Staph and Strep Flashcards
(118 cards)
1
Q
Staphylococci general characteristics
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nonmotile, do not produce spores, produce catalase (degrade hydrogen peroxide
2
Q
Most common bacterial cause of conjunctivitis
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Staph aureus
3
Q
Staph aureus’ distinguishing lab features
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Production of coagulase and sensitive to novobiocin
4
Q
Common source of staph aureus infection in neonates
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carriage by health care personnel
5
Q
Carrier state
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individual harbors potential pathogen and can spread it to others, though the carrier is either asymptomatic or has recovered from an infection by the organism already
6
Q
Colonization
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Acquisition of a new organism and it may cause infection or may be eliminated by host defenses
7
Q
Colonization resistance
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Nonpathogenic resistant bacteria occupy attachment sites on skin and mucosa, interfering with colonization by pathogenic bacteria
8
Q
Primary site of colonization for staph epidermidis
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Skin
9
Q
Primary site of colonization for staph saprophyticus
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Skin surrounding GU tract
10
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Primary site of colonization for staph aureus
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nose
11
Q
Reason for yellow color of staph aureus on culture
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Staphyloxanthin
12
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Mechanism by which staph aureus causes necrotizing PNA
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P-V Leukocidin: Pore-forming toxin kills cells, especially WBCs, by damaging cell membranes
13
Q
Protein A
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staph aureus virulence factor; binds to Fc portion of IgG at complement binding site and prevents complement activation; major component of cell wall; no C3b produced so phagocytosis of organisms is greatly reduced
14
Q
Teichoic acid
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staph aureus virulence factor; mediates adherence of staph to mucosal cells; induces release of cytokines (IL-1, TNF) from macrophages
15
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Peptidoglycan
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staph aureus virulence factor; endotoxin-like properties (can activate complement, coagulation cascade, stimulate macrophages to release cytokines); cause of septic shock
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Staphyloxanthin
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causes golden color to staph aureus colonies; virulence factor that enhances pathogenicity by inactivating microbicidal effect of superoxides and other ROS within neutrophils
17
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Coagulase
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staph aureus VF; causes plasma to clot by activating prothrombin to from thrombin which catalyzes activation of fibrinogen to form fibrin clot; serves to wall off infected site, delaying migration of neutrophils to the site.
18
Q
Hemolysins
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Staph aureus VF; hemolyze RBCs and use iron that is required for bacteria to grow; forms holes in host cells; causes necrosis of skin
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Polysaccharide capsule
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staph aureus VF; 11 serotypes with 5&8 most commonly causing infection; it allows bacteria to attach to artificial materials and resist host cell phagocytosis
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Q
Panton Valentine Leukocidin
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Staph aureus VF; pore forming cytotoxin that causes leukocyte destruction by damaging cell membranes and causes tissue necrosis; cell content leak out of pore formed by the toxin causing severe skin/soft tissue infection and necrotizing pneumonia; produced by CA-MRSA
21
Q
Gamma toxin/leukotoxin
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staph aureus VF; lyses phagocytes/RBCs
22
Q
Furuncle
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boil; infection of hair follicle; purulent material extends through dermis into subcu tissue; abscess forms
23
Q
Carbuncle
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Coalescence of several inflamed follicles
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Q
Folliculitis
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Superficial infection of hair follicles with purulent material in epidermis
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Cellulitis
infection of soft tissue; involves deeper dermis and subcu fat
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Furuncle
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Carbuncle
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Paronychia
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Folliculitis
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Cellulitis
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Hordoleum
