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Rheum/Musculoskeletal/Derm Week 3 > Streptococci > Flashcards

Streptococci Flashcards

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1
Q

What is Group A Strep?

A

Mostly Streptococcus pyogenes

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2
Q

What diseases can GAS cause?

A

–Pharyngitis (leading bacterial cause)

–Cellulitis/impetigo/erysipelas

–Necrotizing fasciitis

–TSS

–Scarlet fever

–Puerperal sepsis

–Endometritis

–Rheumatic fever

–Glomerulonephritis

RESPECT PING

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3
Q

How is GAS transmitted?

A

Most strep are part of normal flora (found on skin and oropharynx)

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4
Q

T or F. Strep pyogenes is bacitracin sensitive

A

T.

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5
Q

What are the main virulence determinants of GAS?

A
  • Polysaccharide capsule
  • Hyaluronidase
  • Streptokinase
  • DNase (streptodornase)
  • C5a peptidase
  • Streptococcal chemokine protease
  • Streptolysin O/S
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6
Q

How does the Polysaccharide capsule promote its virulence?

A

It is anti-phagocytic and Abs are not formed against capsule because hyaluronic acid is normal component of body and humans are tolerant to it.

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7
Q

What is the main antigen of human immune response against GAS?

A

M-protein

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8
Q

What does Hyaluronidase do?

A

degrades hyaluronic acid (in subcu tissue);

–known as spreading factor – facilitates spread of GAS in cellulitis/other skin infections

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9
Q

What does streptokinase do?

A

activates plasminogen to form plasmin which dissolves fibrin in clots, thrombi and emboli. Role in GAS infections unclear

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10
Q

What is the effect of DNase (streptodornase)?

A

It degrades DNA in exudates/necrotic tissue. Protect the bacteria from being trapped in neutrophil extracellular traps (NETs).

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11
Q

What is the effect of GAS having C5a peptidase?

A

It cleaves C5a produces by the complement system. Minimizes influx of neutrophils early in infection

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12
Q

What is the effect of Streptococcal chemokine protease?

A

prevents migration of neutrophils into site of infection by degrading chemokine IL-8 which would recruit neutrophils to site

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13
Q

What is the role of SLO?

A

It is cytotoxic and protects GAS from phagocytic killing

•Hemolysin. Oxygen labile. Causes beta hemolysis only when colonies grow under the surface of the blood agar plate.

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14
Q

What is the role of SLS?

A

–More modest effect on virulence.

•Hemolysin. Oxygen stable. Causes beta hemolysis on the surface of the plate

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15
Q

How does this disease present?

A

Pharyngitis presents as inflamed tonsils with pharygneal exudate with systemic symptoms of sore throat, fever, N/V, and enlarged cervical lymph nodes

symptoms of URI absent

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16
Q

How is GAS pharyngitis diagnosed?

A

–Rapid strep antigen test available in 10 minutes

–If rapid antigen test is negative but suspicion is high, do a throat culture

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17
Q

How does the pharygnitis GAS rapid antigen test work?

A

If positive, it causes agglutination of AB bound to latex particles using antigens extracted from a throat swab

highly specific, but low sensitivity

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18
Q

How is GAS treated?

A

•If there is clinical suspicion, do not delay treatment

–Oral Penicillin V 500 mg 2-3 times daily x 10 days

–Amoxicillin 500 mg BID x 10 days

–Cephalexin 500 mg BID x 10 days

If culture is negative, therapy should be discontinued.

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19
Q

How can you treat GAS if the patient is allergic to penicillin?

A

–Azithromycin 500 mg x 1 followed by 250 mg daily on days 2-5

–Clarithromycin 250 mg BID x 10 days

–Clindamycin 600 mg TID x 10 days

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20
Q

What are possible sequelae of untreated GAS?

A
  • Otitis media
  • Sinusitis
  • Mastoiditis
  • Meningitis
  • Peritonsillar/retropharyngeal abscess
  • Rheumatic fever
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21
Q

What is this?

A

Erysipelas- a complication of GAS infection characterized by rapidly spreading erythematous cutaneous swelling that may begin on the face or, less frequently, on the body or an extremity. The rash has a sharp, well-demarcated, serpiginous border and may form a “butterfly” distribution on the face.

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22
Q

What is this?

A

cellulitis- a complication of GAS infection

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23
Q

What is this?

A

Impetigo- a complication of GAS that is characterized by lesions that begin as papules progressing to vesicles then pustules that rapidly break down to form adherent crusts with golden appearance

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24
Q

What is this?

A

GAS necrotizing fasciitis

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25
Q

What M types have been particularly associated with necrotixing fasciitis?

