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Microbiology
Unit 3
| Question | Answer |
|---|---|
| How MUCOUS protects the respiratory system | Produced by mucous membranes, traps microorganisms Predominant antibody is IgA-stimulates inflammatory response. |
| How HAIR protects the respiratory system | The nose has mucous-coated hairs that filter inhaled air & trap microorganisms, dust, & pollutants. |
| How NORMAL MICROBIOTA protect the respiratory system | Suppress pathogens by competitive inhibition in upper respiratory system. Lower respiratory system is sterile. |
| Pharyngitis | Sore throat. Inflammation of mucous membranes. |
| Laryngitis | Infection of the larynx. |
| Tonsillitis | Infection of the tonsils |
| Sinusitis | Infection of a sinus causing heavy nasal discharge of mucous. Acute: S. pneumoniae, H. influenzae, & M. cattarrhalis. |
| Epiglottitis | H. influenzae type b, can cause death within a few hours. Prevention: Hib vaccine given for meningitis. |
| Otitis media | Ear infection. Infects 85% of kids before age 3. 50% of pediatric office visits. Treatment: penicillin. S. pneumoniae, H. influenzae, M. catarrhalis, S. pyogenes, S. aureus. |
| Defenses of the lower respiratory system that helps keep it sterile. | Pleura, Epiglottis, Ciliary Escalator, Coughing & Sneezing, Alveolar Macrophages, IgA Antibodies. |
| Pleura | Double-layered membrane enclosing the lungs. |
| Epiglottis | Covers the larynx during swalowing. |
| Ciliary Escalator | Cells of the mucous membrane of the lower respiratory tract are covered with cilia that move synchronously & propel inhaled dust & microorganisms back toward the throat (1-3cm/hr). |
| Coughing & Sneezing | Speed up the escalator (cigarette smoke & ventilation inhibit the escalator). |
| Alveolar macrophages | Phagocytes. Locate, ingest, and destroy most of invaders. |
| Antibodies (IgA) | In respiratory mucus, saliva, & tears. Identify & neutralize foreign objects. |
| Pertussis (Whooping Cough) | The only vaccine-preventable disease on the rise in the U.S. DTaP. |
| Pathogenic Mechanisms of B. pertussis (causes pertussis-gram-negative coccobacillus, obligate aerobe). | Capsule. Tracheal cytotoxin of cell wall damages ciliated cells. Pertussis toxin enters bloodstream. |
| Stages of pertussis | 1 Catarrhal-like common cold 2 Paroxysmal-violent coughing due to damaged ciliary escalator (1-6 wks). Mucous can block airway. Broken ribs & permanent brain damage can occur in infants due to cough severity 3 Convalescence |
| Diagnosis of Pertussis | Throat swab during coughing fit-difficult to culture. PCR amplifies target DNA through specific primers. Pseudoepidemic-can detect better? |
| Treatment of Pertussis | Erythromycin or other macrolides (not effective after onset of paroxysmal stage). |
| Bronchitis | Inflammation of main air passage. Bacteria, viruses, & fungi cause it. |
| Bronchiolitis | Smallest air passages, viral infections, swelling & mucous. Bacteria, viruses & fungi cause it. |
| Pneumonia | Includes infection of the pulmonary alveoli. Bacteriak viruses, & fungi cause it. |
| Gene | A segment of DNA that encodes a functional product, usually a protein. |
| Genome | All the genetic information in a cell. |
| Genetics | The study of what genes are, how they carry information, how information is expressed, & how genes are replicated. |
| Chromosome | Structure containing DNA that physically carries hereditary information; the chromosomes contain the genes. |
| Plasmid | A circular, double-stranded unit of DNA that replicates within a cell independently of the chromosomal DNA. Plasmids are most often found in bacteria and are used in recombinant DNA research to transfer genes between cells. |
| Base pairs | The pair of nitrogenous bases, consisting of a purine linked by h-bonds to a pyrimidine, that connects the complementary strands of DNA or of hybrid molecules joining DNA and RNA. The base pairs are A-T & G-C in DNA, and A-U and G-C in RNA. |