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Blepharitis
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Conjunctivitis
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Pyogenic infection
Endocarditis, septic arthritis, osteomyelitis, postsurgical wound infections, pneumonia which can lead to empyema/abscess, sepsis, mastitis, abscessess (local and from blood stream)
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MRSA population group
Childcare centers, IV drug users, wrestling teams, prisons
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Cause of scarlet fever
Exofoliatin/Exfoliative toxins A and B; toxin acts as a protease that cleaves desmoglein in desmosomes
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Clinical presentation of scalded skin sydrome
newborns (3-7days), febrile, irritable, diffuse blanching erythema with blisters 1-2 days later in flexural areas, buttocks, hands; serous fluid exudates, dehydration, electrolyte imbalance; mucous membranes are not involved and there is no scarring; lasts 10 days
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Scalded skin syndrome
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Enterotoxin
Toxin in staph aureus that causes food poisoning; it causes prominent vomiting and watery, non-bloody diarrhea; acts as superantigen in GI tracts, stimulates IL-1 and IL-2 from macrophages and helper T cells (cytokines stimulate enteric nervous system to activate vomiting); heat/acid resistant toxin; 1-8 hour incubation period
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Bullous impetigo cause
caused by exfoliative toxin; localized at site of infection
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Clinical presentation of bullous impetigo
Young children; vesicles that have enlarged to form flaccid bullae with clear yellow fluid, which later becomes darker and more turbid; ruptured bullae leave a thin brown crust; usually on the child's trunk
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Bullous impetigo
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Causes of Staph toxic shock
Toxin mediated/superantigen from tampons, nasal packing to stop bleeds, post op infections
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Staph aureus TSS pathogenesis
Toxic shock syndrome toxin enters blood stream and stimulates release of large amounts of IL-1, IL-2, and TNF; blood cultures will be negative becasue the syndrome is caused by the toxin not the bacteria
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Clinical presentation of staph TSS
Fever, hypotension, dizziness/syncope, diffure macular erthroderma that desquamates in 1-2 weeks after onset, V/D, severe myalgias with CPK elevation, renal failure, transaminits or hyperbilirubinemia, thrombocytopenia, AMS
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Treatment options for MRSA
Vancomycin, Ceftaroline, Linezolid, Daptomycin, Bactrim/Clinda(mild)
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Treatment options for MSSA
produces beta lactamase so resistant to some beta lactams; use Nafcillin/oxacillin, Cefazolin, Ceftriaxone, Cefepime, Ceftaroline, Vancomycin, Augmentin (mild)
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VISA/VRSA treatment options
Daptomycin, Linezolid, Ceftaroline
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MRSA resistance mechanism
changes in PBP in their cell membranes; MecA genes on the bacterial chromosome encode these altered PBPs
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Resistance mechanism of VRSA
genes encode enzymes that substitute D-lactate for D-alanine in the peptidoglycan cell wall
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Resistance mechanism of VISA
Due to the synthesis of an unusually thickened cell wall
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Supportive treatment for TSS
Extensive fluid suppression (10-20L/day) and vasopressors (dopamine and NE)
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Surgical treatment of TSS
remove causative agent; if patient is post-surgical, surgical wounds must be explored and debrided
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Antibiotics for TSS
Vanc/Oxacillin plus Clindamycin
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Why Clindamycin is used in treatment of TSS
Clinda suppresses protein synthesis and therefore toxin synthesis; other antibiotics may suppress toxin synthesis too, such as Linezolid
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Prevention of Staph Aureus
For surgery: peri-operative Cefazolin and Vanc if high rate within population
Intranasal mupirocin to reduce colonization with Hibiclens for bathing +/- milds ABX (Doxy, Bactrim)
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Staph aureus micro properties
Catalase positive, coagulase positive, beta hemolytic, ferments mannitol
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Micro properties of Staph epi
Catalase positive, coagulase negative, non-hemolytic, urease positive, does not ferment mannitol, novobiocin sensitive
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Micro properties of Staph Saprophyticus
Catalse positive, coagulase negative, non-hemolytic, urease positive, does not ferment mannitol, novobiocin resistant
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How is coagulase test done
with rabbit plasma
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Most common setting of staph epi infections
