S.

pyogenes
(Integumentary system)

Dr. Asmita Subedi

MBBS, MD Microbiology
• Streptococcaceae are catalase negative gram - positive
cocci, arranged in pairs or chains (due to single plane of
division).

• Important members:
• Streptococcus,
• Enterococcus and
• Pneumococcus
S. pyogenes
 Virulence factors
• Enzymes:
• Cell Wall Antigens • Streptokinase
• Several protein antigens (Fibrinolysin)
such as M, T and R proteins • Streptodornase (DNase)
have been identified in the • Hyaluronidase
outer protein layer. • NADase
• Toxins • Serum opacity factor
• Hemolysins beta hemolytic • C5a peptidase
streptococci such as group
A, C and G produce two
hemolysins- streptolysin O
and streptolysin-S
• Streptococcal pyrogenic
Exotoxin (SPE)
Skin and soft tissue infections

• Impetigo
• Cellulitis
• Erysipelas
• Necrotizing fasciitis
• Streptococcal myositis
Impetigo
• a superficial infection of skin, caused primarily by group
A Streptococcus and occasionally by other streptococci or
S. aureus.
• Most common sites: face (nose and mouth) and legs
• Individual lesions begin as red papules, which evolve
quickly into vesicles and then pustular lesions that break
down and coalesce to form characteristic thin papery
honeycomb-like crusts.
• Painless and not a/w fever.
Erysipelas, cellulitis and fasciitis.

• Result from superficial or deep extension of infection

• Erysipelas and fasciitis are commonly the result of
infection with S. pyogenes, but this etiology is not
exclusive.
• Fasciitis can arise from hematogenous seeding.
• An important common feature of all three entities is severe
pain.
Erysipelas
• superficial cellulitis with prominent lymphatic
involvement, with an indurated, “peau d’orange”
appearance with a raised border that is demarcated from
normal skin.
• often complicates edematous extremities and skin ulcers,
such as in varicose limbs.
• As in impetigo, it may be the result of mixed S. pyogenes
and S. aureus infection.
• Clinical signs of sepsis with high fever are present.
• Prompt empirical treatment should be started with
parenteral antibiotics covering at least both staphylococci
and streptococci.
 Cellulitis
• involves deeper anatomic
structures
• does not produce the typical
geographic skin lesion of
erysipelas
• pain and fever are important signs
• may be from multiple other
organisms, including gram
negative bacteria, especially in
immunocompromised patients.
• broad-spectrum antibiotic therapy
with both anti–gram-positive and
anti–gram-negative coverage.
 Necrotizing fasciitis
• is the most severe condition that
paradoxically presents the least
superficial signs at visual
observation of the skin and soft
tissues.
• The pain may be so intense that it
requires opiate administration for
relief.
• The condition is often the result of
S. pyogenes, but S. aureus may be
involved.
• an absolute emergency that
necessitates immediate and
generous surgical débridement and
drainage.
• also known as hemolytic streptococcal gangrene.
• It involves the superficial and/ or deep fascia invading the
muscles.
• Most common cause: GAS, accounting for nearly 60% of
total cases of necrotizing fasciitis.

• Source of infection:
• 1. Traumatized skin- most commonly caused by GAS
alone or in mixture with S. aureus.

• 2. Gastrointestinal tract breach- It occurs due to

abdominal surgery releasing the bowel flora. It is
polymicrobial, involving anaerobic flora and gram
negative bacilli like E. coli).
Clinical manifestations
• Onset :acute and rapid, and is marked by severe pain with
minimal erythema at the site of involvement.
• malaise, fever, chills, and a toxic appearance

• Later on ( over several hours), disease tends to be more

severe.
• Skin becomes dusky or mottled erythema and anesthetized
(due to infarction of the cutaneous nerves induced by
spreading inflammatory process) with extensive necrosis
of subcutaneous tissue, fascia and muscle (GAS is also
called as flesh eating bacteria).
Toxic Shock Syndrome (TSS)

• Group A Streptococcus producing pyrogenic exotoxins

may cause TSS secondary to soft tissue infection such as
necrotizing fasciitis.

• characterized by shock and multisystem organ failure.

Laboratory Diagnosis

• Specimen Collection and Transport

• depends on the site of the lesion,
• Common specimens: exudates from the lesion,
vesicular fluids
• Transport media: Pike’s transport media
• (composed of blood agar added with crystal violet
and sodium azide)
• Direct Smear Microscopy
• Gram staining  reveals pus cells with gram-positive
cocci (0.5-1 µm) in chains
• Culture:
• S. pyogenes is fastidious, does not grow on MacConkey
agar and basal media like nutrient agar or peptone
water broth.

• grows only in media enriched with blood, serum or

carbohydrate.
• Blood agar:
• Colonies are small 0.5-1 nm, pinpoint, circular,
semitransparent, low convex with a wide zone of beta-
hemolysis.
• Liquid media: glucose or serum broth or brain heart
infusion broth. Growth appears as granular turbidity with
powdery deposit.
Biochemical tests

• Catalase test: catalase negative

• Bacitracin sensitivity testing: Group A Streptococcus is
sensitive to bacitracin 0.04 U disk (any zone of inhibition
around the disk is considered as positive), while most of
other beta- hemolytic streptococci are resistant.
• Lancefield grouping: group A Streptococcus
• Serology: ASO Ab and Anti-DNase Ab
Treatment

• Penicillin is the drug o f choice for pharyngeal infections

as well as for suppurative complications.

• Macrolide, such as erythromycin is given to patients

allergic to penicillin.