Infections of the skin and soft tissue – Flashcards
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Unlock answers| classification of bacterial infections of the skin |
abscess formation spreading infections necrotizing infections |
| abscess formation |
localized collection of pus surrounded by inflamed tissue boils and carbuncles results from infection and inflammation around hair follicles |
| examples of spreading infections |
impetigo erysipelas cellulitis |
| impetigo (pyoderma) |
limited to epidermis presents as a bullous, crusted or pustular eruption of the skin localized cutaneous infection characterized by vesicle on an erythematous base |
| erysipelas |
blocks dermal lymphatics presents as well defined, spreading erytematous inflammation generally on face, legs, or feet localized skin infection with pain, inflammation, lymph node enlargement, and systemic symptoms caused by s. pyogenes |
| cellulitis |
diffuse from of acute inflammation usual presentation if the infection is in the subcutaneous fat caused by s. pyogenes |
| necrotizing infections |
| fasciitis describes the inflammatory response to infection of the soft tissue below the dermis |
| what does S. aureus cause |
| toxic shock syndrome |
| how does s. aureus manifest on the skin |
| rash and desquamation due to toxin |
| what does s. pyogenes cause |
| scarlet fever |
| how does s. pyrogenes present |
| erythematous rash caused by erythogenic toxin |
| what does p. aeruginosa cause |
| septicemia |
| how does p. aeruginosa present |
| ecthyma gangrenosum, skin lesion pathognomonic if infected |
| what does n. meningitidis cause |
septicemia meningitis  |
| how does n. meningitidis present |
| petechial or maculopapular lesions containing bacteria |
| what does treponema palladium cause |
| syphilis |
| how does t. palladium present |
disseminated infectious rash seen in secondary stage of disease 2-3 months after infection |
| what does rickettsia prowazekii cause |
typhus  |
| how does rickettsia prowazekii and rickettsia rickettsia present |
| macular or hemorrhagic rash |
| what does salmonella typhi and salmonella paratyphi B |
| enteric fever |
| how does salmonella typhi and salmonella paratyphi B present |
| rose spots containing bacteria |
| what does blastomyces dermatidis cause |
| blastomycosis |
| what does cyptococcus neoformans cause |
| cryptococcosis |
| how does blastomyces dermatidis present |
| papule or pustule develops into granulomatous lesions containing organisms |
| how does crytococcus neoformans present |
| papule or pustule usually on face or neck |
| what does rickettsia rickettsia cause |
| spotted fever |
| folliculitis |
| impetigo involving hair follicles |
| furuncles or boils |
| large, painful, pus filled cutaneous nodules |
| carbuncles |
| coalescence of furncles with extension into the subcutaneous tissues and evidence of systemic disease (fever, chills, bacteriemia) |
| necrotizing fasciitis |
deep progressive infection of skin that involves destruction of muscle and fat layers patients often die from shock and multisystem failure within 48 hours caused by s. pyogenes |
| osteomyelitis |
destruction of bones, particularly the metaphyseal area of long bones abscess of the bone |
| what bacteria commonly causes folliculitis, boils, and carbuncles |
| s. aureus |
| what structure is involved in folliculitis, boils, and carbuncles |
| hair follicles |
| what bacteria commonly causes impetigo |
| s. pyogenes and/or s. aureus |
| what stucture is involved in impetigo |
| epidermis |
| what bacteria is the common cause of erysipelas |
| s. pyogenes |
| what structure is involved in erysipelas |
| dermis |
| what is the common cause of cellulitis |
| s. pyogenes |
| what structure is involved in cellulitis |
| subcutaneous fat |
| what is the common cause of necrotizing fasciitis |
| anaerobes and microaerophiles, usually mixed infections |
| what structure is involved in the necrotizing fasciitis |
| fascia |
| what is the common cause of myonecrosis gangrene |
| clostridium perfringens and other clostridia |
| what structure is involved in myonecrosis gangrene |
| muscle |
| what is the common cause of ringworm |
| dermatophyte fungi (trichophyton, epidermophyton, and microsporum) |
| what structure is involved with ringworm |
| kerantinized epithelium |
| how is s. aureus arranged |
| grape like clusters |
| is s. aureus gram positive or gram negative |
| gram positive |
| what type of hemolysis reaction does s. aureus have |
| beta |
| what type catalase reaction does s. aureus have |
| catalase positive |
| what type coagulase reaction does s. aureus have |
| positive coagulase |
| S. aureus virulence factors |
