Cross - Staph and Strep Flashcards
1
Q
What are the features of streptococci as a group?
A
- Spherical gram + cocci arranged in pairs or chains
- Catalase negative
- Type of hemolysis is important distinguishing factor
2
Q
What are the medically important streps?
A
- Pyogenes (Group A strep): most frequent cause of pharyngitis, commonly causes skin infections
- Agalactiae (Group B strep)
- Enterococcus faecalis/faecium (Group D strep)
- Bovis (Group D strep)
- Viridans
- Peptostreptococcus
- Streptococcus pneumoniae
- Groups C and G strep (Streptococcus dysgalactiae subspecies equisimilis)
3
Q
What does GAS cause?
A
- Pharyngitis: leading bacterial cause
- Cellulitis/impetigo/erysipelas
- Necrotizing fasciitis
- TSS
- Scarlet fever
- Puerperal sepsis: new mom experiences infection related to birth
- Endometritis
- Rheumatic fever
- Glomerulonephritis
4
Q
How is GAS transmitted?
A
- Found in skin and oropharynx in small numbers
- Most strep are part of normal flora
- Immunologic rxn when Ab against a component of the organism cross-reacts with normal tissue or forms immune complexes that damage normal tissue
5
Q
What are the 3 mechs of GAS disease?
A
- Pyogenic inflammation
- Exotoxin production
- Immunologic
6
Q
What are the 2 anti-phagocytic GAS virulence factors?
A
-
M protein: protudes from outer surface of cell and interferes with ingestion by phagocytes
1. At least 200 emm types (gene encoding the M protein -> reason for ability to cause multiple infections) -
Polysaccharide capsule: made of hyaluronic acid
1. Ab not formed against capsule because hyaluronic acid is normal component of body, and humans are tolerant to it
7
Q
What 5 GAS virulence factor enzymes contribute to inflammation?
A
- Hyaluronidase: degrades HA in subcu tissue, and known as spreading factor bc it facilitates spread of GAS in cellulitis/other skin infections
- Streptokinase: activates plasminogen to form plasmin -> dissolves fibrin in clots, thrombi & emboli (role in GAS infections unclear)
- DNase (streptodornase): degrades DNA in exudates/necrotic tissue; protects bacteria from being trapped in neutrophil extracellular traps (to which are bound neutro serine proteases)
- C5a peptidase: cleaves C5a produced by the complement system, and minimizes influx of neutrophils early in infection
- Streptococcal chemokine protease: prevents migration of neutrophils into site of infection by degrading chemokine IL-8 which would recruit neutrophils to site
8
Q
What are streptolysin O and S?
A
-
Streptolysin O: cytotoxic -> protects GAS from phagocytic killing, and enhances bac virulence (esp. strains that are relatively deficient in HA capsule)
1. Oxygen labile hemolysisin -> causes beta hemolysis only when colonies grow under the surface of the blood agar plate -
Streptolysin S: more modest effect on virulence, so not antigenic/immunogenic (no Ab formed against it)
1. Oxygen stable hemolysin -> causes beta hemolysis on the surface of the plate
9
Q
What are the clinical features of GAS pharyngitis?
A
- Sore throat, fever
- Inflamed tonsils with pharyngeal exudate
- Nausea/vomiting
- Tender enlarged cervical lymph nodes
- ABSENCE of symptoms of URI
10
Q
How do you diagnose GAS pharyngitis?
A
-
Rapid strep antigen test available in 10 minutes
1. High specificity, low sensitivity - Detects bacterial antigen in throat swab specimen
1. Ags are extracted from throat swab and are reacted with antibody bound to latex particles
2. Agglutination of latex particles occurs if GAS is present - If rapid antigen test is negative but suspicion is high, do a throat culture
11
Q
What is the therapy for GAS pharyngitis?
A
- If there is clinical suspicion, do not delay tx:
1. Oral Penicillin V 500 mg 2-3x/day x 10 days
2. Amoxicillin 500 mg BID x 10 days
3. Cephalexin 500 mg BID x 10 days -
Pen allergic: macrolide of clindamycin
1. Azithromycin 500 mg x 1 followed by 250 mg daily on days 2-5
2. Clarithromycin 250 mg BID x 10 days
3. Clindamycin 600 mg TID x 10 days - If culture is (-), therapy should be discontinued
12
Q
What are some of the complications of untreated GAS?
