Micro final

  1. Who was responsible for the initial discovery of the antibiotic penicillin?
    Alexander fleming
  2. inhibits the growth of or destroys microorganisms. These antibiotics contain a beta-lactam ring. The beta-lactam ring interacts with and inactivates transpeptidase, which makes crosslinks between peptide chains in the cell wall. Inactivation results in faulty cell wall synthesis, cell lysis
    Antibiotics
  3. also appear to stimulate autolytic enzymes. is narrow-spectrum and susceptible to microbial counterattacks. Could not penetrate outer membrane ? not effective against Gram ?
    Penicillins
  4. Penicillins can be degraded and inactivated by?
    penicillinase and other beta-lactamases
  5. an antimicrobial agent has been altered and improved upon over the years. overcome the limitations of the original molecule. eg.? Allow for penetration of the outer membrane, and thus can affect some Gram negative bacteria. eg. Are not as easily degraded by beta-lactamases and Achieved by changing functional groups attached to the beta-lactam ring
    Semisynthetic
  6. An antimicrobisal Mimicking defense peptides. Mammalian innate immune system produces peptides that have antimicrobial activity. Bacteria also produce defense peptides called bacteriocins, lantibiotics .These peptides insert into membranes and target other structures in cells
    Synthetic
  7. antibiotic that kills bacteria without reliance on the patient's immune system to help
    Bactericidal
  8. antibiotic is one that prevents the organism multiplying but it is the patient's own immune system which kills off the bacteria and leads to recovery from the infection.
    Bacteriostatic
  9. kill or inhibit the actions or synthesis of molecules in microorganisms but not human host cells. Target structures or processes that differ between the microbe and the host
    selective toxicity
  10. What are some selective toxicity in bacteria?
    Ribosomes; peptidoglycan cell wall; specific anabolic pathways; some aspects of DNA replication
  11. What are some selective toxicity examples in fungi?
    Cell wall; specific anabolic pathways
  12. what are some examples of selective toxicity in viruses?
    Specific viral proteins; receptors that allow recognition of host cells; host pathways necessary for viral replication but not vital to the host
  13. Drugs designed to act on Bacteria are generally ineffective against fungi. More similarities between fungal and human cells (in comparison to Bacteria) means that drugs toxic to fungi may harm
    human tissues
  14. What is the core structure of penicillins that gives rise to their antimicrobial properties? What is the name of the bacterial enzyme that attacks this core structure, allowing for resistance?
    The beta-lactam ring interacts with and inactivates transpeptidase. Can be degraded and inactivated by secreted penicillinase and other beta-lactamases that cleave the b-lactam ring, allow for resistance
  15. bind to the small ribosomal subunit 30S and interfere with protein synthesis by causing misreading of the mRNA. (direct inhibition).
    aminoglycosides
  16. (do what aminoglycosides do), macroslides, and chloramphenicol are static and macroslides bind to the large ribosomal subunit 50S and inhibit peptide elongation during synthesis.
    Tetracyclines
  17. Bind to fungal membranes, causing loss of selective permeability. Specifically interacts with fungi-specific sterols
    Macrolide polyenes (amphotericin B)
  18. Interferes with sterol synthesis, affect membrane integrity of fungi
    Azoles (miconazole and clotrimazole)
  19. Inhibit fungal cell wall synthesis in fungi
    Echinocandins (caspfungin)
  20. Specifically impairs RNA and DNA synthesis in fungi
    nucleotide analogs (flucytosine)
  21. are effective against more than one group of bacteria. Tetracycline antibiotics are an example.
    Broad-spectrum drugs
  22. What is an example of broad spectrun drug?
    Tetracycline
  23. broad spectrum drugs can be useful but also have more potential to cause problems by killing other members of the human microbiome (problems with?
    superinfections
  24. Broad-spectrum antimicrobials destroy
    healthy biota along with pathogens
  25. microbes that were once small in number overgrow when normal resident biota are destroyed by broad-spectrum antimicrobials
    superinfections
  26. Ability of microorganisms to tolerate an amount of drug that would normally be inhibitory. Can be tolerant to low amounts (?intermediate? phenotype) or resistant to higher amounts.
    drug resistance
  27. Microbes become newly resistant to a drug after one of the following occurs:
    Spontaneous mutations or acquisition of new genes
  28. Non-disease-causing flora of humans and animals can harbor antibiotic resistance genes that can be transferred to
    pathogenic bacteria with which they share space
  29. 5 mechanisms of drug resistance.
