Bacterial Skin infections
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| bacterial skin flora are colonized by what type of organisms | predominantly aerobic and facultative anaerobic organisms ranging from 100-10,000
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| factors that effect distribution, composition, and density of bacterial skin flora | climate, moisture, low pH, low temp, chemical composition of surface, exfoliation, bathing habits, antibacterial soaps (not always good)
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| general function of bacterial skin flora? | helps prevent infection by pathogens, resident flora are of low virulence, transient flora re deposited from mucous membrane "fallout" or form the environment, dry areas are colonized with gram positive cocci and aerobic and anaerobic diptherioids,
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| bedridden patients tend to have increased levels of what type of bacteria | gram negative rods
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| most frequent pathogens of bacterial skin flora? | staph aureus, strep pyogenes
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| this causes abscesses, toxic shock and bacteremia | staph aureus (gram positive cocci)
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| this cuases cellulitis, lymphangitis | strep pyogenes (gram positive cocci)
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| causes cellulitis? | H. influenza (gram neg rods)
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| bed sores | E.coli and other enterics (gram negative rods)
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| gas gangrene | C. perfringes (gram positive rods)
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| tularemia | francicella tularensis (gram negative rods)
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| anthrax | bacillus anthracis (gram positive rods)
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| hot tub infection | pseudomonas aeruginosa
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| foot rot | pseudomonas cepacia
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| fish tank cellulitis | mycobacterium marinum (acid fast)
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| leprosy | mycobacterium leprae (acid fast)
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| whats it called when bacteria gain entry through tiny abrasions in skin | exogenous infections
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| examples of when excessive moisture induces skin maceration? | occlusing dressings or wet diapers, obese people (intertriginous folds), constant immersion, hot tubs
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| other ways exogenous infections occur? | trauma-mild abrasions to serious accident wounds or burns, hospital procedures breach the skin, pressure injury (bed sores), compromised blood supply.
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| examples of endogenous infections? | skin becomes infected from th eblood stream or by direct extension of an infection site deep within the tissues. some inf. are accompanied by rashes due to toxin release into the bloodstream (ex: toxic shock syndrome)
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| most common skin infecitons are caused by..? | staph aureus, strep pyogenes
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| staph a characteristics? | spherical, gram positive, non motile, spore forming facultative anerobes. on gram stain easy to spot-frequently grape like clusteres, ferment a wide variety of sugars (acid but no gas),
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| staph a grow well on most lab media provided they are supplemented with... | amino acids and B vitamins
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| staph a grow in the presence of.. | high concentrations of salt(mannitol salts agar)
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| of more than 40 recognized species of staph a, which three are associated with human disease? | staph a, staph epidermidis, staph saprophyticus
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| is staph a coagulase positive or negative | +
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| color of staph colonies? | golden yellow
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| does staph ferment mannitol? | yes
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| this characteristic of staph a is responsible for the shape and rigidity of the cell, serves as chemotractant for polymorphonuclear leukocytes, activates complement by the alternate pathway, has endotoxin like properties | peptidoglycan layer.
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| in staph a, these are polymers of ribotol or glycerol phosphates, help with adherence. in deep seated infections, you have antibodies against these | teichoic acid. it penetrates through the cell membrane.
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| protein embeddd in the cell wall of staph a, anti-opsonin effect. binds the Fc reigon of IgG leaving the Fab portion free to bind with specific antigen | Protein A
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| this part of staph a promotes binding to mucosal cells | fibronectin binding protein (FnBP)
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| this part of staph a allows clumping factor | bound coagulase
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| this property of staph a gives it its antiphagocytic property, predominantly made of polysaccharides | capsule (micro)
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| this property of staph a allows its agglutination in citrated rabbit plasma | bound coagulase. staph a also has free coagulase
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| this property of staph a causes clot formation in citrated rabbit pasma (gold standard) | free coagulase
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| which hemolhysins are found in staph a? | alpha, beta, delta, gamma
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| this is present in mot strains of staph a | leukocidins
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| this property of stpah a hydrolyzes hydrogen peroxide to water and oxygen. It is the primary test used to distinguish staph from strep | catalase
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| this property of staph a catalyzes the hydrolysis of hyaluronic acid | hyaluronidase
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| this property of staph a dissolves fibrin clots | staphylokinase (fibrynolysin)
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| this property of staph a hydrolyzes lipids, ensures survival on the skin and sebaceous glands | lipase enzymes
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| this property of staph a is carried by the mecA gene, a five gene sequence (types I-5) breaks the beta lactam ring | beta lactamase
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| this property of staph causes scalded skin syndrome, and bullous impetigo (A) | exfoliative toxins A and B
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| this is caused by staph a, and results in fever, skin rash, hypotension, peeling of skin upon recovery | toxic shock syndrome
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| this property of staph a (has six antigenic types: A,B,C,D,E,G), causes resistance to gut enzymes and low pH, most common kind of food poisoning in US, ingestion causes vomitting and diarrhea within 2-6 hours. | enterotoxins. they behave as superantigens
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| how do you encounter staph a? | may be normal skin flora (20-40%, colonizes external nares and survive as fomites.