A
-
Local extension:
1. Otitis media
2. Sinusitis
3. Mastoiditis
4. Meningitis
5. Peritonsillar/retropharyngeal abscess -
Immune mediated:
1. Rheumatic fever
13
Q
What is this?
A
- Erysipelas: rapidly spreading erythematous cutaneous swelling that may begin on the face or, less frequently, on the body or an extremity (GAS)
- Rash has sharp, well-demarcated, serpiginous border and may form a “butterfly” distribution on the face
- Involvement of upper dermis and superficial lymphatics
- Same treatment as for GAS pharyngitis
- Remember: case in class that presented kind of differently (AAM w/swelling, little redness)
14
Q
What is going on here?
A
- Impetigo: lesions begin as papules progressing to vesicles, then pustules that rapidly break down to form adherent crusts with golden appearance (GAS)
- Same treatment as for GAS pharyngitis
15
Q
What do you see here?
A
- Cellulitis: dermis and subcu fat (GAS)
- Same treatment as for GAS pharyngitis
16
Q
What is this?
A
GAS necrotizing fasciitis
17
Q
What is this?
A
GAS necrotizing fasciitis
18
Q
How will these patients present? Name some important virulence factors involved in this process.
A
- GAS necrotizing fasciitis
- Clinical features: pain out of proportion to exam
-
Micro: no neutrophils, but 1 gm muscle will grow 109 organisms
1. M protein: filamentous protein anchored to cell mem w/antiphagocytic properties (types 1 and 3 most common)
2. Can also produce one or more pyrogenic exotoxins A, B, or C -> necrotizing fasciitis caused by these strains assoc w/streptococcal toxic shock syndrome in 50% of cases
19
Q
Where in the skin does necrotizing fasciitis infect? Why is this important?
A
-
DEEPER TISSUES
1. Progressive destruction of muscle fascia and overlying subcutaneous fat
2. Infection spreads along muscle fascia due to poor blood supply
3. Initially overlying tissue can appear unaffected –> reason it is difficult to diagnose AND reason for PAIN OUT OF PROPORTION TO THE EXAM
20
Q
What are the predisposing factors for necrotizing fasciitis? What if there is no clear portal of entry?
A
- Skin injury (laceration or burn)
- Blunt trauma
- Recent surgery
- IVDU
- Childbirth
- Occurs in healthy people, any age group
- NOTE: in cases with no clear portal of entry, the pathogenesis of infection is likely hematogenous translocation of GAS from the throat (asymptomatic or symptomatic pharyngitis) to a site of blunt trauma or muscle strain
21
Q
What is the pathogenesis and pathology of necrotizing fasciitis?
A
-
Pathogenesis: different M protein types assoc with nec fasc -> 1 and 3 are most common
1. These strains produces one or more of the pyrogenic exotoxins A, B, or C -
Pathology: paucity of neutrophils at the tissue site of streptococcal infection due to degradation of IL-8 by streptococcal trypsinlike (chemokine) protease, SpyCEP/ScpC
1. 1 gm of muscle will grow 109 organisms
22
Q
What are the clinical findings in GAS necrotizing fasciitis?
A
- SURGICAL EMERGENCY
- Usually acute process which progresses rapidly over several days: diagnosis is clinical
1. Affected area initially appears erythematous, swollen, warm, shiny, exquisitely tender
2. Progresses rapidly over several days – skin changes color from red-purple to patches of blue-gray
3. Crepitus sometimes felt
4. Advanced infection: fever, tachycardia, systemic toxicity are observed - Associated with Strep TSS in about 50% of cases
23
Q
What gyn problems can GAS cause?
A
-
Puerperal sepsis (new mom infection related to birth) and endometritis (endometrial inflammation):
1. Abdominal pain, hypotension, fever
2. 220 cases annually in the US
3. 3.5% case fatality rate
24
Q
What is erythrogenic toxin?
A
- GAS toxin responsible for rash of scarlet fever
- Acts as superantigen
25
Q
What are exotoxin A and B?
