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89 Cards in this Set
- Front
- Back
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what is acinetobacter baumanii?
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- distant relative of pseudomonas
- only nosocomially acquired - causes pneumonia & bacteremia - lots of antibiotic resistance = high mortality |
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what is the leading cause of nosocomial pneumonia?
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- psuedomonas aeruginosa
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what is the phenotypic conversion of P. aeruginosa?
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- motile at first --> colonizes on lines & epithelial cells --> converts to organism that secretes lots of alginate --> intercalates itself into mucus
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why do neutrophils have problems w/ pseudomonas aeruginosa?
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- encapsulated & in mucus layer
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what are the toxins secreted in pseudomonas aeruginosa?
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- hemolysin (phospholipase C) liberate Fe
- exotoxin A: inhibits host protein synthesis via ADP-ribosylation --> inhibits protein synthesis - exotoxin S: disrupts host cell function via ADP-ribosylating - LPS |
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how does legionella replicate? what is the Dot/Icm system in legionella?
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- infects amoebae --> macrophages --> phagosome --> gets into ER (avoids lysosome) --> replication --> macrophage lysis
- intercepts ER to golgi vesicles --> recruited to phagosome --> needed for replication vacuole |
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what is legionnaire's disease vs pontiac fever?
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- legionnaire's disease: 2-10 day incubation, low attack rate, lethal, IC host
- pontiac fever: 1-2 day incubation, high attack rate, non-lethal, healthy host |
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what does borrelia burgdorferi look like? where is it endemic? what kind of tick carries it?
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- spirochete (inner & outer cell membrane like gram -), flagella in b/w membranes = corckscrew motion
- eastern US/midwest (blue state disease) - Ixodes ticks (reservoirs = rodents & birds) |
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borrelia species cause what two diseases?
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- lyme & relapsing fever
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what does outer surface protein A do for borrelia burgdorferi? what
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- binds to midgut in Ixodes tick, don't need it to bind to salivary glands
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what do Ixodes ticks inject in their feeding pit while biting a host? how do they evade the immune system?
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- injects anticoagulants, blocks neutrophils, plasmin to dissolve tissue, bind complement factor H (block alternative pathway)
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how does lyme disease do antigenic variation?
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- VI loci allow for antigenic variation
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what are the clinical stages of lyme?
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1) early disease --> erythema migraines, regional LAD
2) early disseminated disease --> systemic symptoms, fever, arthralgias, myalgias, polyradiculopathy, AV nodal block 3) late --> arthritis, encephalopathy, polyradiculopathy - BAKE = bell's palsy, arthritis, kardiak block, erythema migrans |
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what is garish-herxheimer reaction?
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- occurs w/in first dose of therapy for lyme disease b/c of release of antigens
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what does borrelia recurrentis? who carries it? where is it?
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- relapsing fever
- lice (epidemic) in areas of poor sanitation - ticks (endemic) in north & south america & asia & africa |
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what is the clinical syndrome of relapsing fever? how do you diagnose?
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- clinical: cyclic relapsing fevers
- diagnosis: direct visualization in blood |
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which tick borne diseases have antigenic variation?
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- lyme & RF
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what are the similarities and differences b/w RF & lyme?
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- similarities: both require insect vector, disseminate to multiple organs, treatment = similar
- differences: RF by lice or fast-feeding ticks (lyme by slow-feeding ticks), geography different, RF bacteria titers high in blood (not in lyme), RF relapsing fever higher mortality than lyme |
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what does E. chaffeensis cause? what tick carries it? what cells does it infect? what is the geography?
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- causes erlichiosis, carried by lone star tick (amblyomma americium)
- infects monocytes (HME) - south central & south east US |
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what does A. phagocytophilum cause? who carries it? who is it often co-transmitted with? what cells does it infect? what is the geography?
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- anaplasmosis, carried by Ixodes scapularis
- often co-transmitted w/ B. burgdorferi & B. microti - infects granulocytes (HGA) - northeast & upper midwest = lyme distribution |
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what are the clinical features of erlichiosis/anaplasmosis? how do you treat?