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| can staph a penetrate the skin? | no. they enter through damaged skin or through mucous membranes
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| spread and survival of staph a depends on... | number of organisms, virulence of strain, site of entry, inflammatory response of host, immunological history of patient.
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| staph a causes damage through... | infections, toxinoses
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| primary infections caused by staph a.. | impetigo, scalded skin syndrome, toxic shock syndrome, folliculitis, abscess, boils, carbuncles, cellulitis
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| form of impetigo seen in young children in which the vescles enlarge to form flaccid bullae with clear yellow fluid, which later becomes darker and more turbid; ruptured bullae leave a thin brown crust. | impetigo. due to strins of staph a that produce exfoliative toxin A, a toxin that cuases loss of cell adhesins in the superficial epidermis by targeting the protein desmoglein 1
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| scaled skin syndrome from staph a is caused by... | exfoliative toxins A and B
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| folliculitis is mainly caused by. | pseudomonas and staph a
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| abscesses in skin is called what? | furuncle or boil(carbuncles)
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| staph aureus can spread to subcutaneous tissues and develop... | cellulitis
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| how do you diagnose a minor skin infection? | clinical impression
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| how do you diagnose a skin infection that causes serious illness? | gram stian and culture and follow up with blood culture
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| do minor skin infections require systemic antibiotic treatment? | no, use heat packs
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| how do you treat serious infections-large abscesses (greater than five cm) | incision and drainage, treat empirically to cover for MRSA, TMP-SMX, doxycycline, minocycline, clindamycin
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| what is the treatment for methicillin sensitive staph aureus? | nafcillin, oxacillin
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| what is the primary mechanism for resistance to penicillin? | beta lactamase ring, which breaks the beta lactam ring, alterd penicillin binding proteins (transpeptidase fails to bind methicillin)
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| what are the two primary ways to get MRSA? | hospital acquired (resistant to most other antibiotics), community acquired (resistance limited to penicillins, methicillin, cephalosporin, erythromycin, and sometimes clindamycin. treat with TMP-SMX, doxycycline, or clindamycin if susceptible
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| risk factors for MRSA? | hospitalization within the last 12 months, nursing home residency, surgery, or catheterization. those who have crowded living spaces (homeless shelters, camps, boarding schools, day care centers), those taking drugs by injection, contact sports, using ABX
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| MRSA in community acquired settings is most often transmitted through.. | direct physical contact with an infected person, but it can also be transmitted by contact with contaminated surface items.
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| how to avoid MRSA in community acquired setting.. | wash hand, often, use soap or alcohol gel, use air blowers or paper towels rather than shared towels. don't share personal items such as deep soap razors or clippers, wash linens and clothing in detergent and water for 25 minutes or more,
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| general properties of strep.. | gram + cocci in chains, catalase negative, ferment surgars: lactic acid, low pH, need enrichment with blood to support growth
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| classification of strep? | 20 serological groups based on c carbohydrate (lancefield groups A-U). preliminary grouping is based on hemolysis of 5% sheep blood (beta hemolysis, alpha hemolysis, gamma hemolysis)
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| s. pyogenes: hemolysis of which group | beta
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| strep pyogenes: which lancefield group? | A
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| strep pyogens, what is the lab test? | bacitracin S
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| group A strep has a capsule made of.. | hyaluronic acid.
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| group A strep: fibrils made of what? | M protein and lipoteichoic acid.
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| does Group A strep have peptidoglycan layer | yes
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| what proteins found in group A strep? | T and R
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| soluble virulence factors of group A strep? | streptokinase, streptodornase, hyaluronidase, erythrogenic toxin, NADase, streptolysins (hemolysins)
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| which streptolysin is oxygenlabile, antigenic? | streptolysin O
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| which streptolysin is oxygen stable, nonantigenic? | streptolysin S
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| pathogenesis: encounter of strep A? | acquired from oral secretions or from another infected individual or carrier
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| pathogenesis: spread of strep A? | group A strep highly adapted to resist phagocytosis and spread through tissues
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| pathogenesis: damage caused by strep A? | elicits a strong inflammatory response. causes release of chemotaxins for white blood cells, activate complement by the alternative pathway, resists phagocytosis and kills many of the invading cells.