A
- GAS toxins (strep pyogenes)
- Pyrogenic (fever inducing) exotoxin A: causes most cases of TSS -> superantigen that causes release of large amounts of CYTOKINES
- Exotoxin B (EC cysteine protease): PROTEASE that rapidly destroys tissue and is produced in large amounts by the “flesh-eating” strains of GAS that cause necrotizing fasciitis (exotoxin A and C as well)
26
Q
What is streptococcal TSS? Cx? Dx? Tx?
A
- Occurs most often in setting of GAS infection; most comm portals of entry: skin, vagina, pharynx
- At site of minor trauma pts devo deep infection in 48-72 hrs, many times involving soft tissue extremity
1. Progression to necrotizing fasciitis in 75% - Diffuse erythema in 10%
- Fever, chills, myalgia, n/v/d, hypothermia, hypoTN
1. Can tell this from S. aureus if REALLY BAD SYMPTOMS
2. Can tell this from nec fasc bc nec fasc would not be mildly tender (pain out of proportion) - Complications: DIC, AKI, ARDS
- Diagnosis: isolation of GAS from normally sterile site (blood, CSF, tissue biopsy) and hypotension plus other organ involvement
-
Treatment: Penicillin + Clindamycin (for Strep nec fasc as well, plus surgery)
1. Clindamycin and Linezolid inhibit toxin production
27
Q
What is this?
A
- Scarlet fever: GAS
- Children affected: most commonly ages 3-15
- Erythrogenic toxin
-
Clinical: sore throat w/devo soon thereafter of diffuse erythema on head and neck -> rash spreads rapidly to involve the trunk
1. Skin feels sand-papery (small papules that feel rough when touched)
2. Rash desquamates after several days
3. STRAWBERRY TONGUE
4. Usually in association with, and considered a complication of, pharyngitis
28
Q
What is post-strep glomerulonephritis?
A
- PSGN: caused by nephritogenic strains of GAS
- May be more freq after skin inf. than pharyngitis
1. Latent period b/t GAS and PSGN dependent on site of infection: 1-3 wks post-pharyngitis and 3-6 wks post-skin infection - Ag-ab complexes on glomerular BM
- HTN, facial edema, lower extremity edema, dark urine (RBCs), but many cases are subclinical -> most pts recover completely
- Unclear if early tx of infection can prevent PSGN
- 97% of cases occur in regions of world w/poor SES
29
Q
What is acute rheumatic fever? Dx? Tx?
A
- 2 weeks after untreated GAS pharyngitis (or scarlet fever) -> caused by rheumatogenic strain
1. Abs against GAS proteins cross-react w/host Ags -> probably anti-streptococcal M protein Abs, T cells that cross-react w/cardiac proteins - DIAGNOSIS: Jones Criteria, anti-streptolysin-O (ASO) titer (immunogenic, so Abs formed against it)
1. Remember: streptolysin S is not antigenic, immunogenic -> no Ab formed against it - TREATMENT: even though GAS infection was wks earlier, full course of AB therapy recommended to eradicate any residual GAS, then ->
1. Prevent strep infections with prophylaxis in pts w/hx of RF (PCN IM monthly x many yrs)
30
Q
What are the Jones Criteria for diagnosis of acute rheumatic fever?
A
- Joints: polyarthritis -> affects several joints in quick succession
- Carditis: pancarditis, aortic/mitral valves affected
- Nodules (subcutaneous): firm, painless lesions up to 2 cm in size
- Erythema marginatum: evanescent, pink rash involving trunk most often
- Sydenham chorea: neurologic disorder consisting of abrupt involuntary movements
31
Q
What is the micro for strep agalactiae (GBS)?
A
- Narrow zone of beta hemolysis
- Lack of hydrolysis of bile esculin agar (GDS does hydrolyze bile esculin agar)
- Hydrolyzes hippurate
- Bacitracin resistant (GAS is bacitracin sensitive)
- CAMP test: protein produced that enhances hemolysis on sheep blood agar when combined with beta-hemolysin of S. aureus (see attached) -> note arrowhead formed where they meet
- Induces inflammatory response, but no toxins, enzymes described
- Polysaccharide capsule antiphagocytic
32
Q
What are the clinical presentations and risk factors for strep agalactiae (GBS)?
