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88 Cards in this Set
- Front
- Back
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key symptoms of damaging bacterial infection
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fever greater than 102, thick greenish mucus, headache, stiff neck, sudden onset symptoms
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symptoms of life threatening bact. Infections
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high sustained fever, rapid BP drop, headache and other neuro symptoms, increased HR, increased respers, organ failure
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exotoxin secreting bacteria
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staph. aureus, strep.pyogenes&pneumoniae, clostridium species, bacillus anthracis, bordetella pertussis, vibrio species, corynebacterium diptheriae
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papilloma virus infects what cells
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skin cells
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rotavirus infects what cells
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GI tract cells
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viral infections systemic in nature
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measles virus, mumps virus, smallpox, HIV (even though it infects a limited subset of cells)
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symptoms of viral infections
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fever, muscle pain, headache, general malaise
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differentiating viral/bacterial infections
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culture bacteria, testing for viral ags or abs to ags, tests on genetic sequences, CBC (not always acurate)
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Fc(gamma)RI
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found on neutrophils, receptor for IgG, elevated during an infection. Assay identify either bacterial or viral infection
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CR1 CR3 assay
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found on neutrophils, receptor for complement, elevated during bacterial infection
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steps in infection process
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attachment and entry, local or general spread, multiplication, evasion of host defenses, shedding, [cause damage to the host]
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virulence factors
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genes or gene products a pathogen uses in infection
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Koch's Postulates
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1)organism associated with lesions of disease but not healthy tissue 2)organism must be isolated as pure culture from the lesion 3)experimentally introduced into animal and disease recreated 4)re-isolated from the experimental infection
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Koch's Molecular Postulates
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1)gene found (only) in bacterial strains that cause disease 2)gene isolated by cloning 3)mutation disrupting gene reduces virulence OR transfer of intact gene into no-virulent bacteria makes it more virulent 4)gene expressed by bacterium during the infecious process
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anatomic sites rinsed in a flow of fluid
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GU tract (urine) Eyes (tears) Resp tract (Mucus)
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siderophores
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high affinity iron binding protiens made by pathogens
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stages of bacterial growth (closed system only)
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lag phase, log phase, stationary phase, death phase
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lag phase
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adaptation, no population increase
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log phase
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constant rate of molecular synthesis, doubling time is at max
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stationary phase
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cell growth=cell death, no population increase (stressful conditions due ot lack of nutrients and/or waste build-up
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death phase
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waste products kill cells
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sulfonamides
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antimetabolite, inhibits dihydrofolate reductase for bacteriostatic effect
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sulfamethoxazole
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sulfonamide, inhibits diydrofolate reductase
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drugs: antimetabolites in folic acid pathway
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trimethoprim, dapsone, p-aminosalicylic acid
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nucleoid region
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DNA visualized on electron micrograph as a "wad"
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DNA gyrase
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topoisomerase
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quinolones
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antibacterial agents that bind the alpha subunit of DNA gyrase - inhibits supercoiling
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rifampin
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prevents initiation of transcription in bacteria by binding RNA polymerase, good target specificity, bactericidal
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operons
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encode 2-12 genes, ensure all enzymes in multi-enzyme pathway are made
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Bacterial DNA distinguished from human DNA by..
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random frequency of 5'CG3' recognized by TLR-9
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bacterial ribosomes
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80S made of 30S and 50S.
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aminoglycosides
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irreversibly bind 30S subunits causing misreading of mRNA and premature termination of translation
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tetracyclines
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bind reversibly to 30S subunits, blocking translation by getting in the way of tRNA's
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macrolides
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bind reversibly to 50S subunits and block elongation at the 50S subunit
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clindamycin (Incosamide)
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binds reversibly at 50S subunit and blocks elongation
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quinupristin + dalfopristin
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synergistic combination of streptogramins: dalfopristin binds 50S subunit and blocks peptide elongation AND allows binding of quinupristin which causes ribosome to prematurely release growing protein
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oxazolidinones
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block translation initiation at the 30S subunit
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chloramphenicol
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binds reversibly to 50S subunits to block elongation of growing proteins - also inhibitory effects on human bone marrow cells
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bacteria that lost ability to synthesize a wall
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mycoplasma and ureaplasma
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chlamydia (cell walls)
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cell walls made from different materials than peptidoglycan
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peptidoglycan structure
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made of alternating N-AG and N-AM polymerized into long chains connected by short peptides (8a.acids long or 8a.acids+5gly)
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transpeptidases
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enzymes that join peptides together to strengthen peptidoglycan into a meshwork (act ouside plasma membrane)
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teichoic acid
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polymer woven through fabric of thick peptidoglycan walls, have different R groups
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lipoteichoic acid
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teichoic acid that penetrates all the way through the wall into the cell membrane (has an additional lipid moiety)
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Bacitracin
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antibiotic that interferes with movement of NAG+NAM+shortpeptide units through cell membrane, inhibiting peptidoglycan synthesis (as long as it can reach the cell membrane)
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NAG-NAM bonds
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glycosidic
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beta-lactam antibiotics (mechanism)
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inhibit transpeptidases (enzyme that joins peptides of cell wall together to strengthen it into a meshwork)
