Strep & Enterococci Flashcards
Necrotizing fasciitis symptoms
Pain out of proportion to exam, often overlying edema, cellulitis, skin discoloration, bull, gangrene
Woody feeling of SQ tissues
Crepitus or anesthesia involved skin
Late: sepsis, organ failure, death
Tx of nec fasc
Surgery - dx by easily dissected tissue planes, swollen, dull, gray fascia -> debridement
Broad AB coverage (clinda, linezolid to decrease toxins)
Most common cause of nec fasc
Pts with no risk factors = Strep. pyogenes (GAS)
Common diseases caused by strep/ enterococcus infections
S. pneumo: sinus, ear, pneumonia, menigitis
viridans: endocarditis
Group A (pyogenes): cellulitis, skin infection
Entero: UTIs
Lab dx of strep
G+ cocci in pairs or chains, facultative anaerobes (some capnophilic), blood- or serum-enriched agar, lactic acid production, cat-
Hemolytic patterns
Alpha: breakdown of hemoglobin, appears greenish
Beta: breakdown RBC, appears clear/yellow
Gamma: no hemolysis
Lancefield groupings
Serologic classification based on specific Ag in cell wall; clumping = positive
S. pyogenes (GAS): Lancefield group, hemolysis, bio/phys tests
LG: A
Hem: beta
PYR+, bacitracin sensitive
PYR test
Presence of enzyme L-pyrrolidonyl arylamidase in colony of interest turns solution of PYR broth red when PYR reagent added
S. agalactiae (GBS): Lancefield group, hemolysis, bio/phys tests
LG: B
Hem: weak beta or gamma
CAMP+, bacitracin res, hydrolyzes hippurate
Enterococci: Lancefield group, hemolysis, bio/phys tests
LG: D
Hem: gamma
Growth in bile and 6.5% NaCl, PYR+, hydrolyzes esculin
S. bovis: Lancefield group, hemolysis, bio/phys tests
LG: D
Hem: gamma
Growth in bile, hydrolyzes esculin
S. anginosus (a viridans): Lancefield group, hemolysis, bio/phys tests
LG: F, A, C, G, and none
Hem: beta
Small colonies, group A is PYR+, bacitracin res
Strep viridans: Lancefield group, hemolysis, bio/phys tests
LG: none
Hem: alpha, beta, or gamma
Optochin res, not bile soluble
S. pneumo: Lancefield group, hemolysis, bio/phys tests
LG: none
Hem: alpha
Optochin susceptible, bile soluble
Peptostreptococcus: Lancefield group, hemolysis, bio/phys tests
LG: none
Hem: gamma or alpha
Obligate anaerobe
Strep pyogenes infections
Noninvasive infxns (strep throat, pyoderma)
Invasive infections less common
Can cause rheumatic fever, PSGN
S. pyogenes virulence factors
M protein*: serotype-specific, inhibits complement = dec phago
Streptolysins O, S: hemolysins, toxic to other cells, inh by O2
Capsule, adhesins, exotoxins, C5a peptidase (dec abscess formation); DNAse, hyaluronidase, streptokinase (these 3 dec viscosity, degrade clots & CT = spread)
S. pyogenes prevalence, transmission, immunity
Asymptomatic carriage in kids and adults
Transmitted person-person via resp droplets (crowding is a problem), uncommonly food- or water-borne, not spread by fomites
Serotype-specific long-lasting immunity develops post-infxn
Streptococcal pharyngitis symptoms, complications
Resolves in 1 week
Can have scarlet fever with some strains
Rarely: contiguous or bacteremic spread (suppurative complications)
Non-suppurative complications: RF (1-5 w later), PSGN
Symptoms of scarlet fever
Blanching red rash of sandpaper texture, sparing palms and soles, red strawberry tongue
Rheumatic fever
Affects CT (heart, jj, vessels, SQ tissues), associated with certain M types
Carditis -> chronic rheumatic heart disease, polyarthritis, SQ nodules, chorea, erythema marginatum, fever, arthralgias
3% after untreated strep throat, lasts 3-6 months (but commonly recurs)
PSGN
Post-streptococcal glomerulonephritis
After strep throat or pyoderma
Edema, HTN, proteinuria, hematuria
90% recover completely, recurrence uncommon
Streptococcal pyoderma/impetigo
Discrete purulent skin lesions with thick crusts
Peak: age 2-5 in warmer climates/months
*Can also be caused by S. aureus, so tx is abx to cover both
Erysipelas
Invasive strep skin/ soft tissue infection
Lesions raised above skin with clear demarcation, bright red/ salmon color
Restricted to dermis and lymphatics
Cellulitis
Invasive strep skin/ soft tissue infection
Spreading inflammation of skin and SQ tissues
Most commonly caused by strep in absence of pus or penetrating trauma
