gram + – Chemistry – Flashcards
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| what colony morphology do gram + staphylococci take? |
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| grape-like clusters that divide in 3 planes |
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| what differentiates ALL staphylococi from ALL streptylococci? |
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| staphylococci have catalase which allows them to break down hydrogen peroxide into water and oxygen |
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| where are staphylococci found? |
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| on skin and mucus membranes for humans |
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| which are the coagulase (+) staph? |
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| staphylococcus aureus |
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| which are the coagulase (-) staph? |
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| staphylococcus epidermis and saprophyticus |
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| what is the most pathogenic species of the staphylococcus genus? how do they appear on agar? |
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| staphylococcus aureus. blood agar results in golden colonies and they are beta hemolytic, releasing a hemolysin which lyses RBCS. |
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| what is one way that staphylococcus aureus interacts with IgG? what does the fact that they have coagulase mean in terms of their interaction with fibrinogen? |
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| they have something called protein A that binds the Fc portion of IgG. coagulase A allows staphylococcus aureus to transform fibrinogen into fibrin |
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| how are some strains of staphylococcus able to resist methicillin? |
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| some strains have the mecA gene, (type I-V) located on the staphylococcal chromosome that encodes for PBP2', resulting in MRSA, where an alternative transpeptidase Penicillin Binding Protein makes them resistant to PCN + methicillin. |
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| do staphylococcus have a capsule? any other kind of layer? where do they can they grow? |
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| staphylococcus aureus can grow in high salt and lipid concentrations. they do have a capsule and a slime layer. |
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| where can staphylococcus aureus be found on humans and what % of humans? who is likey to carry it? can it affect internal organs? how virulent is it? |
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| S. aureus can be found transiently on skin, nasal pharynx, urethra, eye and anterior nares of ~30% of humans especially hospital workers. it can infect internal organs if it gets into the blood stream and has many virulence factors. |
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| what is normal body temp in C? |
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| 37 |
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| what are possible symptoms of a staphylococcus infection? temp? swelling? blood count? |
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| fever, (39.4 C), abcess, (swollen w/central softness), and tenderness on the lower spine. a high WBC count. |
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| what would a gram stain positive for staphylococcus aureus show? |
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| gram + cocci in clusters |
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| what might a nuclear bone scane of someone with a staphylococcus aures infection show? |
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| osteomyelitis, (bone infection) |
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| if S. aureus is resistant to PCN, how might this be tested? what is another antibiotic that could work? |
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| the disk diffustion method can give qualitative information on resistance. nafcillin can be successful if PCN doesn't work |
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| why are most, (95%), S. aureus organisms resistant to PCN? |
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| they all make a beta lactamase |
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| what is the toxin that staphylococcus aureus produces? |
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| enterotoxin A |
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| which of these can be caused by S. aureus: skin infection, osteomyelitis, food poisoning? what is the conclusion? |
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| all of them. S. aureus can cause just infection or just intoxication or it can cause infection and intoxication. |
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| what are some general clinical manifestations of S. aureus on the superficial, intermediate, and deep layers of the skin? |
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| folliculitis: pyogenic, (pus), infections in the hair follicle, (sty if in the eye). furuncle: extension of folliculitis, large, painful underlying necrotic tissue, (boil), deep in the skin. carbuncle: multiple interconnected boils that extend into deeper tissue, usually accompanied by fever/chills if spread systemically. all these are considered abcesses, or walled off infections of organ and bone. |
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| what is impetigo? what part does staph play? what does it appear as? |
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| a superficial localized cutaneous infection where staph is usually a secondary invader. a yellow crusting on the skin surface appears with this. |
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| what is bullous impetigo? what causes it? how communicative is it? |
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| large superficial fluid filled blisters caused by strains of S. aureus that produce a toxin called exfoliatin. it is highly communicable, and blisters are culture positive. |