A
- Colonizes genital tract of some women; also found in the colon
1. Infection acquired in utero or during passage through vagina - Main risk factor: premature rupture of membranes (PROM) in women colonized; babies born prior to 37 weeks; children whose mothers lack antibodies
- Causes neonatal sepsis, meningitis, PNA
- Adults: important cause of invasive infections like septic arthritis, cellulitis, osteomyelitis -> diabetes main predisposing factor, also breast cancer
33
Q
How do you dx, tx, and prevent GBS?
A
-
Diagnosis: gram stain/culture
1. Rapid test available in vaginal/rectal samples that detects DNA - Treatment: penicillin/ampicillin (Vanc if allergic)
-
Prevention: screen all pregnant women between 35 and 37 weeks
1. Administer Pen G/Ampicillin IV at time of delivery if positive
34
Q
Enterococcus faecalis/faecium (GDS)
A
-
Hydrolyzes esculin in presence of bile (produce black pigment on bile-esculin agar -> image)
1. Can also grow in hypertonic saline -
Low-virulence, but does have capsule, & produces enzymes to injure host tissue
1. Part of normal colonic flora - CAUSES: hospital-acquired UTIs, blood stream infections (many times line-related), endocarditis, and intra-abdominal infections
- Combo AB tx required: PCN/Vanc (depending on susceptibility) and aminoglycoside
1. Vancomycin Resistant Enterococcus (VRE): more likely E. faecium -> Linezolid or Daptomycin used to tx in these infections
a. Mechanism of resistance: genes encode enzymes that substitute D-lactate for D-alanine in peptidoglycan - Mostly non-hemolytic
35
Q
Strep bovis (GDS)
A
- Hydrolyzes esculin in presence of bile (produce black pigment on bile-esculin agar -> image)
- Causes endocarditis in pts w/colon cancer; very strong association
1. DO A COLONOSCOPY on these people - Will NOT grow in hypertonic saline (unlike enterococcus)
- Treatment: PCN, Ceftriaxone, or Vancomycin
- Mostly non-hemolytic
36
Q
Viridans group strep
A
- Alpha hemolytic, and resistant to lysis by bile and optochin-resistant (distinguishing from S. pneumo)
1. Includes sp anginosus, milleri, intermedius, mutans, sanguis - Normal flora of mouth, colon; enter blood stream after dental sx or in pts w/cavities/poor dentition
- Streptococcus mutans: cause of dental caries bc it synthesizes polysaccharides in dental plaque
- Pathogenesis: no enzymes/exotoxins
1. Can produce glycocalyx allowing for organism to attach to heart valve
2. Brain abscesses, also liver and abdominal abscesses -> most common cause of subacute endocarditis (acute endocarditis: S. aureus) - Treatment: depends on susceptibilities
1. Penicillin or Ceftriaxone
2. Endocarditis w/intermediate susceptibility to PCN -> add Gentamycin
37
Q
Groups C/G Strep
A
- S. dysgalactiae subspecies equisimilis (SDSE)
- Normal commensal flora of the upper airway, frequent asymptomatic colonizers of skin, GI tract, female genital tract
- Emerging causes of human infections, including invasive infections and toxic shock (also skin/soft tissue infections, pharyngitis, bacteremia, meningitis, puerperal infections, etc.)
- Recently acquired virulence factors from GAS, incl. capsule, superantigen, etc -> INC virulence
- Rapid tests do not detect GCS/GGS
38
Q
Peptostreptococcus
A
- Anaerobe
- Members of normal flora of gut, mouth, female genital tract
- Commonly found in mixed anaerobic infections, abscesses -> brain, abdomen, pelvic abscesses
- Treatment: penicillin
39
Q
What is this? Bugs?
A
- ALPHA HEMOLYSIS
- Strep pneumo
- Strep viridans
40
Q
What is this? Bugs?
A
- BETA HEMOLYSIS: clear zone around colonies due to complete lysis of RBCs
- Strep pyogenes
- Strep agalactiae
- GCS/GGS
41
Q
What is this? Bugs?
A
- GAMMA HEMOLYSIS
- S. bovis and Enterococcus sp (GDS)
1. Most non, but some strains display alpha- hemolysis
42
Q
Kid comes in with what looks like strep pharyngitis. What do you do to dx?
A
- Rapid antigen test and culture at the same time
43
Q
What are the anti-phagocytic virulence factors of GAS?
A
Protein M and Polysaccharide
44
Q
What are the possible complications of untreated GAS pharyngitis? How can they be prevented?
