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136 Cards in this Set
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what are some characteristics of streptococcus pyogenes |
Group A b hemolytic strep
causes URI and skin infection gram + catalase - |
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why do we care about URI
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commonly seen in primary care
causes LOTS of AB misuse hard to distinguish pathogen |
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what is...
1. Rhinitis 2. Sunusitis 2. Phayrngitis 4. Epiglotitis 5. Laryngitis |
1. common cold, viral URI
2. acute sinusitis, follows viral rhinitis. Chronic sinusitis- anerobic bacteria usually 3. pharyngitis: viral or bacterial (most common bacteria is GABHS- strep pyogenes) 4. epiglotitis- Hib, lethal. rapid 6-12 hours. also strep pneumonia 5. Laryngitis: no agent 33% of the time. graudual, more self limited |
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what are the most common causes of URT in general
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1. Virus 40%
2. bacteria: 30%, mailly GABHS, s pyogenes |
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wht does x ray look like for epiglotitis
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thumbprint sign
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what are some general features of streptococcus
1. arrangement of cells 2. gram 3. distinguishing tests 4. mobility 5. growth requirements |
1. chains, pairs
2. + 3. Catalase - 4. nonmotile 5. fastidious- enriched media or BAP mesophile (35-37), Capnophile (CO2) |
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so streps lyse RBC? how much
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yep
a- partial b- complete g- none |
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whats the best way to get strep to go
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fastidious mesophile capnophile
35-37* on enriched media in a candle jar |
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what is the lancefield scheme of classification
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1. based on antigenicity of a cell wall carbohydrate. groups A-U
2. GAS = NAG + rhamnose 3. pathogens- A-G |
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what are 6 streptococcus species that are important in human infection
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1. S pyogenes: pharyngitis, skin
2. S agactiace: nenonal meningitis, pneumonia 3. Enterococcus faecalis: UTI 4. Viridans streptococci: endocarditis, dental 5. s pneumonia: pneumonia/meningitis in adults, otitis media in kids 6. s anginosus: pyogenic infectinos, brain abcess |
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what is the morphology of S pyogenes (GABHS) in clinical sample, broth culture
gram, catalase, |
1. Clinical: single diploid short string
2. Broth: string of pearls gram +, catalase - PYR + (L pyrrolidonyl arylamidase) |
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what are the virulence factors of strep pyogenes
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1. Cell Envelope
-M protein -F protein -Capsule 2. Enzymes/Exotoxins -Hemolysins: Streptolysin S/O - C5a peptidase -Strepodornase - streptokinase/fibrinolysin -streptococcal pyrogenic exotoxins |
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what is M protein
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majoy virulence factor of strep pyogenes
-prevents phago and compliment activation **strep pyogenes also has a capsule that resists phago |
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what is protein F and LTA
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cell envelope virulence factor for spret pyrogenes
allows tissue tropism F- binds fibronectin LTA- attaches to pharyngeal epithelium |
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waht allows strep pyogenes to infect the phayrnx
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a virulence factor in the cell envelope called LTA- lets it bind to pharyngeal epithelium
**Protein F lets it bind to fibronectin |
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does strep pyogenes have a capsule
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yep, another one of these cell envelope virulence factors.
**made of hyaluronic acid, inhibits phago (cool! so does M protein, really resistant to phago) |
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what are the hemolysins that strep pyrogenes
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Streptolysin O- can work with O2 present, destroys RBC and WBC, immunogenic, AB can be produced against it in systemic or pharyngeal infections
Streptolysins S- serum induces, lyses WBC & RBC, elaborated in the presentce of Serum |
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which hemolysin is immunogenic
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O- works betterin oxygen
S is NOT immunogeic, works better in serum |
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what do the following virulence factors that strep pyogenes has
1. HA acid capsule 2. LTA 3. M protein 4. Protein F 5. Streptolysin O/S 6. Streptodornase 7. C5a peptidase 8. Streptokinase |
1. HA acid capsule: inhibit phago
2. LTA: helps adhere to our epithelium 3. M protein: interferes with phago, responsible for sequelae 4. Protein F: responsible for attachment to fibronectin on host cells 5. Streptolysin O/S: b hemolysis of RBC and WBC, 6. Streptodornase: enhance spread of bacteria, breakdown host DNA 7. C5a peptidase: destroys C5a, so destroys phago 8. Streptokinase: activates plasmin to dissolve blood clots |
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what does C5a peptidase do? what bug has it
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degrades C5a so that phago wont happen, disrupts inflammation
**seen in strep pyogenes |
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what does streptodornase do?