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| what are the 2 major infections that can be caused by S. aureus if it gets to the bloodstream? |
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| osteomyelitis and septic arthritis. S. aureus is the number one cause of both. |
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| what is osteomyletis? where does it attack in children, adults? |
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| dissemination of S. aureus infections into the bone or secondary infection. in children it can affect long bones, in adults, it can affect vertebral bones, leading to intense back pain w/ fever |
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| can S. aureus cause septic arthritis? how |
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| yes, the most common cause in pts recieving intra-articular injections or those who have mechanical joints |
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| what is staphylococcal skin syndrome? how does it present? who does it occur in? are blisters cx +? |
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| Staphylococcal Scalded Skin Syndrome (SSSS or SSS) is caused by the exfoliatin toxin produced by some S. aureus strains. it presents as clear blisters that pop, (caused by toxin - sp should be cx negative). also erythema and intradermal desquamation, (peeling), can be remote from the lesion. this occurs in the very young, (like the baby of an infected mother) |
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| what is toxic shock syndrome? how does it present? what can cause it? |
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| release of TSST-1, (superantigen), or enterotoxin, (from S. aureus) into the blood. pts suffering from this have high fever, vomiting, diarrhea, sore throat, and muscle pain. this is seen with tampon use or following staph infections of traumtic or surgical wounds. |
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| what can cause staphylococcal food poisoning? what food can contain it? how does the food become contaminated? how does it present. |
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| ingestion of preformed enterotoxin contaminated food. processed ham, salted pork, potato salad, ice cream can all be contaminated by a human carrier. vomiting and diarrhea, (stimulation of vagus nerves) in 1-5 hrs but no fever, and rapid recovery within a day except in the elderly or immune compromised. |
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| how does a primary infection with S. aureus occur? is there anything that can increase the infectious dose? |
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| colonization mediated by surface adhesions that bind fibronectin, fibrinogen, elastin, and collagen. trauma and foreign bodies increase the infectious dose. |
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| how does tissue destruction and localization occur in a primary S. aureus infection? how do abscesses form? |
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| immune response and bacterial toxins can cause tissue destruction. the area is surrounded by a fibrin capsule, (due to fibrin deposition caused by coagulase and stimulation of fibroblasts), the center is full of necrotic host tissue, edema and dead+live staph. |
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| what determines the outcome of a S. aureus infection? where is the most serious place for an infection to occur? |
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| the ability of WBCs to fight off the pathogen, (usually happens in immune competent pts), which depends on the inoculum, (# of bacteria), immune status of the host, and site of entry. the most serious case of infection is found in the bloodstream and distant organs, (osteomyelitis and kidney disease) |
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| in a primary S. aureus infection what can exotoxins do? |
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| exacerbate primary disease, such as enterotoxin. some toxins can exert effects locally or systemically, or take days to act |
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| what does protein A do? |
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| binds the Fc region of IgG, extering an antiphagocytic effect |
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| what does fibronectin-binding protein, (teichoic acid) do? |
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| promotes bacterial binding to host mucosal and tissue matrices |
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| what do cytolytic exotoxins do? |
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| attack host membranes, including RBCs casuing lysis |
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| what do capsules and slime do? |
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| prevent phagocytosis, promote adherence to cells and prothetic devices |
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| what does catalase do? do all bacteria have this enzyme? |
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| catalase facilitates H2O2 into 2H2O + O2. staph does have this strep does not. |
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| what is coagulase? what bacteria make this? how does it work? why is it useful? |
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| an either cell bound or free enzyme that produces blood clumping. S. aureus is the only strain to make this. coagulase cleaves fibronectin to fibrin, clotting plasma. this localizes the organism to protect from phagocytosis. |
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| what do hyaluronidase, staphylokinase (dissolves fibrin clots), and DNas do? why are they important clinically? |
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| enhance bacterial spreading along tissue planes. they are useful in diagnosis. |
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| how are lipases useful to bacteria? |
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| these degrade skin lipids, allowing survival in sebaceous tissue |
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| how is beta-lactamase useful for bacteria? where is it encoded? |