    1)Enzymatic degradation or chemical modification of antibiotics 2) Preventing uptake of antibiotics 3) Efflux (pumping out) of antibiotics form the cytoplasm 4) Alteration of binding site for antibiotics 5) Use of alternative biosynthetic pathways
  30. This techniques ueses Surface of an agar plate is spread with bacteria. Small discs containing a prepared amount of antibiotic are placed on the plate. Zone of inhibition surrounding the discs is measured and compared with a standard for each drug. Antibiogram provides qualitative data for drug selection. Resistant, susceptible, or intermediate. This method is less effective for anaerobic, fastidious, or slow-growing bacteria
    Kirby-Bauer tech.
  31. This technique uses More sensitive and quantitative than the Kirby-Bauer test. Antimicrobial is diluted serially in tubes of liquid medium. Each tube is inoculated with a small uniform sample of pure culture of the organism to be tested. Minimum inhibitory concentration (MIC): the smallest concentration (highest dilution) of drug that visibly inhibits growth. Useful in determining the effective dosage and providing a comparative index against other antimicrobials
    Tube dilution tests
  32. the smallest concentration (highest dilution) of drug that visibly inhibits growth
    Minimum inhibitory concentration MIC
  33. the ratio of the dose of the drug that is toxic to humans as compared to its minimum effective (therapeutic) dose the smaller the ratio, the greater the potential for the drug to have a negative affect on the patient
    Therapeutic index TI
  34. What are some strategies for finding or developing new drugs or methods of treating microbial infections?
    mining for natureal microbes, targeting iron-scavenging capabilities of bacteria, mimiking (synthetic) defense peptides, or using bacteriophages.
  35. What are some general aspects of viruses that make them obligate intracellular parasites?
    Require a host cell for reproduction and all metabolic processes. Free virions are essentially inert (with rare exceptions). Typically have small genomes, often use many enzymes/functions encoded by the host cell
  36. whole, infective virus. Minimally composed of nucleic acid (RNA or DNA) and a protein coat. Nucleic acid may be RNA or DNA, single stranded (ss) or double stranded (ds). ssRNA or ssDNA may be either + strand or ? strand. Nucleic acid content is basis for Baltimore classification of viruses (later). Some viruses also contain a membrane envelope derived form host cell plasma membrane
    Viron
  37. the protein shell that surrounds the genome of a virus particle. Composed of a number of protein molecules arranged in a precise and highly repetitive pattern around the nucleic acid
    capsid
  38. Individual protein subunit of the capsid. Capsomers are groups (usually 5-6) protomers that make up the smallest morphological unit in icosahedral capsids visible with an electron microscope
    Promoter
  39. complete complex of nucleic acid and protein packaged in the virion. Self-assembly of capsid proteins around nucleic acid (mechanism not well understood). Usually structured with a high degree of symmetry
    Nucelocapsid
  40. virus that has a lipid bilayer surrounding the nucleocapsid. Layer itself is derived from the host. However, it is ?decorated? with virus-derived lipoproteins important for attachment to new hosts and other processes. Most enveloped viruses are eukaryotic viruses (not bacterial/archaeal)
    Envelopped virus
  41. Proteins on the outer surface of the virus. Most spikes bind to receptors on specific host cells to allow for attachment (adsorption) and entry
    Spiked proteins or peplomers
  42. What are the 5 major steps in the infection cycle of a generic virus>
    Adsorption, openetration, synthesis, assembly, and release
  43. Lytic phage are only capable of
    lytic cylce
  44. Lysogenic phages can?
    choose to enter lytic cycle upon infection or enter lysogenic cycle, incorporating their nucleic acid into the host chromosome (forming a lysogen or prophage)
  45. What are some differnt outcomes of infection for viruses of eukaryotic cells?
    Acute infections, persistent infections, transformation, cytocidal infections, and cytopathic effects.