A
-
Retropharyngeal abscess, mastoiditis, rheumatic fever (treat it to prevent this)
1. Note - rheumatic fever ONLY follows pharyngitis - PSGN not included in this list because it is very unclear if treatment prevent glomerulonephritis
-
TREATMENT: oral PCN V (10d), Amoxicillin, or Cephalexin
1. PCN Allergy: Azithromycin (2-5d), Clarithromycin, Clindamycin
45
Q
What strep toxin is implicated in scarlet fever?
A
Erythrogenic toxin
46
Q
If you see a stress abscess, what strain should you be thinking about?
A
Think multiple bugs (abscess from dental sx example: viridans and poststreptococcus)
47
Q
What is coagulase (-) staph?
A
- Typically, staph epi
- S. aureus is distinguished from other staph forms by beta hemolysis and coagulase (+)
48
Q
What is the reason for the beta-hemolytic nature of S. aureus?
A
Staphyloxanthin
49
Q
How does arthritis affect your risk of staph infection?
A
- Predisposes you to bacterial seeding
50
Q
Staphylococci: 3 key features
A
- Non-motile
- Do NOT produce spores
- Produce catalase (degrade hydrogen peroxide)
- 30 species of staph total
51
Q
What 3 species of staph are important human pathogens?
A
-
Aureus: normal flora; most important
1. Causes diseases by producing toxins and by inducing pyogenic inflammation
2. Abscesses, septic arthritis, endocarditis, food poisoning, scalded skin syndrome, TSS
3. Hospital-acquired PNA, septicemia, surgical wound infections
4. Folliculitis, impetigo, bacterial conjunctivitis -
Epidermidis: predominant organism of the skin
1. Endocarditis, prosthetic joint/hardware infections - Saprophyticus: predominantly causes UTIs
52
Q
What are normal flora? What does it mean to be a carrier?
A
- Normal flora are all over us -> internal organs are usually sterile
-
Carrier state: individual harbors potential pathogen and can be source of infection to others
1. Typically used for those who have recently recovered from a disease but continue to carry the organism, or who have asymptomatic infection
53
Q
What are colonization and colonization resistance?
A
- Colonization: acquisition of a new organism, and may cause infection or may be eliminated by host defenses
- Colonization resistance: non-pathogenic, resistant bacteria occupy attachment sites on skin and mucosa, interfering with colonization by pathogenic bacteria
54
Q
Staph aureus identifying characteristics
A
- G+ cocci in clusters; catalase/coagulase +
1. Coagulase causes rabbit plasma to clot - Catalase: virulence factor that degrades H2O2 to O2 and H2O so S. aureus can survive killing effect of H2O2 in polys
- Beta hemolysis on blood agar; ferments mannitol
- Vast majority of strains produce beta-lactamase, the enzyme that degrades many penicillins
-
MRSA: strains resistant to beta-lactamase-resistant penicillins (methicillin) by changes in PBP (pencillin-binding protein) in cell mem
1. MecA genes on bacterial chromosome encode altered PBPs
2. Currently >50% of S. aureus strains isolated from hospital patients in US
55
Q
How is S. aureus transmitted?
A
-
Nose is main site of colonization -> 30% of people colonized at any given time
1. Chronic carriers have INC risk of skin infection - Skin is also a common site: hand contact important mode of transmission
- Found in vagina of 5% of women
- Common cause of outbreaks in childcare centers, IVDUs, prisons, and sports teams (e.g., wrestlers)
56
Q
What are the keys to S. aureus pathogenesis?
A
- Produces toxins and induces pyogenic inflammation
57
Q
List the 10 staph virulence factors we need to know.
A
- Staphyloxanthin: causes golden color to colonies
- Coagulase: causes plasma to clot
- Hemolysins: hemolyze RBCs
- Protein A: prevents complement activation
- Teichoic acids: adherence to mucosal cells
- Polysaccharide capsule: resists phagocytosis
- Alpha toxin/hemolysin: necrosis of skin, hemolysis
- PVL: leukocyte destruction
- Leukotoxin: lyses phagos/RBCs
58
Q
What is staphyloxanthin?
A
- S. aureus toxin
- Causes golden color to colonies
- Enhances pathogenicity by inactivating microbial effect of superoxides and other ROS in neutros
59
Q
What is coagulase?