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| beta-lactamase is coded in a plasmid found in ~90& of S. aureus strains. it inactivates beta-lactam antibiotics by degrading the beta-lactam ring, giving bacteria the ability to resist PCN. |
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| what are 5 disease causing toxins found in S. aureus? which of them are superantigens? |
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| enterotoxin, exfoliatin, TSST-1, cytolytic exotoxins, and leukocidins. enterotoxin and TSST-1 are superantigens |
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| which types of enterotoxin are involved in food poisoning? milk products? pseudomembranous colitis? which are heat stable and resistant to gastric juices? is it a superantigen? |
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| types A-G are heat stable and resistant to gastric juices. type A enterotoxin causes food poisoning, C+D are involved with milk products, and B is involved with pseudomembranous colitis. it is a superantigen. |
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| what are 2 types of exfoliatin? what can it cause? how does it work? |
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| ETA+B. this causes exfoliative dermatitis, (SSSS), and bulbous impetigo. exfoliatin is a serine protease that splits intracellular bridges in the epidermis. |
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| what causes TSS, (toxic shock syndrome)? how does it respond to proteolysis? what is a common way to get this? is it a superantigen? |
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| TSST-1, toxic shock syndrome toxin. S. aureus can grow in a localized section of the body, but systemic problems can occur b/c of this toxin. it is a proteolytic-resistant exotoxin. it is often associated with menstruation. it is a superantigen |
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| what are do cytolytic exotoxins do? what is P-V leukocidin? |
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| cytolytic exotoxins are toxic for many cell types: smooth muscle in blood vessels, WBC’s, RBC’s, fibroblasts, and platelets. P-V leukocidin is a pore-forming protein that lyses WBCs, and is encoded by almost all community aquired MRSA. |
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| what are two ways of IDing S. aureus in the lab? |
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| a catalase test will confirm that it is staph, (rather than strep), and a coagulase test will confirm that it is staphylococcus aureus. |
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| is S. aureus beta-hemolytic? what color colonies will it form on blood agar? |
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| S. aureus is beta-hemolytic and forms yellow colonies on blood agar |
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| can S. aureus grow on mannitol-salt sugar? why is this important? |
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| S. aureus can live in high salt conc. and ferment mannitol, (increases pH and turns indicator yellow), which some other staph cannot. |
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| are all S. aureus resistant to PCN? why? what antibiotics do have an effect? |
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| all staph are resistant to penicillin due to the presence of beta-lactamase on plasmids and/or transposons. semi-synthetic penicillins such as nafcillin and methicillin and others are effective, (but not those with the mecA gene -> MRSA) |
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| what is used to treat MRSA? |
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| vancomycin, but resistance is developing |
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| what is immune clearance of S. aureus mediated by? |
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| opsonizing IgG which allows for more efficient phagocytosis. |
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| how long does immunity to S. aureus last? what is the best prevention? |
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| immunity is short and incomplete, so re-infection is a possibility. good handwashing is the best prevention. |
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| what is CoNS? |
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| coagulase negative staphylpcoci which includes S. epidermidis and saprophyricus |
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| is S. epidermidis catalase positive? what about coagulase? is it hemolytic? what color are its colonies on blood agar? where is it found normally? what is its major virulence factor and what is it associated with? |
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| S. epidermis is catalase positive, coagulase negative, it is non-hemolytic and forms white colonies on blood agar. it is normal flora on skin, nose, and throat. its majore virulence factor is high molecular weight polysaccharide slime which enhances its binding to surfaces, causing infections associated with prosthetic devices, shunts, grafts, and catheters, (commonly prosthetic valve endocarditis). for the most part it is an opportunist. |
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| what can S. saprophyticus cause? what is it resistant to, why is this important? |
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| S. saphrophyticus can frequently cause cystitis, (UTIs), in healthy sexually active women. it is resistant to novobiocin which is used to distinguish it from S. epidermidis. |
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| what does novobiocin resistance dermine? |
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| S. saprophyticus is resistant to it and S. epidermidis is sensitive to it |
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| what is used to differentiate streptococci from staphylococci? how do streptococci divide? how do their colonies appear? |
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| strep are gram +, divide in one plane, and do not have catalase, (staph does), and appear as small translucent colonies |
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| how are streptococci classified? |
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| by their serologic/lancefield grouping, hemolysis patterns and biochemical patterns, (species) |
