Generalized morphology of streptococci?
spherical gram (+) cocci in pairs or chains; catalase(-), varying hemolysis
Group A strep also known as?
Group B strep also known as?
3 bugs in Group D strep?
Enterococcus faecalis, Enterococcus faecium, and Strep bovis (gallolyticus)
Diagnosis of GAS?
Do a rapid swab and a culture at time of presentation
Diseases that GAS most commonly causes?
Pharyngitis (most common cause), cellulitis/impetigo, necrotizing fasciitis, TSS, scarlet fever, rheumatic fever, glomerulonephritis
GAS virulence factors (there are 9)
1) Hyaluronidase 2) Streptokinase 3) DNase 4) C5a peptidase 5) Streptococcal chemokine protease 6) Steptolysin O 7) Strepolsyin S 8) Protein M 9) Polysaccharide capsule
Action of Hyaluronidase
Degrades hyaluronic acid in the subQ tissue; known as spreading factor, facilitates cellulitis/skin infection
Action of Streptokinase
Plasminogen-->Plasmin; role in infection unclear
Action of DNase
Degrades DNA exudate to prevent bacteria from being trapped in neutrophil extracellular traps (NETs)
Action of C5a peptidase
Cleaves C5a; significantly impedes influx of neutrophils early in infection
Action of Streptococcal chemokine protease
Prevents migration of neutrophils to infection site by degrading IL-8
Action of Streptolysin O
cytotoxic, protects GAS from phagocytic killing
Strepolysin O hemolysis characteristics (on agar)
Oxygen labile, beta hemolysis only when UNDER the surface of blood agar
Streptolysin S hemolysis characteristics (on agar)
Oxygen stable, beta hemolysis ON THE SURFACE of blood agar
2 distinguishing physical exam findings/symptomology of GAS phraygnitis
Tender, enlarged cervical lymph nodes and ABSENCE of uri symptoms (cough, rhinorrhea)
Specificity/Sensitivity of GAS rapid screen?
High specificity, low sensitivity (false negatives common)
Typical course of GAS pharyngitis abx?
10 days, patient must finish the abx
Why do you treat GAS pharygnitis? Most cases are self limiting
To prevent complications; Rheumatic fever, otitis media, mastoiditis, meningitis, retropharyngeal abscess
What type of GAS illness does rheumatic fever follow?
Only follows a pharyngitis
How does mastoiditis normally occur?
Due to an untreated otitis media and subsequent local spread
What is erysipelas?
A rapidly spreading, erythematous cutaneous swelling on the face. Sometimes in a butterfly distribution
Contrast necrotizing fasciits vs. cellulitis?
The necrotizing fasciitis won't look that bad on physical exam; cellulits looks erythematous, swollen, etc.
Physical exam finding on necrotizing fasciitis (this is on the test)?
PAIN OUT OF PROPORTION TO EXAM
Difference in diagnosis of toxic shock with S. aureus vs. GAS?
S. aureus doesn't require isolation of bactria; for GAS, you must isolate bacteria from a normally sterile site (blood, CSF, etc)
Treatment for necrotizing fasciits?
Surgical debridement (emergency)
What strains of GAS are more associated with necrotizing fasciits?
Protein M types 1 and 3
Immune response at site of necrotizing fasciitis?
Paucity of neutrophils due to GAS degradation of IL-8
Symptoms of advanced necrotizing fasciitis infection?
Fever, tachycardia, systemic toxicty
What does crepitus indicate?
There is a necrotizing fasciits; anaerobes are producing CO2 in the subQ
What toxin causes scarlet fever?
Erythrogenic toxin (superantigen)
What GAS toxin causes TSS?
Pyrogenic exotoxin A
What GAS toxin causes necrotizing fasciits (most commonly)?
Who does scarlet fever affect?
Clinical findings with scarlet fever?
Skin feels like "sand paper" (small papules rough to the touch), rash desquamates, STRAWBERRY TONGUE, normally occurs in association with pharyngitis
Post-strep glomerulonephritis commonly occurs after which type of infection?
Skin infetion, not pharyngitis
Does early treatment of inection prevent PSGN?
It is unclear
Do most cases of PSGN come to clinical attention?
No, most are self limiting and relatively asymptomatic
Physical exam/clinical findings with PSGN
HTN, facial edema, LE edema, dakr urine
Onset of rheumatic fever?
Normally 2 weeks post untreated GAS pharyngitis
Mechanism/Pathophysiology of acute rheumatic fever?
Molecular mimicry, antibodies cross react with host antigens
JONES criteria for acute rheumatic fever diagnosis?
J- Joints, polyarthitis
O-Cariditis (O looks ike a heart)
N- Nodules (subQ)
E- Erythema Nodosum (pink rash on the trunk)
S- Sydenham chorea (abrupt involuntary movement)
What lab finding aids in the diagnosis of rheumatic fever?
ASO titer; correlates to recent GAS infection
Strep agalactiae (GBS) morphology
Narrow zone of beta hemolysis; lacks hydolysis on bile esculin agar; hydrolyzes hippurate; bacitracin RESISTANT; CAMP test (+)
Bacitracin test. What are you distinguishing between?
GAS (sensitive) and GBS (resistant)
Where is GBS normally found?
Genital tract of some women, also the colon
How are neonates infected with GBS?
Acquired in utero or directly when passing through the vagina
What diseases do GBS cause in neonates?
Meningitis, sepsis, and PNA
Prevention of GBS infection in neonates
Screen women at 35-37 weeks gestation; Penicillin G/Ampicillin at time of delivery for those positive
Charactersitic appearance of GDS (enterococcus) on bile-esculin agar?
Hyrdolyzes esculin producing black pigment
Growth in hypertonic saline is characteristic of enterococcus or strep bovis?
S. bovis will not grow in hypertonic saline.
- both will lyse bile
What infections do enterococcus faecalis/faecium commonly cause?
Hospital-acquired UTIs (extremely common), blood stream infections (line-related), endocarditis, and intra-abdominal infection
Patient has a Strep bovis/gallolyticus infection. What do you do next?
Screen them for Colon cancer; extremely high association
Growth of streptococcus bovis/gallolyticus in hypertoni saline?
Will NOT grow
Most common cause of ACUTE bacterial endocarditis?
Virdans group strep morphology
Alpha hemolytic; resistant to lysis by bile; optochin RESISTANT
Where do you normally find virdans group strep?
Normal flora of the mouth and colon
What does streptococcus mutans (Virdans group) commonly cause?
Dental caries and subacute bacterial endocarditis after oral surgery
Optochin test. What are you distinguishing between?
Strep pneumo (SENSITIVE) and Virdans group (RESISTANT)
Most common cause of SUBACUTE bacterial endocarditis?
Virdans group strep
Are abscesses normally monomicrobial or polymicrobial?
Brain abscess from oral source. Which 2 bacteria?
Virdans group or peptostreptococcus
Describe Janeway lesions
Microabscesses caused by septic emboli (seen in endocarditis); NOT PAINFUL
Describe Osler Nodes
Immune complex deposition on the fingers and toes; PAINFUL