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Streptococci

General Characteristics of Streptococci


 Gram positive cocci in chains or
pairs, nonmotile (except for an
occasional
flagellated
strain),
catalase-negative, form capsules
and slime layers.
 Colonies are usually small, nonpigmented, and glistening.
 Normal residents or agents of disease (Pyogenic pathogens) in
humans and animals; others are free-living in the environment.
 Facultative anaerobes that ferment a variety of sugars, usually with
the production of lactic acid (homofermentative).

Classification Systems for Streptococci


(Lancefield grouping)
Rebecca Lancefield
(1895-1981)

 Lancefield grouping based on group


specific carbohydrate antigens
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different

groups

characterized

using an alphabetic system (A, B, C ..)


 Most

and

some

-hemolytic

streptococci can be typed by this


method

Classification Systems for Streptococci


 Hemolysis on blood agar plates
S. pyogenes is -hemolytic (complete)
Viridans streptococci are -hemolytic (incomplete)
Enterococci are -hemolytic (no hemolysis)
S. pyogenes
showing
-hemolysis

S. pneumoniae
showing
greenish zones
typical of hemolysis.

 Biochemical properties
Catalase-negative, facultative anaerobes

Major Species of Streptococcus and Related Genera

Note: Species in bold type are the most significant sources of human infection and disease.
N = none V = varies
*Urinary tract infection.
**Upper respiratory tract.
***No group C-carbohydrate identified.

Species of Streptococci
Streptococcal species

Sites of Colonization

Sites of Infection

S. pneumoniae

Oropharynx , nose

Lungs, sinuses, middle


ear, meninges

S. pyogenes

Oropharynx , rectum

Pharynx, skin, soft


tissue

S. agalacti ae
Gp. B streptococci

GU tract, Oropharynx

Neonatal
infections, CNS,

Viridans streptococci

GU tract, Oropharynx

GU tract, Cardiac valves,


bloodstream

Identification of Streptococci

Streptococcus pyogenes

Diseases caused by S. Pyogenes

Structural components of Streptococcus pyogenes

Virulence Factors of Streptococcus pyogenes

Virulence factors of S. pyogenes


 Structural virulence determinants:
M protein anti-phagocytic, rapid multiplication, molecular
mimicry
Hyaluronic acid capsule antiphagocytic
Heavily encapsulated strains are very mucoid often
associated with rheumatic fever outbreaks
Only weakly immunogenic b/o similarity to connective tissue
Adhesins to host cells
Lipoteichoic acid to fibronectin on epithelial cells
Protein F1- facilitates binding to throat and skin via fibronectin

Virulence factors of S. pyogenes


Enzymes:
Streptokinase, hyaluronidase - liquefy tissue
Streptolysins (S and O) - lyse host cells
Streptolysin O is oxygen-labile
Strains lacking streptolysin S (O2-stable) are -hemolytic
under anaerobic conditions only

Exotoxins:
Pyrogenic exotoxins A-C - function as superantigens
producing a sepsis syndrome
SPE A Structurally similar to the staphylococcal superAgs
SPE B Cys protease that destroys tissue

Toxic Shock-like Sydrome (TSLS)


 Caused by invasive Strep A that produce SPE
 Superantigens stimulate T cells to produce large
amounts of cytokines which damage endothelial
cells causing fluid loss and rapid tissue death from
lack of oxygen
 Characterized by sudden drop in blood pressure,
multi-organ failure, very high fever
 Mortality rate of >30 %

Streptococcal pyrogenic exotoxins (Spe)

Produced by both the scarlet fever strains and invasive


S. pyogenes strains.
More than four serologically distinct toxins (SpeA, B, C and F).
They are superantigens (except for SpeB, which is a cysteine
protease) and may exhibit the following biological activities:
Enhances release of proinflammatory cytokines
(pyrogenicity)
causes skin rash
Spe is associated with streptococcal toxic shock syndrome or
other invasive S. pyogenes diseases.

