STREPTOCOCCUS

Presenter
Dr. satyendra prasad
yadav
Jra-2
INTRODUCTION
 Gram +ve cocci
 Non spore forming
 Arranged in chains; spherical/oval in shape
 Size : 0.5-1.0 µm in diameter
 They are part of the normal flora of humans and animal.
 Streptococcus may causes either pyogenic infection or non
suppurative lesions eg : rheumatic fever and
glomerulonephritis.
 Show poor growth in simple media.
 Growth is enhanced by the addition of fermentable
carbohydrate (eg glucose), blood or serum.
Classification
i. Based on oxygen requirement
a. Facultative anaerobes
b. Obligate anaerobes

ii. Based on haemolysis

a. Alpha haemolysis or haemolytic
b. Beta haemolysis or haemolytic
c. Gamma haemolysis or haemolytic
Alpha Haemolytic Streptococcus

 Produces greenish discoloration with partial

haemolysis around the colonies.
 The zone of lysis is small ( 1 or 2 mm wide)
 They are normal commensals in the throat and may

causes opportunistic infection.

Eg: Streptococcus pneumoniae
Streptococcus viridans
 Gamma haemolytic streptococcus
or Non haemolytic streptococci
 Do not produces hemolysis in the medium.
 Enterococcus Faecalis
Faecium

Beta haemolytic streptococcus

 Produce a sharp, clear, colourless zone of complete

haemolysis
 2-4 mm wide

 Most pathogenic streptococci belong to this group

Beta Hemolytic Streptococcus are further divided
into
i. Lancefield classification
- Based carbohydrate C antigen on the cell wall.

- Includes A to V (except I/J)

ii. Further this group A is divided into 80-100 groups based

on M-Protein called as Griffith typing.

Beta haemolytic streptococcus further classsified into

Group A eg: S.pyogenes
Group B eg: S. agalactiae
Group C eg: S. equisimilis
Group D eg: Enterococcus or non enterococcus
Streptococcus pyogens

A. Morphology
- Gram positive cocci, spherical, oval

- 0.5 to 1.0 micrometer in diameter

- Non sporing

- Arranged in chains

- Chain formation is due to successive cell division occurring in

one plane only and daughter cells failing to separate

completely.
B. Culture
- They are aerobes ,facultative anaerobes
- Best grow at 37 degree Celsius ( 22-42 degree celcius)
- On blood agar, after overnight incubation
- The colonies are
Small ( 0.5 to 1.0 mm)
Pin point
Circular
Semitransparent
Low convex with a wide zone of beta hemolysis around them.
C. Biochemical Reaction
- Catalase negative
- Not soluble in 10% bile
- Hydrolysis of pyrolidonyl naphthylamide

- Oxidase negative

D. Resistance
- Inactivated by heat at 56 degree celcius for 30 minutes

- Rapidly inactivated by antiseptics.

- It is susceptible to sulphonomide and many antibiotics.

E . Virulence factors
 Several antigens along with the cell wall of streptococcus pyogens.
1. Carbohydrate antigen:
- On the basis of the C- carbohydrate antigen, S.pyogenes is

classified under Lancefield Group A.

- Show cross reactivity with some human tissues (leads to post

streptococcal sequelae.
2. Protein antigen
- M- Proteins: Most important protein used for typing as well as for
virulence.
- It acts as a virulence factor by inhibiting phagocytosis and is

antigenic.
- About 80 M protein types have been recognized.
- Rheumatogenic M types are 1, 3, 5, 6,14, 18, 19, and 24.
- M types also pyoderma are 2, 49, 57, 59, 60 and 61
 T- Proteins : Acid labile
- Trypsin resistant antigen.
- R- Proteins: Acts as antigen in many pathogenesis and
virulence.

