Cross - Staph and Strep Flashcards
What are the features of streptococci as a group?
- Spherical gram + cocci arranged in pairs or chains
- Catalase negative
- Type of hemolysis is important distinguishing factor
What are the medically important streps?
- 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)
What does GAS cause?
- 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
How is GAS transmitted?
- 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
What are the 3 mechs of GAS disease?
- Pyogenic inflammation
- Exotoxin production
- Immunologic
What are the 2 anti-phagocytic GAS virulence factors?
-
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
What 5 GAS virulence factor enzymes contribute to inflammation?
- 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
What are streptolysin O and S?
-
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
What are the clinical features of GAS pharyngitis?

- Sore throat, fever
- Inflamed tonsils with pharyngeal exudate
- Nausea/vomiting
- Tender enlarged cervical lymph nodes
- ABSENCE of symptoms of URI
How do you diagnose GAS pharyngitis?
-
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
What is the therapy for GAS pharyngitis?
- 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
What are some of the complications of untreated GAS?
-
Local extension:
1. Otitis media
2. Sinusitis
3. Mastoiditis
4. Meningitis
5. Peritonsillar/retropharyngeal abscess -
Immune mediated:
1. Rheumatic fever
What is this?

- 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)
What is going on here?

- 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
What do you see here?

- Cellulitis: dermis and subcu fat (GAS)
- Same treatment as for GAS pharyngitis
What is this?

GAS necrotizing fasciitis
What is this?

GAS necrotizing fasciitis
How will these patients present? Name some important virulence factors involved in this process.

- 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
Where in the skin does necrotizing fasciitis infect? Why is this important?
-
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
What are the predisposing factors for necrotizing fasciitis? What if there is no clear portal of entry?
- 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
What is the pathogenesis and pathology of necrotizing fasciitis?
-
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
What are the clinical findings in GAS necrotizing fasciitis?
- 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
What gyn problems can GAS cause?
-
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
What is erythrogenic toxin?
- GAS toxin responsible for rash of scarlet fever
- Acts as superantigen






















