S3 Ross Micro – Multifaceted Model – Flashcards

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This microbe is a gm(+) cocci found in clusters, catalase (+), coagulate (+), Beta hemolytic, and resistant to high temperatures, salt and dessication.
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Staph. aureus
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This microbe is usually part of the normal flora in humans and in up 40% of the population can be found in the anterior nares.
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S. aureus. It is noted that healthcare workers, diabetics, and patients on dialysis have higher rates of colonization.
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Why would Wiskott-Aldrich syndrome or diabetes be specific risk factors for S. aurus infections?
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These disorders can cause defects in leukocyte chemotaxis which would make one more susceptible to infection.
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Hypogammablobulinemia or complement deficiencies can increase your chances of S. aureus infection becuase...
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You will not be able to opsonize with antibodies as effectively.
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If you can't activate membrane-bound oxidase systems or superoxide formation, how would it effect your ability to kill microbes?
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You will not be able to perform intracellular killing following phagocytosis.
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Two very common ways to get a Staph infection.
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Skin injuries (burns/surgical incision) and foreign bodies (catheters and prostheses)
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This is touch but try to list all 7 Staph aureus virulence factors.
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Capsular polysaccharides, Peptidoglycan & Teichoic Acids, Protein A, Enzymes, Hemolysins, Toxins, Superantigens.
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How is the capsular polysaccharide a virulence factor for Staph. aureus?
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It prevents phagocytosis
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These virulance factors of Staph aureus are responsible for the activation of complement, monocyte IL-1 production, production of opsonic antibodies and the enhancement of chemotaxis.
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Peptidoglycan & teichoic acid.
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You are a evil North Korean scientist who didn't get the memo that the Iron Curtain has fallen. You are trying to create a biological virulence factor that interferes with opsonization, phagocytosis, and complement activation by binding to the Fc region of IgG1/2/4. There is a second memo that he never got about Staph Aureus. What did it say?
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Protein A binds Fc regions of IgG to interfere with the immune response. He should probably subscribe to some newer journals.
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How do fibrinolysins, haluronidase and lipases help the virulance of Staph. aureus?
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Promotion of bacterial spread in tissues.
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What are two examples of enzymes that enhance bacterial survival in phagocytes?
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Catalase and Carotenoids.
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This enzyme binds prothrombin and becomes enzymatically active, then catalyzes the conversion of fibrinogen to fibrin. Overall it acts as immunological cammo
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Coagulase
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This enzyme acts as a sort of shield over bacterial cells making them resistant to opsonization and phagocytosis.
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Fibrin
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This type of hemolysin lyses PMNs, forms pores that lead to osmotic swelling and is responsible for the zone of hemolysis in BAP.
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Alpha hemolysin
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This hemolysin degrades sphingomyelin
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Beta hemolysin
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Gamma hemolysins + various proteins form this complex. They lyse PMNs and can cause cytoplasmic degranulation.
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Panton-Valentine leukocidin. It is found in MRSA and is responsible for the "flesh eating" scary part of bad staph infections.
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Staphylococcal enterotoxins, TSS Toxin 1, and SPE-A,B,C,F,G,H,J are all examples of what virulence factor?
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Superantigens
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This protein promotes Staph. aureus binding to mucosal cells and tissues matricies.
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Fibronectin-binding protein
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You have a patient who presents with a circumscribed collection of pus. You explain to her that it needs to be drained to allow for access for antibiotics and antibodies. This infection was secondary to a 2nd degree burn. What microbe do you suspect caused the abscess?
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Staph. aureus.
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This microbe is responsible for causing 80% of pyogenic infection.
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Staph. aureus.
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S. aureus can manifest as different types of skin infections. Your patient presents with small erythema which then progressed to bullae which seemed to heal as a honey-colored crust. What is the disease called?
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Impetigo
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Karma has come back to you, and although your infractions were minor, it sure doesn't feel like it. You notice that your hair follicles on your arm are raised, reddish, and painful. What is this called?