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degrages DNA. decreases viscocity and creates purulent exudates
**its an exotoxin that is seen in strep pyogenes |
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what does streptokinase/fibrinolysis do for strep pyogenes
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generates plasmin to break down blood clots
**neat thing, used clinically to treat PE |
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what is the super AG in strep pyogenes? what are they responsible for
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Streptococcal pryogenic exotixin A (SPE a)
**super Ag that leads to massive cytokine release and tissue damage **scarlet fever **also shock |
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what cauess scarlet fever in strep pyogenes
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the SPE a super antigen
can also cause toxic shock |
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what is responsible for B hemolysis in deep cuts in GAS
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streptolysin O
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What does these things in strep pyogenes
type 2 and 3 sensitivity 2, scarlet fever, 3 glomerulonephritis) scarlet fever breaks clot breaks DNA |
M- type 2 and 3 sensitivity 2, scarlet fever, 3 glomerulonephritis)
SPE A- scarlet fever Streptokinase- breaks clot Strepdornase- breaks DNA |
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14 yo recovered form untreated pharyngitis but now has migratory polyarthritis CARDIOMEGALY AND ERYTHEMA. whats going on?
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type II hypersensitivity due to protein antigen AB complex
Type II AB GO AFTER TISSUES |
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MTB virulence
1. what inhibits phagolysosome formation and facilitates intracellular growth 2. induces phagocytosis to help bring virus into cell 3. adjuvent to increase AB, when we put it with cord it forms granuloma 4- inhibit MHC II expression, slows T cells |
1. sulfatides
2. Cord factor- 3. Wax D- 4. LAM- |
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if you have a CXR with small spots near midline in mid lung its... what else will be there?
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Primary TB
**Ghon complex **perihilar, middle/lower lobes |
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what causes the thing where women wont cough so they get crap stuck in their lings
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MAC superinfection- waning immune system, nodular infiltrates, seen in older women who dont cough
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what are some characteristics of the following
Disseminated MAC- Latent TB- Endogenous Reactivation- Miliary- |
Disseminated MAC- wont see granuloma, T cells are too low
Latent TB- needs more patchy infiltrates and a + TB test Endogenous Reactivation- active cavitation and caseous necrosis in apex of lungs Miliary- will be disseminated all over, wont see limited region around perihilar area |
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What are these descriptions associated with
1 homeless, etoh, smoke 2 consolidatinos of lungs, 3. waning immune system, nodular infiltrates, seen in older women who dont cough 4. infiltrate, southwest, subcutaneous, brain abcess, fever, cough, dyspnea. 5. acid fast |
klebsiella- homeless, etoh, smoke
s aeureus- consolidatinos of lungs, not lungs MAC superinfection- waning immune system, nodular infiltrates, seen in older women who dont cough Nocardia asteroides- infiltrate, southwest, subcutaneous, brain abcess, fever, cough, dyspnea. DMAC- acid fast |
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what is the super AG in strep pyogenes? what are they responsible for
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Streptococcal pryogenic exotixin A (SPE a)
**super Ag that leads to massive cytokine release and tissue damage **scarlet fever **also shock |
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what cauess scarlet fever in strep pyogenes
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the SPE a super antigen
can also cause toxic shock |
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what is responsible for B hemolysis in deep cuts in GAS
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streptolysin O
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What does these things in strep pyogenes
type 2 and 3 sensitivity 2, scarlet fever, 3 glomerulonephritis) scarlet fever breaks clot breaks DNA |
M- type 2 and 3 sensitivity 2, scarlet fever, 3 glomerulonephritis)
SPE A- scarlet fever Streptokinase- breaks clot Strepdornase- breaks DNA |
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14 yo recovered form untreated pharyngitis but now has migratory polyarthritis CARDIOMEGALY AND ERYTHEMA. whats going on?
