Micro II-A – Flashcards
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| Acid-fast bacteria are identified by what staining technique |
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| Ziehl-Neelsen |
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| Spirochetes contain which morphological trait |
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| axial filaments (endoflagella) |
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| Corynebacterium diptheriae |
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| Gram + Rod or Club shape humans the only resevoir |
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| Diptheria method of disease |
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| diptheria toxin A-B toxin A- to cytosol B- att. to vesicle membrane |
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| How Diptheria A-B toxin functions |
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| ADP-ribosylation of EF-2 Inactivates EF-2 Inhibiting Protein Synthesis |
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| Domains of diptheria toxin |
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| A- catalytic domain B- binding domain B- transport domain |
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| Bordetella pertussis |
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| Gram - rod aerobic |
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| Pertussis action |
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| adhesins att. to ciliated epi cells pertusis toxin has 5 segments -2,5 binding -1 ADP-ribosylation |
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| pertussis ADP-ribosylation |
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| modifies adenylate cyclase increased cAMP inhibits neutrophile production |
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| Streptococci and Staphylcocci |
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| round gram + |
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| Which bacteria is positive for the catalase test |
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| Staphylcocci |
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| Colonization of streptococci colonization of staphylcocci |
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| string of pearls cluster of grapes |
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| Which bacteria is positive for the coagulase test |
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| Staphylcoccus aureus |
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| Toxin of staphylcocci which can spread to whole body, via bloodstream |
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| exfolatin toxin |
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| How is toxic shock syndrome caused |
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| super-antigen staph aureus toxin Activates many many T/B cells Increases IL-2 + TNF-a = SHOCK |
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| perioral erythema is characterized by what? |
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| a localized rash |
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| How does staph cause food poisoning |
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| Although the bact is killed by heat Toxin is heat labile, and survives |
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| Besides having toxin, what is a virulence factor of staph aureus |
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| Protein A coat -binds Fc receptor of IgG -prevents Ab mediated host response |
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| The three groups of streptococcus are what, and are based on what |
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| alpha, beta, gamma based on hemolysis |
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| What is the main pathogenic group of streptococci |
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beta hemolysins create a clearing for colonization also A-group (for lancefield glyco-classification) |
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| Besides division based on hemolysis, what is another category of streptococci |
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| Cell wall polysaccharides "Lancefield Groups" A-T (A most virulent) |
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| necrotizing fascitis is characterized by: (bact, sympto) |
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| Invasive Group A Streptococci Muscle/Fat destruction along facial plane |
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| Streptococci virulence |
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| M-protein has antiphag behavior binds serum B-globulin factor H this DEGRADES c3b -M has many serotypes |
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| Most GI infections are characterized by what bacteria |
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| Gram - Enterobacteriaceae |
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| E.coli O157:H7 refers to what? |
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| O- surface antigen O(LPS) H- flagella antigen H |
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| Disease of shigella |
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| Dysentry Bloody (+Mucus) Diarrhea |
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| What is similar between salmonella and e.coli |
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| they share ~90% of same DNA makeup |
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| Watery diahrrea characteristics |
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| Colonization of tract production of toxin |
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| Colonization Factors I + II -associated with bacteria -function |
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| diarrhea causing e.coli encoded on plasmid enhance pili adherence to glycoproteins |
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| ETEC and Cholera toxin characteristics |
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| exotoxins which cause diarrhea 2 types: -Heat labile (LT) -Heat stable (ST) 5xB and 1xA subunits |
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| ETEC and Cholera Toxin mode |
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| The A-subunit ADP-ribosylates alpha subunit of G-protein G-protein stims adenylate cyclase cAMP produced activates Protein Kinase Pi's membrane, release of water/electro. |
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| Shigella produces ___ diarrhea by utilizing ____ |
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| Bloody Invasins (adhesins) |
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| How shigella's invasins work |
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| Bind to host integrins Taken up by Phag, but break open vesicle Multiply and spread Mucosal cells die, inflamm. response |
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| Shigella and EHEC toxin and mode |
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| A-B B subunit recognizes host endocytosed A cleaves N-glycosidic bond of 28s rRNA Deactivation = no protein synthesis |
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| Typhoid is caused by ____ and characterized by ____ |
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| salmonella exists in blood, liver, monocytes |
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| Salmonella invasion method |
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| triggers actin rearrangement causes pseudopods to engulf bact. proliferation and breaking-open ("inv") |