A
- S. aureus toxin
- Causes plasma to clot by activating prothrombin to form thrombin, which catalyzes activation of fibrinogen to form fibrin clot
- Serves to wall off infected site, delaying migration of neutrophils to the site
60
Q
What are hemolysins?
A
- S. aureus toxins
- Hemolyze RBCs, and use iron, which is required for bacteria to grow
61
Q
What is Protein A?
A
- S. aureus virulence factor
- Major protein in cell wall
- Binds to Fc portion of IgG at complement binding site and prevents complement activation
- No C3b produced, so phagocytosis or orgs is greatly reduced
62
Q
What are teichoic acids?
A
- S. aureus virulence factors
- Mediate adherence of staph to mucosal cells
- Lipoteichoic acid induces IL-1 and TNF from macros
63
Q
What is the role of the polysaccharide capsule in S. aureus?
A
- Virulence factor
- 11 serotypes; 5 and 8 most commonly cause infection
- Capsule allows bacteria to attach to artificial materials and resist host cell phagocytosis
64
Q
What is peptidoglycan (in the context of S. aureus)?
A
- Virulence factor
- Endotoxin-like properties -> reason for septic shock w/o endotoxin
- Stimulates macros to produce cytokines, activates complement/coagulation cascades
65
Q
What is alpha toxin/hemolysin?
A
- S. aureus virulence factor
- Membrane-damaging, hemolytic toxin
- Forms holes in host cells
- Causes necrosis of skin and hemolysis
66
Q
What is Panton Valentine (P-V) Leukocidin? How does S. aureus aquire it?
A
- S. aureus virulence factor
- Membrane-damaging hemolytic toxin
- Pore-forming cytotoxin that causes leukocyte destruction by damaging cell membranes and causes tissue necrosis
- Cell content leak out of a pore the toxin forms
- Causes severe skin/soft tissue infections as well as severe necrotizing pneumonia
- Produced by MRSA strains, typically community-acquired
-
Emergence: MSSA strain infected and lysogenized by a phage (phiSLT) that harbors lukS-PV and lukF-PV genes, encoding PVL
1. Then, Methicillin resistance cassette (SCCmec IV, V or VT) carrying mecA gene is horizontally transferred into the pvl-positive MSSA strain and integrates into the genome in a location that is distinct from that of the phiSLT integration site
67
Q
What is gamma-toxin/leukotoxin?
A
- S. aureus virulence factor
- Membrane-damaging hemolytic toxin
- Lyses phagocytes/RBCs
68
Q
What is this? What causes it?
A
- S. aureus furuncle (“boil”): infection of hair follicle
- Purulent material extends through dermis into subcu tissue, and abscess forms
69
Q
What is this? What causes it?
A
- S. aureus carbuncle: coalescence of several inflamed follicles
70
Q
What is this? What causes it?
A
- S. aureus paronychia
71
Q
What is this? What causes it?
A
- S. aureus folliculitis: superficial infection of hair follicles with purulent material in epidermis
72
Q
What is this? What causes it?
A
- S. aureus cellulitis: infection of soft tissue that involves deeper dermis and subcu fat
- Can distinguish from Strep cellulitis by devo of micro-abscesses shown in the attached image (this doesn’t always work, but helps)
73
Q
What is this? What causes it?
A
- S. aureus hordoleum: eyelid abscess
74
Q
What is this? What causes it?
A
- S. aureus blephartis: eyelid inflammation that may arise from eyelash follicle or tear gland clogging
75
Q
What is this? What causes it?
A
- S. aureus conjunctivitis: inflammation or infection of outer membrane of eyeball and inner eyelid
76
Q
What 8 pyogenic infections are caused by S. aureus?
A
- Endocarditis
- Septic arthritis
- Osteomyelitis
- Post-surgical wound infections
- Pneumonia: can lead to empyema, abscess
- Sepsis
- Mastitis
- Abscesses: both from local inoculation, and as a result of blood stream infection
77
Q
What is this? What is the pathogenesis/clinical presentation?