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type II hypersensitivity due to protein antigen AB complex
Type II AB GO AFTER TISSUES |
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MTB virulence
1. what inhibits phagolysosome formation and facilitates intracellular growth 2. induces phagocytosis to help bring virus into cell 3. adjuvent to increase AB, when we put it with cord it forms granuloma 4- inhibit MHC II expression, slows T cells |
1. sulfatides
2. Cord factor- 3. Wax D- 4. LAM- |
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if you have a CXR with small spots near midline in mid lung its... what else will be there?
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Primary TB
**Ghon complex **perihilar, middle/lower lobes |
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what causes the thing where women wont cough so they get crap stuck in their lings
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MAC superinfection- waning immune system, nodular infiltrates, seen in older women who dont cough
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what are some characteristics of the following
Disseminated MAC- Latent TB- Endogenous Reactivation- Miliary- |
Disseminated MAC- wont see granuloma, T cells are too low
Latent TB- needs more patchy infiltrates and a + TB test Endogenous Reactivation- active cavitation and caseous necrosis in apex of lungs Miliary- will be disseminated all over, wont see limited region around perihilar area |
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What are these descriptions associated with
1 homeless, etoh, smoke 2 consolidatinos of lungs, 3. waning immune system, nodular infiltrates, seen in older women who dont cough 4. infiltrate, southwest, subcutaneous, brain abcess, fever, cough, dyspnea. 5. acid fast |
klebsiella- homeless, etoh, smoke
s aeureus- consolidatinos of lungs, not lungs MAC superinfection- waning immune system, nodular infiltrates, seen in older women who dont cough Nocardia asteroides- infiltrate, southwest, subcutaneous, brain abcess, fever, cough, dyspnea. DMAC- acid fast |
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what is the super AG in strep pyogenes? what are they responsible for
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Streptococcal pryogenic exotixin A (SPE a)
**super Ag that leads to massive cytokine release and tissue damage **scarlet fever **also shock |
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what cauess scarlet fever in strep pyogenes
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the SPE a super antigen
can also cause toxic shock |
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what is responsible for B hemolysis in deep cuts in GAS
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streptolysin O
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What does these things in strep pyogenes
type 2 and 3 sensitivity 2, scarlet fever, 3 glomerulonephritis) scarlet fever breaks clot breaks DNA |
M- type 2 and 3 sensitivity 2, scarlet fever, 3 glomerulonephritis)
SPE A- scarlet fever Streptokinase- breaks clot Strepdornase- breaks DNA |
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14 yo recovered form untreated pharyngitis but now has migratory polyarthritis CARDIOMEGALY AND ERYTHEMA. whats going on?
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type II hypersensitivity due to protein antigen AB complex
Type II AB GO AFTER TISSUES |
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MTB virulence
1. what inhibits phagolysosome formation and facilitates intracellular growth 2. induces phagocytosis to help bring virus into cell 3. adjuvent to increase AB, when we put it with cord it forms granuloma 4- inhibit MHC II expression, slows T cells |
1. sulfatides
2. Cord factor- 3. Wax D- 4. LAM- |
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if you have a CXR with small spots near midline in mid lung its... what else will be there?
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Primary TB
**Ghon complex **perihilar, middle/lower lobes |
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what causes the thing where women wont cough so they get crap stuck in their lings
|
MAC superinfection- waning immune system, nodular infiltrates, seen in older women who dont cough
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|
what are some characteristics of the following
Disseminated MAC- Latent TB- Endogenous Reactivation- Miliary- |
Disseminated MAC- wont see granuloma, T cells are too low
Latent TB- needs more patchy infiltrates and a + TB test Endogenous Reactivation- active cavitation and caseous necrosis in apex of lungs Miliary- will be disseminated all over, wont see limited region around perihilar area |
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What are these descriptions associated with
1 homeless, etoh, smoke 2 consolidatinos of lungs, 3. waning immune system, nodular infiltrates, seen in older women who dont cough 4. infiltrate, southwest, subcutaneous, brain abcess, fever, cough, dyspnea. 5. acid fast |
klebsiella- homeless, etoh, smoke
s aeureus- consolidatinos of lungs, not lungs MAC superinfection- waning immune system, nodular infiltrates, seen in older women who dont cough Nocardia asteroides- infiltrate, southwest, subcutaneous, brain abcess, fever, cough, dyspnea. DMAC- acid fast |
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whats the cute thing they say about strep
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the only typical thing about it is there is nothing typical about it
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what bacteria is said to be so weird and random the only typical thing about it is there is never a consistent finding
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strep infections
**strep pyrogenes |
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what is the MOST common bacterial throat infection?