usually in the context of a foreign device implant (heart valve, hip), due to organisms on implant
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Pathogenesis of staph epi
Bacterial adherence - adhesins interact with host proteins that cover the prosthetic such as fibringoen and fibronectin; after attachement extracellular polysaccharide matrix or slime is produced which encases the bacteria creating a biofilm
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Treatment options for Staph epi
Vancomycin, (Oxacillin/Nafcillin if MSSE), Rifampin or Gentamicin can be added especially for prosthetic valve endocarditis (high resistance to Gent limits use); remove the device
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Staph saprophyticus presentation
2nd most common CA-UTI in women; most have had sex within previous 2-4 hours
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Treatment of S. saprophyticus
Bactrim or Cipro
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General characteristics of streptococci
Spherical GPCs arranged in pairs or chains; catalase negative, distinguished from each other based on hemolysis
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How group A strep causes disease
Pyogenic inflammation, exotoxin production, immunologic
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Method of diagnosing strep throat (GAS phayngitis)
Rapid antigen test
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How rapid strep antigen test works
high specificity, low sensitivity; takes ~10 min; anitgens are extracted from throat swab and reacted with antibody bound to latex particles; agglutination of latex particles occurs if GAS is present. If high suspicion and negative rapid test, do throat culture
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What does alpha hemolysis look like
green zone around colonies as result of incomplete lysis of RBCs
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What does beta hemolysis look like
clear zone around colonies due to complete lysis of RBCs
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What does gamma hemolysis look like
No lysis of RBCs
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Streptolysin O
hemolysin; oxygen labile; causes beta-hemolysis only when colonies grow under surface of blood agar plate; this is what antibodies exist after infection
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Streptolysin S
hemolysin, oxygen stable; causes beta-hemolysis on surface of plate
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M Protein
antiphagocytic VF of GAS; protrudes from outer surface of cell and interferes with ingestion by phagocytes; 80 serotypes
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GAS Polysaccharide capsule
antiphagocytic VF; it is made of Hyaluronic acid which is a native compound to humans so no antigens are formed against it.
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Hyaluronidase
GAS VF; degrades hyaluronic acid (in subcu tissue); known as spreading factor - facilitates spread of GAS in cellulitis/other skin infections
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Streptokinase
GAS VF; activates plasminogen to from plasmin which dissocles fibrin in clots, thrombi, and emboli; role in GAS infections is unclear
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DNase (streptodornase)
GAS VF; degrades DNA in exudates/necrotic tissue; protect the bacteria from being trapped in neutrophil extracellular traps (NETs)
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C5a peptidase
GAS VF; cleaves C5a produced by the complement system; minimizes influx of neutrophils early in infection
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Streptococcal chemokine protease
GAS VF; prevents migration of neutrophils into site of infection by degrading chemokine IL-8 which would recruit neutrophils to site
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Potential complications of untreated GAS pharyngitis
otitis media, sinusitis, mastoiditis, meningitis, peritonsillar/retropharyngeal abscess, rheumatic fever
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GAS Treatment
Oral Penicillin V, Amoxicillin, or Cephalexin (twice daily for 10 days); if Pen allergy - Azithromycin (Zpack), Clarithromycin (2x10days), Clindamycin (3x10days)
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Skin/soft tissue infections GAS
Erysipelas (rash across cheeks and nasal bridege), Impetigo, Cellulitis
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Erythrogenic toxin
GAS toxin; responsible for rash of scarlet fever, acts as superantigen
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Pyrogenic exotoxin A
GAS toxin; causes most cases of TSS. Superantigen - causes release of large amounts of cytokines
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Exotoxin B
GAS toxin; protease that rapidly destroys tissue and is produced in large amounts by the "flesh eating" strains of GAS that cause necrotizing fasciitis
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Clinical scenario for GAS TSS
In setting of GAS infection (most common entry points are skin, vagina, pharynx) or at site of minor trauma who develop skin infections within 3days; diffuse erythema, fever, chills, myalgia, n/v/d, hypothermia, hypotension, AMS
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Complications of GAS TSS