| Nucleotide | Any of various compounds consisting of a nucleoside combined with a phosphate group and forming the basic constituent of DNA and RNA. |
| dNTP | DeoxyriboNucleotide TriPhosphate |
| Flow of information in biological systems | Central Dogma. DNA-transcription-mRNA-translation-protein. Replication-cell elongation-septum formation-completion of septum w/ formation of distinct walls-cell separation. |
| Bacterial Chromosomes & how they're different from eukaryotic ones. | Appearance-irregular blobs separate from cytoplasm. 4*10^6bp. Most are circular in contrast to linear eukaryotic genomes. Compacted via supercoiling. No membrane separates DNA from cytoplasm (nucleoid). |
| Plasmids | Circular DNA in bacteria with no essential DNA. Can be shared-horizontal DNA transfer. Codes for: antibiotic-resistance, resistance to toxic metals, metabolizing rare food sources, virulence, allowing symbiosis, iron uptake, toxins. |
| Basic Structure of DNA | Sugar, nitrogenous base, and phosphate. Double helix associated w/ proteins. Backbone is deoxyribose-phosphate. Strands held together by H-bonds between AT & CG. Strands are antiparallel. |
| Addition of nucleotides to a growing DNA molecule | 5'-3'. When a nucleoside triphosphate binds to the sugar OH, it loses 2 phosphates. Hydrolysis of the phosphate bonds provides the energy for the reaction. DNA polymerase requires primer-will only bind to ds DNA. |
| Origin of Replication, bacterial DNA | OriC. In bacteria, 2 replication forms move around circular DNA till they meet. |
| Proofreading | DS binding property of DNA polymerase allows proofreading by sensing the local structure of DNA. A mismatch causes a bulge. |
| DNA gyrase | Enzyme that unwinds the ds parental DNA. |
| Helicase | Pulls the DNA strands apart. |
| Primase | The lagging strand is synthesized discontinuously. An RNA primer, produced by the protein primase is used to initiate replication. DNA pol replaces the primer w/ DNA later. |
| DNA polymerase | Synthesizes DNA. 3 at each fork. 1 for each strand & 1 to fill in Okasaki fragments. |
| DNA ligase | Joins the discontinuous Okasaki fragments. |
| Single-stranded binding (SSB) proteins | Bind ss DNA to stabilize it & keep it apart. |
| Okazaki fragments | On lagging strand. |
| If it takes an E. coli cell 40 min to replicate DNA, how does it divide in 20 min? | In fast growing cells, DNA replication doesn't wait until one replication is done before starting another. |
| RNA | Has ribose. Is single-stranded. A h-bonds with U. C with G. 2 OHs on ribose as opposed to 1 on deoxyribose. |
| Transcription | RNA polymerase doesn't require a primer. No proofreading. Makes short segments-1 gene. 5'-3'. Begins at promoter sequence & ends at terminator sequence. No OriC used. One strand transcribed. |
| Sigma factors & promoter sites | Sigma factor tells RNA pol where to bind & begin transcription. Recruits RNA pol to promoters & regulates gene expression. Dissociates after ~12nt. Rho dependent termination-also simple t based on a stem-loop structure in DNA. Promoters: -35 & -10 regions |
| How does the antibiotic Rifampicin block transcription? | Blocks translocation and thus elongation. |
| Four molecules of life | DNA, Protein, Lipids, Carbohydrates |
| Bacterial Ribosomes | ribosomal RNA. Small & large subunits. A, P, & E sites. |
| Translation | mRNA translated into codons (3 nucleotides). Start: AUG. Translation ends at nonsense codons: UAA, UAG, UGA. 61 of 64 codons assigned to 20 amino acids. |
| The genetic code is degenerate | Multiple codons are assigned to one amino acid. Third base degeneracy: reduced specificity at the last base. Minimizes mutation in protein. |
| Synonymous codons | Code for the same amino acid. "Silent" or "synonymous" mutations have no effect on protein. Related codons often code for related aas. Ex. CUU-Leu. AUU-Ile. |
| Shine-Dalgarno sequence with 16S rRNA in translation initiation. | Only in bacteria. We target it with antibiotics. Shine-Delgarno sequence in the mRNA recruits the small subunit of the ribosome. It is spaced 7-10 nts before ATG start so that the initial ATG aligns with Active site of the Ribosome when fully assembled. |