3. Pili :
- These hair like structures project through the capsule of group

A streptococci (GAS)
- The pili consist partly M proteins and are covered with

lipoteichoic acid which is important in the attachment of

streptococci to epithelial cells.
F . Toxins

1. Haemolysins
2. Streptococcal pyrogenic exotoxin (SPE)
3. Streptokinase (fibrinolysin)
4. Deoxyribonucleases ( Streptodornase D Nase)
5. Nicotinamide adenine dinucleotidase ( NADase)
6. Hyaluronidase
7. Serum opacity factor (SOF)
8. Other enzymes
1. Haemolysins
 Two types of haemolysins
- Streptolysin “O”
- Streptolysin “S”

 Streptolysin O
- Antigenic in nature
- Antistreptolysin o appears following streptococcal infection
streptococcal infection.
- Estimation of this antibody (ASO titre) is a standard
serological procedure for the diagnosis of past infection with
S.pyogenes.
- An ASO titre in excess of 200 units is considered significant
and suggests either recent or recurrent infection with streptococci.
Streptolysin S
 Oxygen-stable hemolysin and is responsible for the hemolysin
and is responsible for the hemolysis seen around streptococcal
colonies on the surface of blood agar plates.
 It is protein in nature

 It is not antigenic

2. Streptococcal pyogenic exotoxin (SPE)

- Superantigen in nature.

- They are T-cell mitogen that induces a massive release of

inflammmtory cytokine causing tissue damage, fever and

shock.
3. Streptokinase (Fibrolysin)
- This toxin promotes the lysis of human fibrin clots by activating
a plasma precursor (plasminogen) thereby causing spread of
infection.
 Antistreptokinase antibodies antibodies provide retrospective
evidence of streptococcal infection.
 Streptokinase is given intravenously for the treatment of early

myocardial infarction and other thromboembolic disorders.

4. Deoxyribonucleases
- Causes depolymerisation of DNA

5. Nicotinamide adenine dinucleotidase (NADase)

- Leucotoxic in nature.

6. Hyaluronidase
- Causes breakdown the hyaluronic acid of the tissues,
favouring the spread of infection along the intercellular
spaces.
- Strains that form hyaluronidase in large quantities (M type 4
and 22) are non capsulated.
7. Serum opacity factor
- Acts as a virulence determinant of the organisms.

8. Other enzymes are

- Proteinase
- Phosphatase
- Esterase
- Amylase
- N-acetyl glucosaminidase
- Neurominidase

Their role in pathogenesis is unclear

 Pathogenesis and clinical findings
Streptococcal infections may be localised or diffuse (invasive)
A. Localized infections

B. Toxins mediated infections

C. Non-suppurative sequelae

D. Localized infections include

- Most common streptococcal disease
- May be localized as tonsillitis or may involves the pharynx
more diffusely as pharyngitis.
- Tonsillitis is more common in older children and adults than
in younger children.
- From the throat, streptococci may spread to the surrounding tissues,
leading to suppurative complications such as otitis media, mastoiditis,
quinsy, Ludwig’s angina and suppurative adenitis.
ii. Skin infection :
- Impetigo and pyoderma as localised infections with

induration and pus point.

iii. Erysipelas :
- Rapidly progressing infection with brawny edema and
rapidly advancing margin
iv. Cellulitis
- It is an accute rapidly spreading infection of the skin and
subcutaneous tissue with pain, tenderness and edema
v. Necrotising fascitis
- Most commonly caused by a mixed aerobic and anaerobic
bacterial infection.
- Characterized by extensive necrosis of subcutneous and
muscular tissues and adjacent fascia.
 Treatment
- Penicillin G
-Clindomycin or vancomycin are the drug of
choice in life threatening infection.
13. Toxin mediated infection

i. Toxin shock syndrome (TSS)

- Soft tissue infections with some M types of S. pyogens
(1,3,12,28) may sometimes causes a toxic shock syndrome
resembling staphylococcal TSS.
ii. Scarlet fever
- Pyogenic exotoxin A-C causing scarlet fever may follow
streptococcal pharyngitis or skin and soft tissue infections.
- Rashes on the trunk follow these infections.
Scarlet fever
C. Non suppurative sequelae
i. Acute Rheumatic fever
 The essential lesion in rheumatic fever is carditis including

connective tissue degeneration of the heart valves and

inflammatory myocardial lesions characterised by Aschoff
nodules.
 Rheumatic fever follows persistent or repeated streptococcal

throat infections.
ACUTE RHEUMATIC FEVER
 The lesion are due to reaction of hypersensitivity to some
streptococcal component
ii. Post Streptococcal glomerulonephritis
- Due to antigenic cross reactions between the glomerular
membrane antigen and cell membrane of nephritogenic
streptococci.
- It is an immune complex disease.
Lab diagnosis