  46. two types of persistent infections.
    Latent and chronic
  47. Persistence of the virus in the cell without virus production
    latent infection
  48. virus production w/out cell death
    chronic infection
  49. Virus possesses or encodes an oncogene. Insertion of viral DNA into the host genome activates oncogenes
    Transformation
  50. infections result in cell death
    cytocidal
  51. effects other than lysis can be caused
    cytopathic
  52. Proteins on the outer surface of the virus. Most spikes bind to receptors on specific host cells to allow for attachment (adsorption) and entry. Entry requires adsorption, specific binding of proteins on the outside of the virion
    spiked proteins or peplomers
  53. What are two general modes of entry of viruses of animal cells?
    fusion or endocytosis
  54. Entry of enveloped viruses by fusion of the envelope with the cytoplasmic membrane, resulting in entry of the nucleocapsid
    fusion
  55. Both enveloped and nonenveloped viruses can be taken up by triggering endocytosis of the virion by the cell
    endocytosis
  56. What are three major modes of exit of viruses from host cells? For enveloped viruses, what critical component(s) must be inserted into the host cell membrane prior to budding?
    Lysis of the host cell (common for nonenveloped viruses. Fusion of a membrane vesicle containing virions with the cytoplasmic membrane. Budding from host cell (common for enveloped viruses)
  57. what are the seven major groups of viruses in the baltimore classification system?
    ds DNA viruses, ss Dna viruses, ds RNA viruses, +stranded RNA viruses, - stranded RNA viruses, retroviruses, and reverse transcribing DNA viruses.
  58. What are some major stages of infection of the lytic phage T4 of E. coli?
    Virions attach to cells via tail fibers that interact specifically with polysaccharides on E. coli outer membrane Tail fibers retract and tail core makes contact with E. coli cell surface. Lysozyme forms a small pore in peptidoglycan. Tail sheath contracts and viral DNA passes into cytoplasm After penetration, early genes are recognized by host RNA polymerase. Early genes: Encode proteins that result in covalent modification of host cell RNA polymerase ? anti sigma and new sigma factor. Bind to host cell RNA polymerase and direct transcription of viral genes. Nucleases that specifically degrade host DNA. Additional early-middle genes are recognized by modified RNA polymerase. Replicate T4 DNA (polymerase) Late genes:? Synthesis of capsid proteins, tail proteins.. The virus proteins self-assemble with aid of host chaperones. T4 lysozyme to degrade peptidoglycan ? cell lysis and release of virions
  59. In what way is bacteriophage Mu like a transposon?
    Small genome, mutator phage, can inssert within host genes, replication by tramnsposition, phage is also transposon, DNA sequences that move from one portion to anotherm mediated by a transposase enzyme,
  60. What are some mechanisms by which bacteria can attempt to resist infection by bacteriophage?
    restriction-modification systems and restriction enzymes
  61. CRISPR
    Clustered regulatorty interspaced shoirt palindromic repeats
  62. what are the steps in CRISPR mediated immunity?
    adaption and interference
  63. in this CRISPR stage Cells that survive viral infection can add portions of viral DNA as new spacers in CRISPR loci. Added at one end of the CRISPR, can show history of viral infection
    Adaptation stage
  64. In this crispr stage ? CRISPR regions are transcribed upon viral infection Cas proteins process and associate with individual spacer regions in the CRISPR RNA. Cas/CRISPR complexes bind to and destroy viral DNA/mRNA complementary to CRISPR seqs
    Interference stage
  65. Pox viruses are dsDNA viruses that carry out their entire replication cycle in the animal host cell cytoplasm. What important protein components inside the virion make this possible?
    DNA virus replication, transcripton occurs in the cytoplasm. contains all the necessary genes/functionsm, some already as enzymes in the mucleocapsid, and some activity even before uncoating.