| tRNA | Transfer RNA. An adapter for translating a codon to an amino acid. Stem-loop structure. Anticodon. Acceptor stem. |
| Initiation early in initiation | fMet (formyl met) binds first. Ribosomal subunits come together. |
| Why do antibiotics that target bacterial ribosomes have large side-effects in humans? | Our mitochondria have prokaryotic-like ribosomes. Prokaryote: 30S & 50S. Eukaryote: 40S & 60S. |
| Building the polypeptide chain | Charged tRNAs enter the A site. Peptide bond formation between the amino acids on the tRNAs in the A & P sites. Exit of uncharged tRNAs through the E site. |
| Stopping translation | Stop codons & release factors |
| Why is Peptide deformylase a good antibacterial target? | Bacteria require formyl methionine to start translation. Humans don't. |
| Different ways antibiotics inhibit translations | Inhibit 30S-blocks tRNA attachment. Inhibit 50S-inhibits Catalytic Mechanism (CM). |
| Transcription | RNA pol makes RNA from DNA template. Requires sigma factor to recognize promoter (-35 & -10 regions). RNA is ss & has Us in place of Ts. |
| Translation | Ribosomes make protein from mRNA. Ribosomes are RNA that is catalytic-rRNA. Ribosomes are recruited by Shine Delgarno sequence ~7bp upstream of a start AUG. |
| Importance of Gene Expression | Control allows for antigenic variation (trypanosomes). Also allows for host invasion survivial in dif environments-vibrio cholerae expresses pili necessary for biofilm production/survival in H2O & stomach. After stomach, new pili expressed for intestine. |
| Transcription/translational coupling | Can occur simultaneously. Transcription occurs at the nucleoid/cytoplasm interface. No nucleus. |
| Ways Gene Expression is Controlled | Transcription/translational coupling, multiple sigma factors, mRNA stability, Gene organization (operons), Transcriptional repressors/activators. |
| Multiple Sigma Factors | To recruit RNA pol in response to different stimuli. Expression varies by 10,000 fold. Sigma70 has basal expression. During times of stress, other sigmas are synthesized which recognize new sets of promoters. |
| Gene Organization | In operons so that all genes for one pathway can be controlled together. Polycystronic mRNAs: many genes. Regulatory gene, promoter, operator, genes, terminator. |
| Transcriptional repressors/activators | Lac operon ex: When lactose becomes available, it is converted into allolactose, which inhibits the lac repressor's DNA binding ability. Loss of DNA binding by the lac repressor is required for transcriptional activation of the operon. |
| mRNA stability | Average half life is 30 sec in E. coli. E. coli doesn't make proteins it doesn't need. It is efficient. Our mRNA lasts for days. |
| Regulons: global regulatory system | Regulons are the set of genes affected by a transcriptional regulator. They allow cells to coordinate gene expression in response to a stimuli. Cells send signals to other cells to tell they are present. Make a biofilm together. Quorum sensing. |
| Evolutionary change driving forces | Increase fitness-ability to reproduce. Antibiotic resistance. |
| How can small genetic changes (point mutations) have large effects on protein function? | Protein won't fold right. Folding determines function. We develop cancer this way. |
| Point Mutation | Base substitution, change in one base. |
| Frameshift Mutation | Insertion or deletion of one or more nucleotide pairs. Changes entire reading frame. |
| Silent Mutation | DNA change without amino acid change |
| Nonsense Mutation | An amino acid codon is replace by a nonsense (stop) codon |
| Missense Mutation | Results in an amino acid change |
| Spontaneous Mutation | Natural. Rate=1 in 10^9bp. |
| Mutagens | Increase mutation rate by 1000 fold or more. |
| UV radiation | Causes thymine dimers |
| Ionizing radiation | Causes free radicals that damage DNA bases causing mispairing. |
