STREPTOCOCCI

Prof. (Mrs.)K.Murugananthan
Department of Microbiology,
Faculty of Medicine
 Streptococci
General features
ØGram positive cocci
ØOccur in chains/diplococci
ØCatalase negative
ØNutritionally fastidious - supplemented with blood for
optimal growth
ØFacultative anaerobes
 Streptococci

Classification
ØOxygen requirement
ØHaemolysis on blood agar
ØSerogrouping (Lancefield)
 Staphylococci Streptococci

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 Streptococci
Β Haemolysis α Haemolysis
(Complete lysis of RBC & (greenish zone around the colonies-
clear zone around the incomplete lysis of RBC)
colonies) • S.pneumoniae
1. S.pyogenes • Viridans streptococci
2. S.agalactiae
γ/ non Haemolysis
• S.bovis
Species Lancefield group Typical haemolysis

S.Pyogenes A β

S.agalactiae B β

E.faecalis D α or β

S.bovis D α or γ

S.pneumoniae Not detected or not α

useful for differentiation

Viridans group NA α
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 Streptococcus pyogenes
(Group A)
Virulence factors
ØAdherence to muco epithelium – M protein & lipoteichoic acid
ØM protein –major virulence factor. It protrudes from the outer
surface and blocks phagocytosis and inactivate C3b (opsonin).
ØS. pyogenes without M-proteins are non-pathogenic.
ØCertain M protein types- rheumatogenic and some are
nephritogenic.
ØCapsule composed of hyaluronic acid- anti phagocytic
ØDestruction of tissue by release of toxins & enzymes.
 Enzymes & Toxins
ØHaemolysins
a- Streptolysin “O” – 02 labile -antigenic
b- Streptolysin “S” – 02 stable- not antigenic
ØStreptokinase (Fibrinolysin)
ØDNase (Streptodornase) – degrades DNA
ØHyaluronidase -spreading factor
ØExotoxin B : Proteinase which rapidly destroy the tissue –
responsible for necrotizing fasciitis
ØPyrogenic exotoxin –responsible for Toxic shock syndrome.
ØErythrogenic toxin- causes rash of scarlet fever
 Diseases
1.Pyogenic: pharyngitis , skin and soft tissue infections…..

2. Toxigenic: Toxic shock syndrome, necrotizing fasciitis,

scarlet fever

3. Immunogenic: Rheumatic fever and acute

glomerulonephritis
 Diseases
Direct Action:

ØPharyngitis (sore throat)

ØSkin infection
- Cellulitis
- Impetigo
- Erysipelas
- wound infection

ØSepticaemia
 Pharyngitis (sore throat)
• Throat pain and fever
• Inflamed throat and tonsils,
yellowish exudate
• Accompanied with tender
cervical lymph nodes
• Diagnosis: Culture / Antigen
detection

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Impetigo :Infectious epidermal eruption of pustules which
rupture to form a honey color to brown crust.

Caused by staphylococcus aureus

and
Group A streptococcus(GAS) -
S.pyogenes infection.
Erysipelas : Superficial infection of the skin with lymphatic
involvement
Clinical signs & symptoms:
painful, oedematous and
erythematous lesion.
Systemic features: Fever, malaise
and chills are generally present,
but bacteraemia is uncommon
(<5%)
Cellulitis
• Red, hot, swollen tender
area, not well demarcated,
not elevated.
• Systemic features: Fever,
chills and malaise.
• Regional lymphadenopathy
is common.
 Risk factors for cellulitis

Breach in skin:
• Ulcers
• Eczema
• Burns
• Injury to the skin
Clinical conditions:
• Diabetes
• Varicose veins
• Peripheral vascular disease

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 Diseases

Toxin related infection

ØToxic shock syndrome
ØNecrotizing fasciitis
ØScarlet fever
Scarlet fever

• Associated with pharyngeal

infections.
• Red tongue – Strawberry tongue

• Diffuse red blanching rash. first

appear over upper part of chest
the spreads to trunk and
extremities.
 Deep ( Muscle & Fascia)
Necrotizing fasciitis :
Flesh-eating disease or Flesh-eating bacteria syndrome, very severe
infection of the deeper layers of skin and subcutaneous tissues and
spreading across the fascial plane.
Predisposing factors:
Ø DM
Ø Alcoholism
Ø I/V drug abuse
Diseases

Post streptococcal Sequalae (Nonsuppurative)

• Rheumatic fever

• Acute glomerular nephritis

 1.Acute rheumatic fever (ARF)
Ø Acute rheumatic fever is due to group A beta hemolytic streptococcal
infection.
Ø This is a systemic disease of childhood, often with recurrence.
Ø It is a delayed non-suppurative sequelae to upper respiratory tract infection
with GABH streptococci.
Ø It is an autoimmune response, type 2 hypersensitivity, triggered by a
preceding rheumatogenic strain of S.pyogenes infection (after a period of 1 -
3 weeks), typically pharyngitis (M types l, 3, 5, 6,18 & 24)

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ØMolecular mimicry between Streptococcal M proteins and human tissue
antigens, particularly in the heart, joints, skin, and central nervous system,
leads to the activation of the immune system.
ØTherefore, the antibodies produced against streptococcal M proteins also
cross-react with antigens in the heart., blood vessels, joints, subcutaneous
tissue and CNS
ØThis immune system's cross-reactivity results in inflammation, which causes
the characteristic clinical features of ARF, including carditis, arthritis, and
chorea.
ØThe most significant and serious consequence of ARF is rheumatic heart
disease,
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Epidemiology
Ø Ages 5 - 15 yrs are most susceptible

Ø Rare < 3 yrs

Ø Girls > boys

Ø Common in 3rd world countries

Ø Environmental factors- over crowding, poor sanitation, poverty

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Pharyngitis - produced by GABHS can lead to - acute rheumatic
fever , rheumatic heart disease and post strept. glomerulonepritis

Skin infection - produced by GABHS leads to post streptococcal

glomerulonephritis only.
Ø It will not result in Rh.Fever or carditis as skin lipid cholesterol
inhibit antigenicity.