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| what illness follows an upper respiratory infection of strep? | rheumatic fever
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| localized infections caused by strep pyogenes? | pharyngitis (sore throat), scarle fever, impetigo
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| invasive infections caused by strep pyogenes? | wounds, erysipelas, cellulitis, puerperal fever, endocarditis
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| postinfectious diseases caused by strep pyogenes? | rheumatic fever, glomerulonephritis
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| lab diagnosis of pharyngitis? | throat culture, direct antigen test
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| invasive infections caused by strep pyogenes? | gram stain and culture, blood culture if bacteremia is suspected?
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| antibodies to strep pyogenes? | streptozyme test: screens for ASO, anti DNase B, AHase, and anti-NAD, antistreptolysin O titer: quantitative antibodies to streptolysin O
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| this illness happens when erythrogenic toxin produced by lysogenic Group A strep causes rash, strawberry tongue | scarlet fever
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| treatment of strep? | penicillin: pen G used for prevention against rheumatic fever. use long acting penicillin G, oral penicillin for 10 days.
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| non-bullous disease caused by strep pygenes,and this is the most common form. may be mixed with staph a. lesions begin as papules that progress to vesicles surrounded by erythema. subsequently they become pustules that nelarge and break down | impetigo. vesicles evenually break down to form thick, adherent crusts wth a characteristic golden appearance; this evolution usually occurs over about one week. lesions usually involve the face and extremities.
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| some infections caused by strep pyogenes | erysypelas, ecthyma, wound infections, streptococcal cellulitis, cellulitis via flesh eating bacteriu
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| treatment of cellulitis? | penicillin. also used for prevention agianst rheumatic fever (long acting penicillin G, oral penicillin for 10 days)
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| these are opportunitstic pathogens that do not ferment gluocse | gram negative nonfermenters
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| general characteristics of pseudomonas aeruginosa | motile with polar flagella, oxidase positive that are obligate aerobes, grow at 42 degrees C (which allows ID), colonies produce a fruity odor.
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| are colonies of pseudomonas aeruginosa pigmented? | yes-green
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| virulence factors of pseudomonas aeruginosa? | pilli, polysaccharide capsule (slime layer)-biofilm resists killing by antibiotics, endotoxin, many extracellular enzymes, exotoxin A
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| this toxin of pseudomonas aeruginosa causes ADP ribosylation of elongation factor 2, which inhibits protein synthesis. Eschar formation with tissue necrosis. | exotoxin A
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| disesaes caused by pseudomonas aerugiosa...(infect immunocompromised or those with compromised physical barriers) | skin infections following burns, super infections following use of braad spectrum antibiotics, wounds, colonize respirators pneumonia, colonize respiratory tract in patients with cystic fibrosis pneumonia, conjunctivitis, otitis externa (swimmers ear)
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| prevention and treatment of pseudomonas aeruginosa? | clean rooms and sterilize hospital equiptment, replace plastic tubing in respoirators where possible, minimiz eunnecessary broad spectrum antibiotic therapy, use AG+pipercillin for serious infections
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| oxidase negative (aerobic), nonfermentative nonmotile short gram negative rod, lacks cytochrome C. cause a variety of opportunistic nosocomial infections similar to pseudomonas in temperate climates. prevalent among american soldiers wounded in iraq | actinobacter-tend to colonize in in the skin in humid, tropical environments
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| most common cause of all skin disorders. mech: excessive sebum production secondary to androge stimulation, abnormal follicular keratinization (folllicular plugging), proliferation propionibacterium acnes, inflammation and release of proinflammatory med | acne vulgaris
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| causes complications from cat or dog bites | pasteurella multocida
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| causes erythrasma | cornybacterium minutissum. can be diagnosed via red appearance under woods lampm
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| mixed infection of staph a, strep pyogenes, and enteric organisms | decubitus ulcer
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| diabetic foot results from... | mixed infection: one of the main reasons for amputation
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| causes purpura secondary to vasculitis | neiseria meningitidis
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| causes primary syphillus | treponema pallidum
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| causes skin rash, lesions are infectious, rash will resolve with or without treatment, one third will cure spontaneously | secondary syphillis
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| caused by mycobacterium leprae | leprosy
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