who gives it to us when? what ages gets it |
sterp pyogenes
we give it to each other, human is ONLY resevoir 5-15 yo seen in winter/early spring |
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what is the transmission of strep pyogenes
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person to person
**ppl are the ONLY resevoirs (contrast to flu!) **doesnt survive on fomites **seen in kids 5-15 in the winter/early spring **its the most common cause of bacterial laryngitis |
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what are the 3 mechs of strep pyogenes pathogenesis
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1. pyogenic infection: pharyngitis
1. Toxin Mediated: scarlet fever 3. immunologic disease: rheumatic fever, poststreptococcal acute glomerulonephritis :) |
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is a sore throat the only thing we need to worry about with a strep pyogenes throat infectiondo
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nope, scarlet fever from exotoxin SpeA
Rheumatic fever Poststreptococcal acute glomerulonephritis |
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hoe does strep pyogenes present in infants/small kidds
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strep throat!!
middle ear persists for several weeks **then the expected cervical lymphadenopathy and subacute nasopharyngitis with serus discharge |
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how does strep present in older kids and sdults
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acute nasopharyngitis, tonsilitis
erythema, edems purulent exudate cervical lymphadenopathy fever self limitied **in babes it last longer has ear infections adn nasopharyngitis is subacute. in adults its 3-5 days, fever, and acute nasopharyngitis |
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whats the ddx for strep throat
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1. Mono (EBV)
2. Dipthelia 3. Adenovirus 4. Gonococcal infection |
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tell me a little about scarlet fever
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-seen after strep infections: requires lysogenized s pyrogenes and release of SpeA exotoxin
-erythema rash that blanches -sandpaper rash that later deaquamates -pastia lines (thompson sign) red in flexor folds -strawberry tongue |
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if you have a kid with pastia lines (thompson sign) and a rash that turns white when you push it and later the rash falls off what disease? what was initial? what other signs and sx
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Scarlet fever
After strep pyogenes infection Also see sandpaper rash SpeA exotoxin rlease blanching around the mouth strawberry tongue |
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whats the relationship bten strep pyogenes scarlet fever and rheumatic fever
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rheumatic fever can be caused by: strep pyognes OR scarlet fever
Scarlet fever can be caused by strep pyogenes |
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after a strep pyogenes infection what are we on the look out for as far as sequelae are concerned
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1. Rheumatic fever (can follow strep or scarlet fever)
2. Acute glomerulonephritis |
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what is going on with acute rheumatif fever? ARF
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AB mediated cytotoxic type II hypersensitivity
**Protein M AB cross react with the joints and heart **pretty serious |
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what is the serious sequelea of strep pyogenes that is caused by a type II hypersensitivity
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Acute rheumatic fever
**Protein M (the one that inhibits phago) AB cross react with the heart and joints |
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why might one suspect ARF
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if pt had UNTREATED GABHS in the past 1-4 weeks
**rheumatic fever is a type II hypersensitivity mediated by protein M AB cross reacting in our joints and heart |
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what are 5 key manifestations of ARF seen after GABHS (caused by type II hypersensitivity with protein M AB that cross react)
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1. Pandarditis: inflammation of all parts of the heart
2. Joint swelling: migratory polyarthritis 3. Chorea 4. Subcutaneous nodulesrubbery nodule under skin 5. Rash: transient red rings with raised edge also see: arthralgia, ESR/CRP increase, fever, prolonged PR interval |
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what is this classic of?
