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81 Cards in this Set
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staphylococci morphology |
gram positive, non motile, diameter of 1 micron; individual cocci of pathogenic strains appear smaller than non pathogens; they grow in clusters on solid media and in shot chains and clusters in liquid media |
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colonies of staphylococci aureus and epidermidis appear |
usually golden yellow due to the production of the carotenoid pigment while those of staphylococcus epidermidis are chalky shite |
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staphylococci are present where on humans |
on the skin and mucus membranes of humans |
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staphylococci species associated with diseases include |
staphylococcus aureus, methicillin sensitive (MSSA), and methicillin resistant (MRSA); S. epidermidis, S. haemolyticus, S. lugdunensis, S. saprophyticus |
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metabolism of staphylococci |
they are among the hardiest of all non spore forming bac; most strains are relatively heat stable; facultative anaerobes and produce catalase which breaks hydrogen peroxide down into water and oxygen; can either be coagulase positive or negative |
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coagulase positive staphylococci |
coagulase positive staphylococci produce coagulase which is an enzyme that converts fibrinogen to fibrin resulting in clot formation; these are primarily S. aureus |
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coagulase negative staphylococci |
do not produce coagulase and are referred to as CoNS as a group; priamrily S. epidermidis, S. haemolyticus, S. lugdunensis, and S. saprophyticus |
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structure of staphylocci |
capsule and slime layer; many staphylococci are covered with a polysaccharide capule which can be used for serotyping; S. aureus has 11 capsular serotypes but only 2 serotypes (5 and 8) are associated with human infections; slime layer is a loosely bound, water soluble film consisting of monosaccharides, proteins, and small peptides and it is involved in biofilm formation; are gram positive so have thick peptidoglycan layer (alternating subunits of N-acetylmuramic acid and N-acetylglucosamine); use PCN binding proteins to build it so PCN and other beta lactams can kill it |
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the surface adhesion proteins of staphylococci |
important for adherence to host matrix proteins including fibrinogen, elastin, and collagen; most of these proteins are covalently bound to the cell wall peptidoglycan; they are designated MSCRAMM, microbial surface components recognizing adhesive matrix molecules; include protein A which binds to the Fc receptor of immunoglobulin, fibronectin binding proteins, and clumping factor proteins (coagulase |
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staphylococcus aureus virculence factors |
capsule, slime layer, peptidoglycan, teichoic acid, and protein A; protein A is important because it binds to the Fc portion of antibodies and the Fc portion usually binds to a phagocyte after the antibody has picked up a bac; so know the Fc portion is obscured and cannot bind to a phagocyte so the bac is saved; bac can also release a bunch of protein A into the environment so that it binds up all the antibodies and leaves the bac alone |
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the capsule- virulence |
inhibits chemotaxis and phagocytosis; inhibits proliferation of mononuclear cells |
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slime layer- virulence |
facilitates adherence to foreign bodies; inhibits phagocytosis |
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peptidoglycan- virulence |
provides osmotic stability; stimulates production of endogenous pyrogen (endotoxin like activity); leukocyte chemoattractant (abscess formation); inhibits phagocytosis |
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teichoic acid- virulence |
binds to fibronectin |
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protein A- virulence |
inhibits antibody mediated clearance by binding IgGa, IgG2, and IgG4Fc receptors; leukocyte chemoattractant; anticomplementary; protein A is important because it binds to the Fc portion of antibodies and the Fc portion usually binds to a phagocyte after the antibody has picked up a bac; so know the Fc portion is obscured and cannot bind to a phagocyte so the bac is saved; bac can also release a bunch of protein A into the environment so that it binds up all the antibodies and leaves the bac alone |
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staphylococcal toxins |
cytotoxins= alpha, beta, delta, and gamma toxins, panton-valentine leukocidin (PVL) present in virtually all MRSA strains associated with community acquired infections; exofoliative toxins (staphylococcal scalded skin syndrome or SSSS)= ETA and ETB; enterotoxins (18 enterotoxins, A-R); toxic shock syndrome toxin (TSST-1) |
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cytotoxins- alpha toxin |
encoded ont he chromosome and a plasmid; produced by most S. aureus strains that cause human disease; integrates into the host cell membrane forming pores, which leads to osmotic swelling and cell lysis |
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cytotoxins- beta toxin |
heat labile protein that catalyzes the hydrolysis of membrane phospholipids in a variety of susceptible cells |