| Pathways for DNA damage repair | Photolyases separate thymine dimers. Nucleotide excision repair. |
| Chemical Mutagenesis | Mispairing or frameshifting. Make bases look different & cause problems. |
| The Ames test | Plate Histidine-dependent Salmonella. Spot a potential mutagen in the middle. Check to see if more growth occurs with mutagen than in control. Will grow more around mutagen. Revertants: problem mutated to repair. |
| Horizontal Gene Transfer | Cells of same generation. 3 mechanisms: Transduction, Transformation, & Conjugation. |
| Transduction | Transfer by viral delivery |
| Transformation | Uptake of free/naked DNA from environment. Griffith: Non pathogenic rough, live bacteria mixed in mouse with dead, pathogenic, smooth bacteria killed the mouse. Avery, MacLeod, McCarty found that DNA was transferred by using DNAse, RNAse, & Proteinase. |
| Conjugation | Plasmid transfer through the pilus from one bacterial cell to another. One F-, one F+. Replicate plasmid during transfer so both have it, both F+. F factor can be inserted into chromosome. |
| DNA integration through recombination | Newly aquired DNA can be integrated into host genome by recombination. Exchange of genes between 2 DNA molecules. Crossing over occurs when 2 chromosomes break & rejoin. |
| How can recombination lead to greater genetic changes? | Greater variation. Different from 2 parents. |
| How do genetic changes lead to new phenotypes that allow bacteria to adopt new lifestyles? | Antibiotic resistance, ability to live somewhere new, etc. |
| R Factor | A type of plasmid that encodes antibiotic resistance genes |
| Generalized vs. Specialized Transduction | G: Phage degrades chromosome & takes a piece with it. Can't make new phages. S: Phage goes into lysogenic cycle. Integrates into host chromosome. When it leaves, it takes a piece of host w/ it. Can make new phages. New bacteria pathogenic during lysogeny. |
| Disease progression for a Yersinia pestis infection | Bubonic, septicemic, & pneumonic plague. B=swelling lymph nodes-bacteria make a soup of them. Get into bs & cause S=coagulation=blackness on extremities. Lung if you live long enough. VERY contagious-cough. |
| How do you become infected with plague? | 90% bubonic from fleas. Infects flea preventriculus. Blocks tummy. They are hungry more & regurgitate blockage into host. They spit a biofilm into us that is hard for us to phagocytize. |
| Type 3-secretion system to inject toxic proteins directly into human cells. | Needle & syringe. Toxic YOPS proteins paralyze cell. Prevent infected cell form calling for help. Make immune cells commit suicide. Suppress inflammation by downregulating cytokines. |
| Why are there only ~10 infections/yr in the U.S. today? Why is plague still important to study. | A different, less pathogenic strain lives today. Plague caused three historical pandemics. We can learn about other plagues as well as this one by using Yersinia pestis as a model. |
| Biotechnology | The use of microorganisms, cells, or cell components to make a product. Foods, antibiotics, vitamins, enzymes. |
| Recombinant DNA (rDNA) technology | Insertion or modification of genes to produce desired proteins. |
| Cloning (Genetic Modification) | Clone: Population of cells arising from one cell, each carries the new gene. |
| What are plasmids and how are they used in rDNA technology? | Small, circular piece of DNA. Used as vectors for cloning. Carry new DNA to desired cell. Plasmids & viruses can be used as vectors. |
| Polymerase Chain Reaction (PCR) | DNA replication in a test tube. A way to isolate genes. Uses enzymes & temperature. |
| Necessary Materials for PCR | DNA polymerase, a primer, DNTPs, & a template. |
| Uses for PCR | Clone DNA for recombination. Amplify DNA to detectable levels. Sequence DNA. Diagnose genetic disease. Detect pathogens. |
| PCR Steps | Incubate target DNA at 94C for 1 min-strands separate. Add primers, dnts, & DNA pol. Primers attach during incubation at 60C for 1 min. Incubate at 72C for 1 min. 2 DNA copies formed. Repeat. |