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 2)Acute post-streptococcal glomerulonephritis
(PSGN)
Ø This is an antibody-mediated inflammatory disease of the glomeruli of
the kidney.

Ø It occurs about one week after infection of either the pharynx or skin
by nephritogenic (having the ability to cause glomerulonephritis)

Ø Only a few strains of beta-hemolytic group A streptococci are

nephritogenic.

Ø Certain antigens(M protein) from these nephritogenic streptococci

induce an antibody response. The resulting antigen-antibody
complexes travel to and are deposited in the glomerular basement
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membrane.
Ø This deposition leads to the activation of the complement system
and subsequent inflammation and cell medicated immune response.

Ø The inflammation results in damage to the glomerular basement

membrane.

Ø Results in RBC casts and protein in the urine

Ø Leads to clinical manifestations such as haematuria, proteinuria,

oedema, and hypertension- most patients recover without long-term
consequences.

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Lab Identification of Pharyngitis

Ø Throat swab culture

Ø Rapid Antigen detection (RADT) from the throat swab

[ S. pyogenes can be identified with β haemolysis on
blood agar and Bacitracin sensitivity]

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Lab Identification of Rheumatic fever

Ø Diagnosed based on clinical suspicion and past history

of pharyngitis

Ø ASOT, Anti-DNase
 Lab Identification of post streptococcal
glomerulonephritis
Ø Evidence of renal failure with glomerular damage.

ØPast history of pharyngitis or impetigo

 Prevention of ARF
Ø The most effective way to prevent ARF is promptly treating Streptococcal
pharyngitis with oral phenoxymethyl penicillin or co-amoxiclav, for 10 days.
Ø This treatment helps to eliminate Streptococcus pyogenes before the immune
response can trigger ARF.
Ø If patient is allergic to penicillin, clarithromycin (erythromycin)/ cefalexin
Ø For patients with ARF, continuous prophylactic antibiotics (secondary
prophylaxis) are prescribed to prevent recurrence.
Ø Ensuring good hygiene practices
Ø Reducing overcrowding, ensuring adequate ventilation, and improving
sanitation are important measures to minimize the risk of streptococcal
infection and transmission

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 Prevention of PSGN

ØAvoiding overcrowding and personal hygiene to decrease the risk of

catching streptococcal infections.

ØUnlike for ARF, treating streptococcal pharyngitis/skin infection with

penicillin is not effective in preventing the development of PSGN in
that patient.
ØHowever, treating PSGN patients and their colonized family contacts
with penicillin for 10 days will eradicate nephritogenic strains of S
pyogenes in the community which will prevent PSGN in others

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 Treatment

Penicillin remains as the drug of choice for treatment of all

Streptococcus pyogenes infections
Impetigo : Clean and dry the affected area (removal of the
crest by soaking with soap and water /Normal saline)

• Topical Abcs (Mupirocin/ fusidic acid cream)

• Oral Abcs ( Flucloxacillin/doxycycline)

 Treatment……

ØErysipelas : Amoxicillin /cephalexin /flucloxacillin

ØCellulitis : Flucloxacillin/ Co-amoxiclav

ØSevere infections: Necrotizing fasciitis, myonecrosis and

streptococcal toxic shock syndrome - with intensive care
support Combinations of antibiotics specially clindamycin to
suppress toxin production.
 Streptococcus agalactiae
(Group B)
• Asymptomatically colonize the lower GIT or genital tract of 25-30% of
woman.
Diseases
1.Early onset of neonatal diseases : rapture of membranes in women who
colonized with this.
Age : <7days
Sources : in utero/at delivery
Presentation : neonatal septicemia, pneumonia &
meningitis
Mortality : high

Treatment : Benzylpenicillin + Gentamicin I/V

2. Late onset neonatal diseases
• Age : 1week to 3 months
• Sources : environment
• Presentation : bacteraemia, pneumonia,
osteomyelitis(rare)
Treatment : Cefotaxime I/V
3. Postpartum sepsis
• Adults : puerperal sepsis

Prevention
Intrapartum antibiotic prophylaxis to colonized women are screened at 35 to
37 weeks of gestation and treat with benzylpenicillin or ampicillin at the
time of delivery
Other β Haemolytic streptococci

• Group C & G – sore throat, puerperal sepsis

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Viridans group streptococci

ØS. mutans, S. sanguis, S. mitis, S. milleri and S. intermedius

Ø α Haemolysis
ØMost common cause of Infective endocarditis in patients with heart
diseases:
ØRheumatic heart disease/ Congenital heart disease/ mitral valve prolapse…

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Viridans group streptococci

Pathogenesis
Ø Normal flora of mouth & teeth
Ø Adhere to tooth enamel & damaged heart valves
During dental manipulations these organisms get into the
bloodstream and subsequently, they can implant on the
endocardial surface of the heart, most commonly on a
previously damaged

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 Viridans group streptococci
Diseases
Bacteremia, endocarditis, Dental caries.
S.milleri – Brain abscess formation
Treatment
Penicillin (first line therapy)
Cephalosporins and vancomycin (second line therapy)

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 Viridans Streptococcus is eating heart valves slowly,
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while Staphylococcus aureus is eating fast.