A

Many M types of GAS have been associated with necrotizing fasciitis; types 1 and 3 are most common. These strains can produce one or more of the pyrogenic exotoxins A, B, or C . Necrotizing fasciitis caused by these strains is associated with streptococcal toxic shock syndrome in about 50 percent of cases.

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26
Q

What causes necrotizing fasciitis?

A

This is an infection of deeper tissues that results in progressive destruction of muscle fascia and overlying subcutaneous fat

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27
Q

Why is necrotizing fasciitis hard to diagnose?

A

Infection spreads along muscle fascia due to poor blood supply and initially overlying tissue can appear unaffected – reason it is difficult to diagnose AND reason for PAIN OUT OF PROPORTION TO THE EXAM

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28
Q

In cases with no clear portal of entry, the pathogenesis of infection likely comes from what route?

A

consists of hematogenous translocation of GAS from the throat (asymptomatic or symptomatic pharyngitis) to a site of blunt trauma or muscle strain

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29
Q

Even though necrotizing fasciitis can affect any age group and even healthy people, there are predisposing factors. Name some:

A

skin injury (laceration or burn), blunt trauma, recent surgery, IVDU, childbirth

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30
Q

How does GAS Necrotizing Fasciitis present clinically?

A

It is usually an acute process which progresses rapidly over several days. Initially, the affected area may appear erythematous, swollen, warm, shiny, exquisitely tender

–Process progresses rapidly over several days – skin changes color from red-purple to patches of blue-gray

–Crepitus sometimes felt

–Advanced infection: Fever, tachycardia, systemic toxicity are observed

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31
Q

What is puerperal sepsis?

A

any bacterial infection of the female reproductive tract following childbirth or miscarriage.

Characterized by abdominal pain, hypotension, and fever

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32
Q

What are some exotoxins used by GAS?

A
  • Erythrogenic toxin
  • Pyrogenic (fever inducing) exotoxin A
  • Exotoxin B (extracellular cysteine protease):
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33
Q

What does erythrogenic toxin do?

A

responsible for rash of scarlet fever. Acts as superantigen

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34
Q

What does Pyrogenic (fever inducing) exotoxin A do?

A

•causes most cases of TSS. Superantigen – causes release of large amounts of cytokines.

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35
Q

What does Exotoxin B (extracellular cysteine protease) do?

A

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)

36
Q

Streptococcal TSS

A

•Occurs most often in setting of GAS infection.

–Most common portals of entry: skin, vagina and pharynx

•At site of minor trauma patients develop deep infection within 48-72 hours, many times involving soft tissue of an extremity

–Progression to necrotizing fasciitis in 75%

37
Q

What are the symptoms of Strep TSS?

A
  • Diffuse erythema in 10%
  • Fever, chills, myalgia, n/v/d
  • Hypothermia, hypotension, AMS
38
Q

What are the potential complications of Strep TSS?

A

DIC, AKI, ARDS

39
Q

How is Strep TSS diagnosed?

A

•Diagnosis includes isolation of GAS from normally sterile site (blood, CSF, tissue biopsy) and hypotension plus other organ involvement

40
Q

How is Strep TSS treated?

A

Penicillin plus Clindamycin (for Strep nec fasc as well, plus surgery)

41
Q

Describe Streptococcus agalactiae (GBS)

A

–Narrow zone of beta hemolysis (below)

–Lack of hydrolysis of bile esculin agar

–Hydrolyzes hippurate

–Bacitracin resistant (GAS is bacitracin sensitive)

42
Q

What is a CAMP test?

A

CAMP test: protein is produced that enhances hemolysis on sheep blood agar when combined with beta-hemolysin of S. aureus

43
Q

Virulence of GBS?

A

Organism induces inflammatory response (no toxins/enzymes described). Polysaccharide capsule is antiphagocytic

44
Q

How does GBS infection occur?

A

GBS colonizes genital tract of some women; also found in the colon and infection is commonly acquired in utero or during passage through vagina

45
Q

What are the main risk factors of GBS infection in neonates?

A

PROM in women colonized; also babies born prior to 37 weeks; children whose mothers lack antibodies

46
Q

What diseases can GBS cause?

A

neonatal sepsis, meningitis, PNA

–Adults: important cause of invasive infections such as septic arthritis, cellulitis, osteomyelitis.

47
Q

What are the main risk factors for GBS infection in adults?

A

Diabetes and breast cancer

48
Q

How is GBS diagnosed?

A

Rapid test available in vaginal/rectal samples, detects DNA

49
Q

How is GBS treated?

A

Penicillin/ampicillin (Vanc if allergic)

50
Q

How can neonatal GBS infection be prevented?