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cytotoxins- delta toxin |
wide spectrum of cytolytic activity; may function as a surfactant (detergent) disrupting the host cell membrane |
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cytotoxins- gama toxin and PVL |
bi component toxins composed of 2 polypeptide chains that mediate pore formation and osmotic lysis; PVL induces rapid cell death in human neutrophils but not in mouse or simian cells; HE WANTS US TO REMEMBER PVL BECAUSE OF ITS ASSOCIATION WITH COMMUNITY ACQUIRED MERSA |
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exfoliative toxins- ETA and ETB |
serine proteases that split desmoglein 1 which is responsible for forming the intercellular bridges in the stratum granulosum epidermis; ETA is heat stable and its gene is phage associated; ETB is heat labile and its gene is located on a plasmid; the toxins do not cause cytolysis or inflammation; scalded skin syndrome is an intoxcation neither staphylococci nor leukocytes are present in the involved layer of epidermis; the toxic process resolved by the development of the protective neutralizing antibodies |
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enterotoxins |
the enterotoxins are superantigens that are stable to heating at 100 C for 30 mins (not destroyed by mild reheating of cooked food) and resistant to hydrolysis by gastric enzymes <-- THESE 2 THINGS ARE IMPORTANT TO REMEMBER because when you have these symptoms they are from intoxication and not infection; stimulate release of inflammatory mediator in mast cells, increasing intestinal peristalsis and fluid loss, as well as nausea and vomiting (emesis) NO FEVER |
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enterotoxin A |
commonly associated with food poisoning |
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enterotoxin B |
causes staphylococcal pseudomembranous enterocolitis |
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enterotoxins C and D |
are found in contaminated milk products |
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superantigens |
activate 2-20% of ALL CD4+ T cells instead of the normal number of 0.001-0.01%; activated CD4+ T cells produce TNF, IL-2 (stimulates proliferation of T cells) and IFN gamma; massive overproduction of TNF leads to toxic shock= edema, intravascular volume depletion, hypotension, shock, multiple organ failure, death |
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toxic shock syndrome toxin 1 |
produced by about 90% of the S. aureus strains responsible for menstruation associated toxic shock syndrome (TSS) and other forms of TSS (e.g. wound associated); chromosomally mediated, heat and proteolysis resistant, superantigen (so the 2 superantigens are TSST1 and the enterotoxins); able to penetrate the mucosal barrier; while the infection is localized to the vagina or the wound site the toxin enters the blood and lymph fluid producing the systemic effects of TSS (so the toxin (the thing causing the symptoms) is systemic); death results from hypovolemic shock that leads to multi organ failure |
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Staphylococcus aureus virulence factors |
cytotoxins, exfoliative toxins (ETA, ETB), enterotoxins (A-R), toxic shock syndrome toxin-1 |
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cytotoxins- virulence factors |
toxic for many cells including erythrocytes, fibroblasts, leukocytes, macrophages, and platelets |
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exfoliative toxins (ETA, ETB) |
serine proteases that split the intercellular bridges in the stratum granulosum epidermis |
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enterotoxins (A-R) |
superantigens (stimulate proliferation of T cells and release of cytokines); stimulate release of inflammatory mediators in mast cells, increasing intestinal peristalsis and fluid loss as well as nausea and vomiting |
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toxic shock syndrome toxin 1 |
superantigen (stimulates proliferation of T cells and release of cytokines); produces leakage of cellular destruction of endothelial cells |
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scalded skin syndrome |
staphylococcus aureus- toxin mediated disease; staphylococcal scalded skin syndrome (Ritter Disease or SSSS) caused by ETA and ETB; abrupt onset of perioral erythema and spread over the entire body within 2 days followed by formation of cutaneous blisters and the desquamation of the epithelium; the blisters contain no bacteria or leukocytes; within 7-9 days the epithelium becomes intact due to the development of neutralizing antibodies; primarily a disease of neonates and young children; infection in adult immunocompromised hosts may result in a mortality rate as high as 60% |
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bullous impetigo |
staphulococcus aureus- toxin mediated disease; this is a localized form of SSSS; superficial skin blisters; the blisters are localized and culture positive (so you do find the bac in this one even though not in SSSS); occurs primarily in infants and young children; highly communicable |
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staphylococcal food poisoning |
staphylococcus aureus- toxin mediated disease; INTOXICATION AND NOT INFECTION; most commonly contaminated food processed meat such as ham and salted pork, potato salad, and ice cream; reheating the contaminated food kills the bacteria but does not inactivate the toxin; rapid onset; 4 HRS INCUBATION PERIOD; severe vomiting; watery diarrhea; abdominal pain; nausea; NO FEVER symptoms; generally LASTING LESS THAN 24 HRS |