Streptococcal toxic shock syndrome
Any GAS infxn a/w shock and organ failure, usually serotypes M1, M3
Primarily exotoxin-mediated
Phases: 1) flu-like prodrome, confusion, pain; 2) tachycardia, tachypnea, fever, inc pain; 3) shock, organ failure
Tx: source control, fluids, abx (PCN + clinda), ICU care, +/- dialysis and IVIG
Lab dx of S. pyogenes
Strep throat: rapid Ag detection test; throat culture*
Invasive infxn: blood/tissue culture; clinical for pyoderma, erysipelas, cellulitis
RF: Jones criteria, evidence of previous GAS infxn
PSGN: clinical picture + evidence of previous GAS infxn
Jones criteria for RF
Major: migratory arthritis, carditis, valvulitis, CNS involvement, erythema marginatum, SQ nodules
Minor: arthralgia, fever, elevated APRs, prolonged PR interval
ASO titer
Used to detect previous strep infection for RF and PSGN
Abs take weeks to develop, so this is not for acute infection
Tx of S. pyogenes infections
Strep throat: pen or another abx
Invasive infxn: longer course abx
RF: ASA, steroids, pen prophylaxis for 5-10 y to prevent recurrence
PSGN: pen (as for strep throat)
Lab dx of GBS/S. agalactiae
Beta-hemolysis, bacitracin resistant, +CAMP test, hydrolyzes hippurate
S. agalactiae/GBS normal colonization sites, infections, and main virulence factor
Colonizes GI, oropharynx, vagina (20% women)
Source of sepsis for babies and elderly w comorbidities (DM, liver disease), meningitis
Main: polysaccharide capsule to interfere w phagocytosis
GBS in pregnancy
50% neonates colonized if mother not treated
Pregnant women screened at 35-37 weeks and given intrapartum pen prophylaxis if positive
Infants: 1-7d bacteremia, sepsis, pneumonia, meningitis; 1-13w bacteremia, meningitis, focal infxn (osteomyelitis, cellulitis)
GBS infections in adults, dx, and tx
Pregnant: chorioamnionitis, miscarriage, endometritis, postpartum UTI
Elderly w comorbidities: bacteremia, pneumonia, osteomyelitis, arthritis, cellulitis
Dx: culture or PCR
Tx: pen or another abx
Viridans group of strep
Genetically related, mostly a-hemolytic but any hemolysis and Lancefield group possible; treat different strains diff for testing and clinical purposes
Normal flora of oropharynx, GI, upper resp, female GU
Viridans strep groups
Anginosus, mitis, mutans, salivarius, sanguinis
Virulence of viridans strep
Low virulence, no exotoxins except S. anginosus group
S. anginosus infections and virulence
Invasive pyogenic abscess (in 50-80% brain abscesses; dental, liver, lung)
Vir: exotoxins, hydrolytic enzymes, polysaccharide capsule
Species in viridans strep anginosus group & shared phenotype and metabolic features
S. constellatus, intermedius, anginosus
Small colonies with caramel odor
Growth enhanced by anaerobes
Clinical syndromes of viridans strep
Infective endocarditis (20% of cases), bacteremia, aspiration pneumonia with anaerobes
Symptoms and tx of infective endocarditis
Subacute; fever, murmur, fatigue, weight loss, splenomegaly
Janeway lesions, Osler’s nodes, splinter hemorrhages, Roth’s spots
Tx: pen or ceftriaxone +/- gentamicin (sensitivities)
Viridans strep bacteremia
Primarily in neutropenic fever; 25% fulminant shock, 6-12% mortality
Lab dx S. pneumoniae
G+ cocci in pairs or chains, large a-hemolytic colonies, Lancefield non-typeable, optochin sensitive, bile soluble, 91 serotypes, + quellung reaction
Quellung reaction
Polyvalent anticapsular Abs + bacteria, examine microscopically for increased refractiveness around bacteria = + reaction = pneumococcus
S. pneumoniae colonization and infections
5-70% people colonized (nasal carriage), normal flora of oropharynx, obligate human parasite
Leading bacterial cause of meningitis, pneumonia, sinusitis, otitis media
Pneumococcus/ S. pneumo virulence factors
Surface adhesins (attach) IgA protease and pneumolysin (evade removal by cilia) Pneumolysin, teichoic acid, peptidoglycan fragments, hydrogen peroxide, phosphocholine (tissue destruction) Polysacch capsule (prevent phago), pneumolysin (suppress killing by phago)
How do pneumolysin, teichoic acid, peptigoglycan fragments, hydrogen peroxide, and phosphocholine help S. pneumo destroy tissue?