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| serologically/lancefield? |
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| what is serologic/lancefield grouping based on? what are medically important strains? examples? |
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| major cell wall carbohyrates, and includes medically important A,B,C,D, and G. for example, S. pyogenes is GAS, (group A strep) or GABHS, (group A beta-hemolytic strep) and S. agalactiae is GBS, (group B strep) |
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| what group did enterococci used to be a part of? |
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| group D strep |
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| what are streptococci not able to be grouped with the lancefield system? |
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| vivridan strep, S. mutans and S. sanguis, (common cause of acute endocarditis), and peptrostreptococcus |
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| what are the three ways that streptococi can be classfied accordng to the hemolysis they exhibit on blood agar? what do alpha, beta, and gamma hemolysis look like? |
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| alpha hemolysis is incomplete, surrounded by a green halo. beta is complete hemolysis, surrounded by a clear zone. gamma is no hemolysis. |
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| why are streptococcus pyogenes considered group A? are they hemolytic? are they particularly sensitve to any antibiotics? what kind of antigens do they have? what kind of antigen do they have? |
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| streptococcus pyogenes are GAS, espressing a group A specific carbohydrate, (N-acettlyglucosamine+rhamanose). they are beta-hemolytic and very sensitive to bacitracin. they have an M-type specific antigen. |
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| what does the M protein expressed on streptococcus pyogenes do? where is it exactly found on the bacterial surface? |
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| this M protein is only associated with S. pyogenes, it is needed for virulence. it is involved in adhesion to keratin containing epithelial cells, (but not pharyngeal tissue). it also has antiphagocytic proterties, (prevents C' deposition in the absence of specific antibody) and has antigenic epitopes similar to human cardiac muscle tissue. |
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| is the M protein found on S. pyogenes highly variable? what are the implications of the fact that it has antigenic epitopes similar to human cardiac tissue? |
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| the M protein found on S. pyogenes is highly variable, with hypervariable regions eliciting specific immunity. fact that it has antigenic epitopes similar to human cardiac tissue means that there is cross-reactivity, leading to immune problems and acute rheumatic fever and post streptococcal glomerulonephritis |
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| what do streptococcal pyrogenic exotoxins do? are they superantigens? what are the 3 immunological forms? what are they encoded by? |
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| cause direct damage to skin, responsible for scarlet fever rash. the are superantigens, (non specific mitogen of T-cells, causing exaggerated production of cytokines). the 3 immunological forms are SPE A,B, and C. they are encoded by temperate phage, (A+C), tox-strains can be converted by aquistion of a phage, (lysogenic or phage conversion) |
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| what does the hyaluronic acid capsule of S. pyogenes do? |
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| it is non-immunogenic, (looks like host), and anti-phagocytic |
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| what are streptolysin S and O? why are they important? |
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| both are hemolysins which lyse leukocytes, platelets and erythrocytes but S is non-immunogenic and O is. these are important because there is an ASO test for antibodies which is diagnositic for previous strep infections |
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| what is hyaluronidase? |
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| this hydrolyzses |
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| what does hyaluronidase (found in S. pygenes) do? why else is it important? |
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| hydrolyzes hyaluronic acid in ground substance of host tissue, and capsule of organism. it is also important b/c antibodies for it can be tested for later on |
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| what does streptokinase (found in S. pygenes) do? why else is it important? |
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| activates palsminogen to plasmin, (plasmin dissolved fibrin clot). it is also important b/c antibodies for it can be tested for later on. |
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| what does DNase, (streptodornase), (found in S. pygenes) do? why else is it important? |
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| degrades DNA in purulent material. anti-DNase B elevated after skin infections can can be tested for |
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| what are suppurative diseases caused by streptococcus pyogenes? |
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| diseased involved with the formation of pus. pharyngitis, scarlet fever, impetigo, erysipelas, cellulitis, necrotizing fascitis, and streptococcal toxic shock syndrome |
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| what is the #1 cause of bacterial pharyngitis? how does it present? what are considerations for antibiotic tx? |
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| streptococcal pyogenes. it presents with inflammation of posterior oropharynx and tonsillar area; strawberry tongue. antibiotic treatment is recommended to prevent acute rheumatic fever or poststreptococcal glomerulonephritis |
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| what is scarlet fever? how is it caused? how does it present? |