Role of M Protein in Disease


 Antigenic variations in M proteins are used to type
Group A streptococci (> 80 types)
Pharyngitis and impetigo strains differ in gene sequence

 Antibody against M protein is durable and protective


but is type-specific
 Strains lacking M protein are avirulent
 M protein is anti-phagocytic, inhibiting (C3b)
activation of complement via the alternate pathway
 M protein positive strains multiply rapidly in fresh
human blood

Epidemiology of Group A Streptococcal Pharyngitis


Humans are the natural reservoir
S. pyogenes can transiently colonize the oropharynx and skin.
Diseases are caused by recently acquired strains that can
establish an infection of the pharynx or skin.
Primarily seen in 5-15 year olds
More common in temperate/cold climates - winter
Different strains (M-protein types) are generally responsible
for pyoderma and pharyngitis
There can be relatively rapid changes in prevalent M type
strains in different areas
Asymptomatic pharyngeal carriage is relatively common

Disease caused by S. pyogenes


Suppurative
Non-Invasive
Pharyngitis (strep throat)-inflammation of the pharynx
Skin infection, Impetigo

Invasive
Scarlet fever-rash that begins on the chest and spreads
across the body
Pyoderma-confined, pus-producing lesion that usually
occurs on the face, arms, or legs
Necrotizing fasciitis-toxin production destroys tissues and
eventually muscle and fat tissue

Clinical Features of Group A Streptococcal


Pharyngitis
 Difficult to distinguish from pharyngitis caused by
other pathogens
The most common cause of bacterial pharyngitis in children
Overall responsible for a small percentage of cases of
pharyngitis seen by physicians

 Findings suggestive of GpA strep:


- Sore throat sudden onset, fever, headache, lymphadenitis,
tonsillar exudates

 Findings not suggestive of GpA strep:


- conjunctivitis, coryza, cough, diarrhea
 Suppurative sequelae - abscess, sepsis, dissemination

Nonsuppurative Sequelae of Pharyngitis


 Invasive Strep A disease involve specific virulent
strains (M-1 and M-2 serotypes)
 Acute Rheumatic fever:
Carditis, polyarthritis, subcutaneous nodules, chorea
Life threatening inflammatory disease that leads to damage
of heart valves muscle

Pathogenesis believed to involve molecular mimicry


Cross reactive epitopes with myosin and M protein

 Glomerulonephritis:
Immunologically mediated damage perhaps resulting from
streptococcal antigens that cross react with kidney tissue

Inflammation of the glomeruli and nephrons which obstruct


blood flow through the kidneys

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Coiled-coil structure of M protein


 Most variable parts of
M protein are oriented
towards outside and
provide
the
antiphagocytic effect
and
serologic
specificity.
 Conserved
portions
are rooted in the cell
wall.
 All four types contain
epitopes which may
stimulate the crossreactive
immune
reactions
seen
in
rheumatic fever.

Acute Rheumatic Fever (ARF)


 Autoimmune state characterized by inflammation of heart
valves, joints, subcutaneous tissues and CNS
 Antigenic similarities between streptococci and human
tissue antigens
 Antigens stimulating Abs: most probably M protein, but
the group A carbohydrate is also a possibility
 M protein epitopes involved differ from antiphagocytic
domains
 Antibodies against dominant epitope of group A
carbohydrate (N-acetylglucosamine) may play role in
injury to valvular endothelium
 Genetic factors are probably also important in ARF
Only a small proportion of individuals infected with Gp A
Strep

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Acute Glomerulonephritis
 Caused by deposition in the glomerulus of antigen
antibody complexes with complement activation and
consequent destruction of glomerular membrane,
allowing blood and proteins to leak into urine
 Type II hypersensitivity reaction
 M proteins of some nephritogenic strains share
antigenic determinants with glomeruli
 Streptokinase also been implicated both through
molecular mimicry and through its plasminogen
activation capacity

Pathogenesis of Streptococcal Pharyngitis


 Bacteria are spread by droplets or nasal secretions.
Crowding increases the risk of spread
 Strains rich in both M protein and hyaluronate
appear to be more easily transmitted
 Streptococci adhere to epithelial cells using adhesins
- protein F1 and lipoteichoic acid
 Susceptibility to infection is determined by the
presence of type-specific antibody to M protein

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Diagnosis
As noted clinical criteria for streptococcal
pharyngitis of limited value
Culture remains the gold standard
Rapid streptococcal antigen detection kits
based on carbohydrate recognition are highly
specific

Treatment/Prevention of S. pyogenes
Infection
The species remains exquisitely sensitive to penicillin
The use of antibiotics that are protein synthesis
inhibitors (e.g. clindamycin) that inhibit protein
synthesis may improve outcome
Soft tissue infections often require surgical
debridement
Intravenous immunoglobulin may also have a
beneficial role
Prophylactic antibiotics
Vaccines - under investigation

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