protein a coagulase hyaluronidase staphylokinase lipases enterotoxins hemolysins toxic shock syndrome toxin exfoliatin leukocidins |
| protein a |
binds the Fc portion of IgG preventing opsonization and Fc-mediated phagocytosis  |
| what can protein A bound IgG activate |
| complement inducing inflammation and/or septic shock |
| what does coagulase do |
activate thrombin cause clotting of plasma which contributes to the ability to localize and form abscesses |
| what does hyaluronidase cause |
| causes depolyermization of hyaluronic acid which facilitates the spread of the organism |
| what does staphylokinase (fibrinolysin) activate |
| plasminogen to plasmin which may be important in the breakdown of tissues and blood clots facilitating the spread of organisms |
| what does lipases do |
enhance growth by the breakdown of complex lipids to simpler compounds important with infection of skin around sebaceous glands and hair follicles where the concentration of lipids and fatty acids are high |
| enterotoxins |
produce about 50% of all coagulase positive S. aureus strains in staphylococcal food poisoning, induces diarrhea and stimulates the vomit reflex by interaction with neural receptors in the upper GI tract |
| hemolysins |
| destroys red blood cells and a variety of other cell types |
| toxic shock syndrome toxin (TSST-1) |
| a superantigen that induces the excessive release of cytokines from the T lymphocytes and monocytes |
| exfoliatin (epidermolytic toxin) |
| cleaves the stratum corneum causing separation and loss of the superficial layers of the epidermis to cause the condition, staphylococcal scalded skin syndrome (SSSS) |
| leukocidins |
| kills polymononuclear cells (PMN) and macrophages |
| examples of s. aureus infections of soft and hard tissues |
acute infective endocarditis deep organ abscesses pneumonia osteomyelitis |
| examples of s. aureus toxic syndrome |
scalded skin syndrome toxic shock syndrome food poisoning |
| Scalded Skin Syndrome (SSS) |
| skin diseases in which there is a demonstrable exfoliatin toxin |
| Scalded Skin Syndrome Diseases |
classic scalded skin syndrome ritter's disease bullous impetigo staphylococcal scarlet fever |
| classic scalded skin syndrome |
| desquamation of skin; usually associated with neonates and young infants |
| ritter's disease |
| a severe form of SSS in neonates |
| bullous impetigo |
| a development of large blisters that may rupture |
| staphylococcal scarlet fever |
| nondesquamative, eryematous rash that rarely involves the tongue and palate |
| toxic shock syndrome |
febrile illness characterized by vomiting, diarrhea, an erythematous rash, muscle pain and hypotension may lead to organ failure and death associated with menstruting women and the use of highly absorbent tampons S. aureus releases toxic shock syndrome toxin (TSST-1) during infections of the vagina |
| superantigens |
| group of toxins that activate T cells by simultaneously binding to t cell receptor and MHC II |
| infections of soft and hard palates by s. aureus |
| disseminate from a primary site of infection via blood stream to other body tissues |
| who does osteomyelitis most commonly infect |
| children under 12 |
| what is the most common bacterial cause of acute osteomyelitis |
| s aureus |
| how do you differentiate s. aureus from beta hemolytic group A streptococci |
catalase test s. aureus is catalase positive |
| are there other staphococcyl species that are coagulase positive besides s. aureus? if so which ones? |
| no |
| does s. aureus grow on mannitol salt agar? |
| yes |
| does s. aureus ferment mannitol |
yes, turns the plate from pink to yellow |
| how do you treat s. aureus |
start with beta-lactamase resistant penicillin  |
| examples of beta lactamase resistant penicillin |
methicillin cloxacillin oxacillin nafcillin |
| how do you treat MRSA |
vancomycin linezoid quinospristin-dalfopristin daptomycin |
| what populations are at the highest risk for s. aureus infections |
drug abusers immunocompromised individuals |
| what bacteria is one of the major causes of nosocomial infections |
| s. aureus |
| how is streptococcus arranged |
| long or short (diploccocci) chains |
| is streptococcus gram positive or gram negative |
| gram positive |
| is streptococcus catalase positive or catalase negative |
| catalase negative |
| what is an example of group A strept |
| s. pyogenes |
| what type of hemolysis does s. pyogenes does |
| beta hemolysis |
| examples of diseases caused by s. pyogenes |
uncomplicated pharyngitis, impetigo and erysipelas severe, invasive and often fatal necrotizing fasciitis/myositis and toxic shock syndrome rheumatice fever, scarlet fever, and bacteremia |
| what are some virulence factors of group a strept |