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| a complication of strep. pharyngitis or skin infection, will occur if infecting strain lysogenized to produce SPE's 1-2 days after pharyngitis symptoms. there is an extensive rash, (except around the mouth), and strawberry tongue), and usually happens in a child with infection that has a phage encoding for strep. pyrogenic exotoxins. (SPE = streptococcal pyrogenic exotoxins) |
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| what is impetigo/pyoderma? |
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| confined purulent infection of the skin, can be caused by strep. pyogenes |
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| where is erysipelas? is it specific to S. pyogenes? what is it a form of? what does it present as? what is a general concern for cellulitis? |
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| erysipelas is a skin infection specific to strep. it is a form of streptococcal cellulitis that presents as a fiery red erythema of dermal tissues, usually on face and legs. it can have systemtic effects. with any kind of cellulitis, the specific bacteria should be IDed |
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| what is necrotizing faciitis? where does it occur? what is it characterized by? what needs to be done to treat it, what can happen if not treated? is super antigen involved? |
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| necrotizing fasciitis, (streptococcal gangrene, can happen w/other bacteria), occurs deep in subcutaneous tissues and spreads along fascial planes. it is characterized by extensive destruction of muscle, fat, and skin. if infected tissue is not removed, systemic toxicity, multiorgan failur, and death, (50% rate), is possible. several of these problems is a result of pyrogenic exotoxin - SUPER ANTIGEN |
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| what is streptococcal toxic shock syndrome? what is it characterized by? does it occur with necrotizing fasciitis? |
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| invasive group A streptococcal disease. there is inflammation at the site of infection, followed by shock and organ failure. the difference between this and staph TSS is both the strep organism and its toxin are in the blood. it can occur with or without necrotizing fasciitis. |
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| what are 2 non-suppurative complications, (sequelae) associated with streptococcus pyogenes? |
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| acute rheumatic fever, (ARF), and acute glomerulonephritis. |
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| what happens with acute rheumatic fever, (ARF)? what kinds of infections does it follow? |
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| ARF is an autoimmune type II hypersensitivity response based on cross-reactivity of streptococcal antigens and the human heart, joint, and nervous tissue. certain M proteins serotypes are considered rheumatic. it follows respiratory but not skin infections and is characterized by carditis and arthritis. |
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| what is acute glomerulonephritis? what types of infections can this follow? what are clinical features? |
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| in the kidneys, autoimmune type III hypersensitivity can occur where antigen-antibody complexes deposited in the kidney fix complement and damage glomeruli. this can follow respiratory or skin infections. clinical features include facial edema, dark urine, and HTN. |
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| what are methods of diagnosis for streptococcus pyogenes? in terms of gram, hemolytic ability, antibiotic resistance, previous infections? |
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| direct gram smear or cx on blood agar. catalase test should be negative for strep. sensitivity to bacitracin and CAMP negative differentiates from group B strep, (B are bacitracin resistant). ASO test for antibody to streptolysin-O, ADB test for DNase B, (or streptokinase, Hyaluronidase, and NADase), can be done to test previous strep infection status. |
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| is immunity M type specific? how is immunity enacted? |
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| immunity is type specific, and is usually enacted via antibody dependent phagocytosis |
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| are most bacteria still sensitive to PCN G? |
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| yes |
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| what can prevent initial attack of rheumatic fever, but not glomerulonephritis? |
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| prompt and adequate antibiotic treatment |
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| are there vaccines currently available for strep? |
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| no, but specific M-protein vaccines are being investigated |
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| what defines streptococcus agalactiae in terms of antibiotics? what kinds of colonies/zones of hemolysis do they have in comparison to group A? what disease is strep. agalactiae a leading cause of? what kinds of long term problems is this associated with? |
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| streptococcus agalactiae are group B strep, which means they are bacitracin, (differentiates them from group A). they have larger colonies, and a more narrow zone of hemolysis than group A. strep. agalactiae is a leading cause of neonatal sepsis and meningites, causing long term problems such as seizures, deafness, developmental delay, and motor deficits. |
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| is strep. agalactiae, (GBS), a part of normal flora? how can this be problematic? |
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| strep. agalactiae is a part of normal flora, so it can be passed from mother to child. it can also cause UTIs and disease in immunocompromised individuals. |
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| what are 3 ways of testing for strep. agalactiae, (GBS)? |