  66. What enzyme critical for replication of RNA viruses is not normally present in animal host cells?
    RNA replicase
  67. For which types of RNA viruses (dsRNA, +ssRNA, -ssRNA) is the replicase enzyme required in the virion?
    ds and -ss RNA
  68. For which of these types of viruses is the RNA genome itself infective?
    +SSRNA
  69. example of a lysosome virus
    Mu
  70. Is the virus that cuased SARS, enveloped replication occurs in cytoplasm. Genome has a 5? cap, 3? poly-A tail. Virions are assembled in the Golgi apparatus
    Corornavirus
  71. examples of -Stranded ssRNA? All must contain rna replicase
    Rabdoviruses Rabies virus Orthomyxoviruses Influenza Ebola virus
  72. Usually infect cells in upper respiratory tract. Enveloped; replicates in the host cell nucleus Genome is segmented: 8 segments encoding 10 genes
    Influenza
  73. Enzymes in the influenza?
    RNA replicase, RNA endonuclease, neuraminidase, and hemagglutinin
  74. Mutations in genes encoding N and H during replication result in small differences in N and H structure. Antibodies developed by exposure to previous (unmutated) versions recognize the new, mutated versions less effectively (or not at all)produces yearly variation in most influenza strains. This is the reason why flu vaccines are revised yearly
    Antigenic drift small changes un individual genes by point mutation
  75. ?Large? changes due to recombination of genome segments
    Antigenic shift
  76. What are the three important enzymes that are present in the HIV viron?
    Reverse transcriptase, integrase, and protease
  77. This HIV enzyme converts RNA genome to DNA
    Reverse trasncriptase
  78. this HIV enzyme integrates viral DNA into host cell chromosoeme
    Integrase
  79. THis HIV enzyme processes/cleaves viral proteins for selectiveely toxic anti-HIUV drugs
    protease
  80. what are some selectivey toxic drug interactions for HIV?
    Fusion inhibitors, Reverse transcriptase inhibitors, integrase inhibitorsm and protease inhibitors.
  81. Some retro viruses can cause cancer. how?
    integration near proto-oncogenes, resulting in chages in expression
  82. What is the great plate count anomaly?
    plate counts are typically much less than direct counts. 1% 0.1% or even 0.01%
  83. why is there such a difference in plate counts and direct counts?
    abundace of unculturable microbes in various environment.
  84. what are some reasons that microbes might not be grown in isolation easily?
    Slow growing, low abundance, inhibition by other microbes, fastidious growth requirment, crossfeeding or signals from other microbes needed, and triggers for growth from a dormant state are not present.
  85. whay use 16s/18s rRNA genes?
    all cells have them, 1500bp long, contain both conserved and variable regions, promers for PCR can target conserved regions, and sequencing into variable regions can identify differnt organisms.
  86. Typically 16S rRNA gene sequencing cannot easily identify a given microbe down to the
    species-level
  87. what method will offer a higher taxonomic resolution>
    genome sequencing.
  88. Analysis of the whole mixture of environmental DNA
    Metagenomics
  89. Benefits of cultivation-independent genomics techniques
    Typically, only 1% or fewer of microbes in a given environment can be cultivated using standard techniques. Standard genomics techniques require cultivation. Metagenomics and single-cell genomics allows application of genomics techniques to this "uncultured majority".
  90. Limitations cultivation-independent genomics techniques
    Often only incomplete genomes are obtained from a given organism. Much more sequence data is generally required than for standard genomics
  91. What is FISH and what does it target?
    Fluorescence in situ hybridization. Target is the ribosomes (100?s-1000?s copies in active cells), not the genes (few copies
  92. What is stable isotope probing?
    Like FISH-nanoSIMS, but just analyzing DNA (or RNA), not with microscopy and labeled probes
  93. How might you use stable isotope probing to determine which microbes in an environmental sample are capable of uptake of a specific compound, e.g. pectin or estrogen?