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Folliculitis. Follicle + inflammation = folliculitis.
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Describe the difference between a furnucle and a carbuncle.
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A furnucle is a single red painful lesions that has a yellowish center. A carbubcle is collection of furuncles which could spread into the subcutaneous tissues.
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This is a pyogenic infectino of the apocrine sweat glands which looks like a small bunch of furnucles.
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Hidradentis Suppurativa.
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erythematous skin lesion enlarges rapidly and has a sharply demarcated raised edge. It appears as a red, swollen, warm, hardened and painful rash, similar in consistency to an orange peel.
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Erysipelas
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This appears as a large rashed area which is disproportionately painful upon touch and can spread into the blood stream
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Cellulitis and fasciitis
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Your patient, Jude Law, presents today with symptoms of acute septic syndrome. Heart auscultation revealed a murmur. You also note petechiae and Janeway lesions. You think, man I am so glad Sloma put all of this on one slide for us. You then inform Jude Law that he probably has...
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Endocarditis secondary to a Staph. aureus infection.
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If Staph a. infects in this particular area it can be quite lethal.
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Pulmonary infection.
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A superficial Saph a. skin disorder that can lead to blistering or scaling that is usually seen in neonates.
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SSSS (Staphlococcal Scalded Skin Syndrome)
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These toxins are responsible for the pathogenicity of SSSS. They are serine proteases which dissolve mucopolysaccharide matrix and splits cellular linkages but does NOT involve the mucosa.
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Exfoliatins A & B (ET-A & ET-B). These toxins look for GM4 in the stratum granulosum, which is only in children and people with weird diseases.
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What are some differences between Generalized and Localized (bullous impetigo) forms of SSSS?
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Generalized has toxin spread all over the body and you will see scaling but the microbes will NOT be in the lesions. It goes away in 4-7 days. Bullous Impetigo is in people who have some immunity against it so you will see antibodies and blisters with bacteria in it.
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These proteins can activate up to 20% of the total T-cell pool by binding to MHCII and the V-beta region of the TCR.
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Superantigens. Binding causes MASSIVE cytokine release subsequent inflammation leading to endothelial leakage, hemodynamic shock and multiorgan failure. Pretty much the worst parts of the bible.
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These are a part of a group of 15 staphylococcal enterotoxins which cause food poisoning and are pyrogenic.
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superantigens.
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Toxic shock syndrome is caused by this toxin.
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Toxic show syndrome toxin-1
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What are SEA (E,H,I), SEB, and SEC?
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Heat-stable enterotoxins produced by S.A. which cause food poisoning. They can indirectly induce the emetic reflex and can increase intestinal peristalsis.
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What are the two forms of TSS?
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Menstural TSS and Non-menstrual TSS. The former is usually caused by high-absorbency tampons. The latter by TSST-1, SEB, and SEC.
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What conditions are needed for Menstrual TSS?
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Elevated protein, pCO2, pO2 and neutral pH. These specific conditions lead to the production of TSST-1. Also note that blood cultures will be negative.
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Your patient is febrile, hypotensince, has non-pitting edema, hypoalbumenemia, and a morbilliform rash. What is the syndrome?
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TSS.
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Vancomycin, nafcillin, and oxacillin are the three drugs mainly used to treat S. aureus infections. When would you use each?
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Vanco for severe infections where you don't know the susceptibility. If you know it is susceptible to methicillin, then you give them nafcillin or oxacillin.
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You will find this bug in hospitals, usually in catheters infecting immunocompromised hosts.
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S. epidermidis. Note that it forms a biofilm making it very resilient.
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Young promisCOUS women are usually seen with UTIs involving this bug.
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S. saprophiytiCUS.Virulence factors include urease and hemagglutinin.
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You have two CoNS (Coagulase Negative Staph). Which one will will resistant to Novobiocin?
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Saprophyticus is resistant. Epidermidis is susceptible to novobiocin.
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The DOC for CoNS infections.
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Vanco. More than 80% of CoNS are resistant to methicillin and penicillin.
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