inflammation of all layers of the heart, migratory polyarthritis, chorea, rubbery nodues, transiend red rings with raised edges' wht other things are seen |
acute rheumatic fever
**caused by a type II hypersensitivty. Protein M AB cross react with the ehart and joints *also see arthralgia elevated ESR/CRP, fever, prolonged PR |
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what is Reactivated ARF
caused by? damage? tx? dx feature |
caused by recurrence of GABHS (strep pyogenes)
damages mitral valve- murmur, increased risk for infection prophylactic penecillin aschoff bodies |
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what are aschoff bodies
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its a thing found in the heart after reactivated rheumatic fever
Dx of reactivated ARF (also see mitral valve daage- murmur) |
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what is teh type III immune complex mediated hypersensitivity that is seen in strep pyogenes
who gets it? |
Acute poststreptococcal glomerulonephritis
**immune complex mediated- AB/AG comlpex is deposited in BM of glomeruli **seen in kids |
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what is the pathogenesis of AGN (acute poststreptococcal glomerulonephritis)
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type III hypersensitivity
**AB/AG complex is deposited in BM of glomeruli **this stim PMN to secrete proteolytic enzymes **the glomeruli are destroyed by proteolytic enzymes |
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if a kid comes in after a strep infection what makes you think they may have a type III hypersensitivity thing going on
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acute glomerulonephritis
**puffy face (fluid retention) **hematuria **hypercolemis (2 to fluid retention) Not serious, good prognosis |
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is it important to distinguish if a sore throat is viral or bacterial
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YES!!!
prevent overuse of AB prevent disease transmission (virus spread like wild fire, strep is not spread by fomites) decrease duration/severity of sx PREVENT RF AND AGN |
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what are the tests to dx strep pharyngitis
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1. RADT (rapid AG detection test) Swab, high sensitivity. all + are true + BUT a - may really be a +
-tests the A AG of C carbohydrate 2. Confirmatory throat culture: only done if RADT is - NO false + here, high specificity. plate on BAP and look for anerobic b hemolysis |
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what is the RADT testing for
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A AG from carb C of strep pyogenes
**super sensitive test, no false -, all true + **if this is neg get a culture adn look for anaeribic b hemolysis **BAP- bacitracin will inhibit growth |
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when we do a throat culture fo rstrep why does the lab grow on blood agar in anerobic ocnditions
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bc strep pyogenes likes CO2 so removing the O2 will help it do the complete b hemolyiss we expect
bacitracin inhibits growth |
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what AB is used in BAP to determine strep pyogenes
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bacitracin
99% of GABHS are inhiited by bacitracin, |
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what does bacitracin do to GABHS
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it inhibits growth of GABHS
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what is the PYR test
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when + it identifies group A b hemolytic strep from other types of b hemolytic streps
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how can we determine if a b hemolytic stres is in fact group A
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a + PYR test
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what are the post strep infection dx tests that they have
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Serological tests, ASO AG (anti streptolysin O, seen after recent infections or current RF)
**not done often, time and $$ |
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what is the DOC for strep Pyrogenes infection
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Penecillian VK, b lactamase
**if you are allergic cephalosporin, or mAColidEs- Azithromycin, Clarithromycin, Erythromycin **clindamycin if regional resistance is an issue |
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so if the DOC for strep pyrogenes is penecillin why mught you use a dif drug
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Allergies: instead use
2/3 generation cephalosporin Macrolides: azithromycin, clarithromycin, erythromycin 2. Resistance -use clindamycin instead |
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whats the goal of tx of strep
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not really to help sx, they clear in 3-5 days if you are an adult
**it eliminated AG stimuli, prevents RF (II) nad AGN (III) |
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is there a strep vaccine? what would be in it
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nope
**M protein |
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1. whats the most common bacterial infection of the throat?
2. What is the gram stain and cell shape 3. What is the major virulence factor 4. What age is affected 5. whats the disease prognosis 6. Dx 7. tests to comfirm Dx 8. Sequelea dx 9 DOC |
1. whats the most common bacterial infection of the throat?strep pyogenes
2. What is the gram stain and cell shape: gram + coccal chains 3. What is the major virulence factor. M protein, inhibit phage 4. What age is affected 5-15 5. whats the disease prognosis: good but can lead to -RF (II) -AGN (III) -Scarlet fever (SpeA) 6. Dx: RADT, Culture (anerobic b hemolysis) 7. tests to comfirm Dx: bactracin sensitive, PYR positive (groupA) 8. Sequelea dx: detect AB in serum (ASO) 9 DOC: penicillin VK |
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what are the most common causes of bacterial otitis externa?