| Restriction Enzymes | Cut specific sequences of DNA. Destroy phage DNA in bacterial cells. Can't digest host DNA with methylated cytosines. |
| Restriction modification systems | Found in most bacteria to protect against foreign DNA. |
| How do molecular biologists use restriction enzymes to manipulate DNA? | We use them to cut open plasmids that we can then insert our PCR product into. "Gene of Interest." |
| Uses of Cloning (Genetic Modification) | Make a protein product of a gene-insulin! Make copies of a gene. Pest resistance gene, Gene that alters bacteria to clean up toxic waste. Subunit vaccines (protein portion of pathogen). DNA vaccines. Gene therapy-replace missing or defective. |
| Properties of E. coli that make it a great organism for producing proteins | Easily grown. Its genomics are known. It eliminates endotixin products. Cells must be lysed to get product. E.coli doesn't. |
| Why are eukaryotic cells sometimes necessary to produce proteins? | Sometimes yeast cells are used because they have properties more similar to human cells. Saccharromyces cerevisae expresses eukaryotic genes easily. Plants are easily grown. Mammalian cells are harder to grow, but express eukaryotic genes easily. |
| Ti plasmid | Agrobacterium tumefaciens transfers the tumor-inducing (Ti) plasmid by conjugation to plant cells. We use it to put new traits into plants. Pesticide resistance, vitamins, etc. |
| Methods used to insert foreign DNA into cells | Conjugation. Electroporation (increase cell membrane permeability w/ an electrical current). Transformation-uptake of DNA often induced by chemicals. Protoplast fusion-digest away cell walls, let membranes fuse. Micro injection. |
| How does knowing the whole genomic sequence for an organism aid in our understanding of organisms and diseases? | The Human Genome Project-nts sequences in an international 13-year effort. Finished 2003. Human Proteome Project may provide diagnostics & treatments. Reverse genetics-block a gene to determine function. |
| Why is Tuberculosis a major world concern? AKA Consumption. | WHO: A global health emergency. 1 new case per second. Kills 50% if untreated. 1/3 of world infected. Rising by 2%/year. #4 infectious disease killer in the world. Single agent. |
| Acid-fast cell wall of Tuberculosis advantages & disadvantages. | High lipid content of cell wall protects cells from drying out & from antimicrobials, BUT it stimulates a strong immune response. Inflammatory response damages lung tissue. T cells create memory |
| Step 1 in the pathogenesis of Tuberculosis | Inhalation into lungs. Ingested by macrophage. Inhibits formation of the phagolysosome & grows in macrophage. Protected from detection. |
| Step 2 in the pathogenesis of Tuberculosis | Tubercle bacilli multiply in macrophage causing chemotactic response that brings more macrophages & defensive cells to area. Form layer & early tubercle. Most macrophages don't destroy bacteria but release enzymes & cytokines that cause inflammation. |
| Step 3 in the pathogenesis of Tuberculosis | Few wks, symptoms appear as macrophages die, releasing tubercle bacilli & forming caseous center in tubercle. Aerobic bacilli don't grow well. Many remain dormant 7 serve as a basis for later reactivation. Maybe arreseted at this stage-lesions calcified. |
| Step 4 in the pathogenesis of Tuberculosis | In some, disease symptoms appear as mature tubercle is formed. Disease progresses as the caseous center enlarges-liquefaction. Air-filled tuberculous cavity in which aerobic bacilli multiply outside the macrophages. |
| Step 5 in the pathogenesis of Tuberculosis | Liquefaction continues until tubercle ruptures allowing bacilli to spill into a bronchiole &be disseminated throughout the lungs & then the circulatory & lymphatic systems. |
| 2 pathogenic mechanisms for tuberculosis | Inhibits formation of the phagolysosome-able to grow in macrophages & can multiply outside macrophages in caseous center. |