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| Neisseria gonorrhoeae |
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| Gram - Diploic (paired, like coffee bean) |
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| Bacteria characterized by having LOS (lipo-oligo-saccharide) |
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| Neisseria gonorrhoeae -triggers inflammation |
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| Neisseria gonorrhoeae method |
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| tight adherence to mucosal cells (like endocervical columnar epi) PII/Opa directs this tight jct. P1 protects bact. from PMNs |
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| Neisseria gonorrhoe avoidance of immune system |
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| serotypes- multiple Ag pili phase variance- not all of its surface components turned on IgA Protease- enzyme inacts. Ab |
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| Treponema pallidum |
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| Syphilis spirochete Needs darkfield or staining to see |
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| 3 stages of syphilis |
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| 1: lesion, chancre 2: mucosal membranes, blood 3: rare, musculoskeletal and organs (only non-contagious stage) |
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| syphilis method |
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| surface coated with: -IgG heavy chain -MHC-I |
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| Chlamydiae trachomatis |
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| obligate intracellular pathogen very small small genome |
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| Chlamydia life cycle |
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| Small elementary body (EB) -spore-like, infectious Reticulate Body(RB) -exists only in cell, proliferates |
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| Treatment of chlamydia |
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| azithro, doxy, erythro -pregnant: ONLY azithro |
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| Helicobacter pylori |
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| Gram - Rod, spiral shaped |
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| Helicobacter pylori disease and location of colonization |
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| Gastritis, duodenal ulcers The acidic antrum of stomach |
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| Helicobacter pylori virulence |
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| Urease on surface, makes NH3: neutralizes LPS inhibits glycosylation of mucus -lipid A has low Pi, not seen as Ag -LPS stims. pepsinogen, weakens walls |
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| People with Helicobacter pylori might have high levels of: |
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| IgG antibody -because bact. causes high IL-8 -induces immune response |
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| Borrelia burgdorferi |
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| Lyme disease Spirochete axial filaments |
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| Borrelia burgdorferi mode of motility |
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| axial filaments (in periplasmic space) -corkscrew movement |
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| Initially lyme disease seen as... |
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| Juvenile rheumatoid arthritis |
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| Mycobacterium tuberculosis |
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| acid-fast stain mycolic acid (B-hydroxy F.A.) |
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| Potential carriers for Tb |
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| HIV/Aids Compromised immunity |
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| Why is Tb easily spread? |
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| Pulmonary lesions easily ejected Mycolic acid makes it resistant to drying when in air/dust |
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| Main cause of lung problems of Tb |
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| Inflammatory response releases TNF-a |
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| How Tb skin test works |
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| delayed hypersensitivity injection with Tb protein fragments (if body infected, then its Ab would elicit response) |
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| Treatment of Tb |
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| 6 months (rifamp, isoniazid) 1st 2 months (pyrazinamide) |
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| Name 6 common Virulence Factors |
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| Adherence/colonization Invasion of Host Cell/Tissues Avoiding defenses Toxins Hydrolytic enzymes Tissue damage (via immune response) |
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| General adherence is mediated by ___ Tightened adherence by ____ |
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| pili/fimbriae afimbrial adhesins |
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| Name two examples of afimbrial adhesins |
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| Gonorhea: PII e.coli: Colonization Factors I, II |
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| Intra/Extra-cellular facultative bacteria often involved with which type of virulence |
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| Invasive |
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| Examples of avoiding defenses (virulence) |
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| Inhibit complement Antiphag activity Ag variation Superantigen |
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| Bacteria inhibiting complement |
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S.aureus: hides surface Ag in capsule meningococci: coated by protein A (IgA) S.pyogenes: degrades c5A salmonella/e.coli: blocks MAC (LPS doesn't allow access) |
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| Example of endotoxin |
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| Gram - LPS (A-in O-out) Induces IL's and TNF-a |
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| A-B toxins and ADP-ribosylation |
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| cholera: g-protein, increased camp diptheria- EF2, inactivates |
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| Where many virulence genes are located |
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| Plasmids and Phages |
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| A bacteria with chromosomally located virulence genes |
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| Cholera (for cholera toxin) |
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| Pathogenicity Island |
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| group of virulent genes on chromosome distinct structural and functional units |
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| Common position of pathogenicity islands |
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| at a tRNA locus (source for phage introduction) |
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| Possible explanation for similarity between cholera toxin + ETEC toxin |
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| horizontal gene transfer |