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staphylococcal enterocolitis |
staphylococcus aureus- toxin mediated disease; watery diarrhea, FEVER occurring mainly in pts receiving antibiotics that suppress the growth of normal colonic flora; abundant S. aureus in the stool <-- very characteristic (many gram positive cocci in stool sample) and absence of other normal stool bac; white plaques with ulcerations on the colonic mucosa; be able to distinguish from food poisoning |
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what do you see in a gram stain of staphylococcal enterocolitis |
presence of pus cells (PMNs) and gram positive cocci in clusters to the exclusion of almost all other normal flora (should be mixed morphotypes- gram negative and positive bacilli of many shapes of gram positive cocci) |
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toxic shock syndrome |
staphylococcus aureus- toxin mediated disease; initiated by the localized growth of TSST-1 producing S. aureus in the vagina (the bacteria multiplies rapidly in hyper absorbent tampons and release the toxin) or a wound; clinical manifestations which start abruptly involve fever, hypotension, and a diffuse erythematous rash; multiple organ systems may be affected (GI, CNS, renal, musculature); purpura fulminans= virulent form of TSS with larger purpuric skin lesion, fever, disseminated intravascular coagulation; unless the pt is treated with antibiotics the risk of recurrence is more than 50%; fatal case= cutaneous and soft tissue involvement; mild case= desquamation of the skin occurring particularly on the palm and soles; REMEMBER PALMS AND SOLES b/c with other rashes these areas are usually spared |
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cutaneous localized pyogenic infections |
staphylycoccus aureus- suppurative infections; impetigo, folliculitis, furuncles, carbuncles, staphylococcal wound infection |
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impetigo |
a superficial infection, occurs primarily on the face and limbs, a small flattened red spot (macule) appears first followed by a pus filled vesicle (pustule) develops, multiple vesicles at different stages of development are common |
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folliculitis |
a pyogenic infection of the hair follicles, the base of the follicle is raised and red, pus may accumulate in the epidermal surface |
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furuncles |
an extension of folliculitis, large raised painful nodules with underlying necrotic tissues |
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carbuncles |
coalescence of furuncles and their extension to the deeper subcutaneous tissues; in contrast to pts with folliculitis and furuncles, pts with carbuncles may develop chills and fever (system infection); the issue is that these form biofilms in the wound and so you might try to treat them with antibiotics but that won't fix the issue so you need to go in with surgical debridement (cut it all out) |
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staphylococcal wound infection |
occurs in pts after surgical procedures or trauma; in immunocompetent person, the presence of foreign bodies (stitches, splinters, dirt) helps S. aureus establish an infection; if the foreign body is not removed and the purulence is not drained, systemic infection may occur |
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suppurative infections- systemic |
staphylococcus aureus; pneumonia ane empyema; aspiration pneumonia, hematogenous pneumonia, necrotizing pneumonia, empyma, osteomyelitis, hematogenous infection, trauma related osteomyelitis, septic arthritis, bacteremia, endocarditis, endocarditis in parenteral drug abusers |
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aspiration pneumonia |
results from the aspiration of oral secretions; occurs primarily in very young children, elderly, pts with cystic fibrosis, and pts with obstructive pulmonary diseases; localized abscesses may develop |
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hematogenous pneumonia |
common in pts with endocarditis or bacteremia (infection coming from the blood stream) |
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necrotizing pneumonia |
a severe form of necrotizing pneumonia can be caused by MRSA but this is not very common; this may lead to shock and a high mortality rate |
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empyema |
a collection of pus within the pleural cavity, occurs in 10% of pts with pneumonia |
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osteomyelitis |
from hematogenous dissemination to the bone or a secondary infection from trauma |
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hematogenous infection |
hematogenous so bac coming from the blood; in children generally results from cutaneous infection and involves the highly vascularized area of long bones (epiphyses); in adults it commonly occurs as vertebral hematogenous osteomyelitis |
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trauma related osteomyelitis |
accompanied by inflammation and purulent drainage from an infected wound or the sinus tract overlying the infected bone |
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septic arthritis |
primary cause of septic arthritis in children; occurs in adults who are receiving intra-articular injections; characterized by painful erythematous joint and purulent aspirated synovial fluid |
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bacteremia |