what is the biggest predisposing factor sx |
Pseudomonas aeruginosa
Staphylococcus aureus **moisture. "swimmers ear" ear pain- otalgia, ear exudate- otorhea |
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if you were in a pool that was infested with p aeuroginosa and s auerues and you have a fever whats the deal
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its NOT just otitis externa, fever indicated more than just local infection, need systemic AB
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what gram - bacillus is assocated with a pigment, whats the pigment and what color
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Pseudomonas aeruginosa
Pyocanin- blue Pyoverdin- green **bandaids and things can flouresce. **if you are a swimmer maybe you have otitis externa and your ear will flouresce |
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pseudomonas aeuriginosa
1. gram stain 2. shape 3. characteristic |
1. neg
2. bacillus 3. pyocyanin (blue) pyoverdin (green) **otitis externa |
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staph aeurus
1. gram 2. shape 3. characteristic |
1. Positive
2. cluster of cocci (strep pyogenes is chain of coci) 3. coagulase +, b hemolytic |
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6 yo female with external exudate that is thick adn nasty and a little green. gram reveals a gram - bacillius. whats the pathogen
1. P aeuroginosa 2. s aerus 3. moraxella catarrhaiss |
P aaeuroginosa
its swimmers ear, otitis externa, it can be caused by S aeurus but then it wouldnt be green and it would be a gram + cluster of cocci Moraxella catarrhalis is otitis media |
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how can you dx otitis externa caused by p aeuroginosa or s aerus
whats the tx |
1. gram stain + for straph - for pseudomonas, pseudomonas will lite with black light
2. Topical AB, systemic pain releif If there is a fever tx systemic AB |
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whats the deal with otitis media, bacterial or viral
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most is viral but we will look at the bacterial causes via
strep pneumonia h influenzia moraxella catarrhalis |
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what are the most and least common causes of otitis media/sinusitis
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1. strep pneumonia
2. haemophilus influenzea 3. Moraxells catarrhalis |
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streptococcus pneumonia
1. gram 2. shape 3. characteristis 4. causes |
1. Gram +
2. diplococcus 3. virulent strains have capsule, a hemolytic, sensitive to opticicin causes otitis media and sinusitis |
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what bacteria is sensitive to optocin
what bacteria si sensitive to bactracin |
streptococcus pneumonia, also a hemolytic
GABHS Strep pyogenes |
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is is killed by bactracin what is it
if a bug is killed by optichin what is it |
GABHS
Strep pneumonia, a hemolytic |
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H influenzea
gram shape |
gram -
coccibacilli **causes sinusitis and otitis media (second most common, S pneumonia is most common) |
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moraxella catarrhalis
gram shape characteristic |
neg
diplococci osidase + **3 most common cause of bacterial otitis media and sinusitis |
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waht is the dx of bacterial otitis media
wht is the DOC WHat do you do for chronic infectins what the most common bacterial cause |
cilincal presentation, can take fluid but not common
tx: Amoxacillin tympanostomy tubes strep pneumonia |
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most common cause of bacterial sinusitis
whts the dx whts the tx |
strep pneumonia (same as otitis media)
clinical presentation, CT scan, allergy tests, nnasal biopsy Nasal steroids, surgery, OTC decongestant, AB |
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what bug looks like chinese letters
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coyrnebacterium diptheriea
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Corynebacterium diptheria causes what 2 diseases
gram? cell morphology? |
respiratory and cutaneous diptheria
gram + chinesse letters |
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are all corynebacterium virulaten
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nope, need the phage encoded diptheria toxin
AB toxin that is made when Fe is LOW B binds heparin binding EGF receptor, T inserts into endosome, A is catalytic and inactivates EF2 and halts protein synthesis |
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what is teh mech of the phage encoded diptheria toxin
include the type of exotoxin, the receptor that it binds and how it kills host |
its and AB exotoxin that is made when Fe is low
1. B subunit binds to hepatin binding EGF receptor 2. T inserts into endosomal membrane 3. A subunit inactivates EF2 and stops protein synthesis |
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what has happened
pt presents with bull neck and pharyngitis, they have a sudden onset of malsise and low grade fever |
respiratory diphteria
**also will have pseidomembrane **recall the mech of diptheria toxin is to stop protein synthesis via phage endoced AB exotoxin |
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what is the pathogenesis of diptheria
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1. Adherence/Proliforation (person to person spread)
2. 2-6 day incubation. localized damage due to exotoxin leads to grey pseudomembrane **if infection continues you get systemicc toxicity that can lead to myocarditis and demylenation |
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who gets diptheria
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ppl NOT in US
uncommon due to vaccien!!! person to person spread |
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what are 2 KEY things to see on PE for diptheria