m protein fibronectin-binding protein capsular polysaccharide toxins and superantigens hemolysins |
| what is the MAJOR virulence factor in group a strept |
| m protein |
| m protein |
an adhesin which promotes attachment to epithelial cells containing keratin but not pharyngeal tissue antiphagocytic and anticomplement properties more than 100 different antigen types immunologically cross-reactive with human cardiac tissue |
| what does s. pyogenes pili contain |
| complex of m protein and lipoteichoic acid (LTA) |
| f protein in s. pyogenes |
| an adhesin which binds fibronectin and promotes adherence to fibronectin containing tissues |
| examples of fibronectin containing tissues |
upper respiratory tract female genital tract |
| how many different forms of pyrogenic (erythogenic) toxin are there |
three different immunological forms A, B, C (SPE A, B,C) |
| what does pyrogenic (erythogenic) toxin cause |
direct toxic damage to the skin produce a delayed hypersensitivity response responsible for the rash seen in scarlet fever |
| how does pyrogenic (erythogenic) toxin act |
| act as superantigens to stimulare the production of excessive amounts of TNF and IL-1 |
| SPE A and C |
encoded by a gene on a temperate phage only phage containing cells produce toxin |
| how can tox- strains of s.pyogenes be converted to tox+ strains |
| by a process called phage conversion or lysogenic conversion |
| s. pyogenes capsule |
| nonimmunogenic, antiphagocytic capsule made of hyaluronic acid |
| examples of hemolysins in s. pyogenes |
| streptolysin O and S |
| streptodornase (DNAase), Streptokinase, and Hyaluronidase |
| facilitates invasion of tissues and spreading |
| what is the most common bacterial cause of pharyngitis or tonsillitis |
| s. pyogenes-transmitted by droplet infection(respiratory secretions) |
| symptoms of s. pyogenes pharyngitis or tonsilitis |
malaise, fever, headache and sore throat tonsils are enlarged and erythematous anterior cervical nodes may be swollen  |
| s. pyogenes impetigo |
erthema, blisters followed by eruption and crusting transmitted by direct contact or sharing of contaminated items also caused by s. aureus |
| scarlet fever |
can accompany pharyngitis or streptococcal skin infections generalized punctate erythematous rash sometimes described as sandpaper rash and strawberry tongue accompanied by fever rash caused by pyrogenic toxin transmitted by droplet infection (respiratory secretions) |
| streptococcal toxin shock syndrome |
| symptoms due to the release of TNF, IL-1, IL-2 and possibly IL-6 due to the superantigen activity of pyrogenic toxins and B (SPE A and B) |
| S. pyogenes rheumatic fever/rheumatic heart disease |
autoimmune condition caused by cross reactivity of streptococcal antigens and human heart, joint and nervous tissue characterized by inflammation of the myocardium or endocardium, especially the mitral and or aortic valves arthritis (inflammation of joints) and neurologica symptoms (uncontrolled involuntary movements) follows respiratory but not skin infections |
| s. pyogenes glomerulephritis |
streptococcal antigen-antibody complexes are deposited at the basement membranse of the kidney glomeruli and injury to the glomerulus occurs as a result of an excessive inflammatory response may follow cutaneous or respiratory infection |
| how do you differentiate group a strept from group b strept |
bacitracin sensitivity CAMP test will be negative this is for group a |
| s. pyogenes immunity |
host defense is dependent on complement and opsonization, phagocytosis antibodies are directed to pili and the M and F proteins to prevent attachment and enhance phagocytosis type specific |
| is C. perfringens gram positive or gram negative |
gram positive anaerobic bacilli spores are rarely seen |
| s. pyogenes treatment |
penicillin erythromycin if allergic to penicillin will not prevent glomerulonephritis |
| who are most group a strept infections seen in |
| children 10 years of age and younger |
| how is s. pyogenes maintained in nature |
| asypmtomatic nasal and pharyngeal carriers |
| C. perfringens |
major infections are soft tissue infections (cellulitis, suppurative myositis, myonecrosis (gas gangrene) and gastroenteritis (food posioning) Â |
| what does C. perfringens infections usually result from |
| infection of traumatic or surgical wounds with organisms in soil or in human or animal feces |
| what is the most important virulence factor in c. perfrigens |
| alpha toxin |
| alpha toxin |
| a lecithinase (phospholipase C) which hydrolyzes the lipids in cell membranes resulting in cell lysis and death |
| c. perfringens treatment |
| serious infections require surgical debridement and high dose penicillin therapy |
