STREPTOCOCCUS
Pavithra G. Palan
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Streptococci are Gram positive cocci.
Arranged in chains or pairs.
The name streptococci (streptos meaning
twisted or coiled) was given by Billroth.
CLASSIFICATION:
Streptococci
02 requirement
Obligate anaerobes
Eg: Peptostreptococci
Aerobes & facultative
anaerobes
Haemolysis
Alpha haemolytic
Eg: Viridans streptococci
Beta haemolytic
Gamma haemolytic
Eg: Enterococcus group
Serological Grouping (C carbohydrate antigen)
20 Lancefield groups
(ABCDEFGHKLMNOPQRSTUV)
Group A- Streptococcus pyogens
Serological typing (M Protein)
80 Griffith types
(1,2,3,etc. up to 80)
Streptococcus pyogens
MORPHOLOGY:
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Gram positive spherical
or oval cocci arranged
in chains.
Individual coccus will
be 0.5-1.0μm in
diameter.
They are nonmotile
and nonsporing.
Some strains have
capsule composed of
hyaluronic acid.
CULTURE:
Media used:
1. Non selective media:- Sheep blood agar
2. Selective media:- Crystal violet blood agar
PNF medium
Cultural characteristics: On blood agar, after
overnight incubation, the colonies are small,
circular, low convex with an area of
β-haemolysis around them.
Biochemical reactions:
1. Catalase test: Negative
2. Bile solubility test: Negative
Positive
Negative
3. PYR test: Positive
4. Ribose is not fermented.
PATHOGENICITY:
Source of infection:
1. Patient
2. Carriers
Mode of transmission:
1. Contact: direct or indirect( through fomites)
2. Inhalation of air borne droplets
Antigenic structure:
1.Capsular hyaluronic acid:
2.Cell wall antigens:
a) Inner layer of peptidoglycan
b) Middle layer of group specific C carbohydrate
c) Outer layer of protein (fimbriae) & lipoteichoic acid
3.Type specific antigens:
a) M protein
b) T protein
c) R protein
Antigenic structure of S. pyogens
Virulence factors:
These include
A) Toxins
B) Enzymes
A) Toxins:
1. Haemolysins
a) Streptolysin ‘O’
b) Streptolysin ‘S’
2. Pyrogenic exotoxin( Erythrogenic toxin)
B) Enzymes:
1. Streptokinase (Fibrinolysin)
2. Deoxyribonuclease (Streptodornase)
3. NADase
4. Hyaluronidase
Diseases:
Diseases caused by S. pyogens is studied
under 2 groups
1. Suppurative infections
2. Non suppurative complications
1. Suppurative infections:
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Pyogenic infections.
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Spreads locally, along lymphatics and
through the blood stream.
Common suppurative infections are:
A) Respiratory infections:
Tonsillitis
sore throat
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Pharyngitis
Otitis media
Mastoiditis
Quinsy
Ludwig’s angina
Rarely it may cause pneumonia & meningitis
Scarlet fever (sore throat & skin rash)
Tonsillitis
Pharyngitis
Otitis media
Mastoiditis
Quinsy
Ludwig’s angina
Skin rashes in Scarlet fever
B) Skin infections:
Infection of wounds & burns
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Impetigo
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Erysipelas
Impetigo
Erysipelas
C) Soft tissue infections:i) Cellulitis
ii) Necrotising fasciitis
iii) Soft tissue infections with some M types of
strains may sometime cause toxic shock
syndrome resembling staphylococcal TSS.
D) Genital Infections:-Puerperal sepsis
E) Other suppurative infections:
Pyemia
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Septicemia
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Abscesses in internal organs such as brain,
lungs, liver and kidney.
2. Non suppurative complications:
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It is also called as post streptococcal
complications
Non suppurative complications of S.pyogens
occur 1-4 weeks after the acute infection.
The organism may not be detectable when
these complications set in.
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These complications are believed to be the
result of hypersensitivity to some
streptococcal components.
The complications are1. Acute rheumatic fever
2. Acute glomerulonephritis
1. Acute rheumatic fever: It occurs after repeated
sore throat caused by S. pyogens.
Mechanism of pathogenesis:
During primary infection antibodies will be produced
against some streptococcal antigen.
Since streptococcal antigen has similarity with cardiac
tissue antigen, the antibodies will cross react with
cardiac tissue antigen causing destruction.
Leads to clinical symptoms such as Aschoff’s nodules,
carditis, fever and malaise.
2. Acute glomerulonephritis: It follows after skin
infection caused by S. pyogens nephritogenic types.
Mechanism of pathogenesis:
During skin infection caused by nephritogenic types of
S. pyogens, the antibodies will be produced against
cell membrane antigen.
These antibodies cross react with glomerular
basement membrane antigen causing destruction.
Leads clinical symptoms such as proteinuria,
haematuria & hypertension.
LABORATORY DIAGNOSIS:
A) In acute suppurative infection
Specimens to be collected:
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Throat swab,
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Pus,
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Tissue material,
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Blood,
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Swab from nose for detection of carriers.
