37. Streptococcus

Question 1

streptococci are what type of bacteria under microscope?

Answer 1

gram+ cocci in pairs and chains

catalase -

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

Question 2

alpha hemolysis

Answer 2

partial hemolysis : green discoloration

vidirans streptococci

Question 3

beta hemolysis:

Answer 3

complete hemolysis (clear zone around colony)

B-hemolytic streptococci

Question 4

gamma hemolysis:

Answer 4

no hemolysis

vidirans streptococci

Question 5

what is the only clincally important GAS?

Answer 5

strep. pyogenes

Question 6

suppurative vs non-suppurative? (re: GAS)

Answer 6

suppurative: pharyngitis and skin infections (pus)

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

Question 7

M protein?

Answer 7

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

Question 8

somatic virulence factors of GAS?

Answer 8

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)

Question 9

toxins from GAS?

Answer 9

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)

Question 10

GAS enzymes?

Answer 10

play a role in rapid spread through tissues

DNAses

Hyaluronidase

Streptokinase (degrades fibrin, used as a Rx)

Question 11

GAS avoidance of innate immune response?

Answer 11

C5a peptidase (disrupts C’ chemoattractant)

SpeB (cleaves IgG)

Question 12

GAS epidemiology?

Answer 12

• 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)

Question 13

GAS respiratory tract suppurative disease?

Answer 13

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

pneumonia (rare)

Question 14

GAS skin suppurative disease?

Answer 14

impetigo (pyoderma)

erysipelas

necrotizing fasciitis (streptococcal gangrene)

streptococcal toxic shock syndrome

Question 15

pharyngitis diagnosis?

Answer 15

rapid antigen tests:

• convenient
• good specificity
• negative requires culture

culture:

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

Question 16

pharyngitis treatment?

Answer 16

• 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)

Question 17

scarlet fever (scarlatina)

Answer 17

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

Question 18

impetigo (pyoderma)

Answer 18

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)

Question 19

erysipelas?

Answer 19

form of cellulitis

highly characteristic of B-hemolytic streptococcus

bright erythema

edema

sharp raised edges

regional lymphadenopathy

systemic sxs

Question 20

cellulitis w/lymphangitis?

Answer 20

s.pyogenes has peculiar relationship w/lymphatics

cellulitis often complicated by lymphangitis

those w/damaged lymphatics predisposed to recurrent strep cellulitis

Question 21

necrotizing fasciitis

Answer 21

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

Question 22

streptococcal toxic shock syndrome

Answer 22

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

Question 23

pathogenesis of streptococcus pyogenes nonsuppurative infections?

Answer 23

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

Question 24

clinical syndrome of acute rheumatic fever?

Answer 24

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)

Question 25

therapy for acute rheumatic fever?

Answer 25

symptomatic w/asa or corticosteroids primary preventio: tx of pharyngitis secondary prevention: benzathine PCN G or oral pcn daily

Question 26

post-streptococcal glomerulonephritis

Answer 26

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

Question 27

Group B strep

Answer 27

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

Question 28

Group C, F, and G

Answer 28

share virulence factors with group A cause pharyngitis, cellulities, bacteremia without identifiable focus dx, tx same as other strep

Question 29

S. anginosis

Answer 29

Group F strep B-hemolysis, a-hemolysis, or g-hemolysis abscesses in liver, brain, periodontal