most likely infection spreads from a skin infection to the blood; more than 50% of S. aureus bacteremias are acquired in the hospital following surgical procedures or from contaminated intravascular catheters |
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endocarditis |
the mortality rate from acute S. aureus endocarditis may reach 50%; initial symptoms are non specific influenza like symptoms however the pts condition deteriorates rapidly; immediate medial and surgical intervention is necessary |
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endocarditis in parenteral drug abusers |
right sided disease (tricuspid valve) rather than left; generally presents as sudden onset of fever, chills, and pleuritic chest pain caused by pulmonary emboli |
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clinical disease: S. epidermidis and other CoNS |
endocarditis, IV catheter and shunt infections, prosthetic joint infection, urinary tract infection |
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endocarditis |
artificial valves= introduced during valve replacement, abscess may develop and lead to separation of the valve and mechanical heart failure, mainly S. epidermidis; native valve= not commonly caused by staphylococci, S. lugdunensis |
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IV catheter and shunt infections |
S. epidermidis and other CoNS; long dwelling catheters in critically ill pts; associated with bacterial biofilms on the surface of the catheter; access of the bacteria to blood leads to persistent bacteremia |
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prothetic joint infection |
S. epidermidis and other CoNS; mainly infection of artificial hip with local pain and failure of the joint; no symptoms of systemic infection, high risk of re-infection |
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urinary tract infection |
S. saprophyticus and other CoNS; young sexually active women who develop dysuria (pain on urination) and pyuria (pus in urine) |
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inhibition of staphylococcus aureus biofilms on hemodialysis catheters |
organoselenium compound |
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lab diagnosis |
microscopy of a gram stain but detection of bac in clinical specimens depends on the type of infection and the quality of the submitted materials; PCR (DNA amplification) primarily used for nasal carriage of MRSA but may be used with other clinical specimens (e.g. wound); culture on either sheep blood (s. aureus makes large smooth colonies surrounded by zone of hemolysis) or mannitol salt agar for selection of S. aureus and S. epidermidis from mixed flora (aureus can grow but nothing else can) |
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identification of S. aureus by the lab |
coagulase+, protein A+, heat stable nuclease+; coagulase slide test where the bacterial suspension is mixed with a drop of plasma and examined for clumping of bacteria; coagulase tube test where bac are inoculated in a test tube containing plasma and examined after 24 hrs for clot formation; fluorescent in situ hybridization (FISH) were you have a probe for aureus that is fluorescently labeled |
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treatment |
strains that produce penicillinase (beta-lactamase) occur frequently especially in the hospital environment so they are resistant to ordinary PCNs and may be susceptible to semi synthetic penicillinase resistant PCNs such as oxacillin and nafcillin (methicillin not used clinically); MRSA have become a big problem in hospitals and in the community usually susceptible to vancomycin but now vancomycin resistant isolates have occurred; CoNS often produce beta-lactamase, are methicillin resistant, and now some are also resistant to vancomycin |
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MRSA and the mecA gene: where is it found and what does it encode |
mecA is found on the staphylococcal cassette chromosome mec (SCCmec) that carries the gene into the chromosome; mecA encodes PBP2 which is an alternative PCN binding protein (PBP) that has low affinity for beta-lactam antibiotics thus allowing the catalytic action necessary for cell wall synthesis (peptidoglycan layer) to continue in the presence of the drug; all MRSA strains carry at lease one SCCmec element in the chromosome |
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the number of defined SCCmec |
has grown from IV (2005) to VIII (2010) to XI (2012); types I, II, and III (which carry additional resistance genes) are usually seen in hospital acquired (HA) MRSA; types IV, V, and VI are generally present in community acquired (CA) MRSE; type IV has become 'the' genetic marker for Ca MRSA in the US |
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the line between HA MRSA and CA MRSA |
unfortunately are blurring |
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MRSA and the mecA gene: the current PCR tests for |
mecA sequences and/or the junction of SCCmec/orfX |
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MRSA and the mecA gene: multiplex tests |
are in use that detect additional genes found in S. aureus only as SCCmec is also found in CoNS |
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treatment |
alternative antibiotics to oxacillin and vancomycin have been developed= linezolid and quinupristin/dalfopristin; some older antibiotics still work for some isolates especially community acquired strains= tetracycline and clindamycin; antibiotic susceptibility of the infecting staphylococcus isolate should be determined |