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- no rash or non-spectific rash
- fevers & non specific systemic symptoms - key: ***early leukopenia & thrombocytopenia, increased transaminases - doxycycline or tetracycline |
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what does B. microti & B. cause? what tick carries it? in what cells does it live/what unique characteristic does it to in these cells? what is the geography?
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- babesiosis, carried by Ixodes tick
- small intra-erythrocytic parasites form maltese crosses - geography = lyme disease |
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what are the clinical symptoms of babesiosis? how do you treat it?
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- viral like illness
- can be severe in elderly, splenectomized & immunocompromised - azithromycin or clindamycin |
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what does rickettsia rickettsii cause? what is the geography?
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- rocky mountain spotted fever
- east coast mainly |
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what are the clinical features of rocky mountain spotted fever? how do you treat it?
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- triad: rash (palms/soles), fever, severe headaches
- treat w/ doxycycline, chloramphenicol |
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what special medium does bordetella pertussis have to be grown on?
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- charcoal cephalexin blood agar for 3-7 days
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how does the filamentous hemaglutinin (FHA) toxin of bordetella pertussis work?
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- FHA: binds galactose on sulfatide (membranes of ciliated cells) so able to colonize trachea
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what 3 toxins does bordetella pertussis have?
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- pertussis toxin: AB toxin, inactivates Gi --> increased cAMP --> chemotaxis impaired
- adenylate cyclase: pumps in it's own, impairs phagocytosis, chemotaxis, etc. - tracheal cytotoxin: kills ciliated cells & inactivates cilia from clearing debri |
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what happens during the prodromal, catarrhal, convulsive & convalescence phases of bordetella pertussis?
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- prodromal (7-14): before symptoms, contagious, culture (+)
- catarrhal (7-14): highly contagious, symptomatic - convulsive (15-60): recovering, less infectious, harder to culture (+), die from secondary infections - convalescence (1-2mo): recovering, not contagious - main point = culture (+) infrequent later in disease |
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how do you treat bordetella pertussis?
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- macrolides
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what 2 cancers is H. pylori a risk factor for?
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1) gastric adenocarcinoma
2) mucosal associated lymphoid tissue lymphoma (MALT) |
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what does urease do for H. pylori?
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- generates higher pH around it --> doesn't love low pH of stomach
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what are the two variants of H. pylori? what kind of secretion system does it have?
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- CagA (+) & CagA (-) --> CagA encodes type IV secretion system & more frequently associated w/ disease b/ inject toxins --> pro-oncogenes
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what is the 1st line treatment for ulcers?
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- triple therapy = LAC --> lansoprazole/omeprazole, amoxicillin, clarithromycin
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what can neisseria meningitidis ferment?
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- maltose & glucose (b/c M & G in the name)
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what age group is neisseria meningitidis the leading cause of meningitis?
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- ages 2-18 (teenagers)
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what are the spinal fluid characteristics of bacterial vs Tb vs viral meningitis?
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- bacterial: high PMNs, high protein, low glucose
- Tb: low PMNs, high protein, low glucose - viral: low PMNs, slightly elevated protein, normal glucose |
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how do you treat neisseria meningitidis?
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- IV ceftriaxone or beta-lactam
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what does neisseria meningitidis look like?
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- gram (-) diplococci, encapsulated
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what syndromes does haemophilus influenzae cause?
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-haEMOPhilus = epiglottitis, meningitis, otitis media, pneumonia
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what does H influenzae look like?
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- gram (-) coccobacillus, encapsulated
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how do you treat H influ?
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- IV ceftriaxone & beta-lactam
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what kind of epithelium does neisseria gonorrhea populated? what are the virulence factors?
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- non-ciliated columnar epithelium
- type IV pili attach to epithelium, Opa proteins --> all aggregate together - IgA protease to evade immunity, take sialic acid from host & coat LPS to avoid complement recognition |
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how do you treat gonorrhea?