| How is Tuberculosis detected/diagnosed? Skin tests & Metabolic Assays. | Positive skin test means current or previous infection. Are false +s. T-cells react w/ tuberculosis protein injected into arm. Follow w/ X-ray or CT exam, acid-fast staining of sputum, culturing of bacteria (3-6wks) & PCR analysis for detection, etc. |
| Describe how being infected w/ M. tuberculosis is different from having Tuberculosis. | Almost 1/3 of earth's population is infected w/ M. tub. Can test positive w/ vaccine, previous infection-T-cell memory. |
| Describe why the long antibiotic cocktail treatment is necessary for Tuberculosis. | Includes isonaizid, rifampin & 1-2 others for 6 mo. isonaizid inhibits lipid (mycolic acid) biosynthesis. Rifampin inhibits RNA pol. Ethambutol inhibits mycoli8c acid synthesis. MDR: multidrug resistant. XCR Extensively drug-resistant. |
| Describe the difficulties w/ the Tuberculosis vaccines. | Bovine only works in kids. Tuberculosis is slow growing. Hard for antibiotics to kill. Many hosts in good living conditions are resistant. |
| Identification scheme for selected species of Mycobacteria Metabolic assays | Slow growing-urease test-nitrate reductase test-M. tuberculosis test. |
| Describe the magnitude of the Malaria problem & how this parasite continues to affect the wellbeing & economy of the world. | 60,000 U.S. troops died from Malaria due to lack of quinine for treatment-WW2. 800mil cases/yr. 1-2mil deaths/yr.-mostly <5y.o. kids-Africa. Over 40% of world is at risk in endemic countries. Resistance widespread. Vaccines problematic. |
| Four species of Plasmodium that cause Malaria in humans | Plasmodium falciparum, vivax, ovale, & malaria. |
| Plasmodium falciparum | Causes most fatalities. Drug resistance common. Predominant in tropics. |
| Plasmodium vivax | Relapsing. Common in subtropics & temperate. |
| Plasmodium ovale | Relapsing. Found in W. Africa. |
| Plasmodium malaria | Uncommon. Temperate or subtropics. |
| How was quinine discovered? (The top drug for treating Malaria) | 1st effective treatment was bark of cinchona tree, which contains quinine. Originally used by Peruvians to control malaria, the Jesuits introduced this practice to Europe in 1640s. It was not until 1820 that the active ingredient quinine was extracted. |
| Describe the complex life cycle of Plasmodium falciparum Part 1 | When a mosquito takes a blood meal it injects salivary fluid to keep the blood from clotting. During this process sporozoites (which have been developing in the mosquito salivary glands) are injected into the host. |
| Describe the complex life cycle of Plasmodium falciparum Part 2 | The malaria parasite has many different stages in its life cycle. The sporozoite stage infects humans. The gametocyte stage infects mosquitoes. |
| Describe the complex life cycle of Plasmodium falciparum Part 3 | While in a human, a single malaria sporozoite can develop into 40,000 parasites. Each one these is capable of infecting a human red blood cell. |
| Describe the complex life cycle of Plasmodium falciparum Part 4 | Infected red blood cells are lysed (broken open) by the malaria parasite. This spills hemoglobin and other cellular contents into your blood stream as well as parasites and parasite waste products. This results in a fever. |
| Describe the complex life cycle of Plasmodium falciparum Part 5 | The "stickiness" of malaria infected cells is a main factor, giving rise to complications of malaria. The blockage of vessels by malaria infected red blood cells causes the occlusion of vessels in the placenta and brain. |
| Describe the complex life cycle of Plasmodium falciparum | Human Liver Schizont ruptures. Human Blood immature trophozoite matures into gametocytes. Taken by mosquito-microgamete enters microgamete. Ookinete. Oocyst. Ruptured oocyst into sporozoites injected into human by mosquito. Back to liver. |
| Malaria Immunity-It's complex life cycle interferes w/ vaccine development. | w/ Chicken Pox you generally get over it & don’t get it again-sterile immunity. This doesnt happen w/ Malaria. You generally don’t get over it. Develop low level of immunity that protects from severe infection. Low level of immunity wanes if cured. |