1. Specimen
- Swab or aspirates from the affected site are collected
aseptically.
- Serum is collected for serology in rheumatic factor and
glomerulonephritis.
2. Microscopy
- Gram stained slides from pus show gram positive cocci in

chains
.
3. Culture
Colony on blood agar show
- Small
- Circular
- Semitransparent colonies with clear hemolysis around them.
 4. Identification
i. Antigen detection
Rapid diagnostic test kits using specific antisera are available
commercially for the detection of streptococcal group A antigen
from throat swabs.

ii. Bacitracin Sensitivity

A wide zone of inhibition is seen around a 0.04 unit bacitracin
with S.pyogens, but not with other streptococci.

iii. Biochemical reaction

- Hydrolysis of pyrrolidonyl beta naphthyl amide (PYR test)

- Failure to ferment ribose

5. Serology
- InRheumatic fever and glomerulonephritis, a retropective diagnosis a
streptococcal infection may be established by demontrating high level
of antibody to streptococcal toxins.

i Antistreptolysin O (ASO)
- High levels are usually found in acute rheumatic fever
- In glomerulonephritis titres are often low.

ii. Antideoxyribonuclease B ( anti DNAase B)

- Antibody to DNAase
- Titres greater than 300 are significant
- Anti-DNAase B is very useful for the retrospective diagnosis of
streptococcal pyoderma.
Treatment :

- All beta haemolytic Group A streptococci are

sensitive to
penicillin G.
- Erythromycin
- Cephlexin may be used
- Bacitracin used for local application on skin lesions.
Group “B” Streptococci (GBS)
 Streptococcus agalactiae is an important pathogen of Bovine
mastitis in cattle.
 Most important pathogen in neonates causing neonatal
septicemia and meningitis.
 Also causes septic abortion.
 Streptococcus is a commensal of female genital tract.
 Other infections caused by Group B streptococcus are
Osteomyelitis
Arthritis
Conjunctivitis
Respiratory infections
Endocardititis and Peritonitis
Laboratory Diagnosis
1. Hydrolyze hippurate
- Hippurate positive bacteria produces a deep purple colour,

where as hippurate negative organisms produces a slightly

yellow pink colour or fail to produce any colour.
- Group B streptococcus possess the enzyme hippuricase ( also

called hippurate hydrolase) which hydrolyses sodium

hippurate to form sodium benzoate and glycine.
2. CAMP Test
 Christie, Atkins and Munch-Peterson

 When S. agalactiae is inoculated perpendicular to a streak of

S.aureus grown on blood agar an accentuated zone of

hemolysis occurs
 3. Resistance to SXT ( trimethoprim- sulphomethoxazole)
Group C streptococcus

Eg: Str. dysgalactiae sub species equisimilis

- Most commonly affect animals.
Group D streptococci
 Classified into enterococci ( faecal streptococcus) and non enterococci
( non faecal streptococci)
 Enterococcus: eg: E.faecalis

E. faecium
- Normal commensale of the gut
 Non enterococcus eg: S,bovis

S. gallolyticus
- Causes colon cancer
Enterococcus
 Positive for Bile aesculin hydrolysis test.

 Relatively heat resistant and can withstand heat at 60 degree celcius for 30

minutes.
 Grow in the presence of 6.5% Nacl.

 Can grow at 45 degree and at pH 9.6

 They are PYR test positive

 They are resistant to SXT

 Enterococcal species have been
divided into five group (Group
i to Group v) based on acid
formation from mannitol and
sorbitol and arginine
hydrolysis.

 E.faecalis and E. faecium

belongs to group ii culture.

 On Mac Conkey’s medium they

grow as tiny deep pink
colonies.
 On Gram Staining

•On Gram is staining enterococcus appear as pairs of oval cocci and

short chains.

•Enterococcus faecalis identified by fermentation of mannitol, sucrose,

aesculin and sorbitol and by producing black colonies when grow on
tellurite blood agar.
Pathogenesis
 Hospital acquired infections
 Causes urinary tract infection and wound infection

 They may causes SABE, endocarditis , septicaemia, peritonitis

and infection of Biliary tract.

Treatment
 In Penicillin sensitive strains

treated with a combination of penicillin (ampicillin) and

aminoglycoside ( gentamicin)
 In case of resistance to penicillin and aminoglycoside.

 Vancomycin in the DOC.

THANK YOU