bacteria.
  120. Antibiotic combinatorial therapy.
    Using combination of different antibiotics to get a synergistic effect to enchance the effectivness of the drug.
  121. 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.
  122. Basic mechanisms of antibiotics
    1. Inhibit cell wall synthesis. 2. DNA replication 3. RNA synthesis. 4. Protein synthesis 5. Antimetabolities (disrupt metabolic processes)
  123. 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).
  124. 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.
  125. Bacitracin
    G- are resistant. MECHANISM. Prevents the movement of the precursor peptidoglycan to the cell wall. 2. Damages cell membrane increasing permeability
  126. Polymyxin B
    Similar to Bacitracin and increases permeability of outer membrane. More effected by osmotic pressure.
  127. 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
  128. 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.
  129. 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.
  130. 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
  131. 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.
  132. 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
  133. Metronidazole
    Inhibition of Nucleic Acid Syntheis. TARGET. cytotoxic to DNA. Resistance. 1. Efflux pump. 2. Decrease uptake.
  134. 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
  135. Major groups of pathogens
    1. Viruses. 2. Bacteria 3. Fungi 4. Parasites
  136. Immune system response to Intittial Infection 3 phases
    1. Innate immune response. 2. Early immune response. (first two are general) 3. Adaptive immune response.
  137. 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
  138. 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.
  139. 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.
  140. 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.
  141. 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
  142. 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.
  143. 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.
  144. Innate cell mechanism
    Use phagocytosis by recognizing components on pathogen. They are broken down by chemicals in the lysozymes.
  145. 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
  146. 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.
  147. 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.
  148. 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.
  149. 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.
  150. 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.
  151. 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.
  152. 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.
  153. 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
  154. 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.
  155. 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
  156. 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.
  157. 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.
  158. 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.
  159. Cytokines
    Are chemcial messengers. Can cause a bunch of different responses in cell. Are used to help fine tune and activate the immune response.
  160. Cytokine storm
    Super antigens induce an overactive response of immune system. Is abundant release of cytokines activating T cells.
  161. 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.
  162. Resisting phagocytosis
    1. Capsules make bacteria slippery and cant bind to bacteria. 2. Produce leukocidins that destroy phagocytes.
  163. 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.
  164. Defense against viruses
    1. Cytotoxic T cells 2. Interferon (a cytokine) makes other cells go into a antiviral state.
  165. 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.
  166. Type IV hypersensitivity
    Delayed type hypersensitivity. The first exposure nothing happnes. During second exposure is must more severe. Inflammation.
  167. Vaccine
    Stimulate the immune system to create a response and induce memory of a pathogen. First vaccine was small pox created by Edward Jenner.
  168. 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.
  169. 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.
  170. Louis Pasteur vaccines
    Chicken cholera. Antrhax. Rabies.
  171. Pyogenic Cocci
    Pus forming. Are staphlococcus and micrococcus. Are infections that cause pus. Pus is dead white blood cells.
  172. 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
  173. S. aureus
    Colonies turn a gold color as the stay longer on the media. Called old gold. Also Beta hemolytic.
  174. 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).
  175. M lutues colony color
    Has a bright yellow pigmented colony. Often confused with S. aureus but NO HEMOLYTIC.
  176. 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.
  177. Staphlyococcus Epidemiolgoy
    Can survive on surfaces for a long time. Person to person spread by direct contact or fomite. Opportunistic pathogen.
  178. 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)
  179. Exfollative toxins
    ETA and ETB. Are proteases that destroy the ECM and skin peels off. 5-10% strains. Cause Staphylococcal scalded skin syndrome (SSSS).
  180. 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.
  181. 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.
  182. 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.
  183. 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.
  184. 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)
  185. Staphylococcus epidermidis
    Frequent contaminant of blood cultures. Causes of nosocomial infections. Causes biofilm on catheters which are very antibiotic resistant.
  186. Staphylococcus saprophyticus
    2nd most common cuase of UTI. RESISTANT TO NOVOBIOCIN. Distinguishes from S. aureus and S. epi
  187. 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).
  188. S aureus is identified by
    1. Yellow colonies on MSA. 2. Coagulase positive. 3. Staph latex agglutination test.
  189. 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.
  190. MRSA
    Majority of nosocomial and community acquired infections. Treat wtih intravenous vancomycin ororal antibitoics clindamycin. sulfa drugs. doxycycline. VISA and VRSA.
  191. 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
  192. Differenttiation of species of Strep/Entero
    1. Lancefield groupsn (carbohydrates on cell wall). 2. Hemolytic patterns on BA. 3. Biochemical properties.
  193. Group A strep
    Streptococcus pyogenes. Most poteint pathogen. Rarely normal flora. ONLY HUMAN organism. Reseviors are humans who carry the bacteria. Beta Hemolytic
  194. 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.
  195. 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)
  196. Necrotizing fasciitis
    Very rare disease caused by S. pyogene. Super antigen exotoxins. begin like cellulits but does massive tissue damge. Needs debreedment to remove.
  197. 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.
  198. 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
  199. 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.
  200. 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.
  201. S. agalactiae and menigitis
    Causes meningitis in newborns
  202. 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.
  203. 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.
  204. 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.
  205. 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.
  206. Diseases caused by Enterococcus
    UTI. endocarditis from bacteremia. Polymicrobial wound and abdominal infections. Cause a lot of post infections. IS A POLYMICROBIAL INFECTION.
  207. 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.
  208. 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
  209. General characteritics of coynebacterium. listeria. erysipelothrix
    Gram positive bacilli. Aerobic or faculatavie. NON-SPROREFORMING. INclude outright pathogens. opportunists. and zoonotic pathogens.
  210. 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.
  211. 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.
  212. 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.
  213. 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.
  214. 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.
  215. 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.
  216. 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.
  217. Erysipeloid
    Localized skin infections. NO PUS PRODUCTION.
  218. C. diptheriae