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28 Cards in this Set

  • Front
  • Back
Streptococci group characteristics
-GP cocci chains
-fail to produce catalase (in contrast to staph)
-grow best on blood agar> can use to determine alpha vs beta hemolysis
alpha vs beta hemolysis
-seen in strep
-B- complete hemolysis, clear around colonies on blood agar
-a- hazy, green on blood agar due to incomplete hemolysis
3 major groups of streptoccci
-pyogenic (B-hemolytic, group Ags)
-pneumococci (a-hemolytic, capsule, no group Ags)
-Viridans (a hemolytic, no group Ags, no capsule, part of normal oral flora)
>>>>>Enterococcus is no longer in this group (has group D Ag)
Group A Strep (GAS)
-name the 2 toxins that cause b-hemolysis
-streptolysin S
-streptolysin O (oxygen stabile)
Structures of GAS cell wall
-M protein (80 diff serotypes)
-F protein
-lipotechoic acid
-pili
M protein
-on GAS
-on cell wall, extends out and serves as Ag for serotyping (>80 serotypes)
-biologic funtion assigend to specific domains such as antigenicity or capacity to binds molecules like fibrinogen, serum factor H, and Igs
Streptolysin O (SLO)
Exotoxin of GAS
-pore forming
-causes B-hemolysis
-is antigenic and is the basis for the serologic test antistreptolysin O (ASO)
StrepSAgs
-strep super antigens
-made by about 10% GAS
-similar to StaphSAg
-multiple effects such as fever rash, scarlet fever, T-cell proliferation, B-cell supression
-cytokines released through super Ag mechanism
Dz caused by GAS
-pharyngitis
-impetigo
-wound and puerperal infections
-strep TSS
-post strep dz (acute rheumatic fever and rheumatic dz)
-poststreptococcal glomerulonephritis
Impetigo
-what organism
GAS
-transient skin colonization with GAS combined with minor trauma, insect bite
-spreads locally by scratching and to others by direct contact
Streptococcal TSS
-what bug
GAS
-severe invasive for of GAS soft tissue infection
-rapid progression to death
-multiorgan involvement> spreads to blood
Poststreptococcal sequelae of GAS (2)
1) ARF (acute rheumatic fever)> does not follow skin or other non-respiratory infections of GAS
-recurrances can be triggered with any GAS infection
-injury to heart by common recurrences leads to rheumatic heart disease
2) Poststreptococcal glomerulonephritis> can follow respiratory or cutaneous GAS> involves only certain nephritogenic strains though
Acute GAS infection pathogenesis
-nasopharynx vs skin
-name 3 adhesins on cell wall surface and function
-3 adhesins of GAS
-M protein, F protein, LTA (lipotechoic acid)
-all 3 involved in nasopharynx infection> attach to fibronectin> M protein provides scaffold for LTA
SKIN
-M protein binds directly to subcorneal keratinocytes
-F protein involves adherence to Ag- presenting langerhans cells
How are some GAS resistant to phagocytosis?
-what is the major molecule for this?
M protein essential
-binds fibrinogen and factor H> diminished alternative pathway
-in presence of M specific Ab> classical pathway proceeds
Type of HS
-acute rheumatic fever
Type II
Type of HS
-Acute glomerulonephritis (post streptococcal)
Type III
Acute rheumatic fever follow what infection?
-bug and specific site
GAS pharyngitis ONLY
(does not follow empitigo)
-due to autoantibodies from M protein
What type of immunity do you develop to GAS?
-Ab against M protein is protective BUT only for same M protein (90 diff serotypes)
-called type-specific immunity
-IgG to M reverses antiphagocytic properties> Ab bind complement C3b by classical mechanism> phagocyte recognition
Streptococcal Pharyngitis
-Clinical, Sx
-what age group?
-where can it spread?
-5-15yo
-fever, malaise, headache, sore, red swollen throat, white-yellow exudate
-effects uvula, tonsillar pillars, and soft palate
-cervical lymph nodes swell
-self-limiting
SPREADS to:
-otitis media, abscesses, suppurative cervical adenitis, acute sinusitis
-rarely goes to bacteremia, pneumonia, meningitis
Impetigo
-what age?
-where on body?
-usually 2-5 yo
-face and lower extremities
-small vesicles surrounded by erythema
Erysipelas
-bug
-Sx
caused by GAS
-AFFECTS DERMIS
-spreading area of edema and erythema, rapid, well-demarcated edges
Scarlet Fever
-3 major charcteristics
-GAS
-any strains that use StrepSAg
-superimposed on pharyngitis
3 characteristics
1) circumoral pallor- cheeks, temples red with pale area around mouth
2) Strawberry tongue- yellow exudate with red papillae
3) Sandpaper rash- appears on second day of illness, spreads from upper chest to trunk then extramities
Streptococcal TSS
-Sx
-Labs
GAS
-starts with vague myalgia, chills, and severe pain at infected site (usually skin or soft tissue) leading to necrotizing fascitis and myonecrosis
-when it involves extrmities referred to as flesh eating bacteria
-continues with nausea vomiting diarrhea> hypotension, shock, organ failure
LABS
-lymphocytosis
-azotemia (impaired renal function)
-bacteremia in 50%
ARF
-Sx
GAS
-fever, carditis, subcutaneous nodules, chorea, migratory polyarthritis
-cardiac enlargement, murmurs> can lead to heart failure
-typically begins 3 weeks after GAS pharyngitis and can last 2-3 months untreated
-repeat infections (diff M proteins) lead to progressive heart damage> damage to heart valves, endocardium, scarring, valvular stenosis> called rheumatic heart disease
Poststreptococcal Glomerulonephritis
-Sx and timecourse
GAS
-primarily children
-1-4 weeks after pharyngitis
-3-6 weeks after skin infection
Sx
-edema, HTN, hematuria, proteinuria, decreased serum C'
Dx GAS
-Culture- demonstrate B-hemolysis on blood agar
-Serologic grouping identifying group A antigen
-Rapid strep test> detect group A Ags directly from throat swab (90% sensitive compared to culture)
-High titers of antistreptlysin O (ASO) are usually found in pts with rheumatic fever
Rx GAS
-susceptible to Penicillin G> resistance unknown> drug of choice
-treatment may not prevent glomerulonephritis
Prevention of GAS
-what scenarios would you use phylaxis?
-penicillin prophylaxis is used to prevent recurrences of ARF during susceptible years (5-15yo)
-people with Hx of ARF use penn prophylaxis if undergoing dental extraction> can lead to bacteremia