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| strep. agalactiae uniquely has enzyme (hippurase)that is able to cleave hippurate, and this can be tested for. the CAMP test which tests production of beta hemolysin, (which acts synergistically with a staph beta toxin), is unique to GBS. and it is bacitracin resistant, which can also be tested for. |
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| how does the CAMP test work? |
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| there should be an arrowhead clearing of hemolysis where staph aureus and GBS streaking meet, (b/c of synergistic relationship with staph beta toxin). test is negative if no arrowhead. |
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| how is strep agalactiae, (GBS) treated? is anyone screened for it? |
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| it is susceptible to PCN G, however the MIC is 10x greater. it is usually treated with PCN and aminoglycoside. all pregnant women are screened at 35-7 wks for it. |
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| what are enterococci? |
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| gram + cocci, usually in pairs, usually nonhemolytic, normal flora of skin, URT, GI, and urogenital tract. they are major opportunistic pathogens, so if pts are treated with broad spectrum antibiotics, enterococci can proliferate and cause disease |
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| what is the major problem with enterococci infections? |
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| they do not have toxins or well-defined virulence factors, but they are resistant to commonly used antibiotics. |
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| where do you see clinical infections with enterococi? |
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| septicemia, (bacteria in blood), wound infections, and UTIs, (infective endocarditis) |
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| how are enterococci IDed in the lab? what is a big differentiator between it can other group D non-enterococci? |
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| they grow in high salt and temperature conditions, high bile conditions, yield a +PYR test, (makes L pyrrolidonyl arylamindase), as well as hydrolzye esulin. these characteristics distinguish it from other catalast neg. gram + bacteria. enterococci's salt tolerance distinguishes it from other non-enterococcal Group D strep. |
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| how are enterococci treated? |
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| usually more than one antibiotic is needed, and it can be resistant to vancomycin. |
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| what are viricans streptococci? where are they found? what problems can they cause? what happens if they gain access to the blood during dental sx? |
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| viricans streptococci are part of non-groupable strep, they are a large group that can be alpha, beta, or gamma hemolytic. they are found in the normal flora of the mouth, gut, etc. they can cause dental caries and periodontal disease, (make dextran sugar that covers teeth and causes plaque). if these organisms gain access into blood during something like a dental surgery, can cause endocarditis, (esp in pts with abnormal heart valves). |
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| what is streptococcus pneumoniae? what is their indivitual shape? are they hemolytic? |
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| gram + diplococci, (lancet shaped in short chains). they are alpha hemolytic on blood agar, (pneumoysin). |
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| are strep. pneumoniae encapsulated? why is this important? |
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| they are, and this has allowed a vaccine to be developed |
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| how do strep. pneumoniae react to optochin? bile? why is this important? |
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| strep. pneumoniae are optochin sensitive and are lysed by bile. this is one way of IDing strep. pneumoniae, (differentiates from other alpha hemolytic virulent strep) |
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| what is sputum? how would you test if for strep. pneumoniae? |
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| mucus from the lungs. if have gram stain of sputum with lancet shaped diplococcic = streptococcus pneumoniae. |
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| what are virulence factors for strep. pneumoniae? |
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| they make a capsule, (antiphagocytic) and pneumolysin, (lyses endothelial cells) |
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| where can infections of strep. pneumoniae come from? |
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| they can be endo or exogenous. b/c they are normal flora of throat/nasopharynx children and elderly have the highest rate of incidence due to low levels of antibodies. |
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| what are common clinical diseases that strep. pneumoniae is responsible for? |
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| typical lobar pneumonia, which is the leading cause, meningitis, which is the most common cause in children/young adults, otitis media, sinusitis, bacteremia |
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| how are strep. pneumonia IDed in the lab? |
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| lancet shaped diplococcus, alpha hemolytic on agar. inhibition by optochin, (differentiates from other alpha hemolytic strep), bile soluble, and quellung rxn,(capsular swelling if mixed w/antibodies |
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| what is strep. pneumoniae treated with? how does it respond to antibiotics, vaccines? |
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| PCN G, but there is increasing resistance to PCN and other beta-lactams. resistant strains are treated with 3rd generation cephalosporins or vancomycin. polyvalent vaccine covers 23 serotypes for those older than 55 and a heptavalent conjugate vaccine is effective in young children, (2-23 mo) |