DIC, AKI, ARDS, puerperal sepsis, endometritis
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Diagnosis of GAS TSS
isolation of GAS from normally sterile site (blood, CSF, tissue biopsy) and hypotension plus other organ involvement
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Treatment of GAS TSS
Penicillin plus Clindamycin
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Post strep glomerulnephritis
caused by nephritogenic strains of GAS, frequently after skin infections; Ag-ab complex form against GBM; present with HTN, facial edema, LE edema, dark urine; early treatment does not stop it and most cases resolve completely
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Acute rheumatic fever
2 weeks after GAS pharyngitis, caused by rheumatogenic strain; antibodies against GAS proteins cross-react with host antigens
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Diagnosis of Rheumatic fever
polyarthritis, carditis, nodules, erythema marginatum, syndenham chorea (neuro disorder consisting of abrupt involuntary movements); ASO titer
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Treatment of Rheumatic Fever
Full course of anitbiotics to eradicate any residual GAS; then prevent further infections with prophylaxis (penicillin IM monthly for many years)
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Peptostreptococcus
anaerobe, members of normal flora of gut, mouth, female genital trac; commonly found in mixed anaerobic infections
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Treatment of peptostreptococcus
Penicillin
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Group D Strep
Hydrolyze esculin in presence of bile (produce black pigment on bile-esculin agar); includes Enterococcus sp, and Strep Bovis
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Enterococcus faecalis/faecium
can grow in hypertonic saline or in bile; low virulence; VF include capsule and enzymes that injure host tissue; part of normal colonic flora; cause hospital acquired UTIs, bactermeia, and endocarditis
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Treatment of Enterococcus faecalis/faecium
combination antibiotic therapy required - PCN/Vanc depending on resistance and aminoglycoside
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VRE
Most likely enterococcus faecium; treat with Linezolid or Daptomycin
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Streptoccocus bovis
causes endocarditis in patients with colon cancer (very strong association); will not grow in hypertonic saline
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Treatment of strep bovis
PCN, Ceftriaxone, or Vancomycin
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Mechanism of resistance for VRE
genes encode enzymes that substitute D-lactate for D-alanine in peptidoglycan
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Streptococcus agalactiae micro
GBS; narrow zone of beta hemolysis; lack of hydrolysis of bile esculin agar; hydrolyzes hippurate; Bacitracin resistant (GAS is sensitive); CAMP Test - protein is produced that enhances sheep blood hemolysis in presence of Staph Aureus; organism induces inflammatory response; polysaccharide capsule is antiphagocytic
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Strep agalactiae clinical scenario
Colonizes genital tract of some women; infection acquired in utero or during passage through the vagina; RF - PROM in women colonized, babies born \<37wks; children whose mothers lack anitbodies
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Complications of strep agalactiae
neonatal sepsis, meningitis, PNA
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Clinical setting of strep agalactiae in adults
important cause of invasive infections such as septic arthritis, cellulitis, osteomyelitis. Diabetes is main predisposing factor, and breast cancer
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GBS diagnosis
Gram stain/culture; rapid test available in vaginal/rectal samples, detects DNA
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Treatment of GBS
Penicillin/Ampicillin (Vanc if resistant0
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GBS Prevention
screen all pregnant women between 35-37 weeks; administer Pen G/Ampicillin IV at time of delivery if positive
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Most common cause of subacute bacterial endocarditis
Viridans group strep
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Veridans strep micro characteristics
alpha hemolytic, resistant to lysis by bile, optochin resistant
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Viridans group strep typical locations
part of normal flora of mouth and colon; enter blood stream after dental surgery or in patients with cavities/poor dentation
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Streptococcus mutans
Cause of dental caries; synthesizes polysaccharides in dental plaque
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Pathogenesis of viridans strep
no enzymes or exotoxins; can produce glycocalyx allowing for organism to attach to heart valve; can cause brain abscesses, endocarditis, and liver/abdominal abscesses
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Treatment of viridans strep
Penicillin or Ceftriaxone; for endocaridits with intermediate susceptibility to PCN, add Gentamicin
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