    Incubate sample with compound labeled with STABLE ISOTOPE. Isolate DNA (or RNA) and separate heavier and lighter DNA fractions by ultra centrifugation.Can investigate the resulting heavy fraction by PCR for specific genes or by ?metagenomics? approaches
  94. What does nanoSIMS mean?
    FISH-nanoSIMS (secondary ion mass spectrometry)
  95. Using FISH-nanoSIMS to assess substrate uptake in ?Caldatribacterium. FISH-nanoSIMS to identify intestinal bacteria that consume mucus (produced from 15N labeled amino acids injected into
    Mouse
  96. What are some things only carrier out by microbes?
    nitrification, nitrogen fixation, and dissimilatory nitrate reduction. Sulfide/sulfur oxidation,
  97. What are some roles that the human microbiota plays that are beneficial to the human host?
    aiding in carbohydrate digestion, production of vitamins (e.g. biotin, K), and preventing colonization of the host by potential pathogens
  98. Where are most opf the bacteria in the human biome?
    skin, Resp. tract, GI, opening of urethram genitalia, vagina, external ear and eye.
  99. sites not colonized in healthy people?
    Organs and sealed systems, bones, neuro, gonads, glands, sinuses, middle and inner ear ma dn interal eye. fluid within and organ or tissues system.
  100. what are the four phyla that make up the human micorbiome?
    Actinobacteria, firicutes, proteobacteria, and bacteroidetes.
  101. what Archea are found in the human biome?
    Methanobrevibacter smithii in the colon.
  102. where does your microbiome come from?
    Breaking of fetal membranes first exposes the infant to microbes.Comprehensive exposure occurs during the birth process itself. Initial colonization of the large intestine depends on how the infant is fed.Colonization continues as the infant comes into contact with family members, health care personnel, the environment, and food
  103. where are most of the bacteria in your biome?
    Colon
  104. What are the jobs of the bacteria in the intestines?
    aide in digestion, produce vitamine K, B12 modifictaion of host steroids.
  105. what are some physical barriers that prevent microbes?
    skin and mucous membranes
  106. Signal molecules found on microbial surfaces recognized by phagocytes and other defensive cells. Molecules shared by many microorganisms, but not present in mammals. Serve as ?red flags? for phagocytes and other cells of innate immunity. Bacterial PAMPs: peptidoglycan and lipopolysaccharide. Viral PAMPs: double-stranded RNA
    Pathogen-associated molecular patterns (PAMPs)
  107. Found on phagocytes, dendritic cells, endothelial cells, and lymphocytes. Recognize and bind PAMPs. Recognition is ?hard wired?. Cells possess PRRs whether they have encountered PAMPs before or not
    Pattern Recognition Receptors PRRs
  108. 7 steps in phagocytosis.
    Chemotaxis, adhesion, engulfment, phagosome formation, phagolysome formation, destruction, exertion
  109. How do inferons work?
    Virus infects cell. Infected cell secrete inferons. picked up by nearby cell. New cells inhibit viral multiplicatiopn and degrage viral rna.
  110. What are three different outcomes of the action of complement?
    Disruption of cell membrane and lysis of pathogens.Increased recognition of pathogens by phagocytes. Stimulation of inflammation
  111. Overall stages in the ?classical? complement cascade resulting in pathogen lysis
    initiation, amplification, polymerization, and membrane attack
  112. Why are iron binding proteins considered to have antimicrobial properties?
    limites growth of bacteria, keeps it from being used by bacteria.
  113. Some types of iron binding proteins:
    Hemoglobin, transferrin, lactoferrin, ferritin
  114. Cationic, short proteins (peptides) produced by humans that can bind to and disrupt bacterial cytoplasmic membranes (causing lysis). Some members of the human microbiome produce similar peptides that can have beneficial effects (attack pathogens)
    antimicrobial peptides
  115. Innate immunity
    Phagocytes
  116. Specific immunity
    Lymphocytes T and B cells
  117. B-Cells produce?
    antibodies and memory cells.
  118. two major tyopes of T-cells
    CD4 and CD8
  119. molecules that stimulate a response by B and T cells
    Antigens and immunogens
  120. The specific structure on an antigen that is recognized
    epitope
  121. B-cell receptors that recognize specific epitopes. These can be bound to B cell membrane or secreted from B plasma cells
    Immunoglobulin or antibodies
  122. Involved in identification of self, presentation of antigens, immunity
    MHC
Author
MagusB
ID
344000
Card Set
Micro final
Description
why look
Updated