Transport media: Pike’s medium
Methods of examination:I) Direct Microscopy:
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Direct microscopy with
Gram stained smear is
useful in case of pus &
CSF, where cocci in
chains are seen.
This is of no value for
specimen like sputum &
genital swabs where
mixed flora are
normally present.
II) Culture:
a) Media used:
b) Cultural Characteristics:
c) Gram’s staining:
Smears are
examined from the
culture plate and
reveals Gram
positive cocci in
chains.
d) Biochemical reactions:
e) Bacitracin (1 unit/ml) sensitivity test:
S. pyogens is sensitive.
f) Lancefield sero grouping: Based on ‘C’
carbohydrate antigen
g) Sero typing: sero typing of S. pyogens is
required only for epidemiological purposes.
III) Antigen detection:
ELISA & Agglutination tests are used for
detection of S. pyogens antigen from throat
swabs
B) In Non-suppurative complications
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Serological tests are useful
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The tests are –
1. Anti Streptolysin O (ASO) test
2. Anti Deoxyribonuclease B (anti-DNAase B) test
3. Anti Hyaluronidase test
4. Streptozyme test
TREATMENT:
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Penicillin G is the drug of choice.
In patients allergic to penicillin; erythromycin
or cephalexin is used.
Antibiotics have no effect on established
glomerulonephritis & rheumatic fever.
EPIDEMIOLOGY:
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Streptococcal infections of the respiratory tract are
more frequent in children5-8 years of age.
They are more common in winter in the temperate
countries.
Crowding is an important factor in the transmission
of infections.
Outbreaks of infection may occur in closed
communities such as boarding school or army
camps.
PROPHYLAXIS:
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Prophylaxis is indicated only in the prevention
of rheumatic fever.
It is done by long term administration of
penicillin in children who have developed
early signs of rheumatic fever.
Antibiotic prophylaxis is not useful in case of
glomerulonephritis.
OTHER HAEMOLYITC STREPTOCOCCI:
Group B: Streptococcus agalactiae
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It is a important pathogen of cattle & causes
bovine mastitis.
In human it inhabitats genital tract.
Clinical significance:
1. Infection in neonates: 2 types
a. Early onset disease- Occurs during first week
of life.
Source of infection- Vagina of the mother &
infection is acquired during birth.
Clinical symptoms- Septicemia, meningitis &
pneumonia.
b. Late onset disease- Occurs during 2nd & 12th
week of life.
Source of infection: It usually acquired from the
hospital environment.
Clinical symptoms- Osteomyelitis, arthritis,
conjunctivitis, respiratory infection, endocarditis
& peritonitis.
2. Infection in adult: It causes bacteraemia,
sepsis , wound infection, septic abortion &
puerperal sepsis.
Laboratory diagnosis:
Specimens collected: Blood, CSF & exudates
from lesions.
Methods of examinations:
1. Detection of antigen in clinical samples.
2. Direct microscopy by doing Gram’s smear.
3. Culture- Blood agar is used for culture.
4. Identificationa. Small β-haemolytic colonies on blood agar
b. Gram staining
c. Catalase test- Negative
d. Hippurate hydrolysis- Positive
e. CAMP test :
f. Lancefield sero grouping is done for
confirmation.
Treatment: Penicillin is used.
Group D Streptococci:
Classified into 2 groups1. The enterococcus group- which have
been reclassified as a separate genus called
Enterococcus, containing- E. faecalis,
E. faecium & E. durans.
2. Non enterococcal group- containing
S. bovis & S. equinus
ENTEROCOCCUS
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1.
2.
3.
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5.
Normal inhabitants of human intestinal
tract.
Possess some distinctive properties likeThey grow in 40% bile,
They resist pH till 9.6.
They grow in 6.5% NaCl solution,
They grow at 45ºC can withstand up to 60ºC for
30 minutes.
They grow in 0.1% methylene blue milk.
Morphology:
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Enterococci typically
appear as pairs of
oval Gram positive
cocci.
The cells in a pair
arranged at an
angle to each other.
Clinical significance:
Source & mode of infection:
1. Endogenous-from colonized site.
2. Exogenous-through direct or indirect contact.
Common infections:
1. Urinary tract infection,
2. Bacteremia,
3. Wound infection,
4. Biliary tract infection,
5. Sub acute bacterial endocarditis.
Laboratory diagnosis:
Specimens collected: Urine, blood, pus &
exudates.
Methods of examination:
1. Direct microscopy- by doing Gram’s smear.
2. Culture- Blood agar and MacConkey’s agar is
used.
3. Colony morphologyi) On blood agar small non-haemolytic colonies
are seen but some strains may show α or β
haemolysis.
ii) On MacConkey’s agar it produces pink
colour colonies.
4. Identificationi)
Gram’s smear
ii)
Catalase test- Negative
iii) Biochemical tests It ferments mannitol, sucrose & sorbitol.
 Bile esculin test- positive
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Treatment:
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Strains resistant to penicillin & other
antibiotics occur frequently.
Vancomycin is the alternative drug to
penicillin.
Vancomycin resistant is also seen.
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