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2. Bull neck, severe lymphadenopathy
2. pseudomembrane- dont rip it off, it bleeds nad spreads infection |
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what is the bug that is a pleimorphic gram + bacilli that has metachromatic granules
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corynebacterium diptheria
Chinese letters |
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what grows as a bloack colony on cystein tellurite agar
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diptheria
**also culture this on 1. Blood agar- rule out hemolytis strep 2. Loefflers- revels colony morphology |
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what 3 agars is diptheira groen on
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1. Blood- rule out hemolytic strep
2. Loefflers- revela morphology 3. Cysteine Tellurite- black colony |
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when we think diptheria we need to test for toxin production (after we grow black colonies etc) how is this done
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1. Elek test: immunodiffusion assay, ppt detects secretion of exotoxin (exotoxin inhibits protein synthesis)
2. PCR- detect TOX gene (phage gene responsible for exotoxin) 3. Elisa: detect toxin 4. Immunochromatographic Strip Assay- sensitive for diptheria |
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what disease is associated with the ELEK test
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its an immunodiffusion assay to detect diptheria toxin
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how is diptheria tx
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treat ASAP, call CDC
neutralize diptheria toxin with antitoxin AB: penicillin or erythromycin Vaccine once recovered |
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if someone has diptheria infection should we vaccine
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ya, for some reason the acutal disease does not promote immunity
**vaccinate AFTER the infection clears (tx with antitoxin and penecillin/erythromycin) |
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what causes whooping cough
gram shape characteristics |
Bordatella Pertussis
1. gram - 2. coccobacilli 3. endo toxin, adhesions, exotoxin. fastidious, aerobic |
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what are the virulence factors with bordatella pertussis
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1. endodoxin (gram -)
2. Adhesions: agglutinins, filamentous hemagglutinate 3. Exotoxins |
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what are the adhesion virulence factors associated with pertussis
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1. Filamentous Hemagglutinin
2. Pertactin= P69 3. Aggluninogens 4. Finbrea **P69 and FHA have RDG sequences hta mediate attachemnt to intigrins on epithelial cells |
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filamentous hemaggluntin and P69 are assosicatied with what
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adhesion virulence for pertussis
**both contain RGD that mediate attachments to epithelium **stop cilia from beathing, bad news for us |
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what are the 4 major exotoxins associated with bordatella pertussis
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1. pertussi stoxin: hypoglycemia
2. adenylate cyclase toxin: decreased chemotaxis/phago 3. Tracheal cytotoxin: inhibits cell movement, regeneratio of damaged cells 4. Dermonecrotic toxin: vasoconstriction and ischemic necrosis |
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exposire to bordatella pertussi causes what to happen in respiratory epithelium
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adhesion toxins and pertussis toxin let bug attach to the respiratory epithelium
**this then leads to proliforation and phago, BUT once phago in the macro the pertussis inhibits intracellular killing and lives |
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what does pertussis toxin do
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1. adhesion
2. lymphocyte leukocytisus by inhibiting extravasiation of lymphocytes. **prevent killing of intracellular pathogens. The pertussis bug is eaten by macro but then inhibits the likkein mech of the macro |
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what are the 3 stages of pertussis (week long incubation
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1. Catarrhal Stage: non specific, highly contagious
2. Paroxysmal Stage: when we get the whoop, epithelial celsl are extruded, impeedes mucus clearing 3. Convalescent stage: can get 2 complicatins like pnemonia, encephalopathy, seizure, death |
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who gets pertussis
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mostly kids, but some adults
STRICTLY HUMAN, no other resevior **workd wide still epidemic |
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how is pertussis grown
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bordget Gengou or regan lowe agar
**dx of pertussis |
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what is grown in Bordget Gengou or Regan Lowe agar
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pertussis
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how can we prevent pertussis
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immunization
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what is the tx for pertussis
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macrolide AB
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macrolide AB can tx what
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pertussis
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Hib can cause what?
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epiglotitis
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what bacteria can cause epiglotitis
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Hib
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