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- quinolones, cephalosporins (ceftriaxone)
- possible co-infection w/ chalmydia treat w/ azithromycin or doxycycline |
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why is chlamydia an obligate intracellular bacterium?
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- because it cannot make it's own ATP
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how is chlamydia similar to gonorrhea?
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- mucous membranes, sexual contact, birthing process, humans = only host, asymptomatic infxn promotes spread
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what is the pathogenesis of chlamydia?
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- elementary body (EB) = infectious form, little metabolic activity, resistant to harsh treatments, binds to heparan sulfate on host cell
- reticulate body (RB) = non-infectious form, fragile, metabolically active - endocytosis --> cytoplasmic inclusion body --> avoid lysosome --> communicate w/ golgi (like legionella) --> re-differentiate into EB so can re-infect |
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how do you treat chlamydia?
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- doxycycline & macrolides (azithromycin, erythromycin)
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what does the structure of treponema palladium look like?
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- spirochete, inner & outer membrane, endoflagellae b/w membranes = motility
- can be visualized by dark-field microscopy |
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in congenital syphilis why is there no local infection and only systemic spread?
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- b/c babies have no immune system so attacks the teeth & bones & brain immediately
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what are the 3 phases of syphilis?
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- 1: chancre
- 2: systemic = rash on palms/soles, systemic symptoms - 3: chronic, vasculitis, gummus (granulomas), aoritis, tabes dorsalis |
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how do you treat syphilis?
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- penicillin
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what does pseudomonas aeruginosa look like?
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- gram (-) rod, aerobic, encapsulated, aerobic
- green-blue color, fruity odor |
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what does legionella look like?
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- aerobic gram (-) rod
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what does bordetella pertussis look like?
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- gram (-) coccobacillus
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what does H. pylori look like?
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- curved gram (-) rod
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what kinds of diseases do not multiply?
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- toxin diseases (ie tetanus, botox, food poisoning)
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what is the only obligate intracellular STD?
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- chlamydia (b/c doesn't make it's own ATP)
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what do integrin & complement receptors recognize? which receptor is important for adaptive immunity?
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- intregrin & complement R: c3bi (innate immunity)
- Fc receptor = adaptive - above + lectin = phagocytic receptors |
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what do RhoGAP proteins do?
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- disrupt signaling to disrupt phagocytosis
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why is LPS not a true toxin?
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- because it is not directed towards host --> host just reacts to it when it sees it
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which organism uses hemolysin phospholipase C? why?
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- P for pseudomonas --> liberates iron for bacteria
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what kind of bacteria have cholesterol-dependent cytolysins?
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- gram (+)
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what neurotransmitters does C. tetani vs C. botulinum inhibit? how do they work? how do you acquire these toxins? what kinds of toxins are these?
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- C. tentai inhibits GABA & glycine --> spastic paralysis, acquired from the soil
- C. botulinum inhibits Ach --> flaccid paralysis, acquired from canned foods (toxins in honey affect babies) - proteolysis of synpatobrevin (snares) = don't allow NTs to fuse - AB toxins |
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what is the normal flora of the skin? teeth? nose? throat? colon? urogenital?
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- skin: staph epidermidis, staph aureus
- teeth: S. viridans = S. sanguis, S. mutans - nose: staph (epidermidis, s. aureus) - throat: staph, strep, neisseria, H. influenza - colon: bacteroides, enterococci, E. coli - urogenital: lactobacillus, E. coli, group B strep |
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which streps are alpha hemolytic? beta? gamma?
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- alpha: viridans, pneumoniae
- beta: group B (agalactiae), group A (pyogenes) - gamma: group D (bovis, enterococcus) |
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which strep group is optochin resistant? sensitive? bacitracin?
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- optochin: viridans resistant, pneumoniae sensitive (OVRPS)
- bacitracin: group B resistant, group A sensitive (B-BRAS) |
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what can group D strep (S bovis) in the blood indicate?
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- B in the blood = cancer in the colon
- can cause subacute endocarditis in these patients |
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what infections does group D strep (enterococcus) cause?
