Properties

Pathogenesis

Clinical findings

Laboratory diagnosis

Treatment & Prevention

Streptococcus pyogenes (Group A)

Gram-positive cocci

Nonmotile

Do not form spores

Arranged in chains or pairs.

Catalase negative.

Form a clear zone around their colonies due to complete lysis of red cells.

Transmission:

- not a commensal, but often carried in the throat.

- commonly spread in respiratory droplets.

Virulence factors:

- surface component – M protein prevents phagocytosis.

- streptokinase activates plasminogen to form plasmin which dissoves fibrin.

- DNAase depolymerizes DNA in exudes or necrotic tissue.

- hyaluronidase hydrolyzes ground substance of connective tissue, which aids its spread.

- erythrogenic toxin causes the rash of scarlet fever.

- streptolysin O & S causes beta-hemolysis; damage host cells & leukocytes.

- exotoxin A is a toxic shock syndrome toxin.

- exotoxin B is a protease that rapidly destroys tissue, causing necrotizing fasciitis.

Diseases:

- pharyngitis

- cellulitis

- scarlet fever

- toxic shock syndrome

- rheumatic fever

- acute glomerulonephritis

Pharyngitis:

- most common bacterial cause of sore throat.

- inflammation, exudate

- fever

- leukocytosis

- tender cervical lymph nodes.

- untreated – spontaneous recovery in 10 days.

- may extend to otitis, sinusitis, mastoiditis, & meningitis.

Scarlet fever:

- general rash (a punctate erythema).

- local complications: peritonsillar abscess, sinusitis, otitis media, mastoiditis.

Skin & soft tissue infections:

- erysipelas: a superficial spreading skin condition.

- impetigo: superficial infection of abraded skin that forms pus or crusts.

- cellulitis: lymphangitis, bacteremia.

Enters uterus after delivery to produce endometritis, sepsis & puerperal fever.

Necrotizing fasciitis: rapidly spreading infection of the fascial plane.

Streptococcal toxic shock syndrome: local infection accompanied by bacteremia, fever & shock.

Poststreptococcal (Nonsuppurative) diseases:

- occur weeks later after acute infection.

- due to a self-limiting autoimmunity attack on body tissues.

Acute rheumatic fever:

- only after pharyngeal infection.

- latent period: 3-4 weeks.

- diagnosis: carditis, polyarthritis, fever, arthralgia, raised ASO titre for serologic evidence.

- pathogenesis: cross-reacting B & T cell responses to strep antigens bind to host components.

- a patient may suffer recurrent attacks of rheumatic fever & cumulative damage to heart valves.

Acute glomerulonephritis:

- more frequent after skin infection than after pharyngitis.

- clinical features: hypertension, edema of face & ankles, ‘smoky’ urine.

- initiated by antigen-antibody complexes on glomerular basement membrane.

- acute renal failure may develop.

Stained smears from skin lesions or wounds that reveal streptococci are diagnostic.

Group A: inhibited by bacitracin disk.

Group B: hydrolyze hippurate.

- Group D: hydrolyze esculin in the presence of bile.

Serologic: high ASO titers after infection.

Sensitive to penicillin.

It is necessary to treat pharyngitis or throat carriage for 10 days with oral penicilin to eliminate S.pyogenes & prevent non-suppurative complications.

Prevention:

- acute rheumatic fever: prevented by prompt treatment of group A streptococcal pharyngitis with penicillin.

- acute glomerulonephritis: prevented by early eradication of streptococci from skin colonization sites but not by administration of penicillin after onset of symptoms.

Streptococcus agalactiae (Group B)

Forms part of normal flora of vagina & bowel.

Neonatal sepsis: complicated by pneumonia or meningitis.

Less sensitive to penicillin; combination with gentamicin or erythromycin.

Group C and group G streptococci

Sore throat, soft tissue infections & invasive sepsis

Group D streptococci

Include members of Enterococcus (E.faecalis) & S.bovis (strongly associated with carcinoma of the bowel).

Enterococci are an important cause of nosocomial infections & cause urinary tract infection.

Enterococci & S.bovis can cause bacteremia & endocarditis.

Enterococci are resistant to penicillin; ampicillin is more effective.

Most strains are sensitive to vancomycin.

S.bovis: penicillin