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beta-lactam antibiotics (drugs)
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penicillins, cephalosporins, cephamycins, carbapenems, monobactams
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vancomycin
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glycopeptide that makes transpeptidase fxn impossible by placing a block on the ends of the peptapeptide units
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major mechanism by which gram (-) bacteria enterobacteria acquire antibiotic resistance
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integrons
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integron components
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integrase gene (encoding enzyme "IntI" responsible for recombo of gene cassettes), "attI" DNA sequence (IntI recognizes and cuts for insertion of gene cassettes), promoter (turns on expression of gene cassettes after "attI")
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gene cassettes
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coding sequence of a gene, often a resistance gene. in integrons. has 59-bp sequence recognized by IntI enzyme
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genomic islands
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large blocks of genes (may contain multiple operons), %GC differes from %GC of rest of chromosome; generally inserts near tRNA genes
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pathogenicity islands
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subset of genomic islands that increase the virulence of a microbe
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operons
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DNA regulated as a unit, by some regulatory protein (ensure all genes in a pathway get made together)
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gene repression
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binding of repressor protein to operator site blocks RNA polymerase from binding and transcribing. genes ON when protein is NOT bound to DNA. small molecule effectors can bind to repressor, affecting DNA-binding (enhancing or discouraging)
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positive regulation
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activator protein binds and enhances RNA polymerase binding and transcription. genes ON when protein IS bound to DNA. small molecule effectors can bind activator, affecting DNA-binding (enhancing or discouraging)
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DtxR repressor (Corynebacterium diphtheriae)
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(negative control) uses iron (FeII) as an effector. when Fe is present, DNA binding is enhanced (cui genes), blocking RNA transcription of Fe acquisition systems
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TetR repressor protein (gram negative bacteria)
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(negative control) binding operator near tetA gene is inhibited by tetracycline, allowing RNA transcription of gene for tetracycline resistance
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polymyxins
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antibiotics that disrupt membrane functionality by associating with LPS molecules, causes leakiness of cell membrane; have serious nephrotoxicity in humans
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penecillin sensitive gram (-) bacteria
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nisseria gonorrhoea
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fimbriae (pili)
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made of protein, and have proteins at tips for specific binding to host cell receptors(act as adhesions) or other bacteria (sex pili). Thinner and stiffer than a flagellum
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flagella
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used for swimming, made of protein, elicit Ab, can act as virulence factors
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flagella virulence factors
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allow movement to a new body site, TLR-5 responsive to flagellin of some pathogens, virulence attenuated by loss of flagella (some strains)
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capsules
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made of polysaccharides, can be immunogenic, key virulence factor (protect against innate immune response)
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endospores
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produced by a limited group of gram (+) rods. Most durable structure in biological world. Genetic material remains viable despite serious stresses
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Type III Secretion Systems (TTSS)
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found in gram (-) bacteria, spanning all 3 cell envelope layers. ex. Shigella's allows for invasion into gut epithelial cells and intracellular survival
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Type IV Secretion System
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found in both gram (-)and(+). Yersinia pestis' alters the physiology of macrophages so they are unable to phagocytize
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Secretion Systems
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complex protein assemblages tha tmove molecules from inside bacteria to outside - even directly through host membrane into host cytoplasm. Variety of roles in virulence
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MtrA
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positive activator. In Neisseria gonorrhoeae. When hydrophobic effector molecule binds MtrA, transcription of mrtCDE operon is activated - the proteins made form efflux pump
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two-component regulatory mechanisms
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cell membrane receptor autophosphorylates, then phosphorylates transducer which binds weak promoter, enhancing transcription
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quorum sensing
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turning on/off (transcriptional regulation) of genes in response to molecules produced by bacterial populations themselves
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regulon
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different operons (separated on the bacterial chromosome) respond to a common activator protein or other transducer
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core region of LPS
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bridges lipid part and antigen part - made of carbohydrates, contains KDO unique to LPS. Common to most gram (-) bacteria
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O-side chain of LPS
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antigenic part, made of repeating units of polysaccharide. Ex. O157:H7
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LPS vs LOS
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lipopolysaccharide vs lipo-oligosaccharide (only a couple of repeating subunits)
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Lipid A of LPS
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*the part responsible for toxicity* attached to KDO of core region, glucosamine backbone with long chain fatty acids attached. Anchors LPS in outer membrane, poor Ag
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effects of LPS
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pyrogenic, complement trigger, blocks corticosteroid receptors, cytokine release, damage to endothelial cells (tightjxns relaxed), disseminated blood clotting, hypotension due to other responses
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MD2
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stabilizes binding of TLR-4(CD14) with LPS
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"gram (+) endotoxin
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teichoic acid
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receptor stimulated by peptidoglycan (or + lipoteichoic acid)
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TLR-2
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receptor stimulated by LPS
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TLR-4/CD14 (stabilized by MD2)
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membrane disrupting toxins
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exotoxin, type II. "-lysins" bind to host cell surface, attacks membrane integrity, host cell becomes leaky and bursts
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A-B type toxins
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exotoxin, type III. Toxin binds host cell via B component, leading to uptake of the A component, which is the active agent against host target enzyme
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superantigens
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exotoxin, type I. produced by relatively few bactera, lead to massive cytokine release from T-helper cells (facilitate non-specific binding of Th cells and MHCII cells)
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petechial lesions
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characteristic of meningococcemia, bleeding out via small vessels
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Waterhouse-Friderichsen syndrome
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adrenal gland failure due to bleeding into the adrenal glands - result from severe meningococcal infection
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neisseria meningitidis serogroups most frequently associated with lung involvment
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Y and W135
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