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- subacute endocarditis, makes biofilms that are very resistant
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what are the GAS toxins?
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- SpeA & C --> TSLS = superantigen, scarlet fever
- Spe B --> necrotizing fasciitis |
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what does glomerulonephritis follow? ARF?
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- glomerulonephritis follows pharyngitis, impetigo (PIG)
- ARF follows scarlet fever, pharyngitis (PSA) |
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what are the virulence factors for GAS?
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- hyaluronic acid (inhibits phagocytosis)
- M protein (most important) --> inhibits opsonization via binding to factor H rendering alternative complement ineffective & fibrinogen |
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what are the toxins secreted by GAS?
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1) streptolysin O = pore forming, binds cholesterol in membrane, lyses neutrophils
2) streptolysin S = beta hemolysis 3) streptokinase 4) DNase B |
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which strain of staph ferments mannitol?
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- S. aureus (turns MSA plate yellow)
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what are the virulence factors of staph aureus: inhibitors of phagocytosis? adhesion molecules? secreted proteins? superantigens?
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1) inhibitors of phagocytosis = protein A, coagulase
2) adhesion molecules = MSCRAMMs 3) secreted proteins = proteases, lipases, DNase, FAME, coagulase, staphylokinase 4) superantigens = enterotoxin (food poisoning), TSST-1 (toxic shock), exfoliative toxin (scalded skin syndrome) |
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which strains of staph are novobiocin resistant? sensitive?
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- "NO StRESs" = saprophyticus resistant, epidermidis sensitive
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what allows B fragilis to be a nanarobe? what allows it to evade the immune system?
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1) SOD = inactivates ROS
2) catalse = degrades H2O2 - evasion of immune system: LPS low toxicity, encapsulated |
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what does V cholerae use to attach to the intestinal epithelium? how does it's toxin work?
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- TCP pili
- AB toxin: transfers ADP-ribose to inactivate Gi --> GalphaS always on --> increased cAMP --> increased Cl & decreased Na loss |
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what are the two AB toxins of ETEC?
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1) HLT --> like cholera activates adenylate cyclase
2) HST --> activates guanylate cyclase |
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what are the AB toxins HST & HLT associated with?
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- ETEC
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what is the pathogenesis of NTS?
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- splash (trigger uptake) --> macrophages in M cells --> type III secretion system --> SPI1 (hijack cytoskeleton) & SPI2 (block NADPH oxidase)
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how do you differentiate typhoid fever from NTS?
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- typhoid has fever, onset/incubation period can be longer, spreads systemically more often than NTS (aka causes systemic symptoms when bacteremic), have a carrier state, treat it w/ antibiotics & vaccine available
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what is the pathogenesis of shigella? what toxin do some strains have?
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- invades M cells --> disrupts tight junctions --> gets actin tails --> invades next cells --> etc
- AB toxin = shiga toxin |
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what toxins does EHEC have? what toxins are injected via the T3SS? what is the pathogenesis of the toxins? what can it not ferment that sets it apart from other E. coli strains?
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- shiga-like toxin encoded on lysogenic bacteriophage, responsible for HUS
- toxins injected: intimin, tir - pathogenesis: attaching & effacing --> disrupt tight junctions, lose microvilli - cannot ferment sorbitol (do not turn sorbitol plates red) |
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why should you never treat EHEC w/ antibiotics?
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- because toxin on a phage so if it sees antibiotics will lyse out and cause more damage
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who has intimin/tir & shiga-like toxin & causes attaching & effacing lesions?
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- EHEC
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what is unique about C. diff diarrhea?
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- it is watery & produces a fever even though it is in the colon & does not invade tissues
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what is unique about EHEC diarrhea?
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- bloody diarrhea w/ no tissue invasion
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what are the toxins present in C diff? what to they do? how do you test for c diff?
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- TcdA: colonic inflammation
- TcdB: actin changes --> pseudomembranous colitis (can lead to toxic megacolon) - cytotoxins in the stool can cause cells to round up when looking for them |