Pneumolysin: activates classical complement TA: alternate complement PG frag: alternate complement H2O2: ROS intermediates PC: helps enter cells
Host defenses vs. pneumococci/ S. pneumo
Mucous and ciliated epithelial cells in lungs move them up and out of resp tract
Spleen clears bact from blood
Anticapsular Ab opsonizes for phagocytosis
Predisposing factors for invasive S. pneumo infection
65 yoa
Native America, AA, Australian aboriginal: 2-10x higher risk
Asplenia/dysfunctional (100x in SCD), DM (6x), COPD (7x), CHF (10x), alcoholics (11x)
Immunodef: HIV/AIDS (47x), solid cancer (33x), hematologic malignancy (56x)
Otitis media and sinusitis
Leading cause: S. pneumo (30-40%), followed by H. flu
Prior resp infection contributes to congestion of sinuses/ ear canal -> obstruction
OM: young children, #1 reason abx in kids
Sin: all ages
Meningitis
Leading cause: pneumococcus (70% of adult, >6 mo)
Direct extension from ear, sinuses, or bacteremia
Sx: fever, nuchal rigidity, AMS, HA, seizures, focal neuro defects, N/V, photophobia, Kernig’s and Brudzinski’s signs
Tx: vanco, ceftriaxone
Kernig’s and Brudzinski’s signs
K: reluctance to allow knee extension with 90* hip flexion
B: spontaneous hip flexion with passive neck flexion
Bacterial vs. fungal/TB vs. viral meningitis CSF parameters
B: >1000 WBC, mostly neutros, low glucose, high protein, elevated opening pressure
F/TB: 10-500 WBC, mostly lymphs, low glucose, slightly high protein, elevated opening pressure
V: 10-500 WBC, mostly lymphs, nrl glucose, nrl-elevated protein, normal opening pressure
Sx of pneumococcal pneumonia
Cough, fatigue, fever, chills, sweats, SOB; tachycardia, tachypnea, crackles +/- dull to percussion, egophany, increased fremitus; infiltrate on imaging
Dx and tx of pneumococcal pneumonia
Dx: resp Gram stain/culture, blood culture, Ag detection (urine or CSF)
Tx: empiric tx covers pneumococcus (ceftriaxone, azithromycin, FQs)
Pneumococcus prevention
Polysaccharide vaccine: T-cell independent immunity, hyporesponsiveness for 1 year, 60-70% efficacy, ineffective in kids
Enterococci features
“Intestine berry”; GPC in pairs and short chains; usually y-hemolytic, can be a or b; can grow in high conc NaCl or bile salt; facultative anaerobes; optochin resistant; PYR+
Enterococcus species of clinical importance
E. faecalis, E. faecium
Pathogenesis of enterococcus, virulence factors
No potent toxins or well-defined virulence factors
Surface adhesins, cytolysin (hemolytic), gelatinase and serine protease
Inherently resistant to many abx, can acquire resistance easily
Tx of choice: ampicillin +/- gentamicin (if sensitive)
Enterococcal infections
Subacute endocarditis (5-20% cases), line infections, UTIs (catheter), intra-abd and pelvic infxns 2-3rd cause of nosocomial infxns in US
Risk factors for enterococcal infections
Recent hospitalization, abx use, SNF residence/stay, immunocompromised (cancer, DM), GI procedure
Strep bovis (GDS) bacteremia tests
HIV ELISA and confirmatory western blot, colonoscopy (assc. w colon cancer), complement levels, Hgb electrophoresis
