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Flashcards in CV ID Deck (28):

Staphylococcus aureus virulence factors and their actions (11)

Biofilm formation, Capsule, Adhesins, pathogenicity islands code methicillin resistance, protein A binds the Fc portion of IgG, Coagulase ->fibrin coat protecting staph from phagocytosis, hemolysins and leukocidins destroy red and white blood cells
Elastin, collagen, & fibronectin (FnbpA) binding proteins


What virulence factors allow staph aureus to invade deep tissue? (3)

Hyaluronidase breaks down connective tissue
Staphylokinase lyses formed clots
Lipase breaks down fat


Virulence factors of strep species (viridans) (2)

Dextran for glycocalyx formation
Surface adhesion proteins (FimA and GspB)


Which organism that causes IE is most frequently found following GU (older men) or OB procedures (younger women)?

Enterococcus (3rd major cause of IE)


Virulence factors of enterococcus species

Pili, surface proteins, biofilm formation
Extracellular enzymes (proteases, hyaluronidases)
Usually resistant to penicillin and carbepenems


Where is enterococcus usually found?

Lines the GI tract.


Strep pyogenes may be a part of normal skin flora. If it causes a localized skin or subcutaneous infection, it presents as ____(3), whereas it can cause ____ or ____ with toxin-mediated infections.

Local: impetigo (pustular lesions and honeycomb crusts)
Sub-q: cellulitis and erysipelas (ery = upper dermis and cutaneous)
Toxic shock syndrome and necrotizing fasciitis


What are patients with strep pyogenes cellulitis at risk for?

Glomerulonephritis but not Rheumatic fever (whereas strep pharyngitis can lead to GN and rheumatic heart disease.


Strep pyogenes virulence factors

Capsule, streptokinase (converts plasminogen to plasmin), M protein (resists phagocytosis), hyaluronidase (breakdown of conn tissue), DNase, Stretolysin O and S (destroy RBCs and WBCs respectively)
*Streptokinase and hyaluronidase from a lysogenized prophage*


How does TSS happen?

Skin infection --> systemic release of pyrogenic exotoxin A (superantigen) --> polyclonal activation of T cells --> acute fever, shock, multiorgan failure


How does strep pyogenes infection lead to necrotizing fasciitis?

Trauma --> deep seated infection --> release of exotoxin B (protease) --> rapid necrosis along fascial planes with no damage to muscles.


Our body producing an antibody to M protein of strep pyogenes that cross reacts with our own heart tissue is what type of hypersensitivity?

Type II
(I = allergy, II = antibody-dependent autoimmune attack, III = Immune complex disease IgG-antigen complex deposits, IV = delayed type, T cell mediated)


Definitive clinical indicator of RHD?

Mitral stenosis following pharyngitis with a rash
- damage due to cross reactive antibodies reacting with meromyosin in heart


How does RHD present?

2-4 weeks post strep infection: pain swelling in large joints, fever, weakness, muscle aches, SOB, CP, n/v, hacking cough, circular rash, lumps under skin.
Treat with penicillin-based ab, aspirin, corticosteroids


Presentation of myocarditis (3)

CP, heart failure, abnormal heart rhythms possible


Major causes of myocarditis. How do they do this?

Coxsackievirus B
Adenovirus (children)
Utilize CAR receptor on heart tissue (coxsackie and adenovirus receptor)


Presentation of pericarditis

CP (irritated pericardium layers rubbing) worse swallowing, supine
3 component friction rub, tachycardia
Frequently ECG changes


Most likely causative organisms for pericarditis

Viruses are major cause: Coxsackie A & B, echo, influenza, entero
Bacterial: staph aureus, strep pneumoniae, h flu, n meningitidis


Artificial valve, pacemaker, defibrillator infections:
- most common cause within 2 weeks
- most common cause within first year
- other culprits

Staph aureus
Staph epidermidis or other coag neg staph
Strep species (viridans) and enterococci species


Treatment of RMSF?



Differentiate between Osler nodes and Janeway lesions

Osler: immunological (though with bacteria found sometimes in early lesions) red-purple, tender, slightly raised lumps usually on fingers and toes.
Janeway: vascular phenom consistent w septic micro-embolism (bacteria inside), usually on palms and soles. Generally non-tender lasting days to weeks


What type of hypersensitivity are Osler nodes the result of?

type III (immune complex-mediated)


What are MSCRAMMs?

microbial surface components recognizing adhesive matrix molecules
- Broad classification of the various attachment proteins utilized by strep and staph in colony formation


Step pneumoniae virulence factors



Neisseria meningitidis virulence factors



Staphylococcus epidermidis virulence factors

SD-repeat containing protein-G (SdrG)
Biofilm formation (various proteins)


COxsackie A and B + adenovirus virulence factors

CAR binding proteins


Rickettsia rickettsii virulence factors

OmpA and OmpB for attachment
Type 4 secretion system (T4SS) for host cell entry