A
-
S. aureus scalded skin syndrome: toxin mediated; exfoliatin toxins A and B
1. Act as proteases that cleave desmoglein in desmosomes -> separation of epidermis at the granular cell layer -
Clinical presentation: very common in newborns, typically 3-7 days of age
1. Febrile, irritable, diffuse blanching erythema with blisters/bullae appearing 1-2 days later (flexural areas, buttocks, hands feet)
2. Serous fluid exudates, dehydration, electrolyte imbalance
3. Flaky desquamation/sloughing occurs as lesions heal
4. Mucous membranes NOT involved
5. Recovery in 10 days - Cleavage plane intraepidermal, so no scars
78
Q
S. aureus food poisoning pathogen/clinical pres
A
- Toxin-mediated
-
Enterotoxin (A): causes prominent vomiting and watery, non-bloody diarrhea -> acts as superantigen in GI tract, stimulating IL-1 and IL-2 from macros and helper T cells
1. Vomiting caused by cytokines that stimulate enteric nervous system to activate vomiting center in the brain
2. HEAT-RESISTANT, so NOT inactivated by brief cooking
3. Resistant to stomach acid/enzymes
4. Incubation period 1-8 hours
79
Q
What is this?
A
- S. aureus bullous impetigo: caused by EXFOLIATIVE toxin; localized at site of infection
- Form of impetigo seen in young children
- Vesicles enlarge to form flaccid bullae with clear yellow fluid -> later becomes darker, more turbid
- Ruptured bullae leave a thin brown crust
- TRUNK more frequently affected
- Chlorhexidine baths and intranasal mupirocin
80
Q
Staph toxic shock syndrome (TSS) pathogenesis
A
- Toxin mediated/superantigen
- CAUSES: tampons (pelvic exam clicker question), nasal packing to stop bleeds, post-op infections, other infections (septic joints, etc)
1. Not as obvious an infection as from Strep - Produced locally in the vagina, nose, or post-op wounds, then enters blood stream, causing toxemia
1. Stimulates release of large amounts of cytokines: IL-1, IL-2, and TNF
2. 5-25% isolates of S. aureus carry TSST gene
3. TSS occurs when people don’t have Ab against TSST - Blood cultures commonly negative: isolation of S. aureus not required for dx (SA recovered from wound/mucosal sites in 80-90% of pts, but blood cultures in only about 5% of cases)
- Treat with Clindamycin -> gets the toxin
1. Vasopressors: can constrict the vessels (loss of leg in the case in class -> DIC + hypotension)
81
Q
What are the signs and symptoms of Staph TSS?
A
- Fever
- Hypotension, dizziness/syncope
- Diffuse macular erythroderma that desquamates 1-2 weeks after onset
- Vomiting/diarrhea
- Severe myalgias with CPK elevation
- Renal failure
- Transaminitis or hyperbilirubinemia
- Thrombocytopenia
- Half of current cases non-menstrual
82
Q
How is MSSA treated?
A
- Most resistant to PCN bc produces beta-lactamase
- Nafcillin/oxacillin
- Some cephalosporins: Cefazolin, Ceftriaxone, Cefepime, Ceftaroline
- Vancomycin
- Augmentin for mild infections
83
Q
How is MRSA treated? VISA/VRSA?
A
-
MRSA: Vancomycin
1. Daptomycin
2. Linezolid
3. Ceftaroline (5th gen)
4. Bactrim/Clinda/Doxycycline (if susceptible) for mild infections - VISA/VRSA: Dapto, Linezolid, Ceftaroline
84
Q
How are MRSA, VRSA, and VISA resistant?
A
- MRSA: changes in PBP in cell membranes -> mecA genes on bacterial chromosome encode the altered PBPs
- VRSA: genes encode enzymes that substitute D-lactate for D-alanine in the peptidoglycan.
- VISA: synthesis of unusually thickened cell wall
85
Q
What is the D test?
A
- Used to evaluate for inducible Clindamycin resistance (macrolide-resistant subpop of bacteria):
1. Agar plate inoculated with bac and 2 drug-impregnated disks (one w/erythromycin, one with clinda) are placed 2 cm apart on the plate
2. If area of inhibition around clinda disk is “D” shaped, test result is (+), indicating inducible resistance – clinda should NOT be used (see attached image)
3. If area is circular, test is (-) – can use Clinda - Necessary bc some bac express MLSB phenotype, in which susceptibility tests will indicate the bacteria are susceptible to clindamycin, but in vitro the pathogen displays inducible resistance
86
Q
What is the treatment for TSS?
