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HDID 2 > 37. Streptococcus > Flashcards

37. Streptococcus Flashcards

1
Q

streptococci are what type of bacteria under microscope?

A

gram+ cocci in pairs and chains

catalase -

classified by hemolysis and serological then biochemical (or now genetic)

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2
Q

alpha hemolysis

A

partial hemolysis : green discoloration

vidirans streptococci

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3
Q

beta hemolysis:

A

complete hemolysis (clear zone around colony)

B-hemolytic streptococci

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4
Q

gamma hemolysis:

A

no hemolysis

vidirans streptococci

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5
Q

what is the only clincally important GAS?

A

strep. pyogenes

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6
Q

suppurative vs non-suppurative? (re: GAS)

A

suppurative: pharyngitis and skin infections (pus)

non-suppurative: rheumatic fever and rheumatic heart disease, acute glomerulonephritis (no pus)

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7
Q

M protein?

A

GAS virulence factor: strongly atiphagocytic, binds serum proteins (like factor H) that inhibit activation of alternative complement components - evades immune system!

but elicits opsonic Abs

> 100 types conferring specific immunity (opsonic abs directed at distal epitopes so can get sick multiple times)

adhesive: binds to numerous serum proteins and CD46 on keratinocytes

certain types can generate Abs that react w/cardiac myosin and sarcolemma

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8
Q

somatic virulence factors of GAS?

A

capsule (hyaluronic acid looks like us and is thus antiphagocytic)

surface adhesins:

  • lipoteichoic acid (binds host cells)
  • M protein (binds keratinocytes)
  • Protein F (binds fibronectin and mucosal cells)
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9
Q

toxins from GAS?

A

hemolysins:

  • streptolysin O (Abs to this suggests previous infection)
  • streptolysin S

streptococcal Pyrogenic Exotoxins (Spe)

  • SpeA, SpeC
  • encoded by bacteriophages
  • superantigens (cause release of CYTOKINES)
  • responsible for characteristic features of SCARLET FEVER and STREPTOCOCCAL TOXIC SHOCK SYNDROME
  • HLA dependent response (not everyone reacts in same way)
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10
Q

GAS enzymes?

A

play a role in rapid spread through tissues

DNAses

Hyaluronidase

Streptokinase (degrades fibrin, used as a Rx)

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11
Q

GAS avoidance of innate immune response?

A

C5a peptidase (disrupts C’ chemoattractant)

SpeB (cleaves IgG)

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12
Q

GAS epidemiology?

A
  • Humans are only host
  • transient colonization of oropharynx/skin normal
  • transmitted person-person via oral secretions or contact w/skin lesions

Non-Suppurative: (primarily pediatric in poor countries)

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13
Q

GAS respiratory tract suppurative disease?

A

pharyngitis
(complication = scarlet fever thanks to SpeA and SpeC)
- kids 5-15, fever, no cough, purulent exudate, cervical lymphadenopathy

pneumonia (rare)

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14
Q

GAS skin suppurative disease?

A

impetigo (pyoderma)

erysipelas

necrotizing fasciitis (streptococcal gangrene)

streptococcal toxic shock syndrome

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15
Q

pharyngitis diagnosis?

A

rapid antigen tests:

  • convenient
  • good specificity
  • negative requires culture

culture:

  • gold standard
  • takes longer (call outpatient pt if cx is positive and give Abx)
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16
Q

pharyngitis treatment?

A
  • in order to prevent non-suppurative complications
  • PCN
  • macrolides or clindamycin for pcn allergies (clindamycin does GP and anaerobes so good rx for oropharyngeal stuff)
17
Q

scarlet fever (scarlatina)

A

uncommon manifestation of acute infection (usu pharyngitis)

manifestation of SpeA or SpeC

rash begins on trunk

capillary gragility (accentuated in skin folds, petechiae elicited w/blood pressure cuff), subsequent desquamation

18
Q

impetigo (pyoderma)

A

superficial skin infection

characteristic “honey colored” crusting from serum exudate

dx clinically or by culture

can treat topically (bacitrain, mupirocin)

systemic for more extensive disease (culture, presumptive therapy w/emoxicillin-clavulanic acid or cephalexin)

19
Q

erysipelas?

A

form of cellulitis

highly characteristic of B-hemolytic streptococcus

bright erythema

edema

sharp raised edges

regional lymphadenopathy

systemic sxs

20
Q

cellulitis w/lymphangitis?

A

s.pyogenes has peculiar relationship w/lymphatics

cellulitis often complicated by lymphangitis

those w/damaged lymphatics predisposed to recurrent strep cellulitis

21
Q

necrotizing fasciitis

A

life threatening deep infection (cuts b/w fascial planes)

clinical clues:

  • pain out of proportion for clinical findings
  • septic shock assoc w/cellullitis
  • hemorrhagic bullae
22
Q

streptococcal toxic shock syndrome

A

features:

  • occurs in context of S.pyogenes infection (skin)
  • fever
  • hypotension, shock
  • multiple organ syndrome dysfunction
  • rash (generalized, macular, may desquamate)

pathogenesis:

  • pyogenic exotoxins, esp SpeC (superantigen)
  • assoc w/certain HLA alleles
  • massive release of pro-inflammatory cytokines
23
Q

pathogenesis of streptococcus pyogenes nonsuppurative infections?

A

rheumatic fever & heart disease:

  • molecular mimicry (specific M proteins have epitopes shared w/cardiac antigens)
  • infiltration of T lymphocytes into heart tissue, inflammatory cytokines, cardiac valve lesions
  • assoc w/HLA-DR alleles
  • after pharyngitis only

Acute glomerulonephritis:

  • deposition of immune complexes in kidney
  • activation of enzymes that damage glomerular basement membrane, with protein loss and decreased renal function
24
Q

clinical syndrome of acute rheumatic fever?

A 
major criteria (2 or 1 plus 2 minor)
- polyarthritis, carditis, chorea, erythema marginatum, subQ nodules

minor criteria:
-arthralgia, fever, elevated CRP or ESR, 1st degree heart block

evidence of recent infection: culture, antigen or serology (anti-streptolysin O)

recurrent attacks lead to rheumatic heart disease (irreversible damage to heart valves)

25
Q

therapy for acute rheumatic fever?

A

symptomatic w/asa or corticosteroids

primary preventio: tx of pharyngitis

secondary prevention: benzathine PCN G or oral pcn daily

26
Q

post-streptococcal glomerulonephritis

A

incubation period 1-2 weeks after pharyngitis, 2-3 weeks after skin infection

result of antigen-Ab complex deposition

manifestations (edema, hypertension, proteinuria, microscopic hematuria, acute renal failure)

differnt strains than those assoc w/acute rheumatic fever

recovery usu complete

27
Q

Group B strep

A

S.agalactiae

colonizes GI and female GU tract

significant disease in neonates

  • early onset at birth or in utero: sepsis, pna, meningitis
  • late onset in 1st month of life: sepsis, meningitis

can cause cellulitis, UTI, sepsis in adults, esp those with underlying disease (Diabetes)

Dx: culture and nucleic acid amplific tests are SENSITIVE and SPECIFIC

tx: pcn (or vancomycin or clindamycin for pcn allergy)

screen all pregnant women and treat colonized women at term

28
Q

Group C, F, and G

A

share virulence factors with group A

cause pharyngitis, cellulities, bacteremia without identifiable focus

dx, tx same as other strep

29
Q

S. anginosis

A

Group F strep

B-hemolysis, a-hemolysis, or g-hemolysis

abscesses in liver, brain, periodontal

HDID 2 (32 decks)

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