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prevention |
proper cleansing of wounds and the use of disinfectant help prevent infections; thorough hand washing and covering of exposed skin helps medical personnel prevent infection or spread to other pts |
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summary for staphylococcus aureus: biology, virulence, and disease |
catalase positive, gram positive cocci arranged in clusters; species characterized by presence of coagulase, protein A, and species specific ribitol teichoic acid with N-acetylglucogamine residues ("polysaccharide A"); virulence factors include strucural components that facilitate adherence to host tissues and avoid phagocytosis and a variety of toxins and hydrolytic enzymes; diseases include toxin mediated diseases (food poisoning, TSS, scalded skin syndrome), pyogenic diseases (impetigo, folliculitis, furuncles, carbuncles, wound infections), and other systemic diseases); hospital and ocmmunity acquired infections with MRSA are a significant worldwide problem |
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summary for staphylococcus aureus: epidemiology |
normal flora on human skin and mucosal surfaces; organisms can survive on dry surfaces for long periods (because of thickened peptidoglycan layer and absence of outer membrane); person to person spread through direct contact or exposure to contaminated fomites (e.g. bed linens, clothing); risk factors include presence of a foreign body (e.g. splinter suture, prosthesis, catheter), previous surgical procedure, and use of antibiotics that suppress the normal microbial flora; pts at risk for specific diseases include infants (scalded skin syndrome), young children with poor personal hygeine (impetigo and other cutaneous infections), menstruating women (TSS), pts with intravascular catheters (bacteremia and endocarditis) or shints (meningitis), and pts with compromised pulmonary function or an antecedent viral respiratory infection (pneumonia); MRSA now the most common cause of community acquired skin and soft tissue infections |
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summary for staphylococcus aureus: diagnosis |
microscopy useful for pyogenic infections but not blood infections or toxin mediated infections; staphylococci grow rapidly when cultured on nonselective media; selective media (e.g. mennitol salt agar) can be used to recover S. aureus in contaminated specimens |
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summary for staphylococcus aureus: treatment, prevention, and control |
localized infections managed by incision and drainage; antibiotic therapy indicated for systemic infections; empiric therapy should include antibiotics active against MRSA strains; oral therapy can include trimethoprim-sulfamethoxazole, doxycycline or mioncycline, clindamycin, or linezolid; vancomycin is drug of choice for intravenous therapy with daptomycin, tigecycline or linezolid acceptable alternatives; treatment is symptomatic for pts with food poisoning (although the source of infection should be identified so that appropriate preventive procedures can be enacted); proper cleansing of wounds and use of disinfectant help prevent infections; thorough hand washing and covering of exposed skin helps medical personnel prevent infections or spread to other pts |
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summary for coagulase-negative staphylococci: biology, virulence, and disease |
catalase positive, coagulase negative, gram positive cocci arranged in clusters; relatively avirulent although production of a slime layer can allow adherence to foreign bodies (e.g. catheters, grafts, prosthetic valves and joints, shunts) and protection from phagocytosis and antibiotics; infections include subacute endocarditis, infections of foreign bodies, and urinary tract infections |
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summary for coagulase-negative staphylococci: epidemiology |
normal human flora on skin and mucosal surfaces; organisms can survive on dry surfaces for long periods; person to person spread through direct contact or exposure to contaminated fomites although most infections are with the pts own organisms; pts are at risk when a foreign body is present; the organisms are ubiquitous sot here are no geographic or seasonal limitations |
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summary for coagulase negative staphylococci: diagnosis |
as with staphylococcus aureus infections |
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summary for coagulase negative staphylococci: treatment, prevention, and control |
the antibiotics of choice are oxacillin (or other penicillinase resistant PCN) or vancomycin for oxacillin resistant strains; removal of the foreign body is often required for successful treatment; prompt treatment for endocarditis or shunt infections is necessary to prevent further tissue damage or immune complex formation |
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a pastry chef cut his finger while slicing a cake. after a week the site of the injury is warm, red, and swollen, and begins to drain pus; while preparing some cream pies he contaminates the custard with drainage from the lesion; the pies were eaten several days later by patrons of the restaurant; within 4 hrs they developed diarrhea and vomiting with no fever; which of the following staphylococcus aureus toxins would be most likely to cause these symtoms? a. P-V laukocidin toxin b. exfoliative toxin A (ETA) c. toxic shock syndrome toxin 1 d. delta toxin e. staphylococcal enterotoxin |
e. staphylococcal enterotoxin |