| What is a simple method for preventing Malaria infection? | Bed nets, sterile mosquitoes? |
| Antimicrobial Drugs | Interfere w/ the growth of microbes w/i a host. |
| Antibiotic | A substance produced by a microbe that, in small amounts, inhibits another microbe. |
| Selective Toxicity | A drug that kills harmful microbe w/o damaging the host. |
| MIC | Minimal inhibitory concentration |
| MBC | Minimal bactericidal concentration |
| Broad Spectrum | Kills different types of bacteria |
| Narrow Spectrum | Kills a smaller range of bacteria |
| Superinfection | Infection with something that's antibiotic resistant. |
| Bactericidal | Kills microbes directly |
| Bacteriostatic | Prevents microbes from growing |
| Describe how Penicillin was discovered & the individuals who were involved. | 1928: Flemming discovered penicillin, produced by Penicillium. 1940: Howard Florey & Ernst Chain performed 1st clinical trials of penicillin. Aided in WW2. |
| How do we discover novel antibiotics today? | From soil bacteria-Actinomyces-Gram-positive, Anaerobic, Some opportunistic pathogens. 81% of soil microbes are bacteria. Most are found in top 3-8 cm. Use the DISK-DIFFUSION METHOD to test for antibiotic sensitivity. |
| Which species gives us half of our antibiotics we use today? | Actinomycetes |
| 5 Main Modes of Antibiotic Action for Inhibiting Microbial Growth | 1 Inhibition of cell wall synthesis 2 Inhibition of protein synthesis 3 Inhibition of nucleic acid replication & transcription 4 Injury to plasma membrane 5 Inhibition of synthesis of essential metabolites. |
| 1. Interfere with cell wall biosynthesis | B-lactams inhibit enzymes required for cell wall synthesis. Penicillin,, cephalosporin, carbapenems, monobactams. Glycopeptides bind to terminal D-Ala residues. Vancomycin, teicoplanin. |
| Penicillin (all in this family have a defining B-lactam ring). | Inhibit cell wall synthesis. Pencillinase-resistant ones. Penicillins+B-lactamase inhibitors. Narrow. Next 2 cards are analogs of penicillin. |
| Carbapenems | Substitue a C for a S, add a double bond. Broad. |
| Monobactam | Single ring. Narrow for gram -. |
| Considerations for choosing an antibiotic | Allergy, side effects, drug interactions-birth control, can cells take up drug where you want it? |
| Cephalosporins | First generation: narrow spectrum, gram+. Second generation: extended spectrum includes gram-. Most widely used penicillins. Cheap & absorbed easily. |
| Polypeptide antibiotics | Vancomycin. Glycopeptide-binds terminal alanine. Important "last line" against antibiotic-resistant S. aureus MRSA). |
| Antimycobacterial antibiotics (tuberculosis) | Isoniazid (INH)-inhibits mycolic acid synthesis. Ethambutol-inhibits incorporation of mycolic acid. |
| Ampicillin | Semisynthetic penicillin. Extended spectrum, many gram-s. |
| Oxacillin | Semisynthetic penicillin. Narrow spectrum, only gram+s, but resistant to penicillinase. |
| Describe how Amphotericin B works in contrast to Echinocandins/Azoles/Allylamines | Antifungal drugs. Amphotericin B inhibits ergosterol synthesis. It is a polene. Others inhibit cell wall synthesis. |
| 2. Interfering with Protein Synthesis | Aminoglycosides, chloramphenicol, macrolides, Strepto-gramins, Tetracyclines/doxycyclin. These antibiotics have side effects because of our mitochondrial ribosomes that look like bacterial ones. |
| Chloramphenicol | Binds to 50S portion & inhibits formation of peptide bond. Blocks Catalytic Mechanism of peptide bond with macrolides. |
| Streptomycin | Changes shpae of 30S portion causing code on mRNA to be read incorrectly. An Aminoglycoside. |
| Tetracyclines | Interfere with attachment of tRNA to mRNA-ribosome complex. |
| Broad Spectrum Inhibitors of Protein Synthesis | Streptomycin, Neomycin, gentamycin, Chloramphenicol, Tetracyclin/Doxycyclin. |
| Gram-positive inhibitors of protein synthesis | Strepto-gramins, macrolides (erythromycin, azithromycin). |