A

Screen all pregnant women between 35 and 37 weeks. Administer Pen G/Ampicillin IV at time of delivery if positive.

51
Q

What does Group D Strep include?

A

Includes Enterococcus sp. (enterococcus faecalis/faecium) and nonenterococcal Group D Strep (Strep bovis)

52
Q

What is characteristic of Group D strep on a bile-esculin agar plate?

A

Hydrolyzes esculin in the presence of bile (produces black pigment on bile-esculin agar)

53
Q

Describe enteroccous faecalis/faecium

A

This GDS bug is part of normal colonic flora that can grow in hypertonic saline or in bile (low virulence but does have a capsule and proudces enzymes to injure host tissue and can cause hospital-aquired UTIs, blood stream infections (line-related), intra-abdominal infections and endocarditis

54
Q

How is Enteroccous faecalis/faecium treated?

A

Combo ABX therapy required- PCN/Vanc if susceptible + aminoglycoside

55
Q

VRE is most likely ______. How do you treat?

A

E. faecium (Linezolid or daptomycin)

56
Q

Notes about Strep bovis

A
  • Causes endocarditis in patients with colon cancer. Very strong association.
  • Will not grow in hypertonic saline
57
Q

How is Strep bovis treated?

A

PCN, ceftriaxone, or vanco

58
Q

Describe viridans group strep

A

alpha hemolytic strep that is optochin resistant (distinguishes from strep pyogenes) that is commonly anormal part of mouth and colon flora and commonly enter blood stream after dental surgery or in patients with cavities/poor dentition

includes: sp. anginosis, milleri, intermedius, mutans, and sanguis

59
Q

What is the most common cause of dental caries?

A

Strep mutans (synthesizes polysaccharides in dental plaque)

60
Q

Pathogeneiss of viridans group Strep? Diseases?

A

–no enzymes/exotoxins

  • Can produce glycocalyx allowing for organism to attach to heart valve (Most common cause of sub-acute endocarditis).Strep sanguis produces dextrans, which bind to fibrin-platelet aggregates on damaged heart valves.
  • Brain abscesses, also liver and abdominal abscesses
61
Q

How is viridans group Strep treated?

A
  • Depends on susceptibilities
  • Penicillin or Ceftriaxone
  • For endocarditis with intermediate susceptibility to PCN, add Gent
62
Q

Groups C and G Strep (S. dysgalactiae subspecies equisimilis (SDSE))

A
  • 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 including capsule, superantigen, etc, increasing their virulence
  • Rapid tests do not detect GCS/GGS
63
Q

What is peptostrepococcus?

A
  • Anaerobe
  • Members of normal flora of gut, mouth, female genital tract
  • Commonly found in mixed anaerobic infections/abscesses
64
Q

How is peptostreptococcus treated?

A

Penicillin

65
Q

What kind of bugs can cause this pattern on a BAP?

A

Alpha hemolysis (Viridans and S. pneumo- do Optochin susceptibility to differentiate)

66
Q

What bugs can cause this pattern of rxn to BAP?

A

Beta hemolysis

GAS, GBS, GCS/GGS

67
Q

What bugs produce gamma hemolysis (non-hemolytic)?

A

GDS: S. bovis and Enterococcus sp. (non strains display alpha hemolysis)

68
Q
A

C. Fastest! At the same time, do a throat culture

69
Q
A

B. Probably GAS causing strep pharyngitis (could also be GBS, GCS, and GGS)

70
Q

What toxins mediate B hemolysis?

A

SLS and SLO

71
Q
A

G.

72
Q
A

F.

NOTE: You can still get PSGN even if you get treated for the pharyngitis (most will completely recover)

73
Q
A

If you dont take the whole course, rheumatic fever is at risk

74
Q
A

B. This is scarlet fever

75
Q

Rheumatic fever ONLY comes after what?

A

GAS pharyngitis

76
Q
A

B. This is PSGN

77
Q
A

F. If you have an abscess, it is likely polymicrobial or staph aureus

78
Q

Periorbital petechiae is a very common assoication with endocarditis!

A

Top left: red macular non-painful lesion (Janeway lesion)

Top right: painful nodule- Ossler nodes (caused by immune complex deposition)

Bottom: Splinter hemorrhages

79
Q
A

Colonoscopy, worried about colon cancer

80
Q

Associations with endocarditis

A
81
Q
A

B.

A= VISA

82
Q
A

D. This is GBS

83
Q
A

Strep viridans (most common cause of ACUTE endocarditis= Staph aureus)

84
Q
A

C. At this point it looks like cellulitis, probably TSS from GAS

85
Q
A

Strep is typically worse than Staph!

Rheum/Musculoskeletal/Derm Week 3 (27 decks)

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