STREPTOCOCCI

BY DR/ MONA RAMADAN

 The important properties of genus Streptococci

1. These are Gram-positive cocci arranged in chains

2. non-motile, and nonspore forming, sometimes capsulated.
3. All Streptococci are catalase negative.
 Classification:

1- According to haemolytic activity on

sheep blood agar:
Beta (ß) haemolytic: cause complete lysis of RBCs e.g.:
S.pyogenes .
Alpha (α) haemolytic: cause incomplete haemolysis of RBCs;
producing greenish discoloration of blood agar e.g. viridians
streptococci & S. pneumoniae.
Non-haemolytic: have no effect on blood agar.
Haemolytic activity on sheep blood agar:
2- According to C carbohydrate antigen (Lancefield classification):
Beta haemolytic Streptococci are further classified into serogroups (A-U) according to
carbohydrate (C) antigen in their cell wall. Group A (S.pyogenes) is the most important
pathogen to man.
3- According to M protein antigen (Griffith classification):
Group A beta haemolytic Streptococci (GABS; S. pyogenes) is further classified into more than
80 serotypes according to a surface protein antigen called M-protein.
Streptococcus pyogenes
 (Group A Beta Haemolytic Streptococci)
Routes of infection
are respiratory droplets, skin contact and food borne (unpasteurized milk)
Virulence factors of S. pyogenes
A) Cell-associated factors:
1. M-protein:
It is expressed by all GABS - it is anti-phagocytic.
2. Capsule:
antiphagocytic but nonimmunogenic.
B- Enzymes and Toxins:
1 Streptolysins:
i) Streptolysin O: It is oxygen labile, It is antigenic i.e. induce antibody formation (anti-
streptolysin O). It increases the ß haemolytic zone diameter on anaerobic culture.
ii) Streptolysin S: It is oxygen stable but non antigenic and it is responsible for the ß haemolytic
zone around streptococcal colonies.
2-Spreading factors:
a) Streptokinase (fibrinolysin): Converts plasminogen into plasmin, which can digest fibrin
threads leading to spread of infection.
b) DNAses (streptodornase): Digests DNA liquefying viscous exudates.
c) Hyaluronidase: dissolve hyaluronic acid, the cement substance of connective tissue, leading
to spread of infection.
3- Pyrogenic exotoxins:
a. Pyrogenic exotoxin A: responsible for most cases of streptococcal toxic shock syndrome.
b. Pyrogenic exotoxin B responsible for extensive tissue destruction in patients with severe
necrotizing fasciitis.
4- Erythrogenic toxin:
It is responsible for the rash in scarlet fever patients. It also acts as a super antigen.
Diseases caused by S. pyogenes:
I- Non-invasive infections: e.g.: Acute pharyngitis, pharyngotonsillitis, Scarlet fever and
impetigo
II. Invasive infections: e.g.: Necrotizing Fasciitis, Cellulitis
III. Post-Streptococcal Diseases:
These diseases occur 2-3 weeks following streptococcal infections in the throat, respiratory
tract, or the skin. Rheumatic fever and acute glomerulonephritis are the
most common post streptococcal complication.
I- Non-invasive infections
II- Invasive infections:
 Laboratory Diagnosis of invasive and non-
invasive diseases
Specimen:
According to the site of infection; pharyngeal swab, skin swab, or pus , Blood culture
should be done in patients with invasive infections.
Microscopic examination of a Gram stained film:
Shows Gram positive cocci arranged in chains between pus cells.
Isolation & identification:
Blood agar incubated aerobically at 370C for 24hrs. The colonies are identified by
their beta haemolytic activity and their small size
Colonies further identified by:
✓ Gram stained film
✓ Catalase test: Streptococci are catalase negative.
Laboratory Diagnosis of invasive and non-
invasive diseases
 III- Post-Streptococcal Diseases:

1. Rheumatic Fever:
 it leads to permanent damage of the heart valves.
 It is more commonly preceded by S.pyogens throat infection.
 The disease is autoimmune in nature
 production of autoreactive antibodies as a result of cross reactivity between S.pyogens M
proteinand human cardiac valves.
 2. Acute Glomerulonephritis (AGN):
 preceded by skin infection.
 There is haematuria (dark urine), albuminuria, edema and hypertension. The majority of
patients recover completely while some develop chronic Glomerulonephritis.
 The disease is initiated by antigen –antibody complexes on the glomerular basement
membrane which activate the complement system resulting in tissue damage (type III
hypersensitivity reactions)
Laboratory Diagnosis of Post Streptococcal Diseases:

A- Specific Tests:
1 Anti-streptolysin “O” test:
Rising antibody titre is diagnostic of active rheumatic fever.
2 Anti-DNase B test:
Titre of anti DNase in diagnosis of acute glomerulonephritis.
B- Non-Specific Tests: Indicate recent infection and tissue damage. C Reactive protein
(CRP) & Erythrocyte sedimentation rate (E.S.R.).
 Viridians group Streptococcus (VGS)

 These are alpha haemolytic Streptococci

 They are members of the resident flora of the oral cavity(including
S. mutans & S. mitis)
 They produce bacteriocins and hydrogen peroxide which inhibit
colonization of oral cavity by many pathogens.
 They are involved in dental caries and sub -acute bacterial
Endocarditis after release into the bloodstream e.g. from tooth
extraction, in patients with predisposing conditions (diseased or
artificial prosthetic heart valves).
 Subacute Bacterial Endocarditis (SABE)

 The normal commensals in the upper respiratory tract and buccal cavity may
enter the blood (e.g. after tonsillectomy or tooth extraction).
 In healthy individuals, such bacteria are cleared from the circulation within
one hour.
 However, they have special affinity to diseased or artificial prosthetic heart
valves,
 It is diagnosed by isolation of the organism from blood by blood culture.
 Prophylaxis of SABE: dental Administration of amoxicillin before any procedure.
 Streptococcus pneumoniae
 Pneumococci are Gram positive cocci arranged in pairs they are capsulated
 The capsule is Polysaccharide in nature
 Pneumococci can be classified into 90 serotypes according to the capsular
polysaccharide.
 5%–50% of the healthy population harbours virulent organisms in the oropharynx,
so pneumococcal infections are not considered to be communicable.
 Diseases caused by S. pneumoniae
 Otitis media and sinusitis.

 Lobar Pneumonia: Pneumococci are the most frequent cause of Lobar Pneumonia.
Occurs as a result of Aspiration of Pneumococci into the lower respiratory tract. The
inflammatory reaction is focused within a single lobule or lobe.

 Meningitis: It is considered one of the leading causes of bacterial meningitis.

Occurs as a result of local spread or hematogenous spread as a result of bacteraemia
associating lobar pneumonia.
Laboratory Diagnosis of Pneumococcal Infections
1 Specimen: sputum, CSF, or blood.
2 Microscopic examination of a Gram stained film: shows Gram-positive diplococci surrounded
by a clear unstained area, which represents the capsule.
3 Quellung reaction(capsule swelling test):
It is a slide precipitation test for rapid identification and typing of S. pneumoniae.
4 Specimens are cultured on enriched media as blood agar or chocolate agar.
Incubate aerobically with 5-10% CO2 at 37ºC for 24 hours.
The colonies are identified by:
o Colonial morphology
o Gram stained film
o Optochin sensitivity
1- Specimen: sputum, CSF, or blood.
2- Microscopic examination of a Gram stained film: shows Gram-
positive diplococci surrounded by a clear unstained area, which
represents the capsule.
3- Quellung reaction(capsule swelling test):
It is a slide precipitation test for rapid identification and typing of S.
pneumoniae.
4- Specimens are cultured on blood agar
Incubate aerobically with 5-10% CO2 at 37ºC for 24 hours.
Show alpha incomplete hemolysis with greenish pigmentation
Comparison between strept.pneumo.&
strept. Viridans
Strept. Pneumo. Strept.viridans
Bile solubility +ve -ve

Optochin sensitivity +ve -ve

Inulin fermentation +ve -ve

Animal pathogenicity +ve -ve

 Common streptococcal species relevant to dental health
WHAT???
They are Streptococcus mutans, S. sanguinis, S. mitis, and S. salivarius.
While S. mutans is associated with caries, other streptococci (S. sanguinis, S. mitis) are more involved in
periodontal disease
WHERE????
They are found in dental biofilms (plaque), saliva, and mucosal surfaces.
They are normal oral flora but can become pathogenic under certain conditions.
HOW ????
1. They converts dietary sugars into acids (via fermentation), leading to enamel demineralization and enamel
breakdown.
2. Produces glucans from sucrose, aiding in plaque formation Central in the initiation and progression of dental
caries.
3. Streptococci are early colonizers in the biofilm that lay the foundation for further bacterial accumulation &
enable more pathogenic anaerobes to thrive
4. Interaction with other periodontal pathogens (Porphyromonas gingivalis, Tannerella forsythia).
5. They can evade host immune responses by producing enzymes (e.g., IgA protease) that degrade
immunoglobulins