| 3. Inhibiting DNA/RNA Synthesis | Fluoroquinolones disrupt DNA synthesis. Inhibit DNA gyrase-opens DNA for replication & transcription. Rifamycin inhibits RNA synthesis. Antituberculosis. |
| 4. Injury to the Plasma Membrane | Polymyxin B-topical, combined with bacitracin & neomycin in over-the-counter preparation. Makes membranes leak. May cause increased bacterial membrane permeability. |
| 5. Inhibiting a metabolic pathway | Sulfonamides & TMP inhibit folic acid synthesis. Sulfa drugs are competitive inhibitors for folic acid synthesis. Broad spectrum. |
| Describe how Vancomycin & isoniazid/Ehambutol (VIE) relate to penicillin. | Inhibitors of cell wall synthesis. |
| Antiviral Drugs | Nucleoside & nucleotide analogs. |
| Acyclovir | antiviral drug. one of most widely used. inhibits the synthesis of DNA. It structurally resembles the nucleoside deoxyguanosine. Only cells affected by the virus will incorporate the analog. |
| Indinavir | Protease inhibitor. The virus makes use of a protease to reproduce (cut its viral proteins). |
| Enfuvirtide/Amantadine | E: Fusion inhibitor. Targets the gp41 region of viral envelope. A: Inhibits uncoating. |
| Raltegravir | Integrase inhibitor. Inhibits viral DNA from integrating into the host chromosome. |
| Zanamivir | Inhibit attachment. |
| Imiquimod | Promotes interferon production. (Stimulates our own immune response. |
| Cholroquine | Antiprotozoal drug. Inhibits DNA synthesis. Malaria. Hard to find antiprotozoal drugs since protozoans are similar to our cells. |
| Metronidazole | Antiprotozoal drug. Damages DNA. entamoeba, Trichomonas. |
| Nitrazoxanide | Antiprotozoal drug. Interferes with metabolism of anaerobes. |
| What was the first drug available for use against parasitic infection? | For hundreds of years, quinine from the Peruvian cinchona tree was the only drug known to be effective for treating a parasitic infection (malaria). Quinine is still used today, but synthetic derivatives, such as choloroquine, have largely replaced it. |
| Four general ways that bacteria become resistant to antibiotics. | 1 Enzymatic destruction of drug. 2 Prevention of penetration of drug. 3 Alteration of drug's target site. 4 Rapid ejection of the drug. |
| Evolutionary processes that lead to the spread of antibiotic resistance. | 1 Already encoded in the genome & confer AR after mutation or activation by mobile elements. 2 Genes acquired by horizontal gene transfer (HGT) "resistome" |
| Factors to consider when attempting to predict antibiotic resistance rates. (Microbial systems allow pathogens to acquire AR from non-pathogens. | 1 HGT genes for AR. 2 Chromosomal mutations allowing AR. 3 Genes that contribute to intrinsic resistance: e.g. eflux pumps. Must take into account: genomic data, microbial phylogenies, mathematical modeling, mutation modeling, advanced systems biology. |
| More factors to consider when predicting antibiotic resistance rates. | Mutation rates & recombination rates to dif domains of bacteria genomes. Interactions between genomes of pathogenic & nonpathogenic bacteria. the processes for expression, selection & spread (fitness costs). |
| How does Vancomycin kill bacteria? | It binds to the terminal D-Alanine. It produces peptidoglcan chains that terminate in D-Ala-D-lactate instead of D-Ala-D-Ala. |
| How do Vancomycin resistance genes vanH, vanA, vanX work to confer resistance? | VanA produces an alternative peptidoglycan to which vancomycin won't bind-modifies the D-alanine. VanH produces the lactate molecule to modify the D-Ala. VanX: D-Ala-D-Ala dipeptidase. |
| How were genes passed from Enterococcus to Staphylococcus resulting in the emergence of VRSA? | Transferred on a plasmid. |
| Malaria Parasite Life Cycle | Sporozoite stage infects humans & gametocyte stage mosquitoes. Mosquitoe ingests gametocytes from humans. Parasite then changes though a bunch of dif forms in the mosquito. When mosquito bites a human, it releases the sporozite. Difficult to make vaccine. |
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