A
-
Supportive: extensive fluid replacement (10-20L/d)
1. Vasopressors (dopamine, norepinephrine): b/c of intractable HOTN, diffuse capillary leak - Surgical: look for/remove tampons in the vaginal canal -> if patient is post-surgical, surgical wounds must be explored and debrided
-
Antibiotics: Vanc/Oxacillin (MRSA/MSSA) PLUS Clindamycin
1. Clinda suppresses protein synthesis, i.e., toxin synthesis; o/ABs may suppress toxin synthesis too, most notably Linezolid
87
Q
What are vasopressors?
A
A powerful class of drugs that induce vasoconstriction, and elevate mean arterial pressure (MAP)
88
Q
How can we prevent S. aureus?
A
- For surgeries: peri-operative Cefazolin +/- Vanc depending on rate of MRSA in that area
- Intranasal mupirocin to reduce colonization + Hibiclens (chlorhexidine gluconate) for bathing +/- antibiotics (Doxy, Bactrim)
1. Usually done for 1 week
89
Q
S. epidermidis defining tests
A
- G (+) cocci in clusters
- Catalase positive and coagulase negative
- Non-hemolytic
- Urease (+): enzyme that catalyzes hydrolysis of urea into carbon dioxide and ammonia (see attached image)
- Does not ferment mannitol (unlike S. aureus)
- Novobiocin sensitive (distiniguishing it from S. saprophyticus)
- Part of normal flora of skin & mucous membranes
90
Q
What are S. epi biofilms? Pathogenesis?
A
- Most S. epi infections in setting of foreign devices
1. Most likely prosthetic materials inoculated with small # of staph at time of implant
2. IV catheters, prosthetic heart valves/joints - General mechanism of virulence is BIOFILM
-
Pathogenesis: bacterial adherence initial step
1. Once in body, foreign materials coated with host proteins –> fibrinogen, fibronectin, etc., potential receptors for Staph surface proteins
2. Surface adhesins critical for interacting with host proteins, and mediating more specific adherence
3. After attachment: EC polysaccharide matrix or slime encases the bacteria -> barrier to AB penetration; may interfere with host defenses
91
Q
What is the tx for S. epidermidis?
A
- Drugs of choice:
1. Vancomycin: assume MRSE; if MSSE, can use oxacillin/nafcillin
a. Main AE w/Vanc is renal failure (can substitute Linezolid or Daptomycin)
2. Rifampin or Gent (lots of resistance -> limit use) can be added and should be added for prosthetic valve endocarditis
3. Remove the device if possible - MRSE same mech of resistance as MRSA (mecA gene producing altered PBP)
- Very commonly causes contaminated blood cultures (REMEMBER: clicker question from class where S. epi was a contaminant and did not need to be treated -> does NOT typically cause cellulitis)
92
Q
S. saprophyticus defining tests
A
- Catalase (+) and coagulase (-); non-hemolytic
- Urease (+): see attached image
- Does NOT ferment mannitol (unlike S. aureus)
- Novobiocin resistant (unlike S. epidermidis)
93
Q
What does S. saprophyticus cause? Tx?
A
- 2nd most common cause of community-acquired UTIs in women
1. Most have had sex in the previous 24 hours - Treatment: Bactrim or Cipro
94
Q
S. aureus microbiologic properties
A
- Catalase (+), coag (-), beta hemolytic, ferments mannitol
- Importance of catalase as a virulence factor: H2O2 microbicidal, and its degradation limits neutrophils’ ability to kill
- Coagulase test done with rabbit plasma
95
Q
S. epidermidis microbiological properties
A
- Catalase (+), coag (-), non-hemolytic, urease (+), does NOT ferment mannitol, novobiocin sensitive
- Importance of catalase as a virulence factor: H2O2 microbicidal, and its degradation limits neutrophils’ ability to kill
- Coagulase test done with rabbit plasma
96
Q
S. saprophyticus microbiological properties
A
- Catalase (+), coag (-), non-hemolytic, urease (+), does NOT ferment mannitol, novobiocin resistant
- Importance of catalase as a virulence factor: H2O2 microbicidal, and its degradation limits neutrophils’ ability to kill
- Coagulase test done with rabbit plasma
