Streptococci. Gram-positive cocci in chains

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Gram-positive cocci in chains (
“Pyogenic cocci” because found in pus forming lesions (also staphylococci).
Group Characteristics.
Gram-positive chain forming cocci.

 Cell division in one direction only.

 Catalase negative

 Facultative anaerobes

 Non-motile

 Require enriched medium (5% added blood).

 Sensitive to benzylpenicillin.

 Killed by heating to 54°C for 30 minutes.

Classified by:
a) Oxygen requirement. Facultative anaerobes (some strict anaerobes).

b)Haemolysis on blood agar:

- haemolysis. Clear zone.

- haemolysis. Partial clearing (green area).

- haemolysis. No visible clearing.

c) Serological typing: Use specific poly-saacharide in cell wall.

 Introduced by Lancefield.

 Called “C” carbohydrate.

 Lancefield scheme includes 20 groups named with letters A-H and K-V.

 Not for S. pneumoniae & Viridans streptococci.

d) DNA hybridisation techniques.
Group A streptococci: S.pyogenes ( β- haemolytic)
Cell Wall Antigens.

  1. C- carbohydrate: Used for Lancefield grouping.

  2. M – protein: Important virulence factor.

  • Anti-phagocytic (protects bacteria from phagocytosis).

  • Host produces antibodies against M-protein.

  • Antibodies bind to M-protein and destroy organism by helping macrophages and neutrophils.

  • More than 60 serotypes of M-protein (thus repeated infections).

  • Other antigens: T and R proteins in cell wall.

Virulence Factors.

  1. Capsule. Prevents phagocytosis.

  2. M-protein. Ability to adhere to surface of host cells and invade cells.

  3. Lipoteichoic acid. Facilitate binding in host.

  4. Toxins and enzymes. Produces many different ones only few described.


  1. Streptolysin O: (Destroys red and white blood cells).

  • Oxygen labile (Sensitive to oxygen).

  • Antigenic. Stimulates anti-streptolysin O antibodies (ASO).

  • Important in diagnosis of Rheumatic fever.

  1. Streptolysin S:

  • Oxygen stable.

  • NOT antigenic.

  • Produces β-haemolysis on blood agar.

  1. Pyrogenic exotoxins (Erythrogenic toxin):

Produced by some lysogenic strains of S.pyogenes in Scarlet fever. Act as “Superantigens” stimulate many cytokines, lead to shock & organ failure.

  1. Fibrinolysin (Streptokinase). Lyses blood clots and aids rapid spread of Streptococci.

  2. Deoxyribonucleases (Streptodornase). De-polymerise free DNA in pus. Reduces viscosity in abscess and helps streptococci in spreading. Four different types known.

  3. C5a Peptidase. Degrades C5a component of complement and so stops activation of phagocytes.

  4. Hyaluronidase. Spreading factor. Breaks down hyaluronic acid found in host connective tissue.

  5. Surface Bound Peptidase. Acts on complement.


  • Colonise oropharynx of healthy children and young adults. Disease usually in children (5 -15 years) but infants and adults may be affected.

  • Colonisation is transient, regulated by the persons ability to mount specific immunity to the M-protein of the infecting strain. Other factors play a role.

  • S.pyogenes disease is caused by recently acquired strains that can establish infection before antibodies are produced

  • Pathogen is spread from person to person through respiratory droplets. Spread is facilitiated in classrooms and daycares.

  • Produces many non-invasive, invasive and non-supurative sequelae (complications).

Clinical Infections.

  • Non-invasive streptococcal disease.

  1. Pharyngitis. (Tonsillitis / Sore throat).

  • Most common S.pyogenes infection.

  • 20-30% of all pharyngitis cases with S.pyogenes. Other agents produce pharyngitis but Group A most frequently.

  • Children more commonly affected.

  • Symptoms: Sudden onset of sore throat. Red swollen tonsils and pharynx with purulent exudate. Pyrexia (high temperature), headache, malaise and swollen lymph nodes.

  • Lasts about 5 days. Antibiotics help recovery and reduce complications (Rheumatic fever).

  • Complications. Rheumatic Fever.

  1. Scarlet Fever.

  • Erythrogenic toxin producing strains.

  • Symptoms:Pharyngitis with diffuse erythematous rash of skin & mucous membranes.

  • Rash 1-2 days after symptoms of pharyngitis.

  • Starts on upper chest area & spreads to extremeties.

  • Area around mouth & soles of feet spared.

  • Yellow-white coating seen on tongue which is shed later revealing red raw surface “strawberry tongue”.

  • Incidence reduced by antibiotic usage.

  1. Impetigo (pyoderma).

  • Mainly in children.

  • Superficial, localised skin infection.

  • Affects face/ arms/ legs.

  1. Erysipelas.

  • Mainly in elderly (sometimes children).

  • Severe infection. In superficial layers with pain and inflamation may involve lymphatics. Systemic signs include fever and chills.

  • Affects face and legs usually.

  1. Cellulitis.

  • Skin and subcutaneous tissue.

  • Other bacteria produce same clinical appearance.

Invasive infections (life threatening).

  1. Necrotising fascitis (NF): Progresses rapidly. Destroys fat & muscle. Enters through skin. Referred to as “Flesh eating bacteria”. Leads to systemic toxicity, organ failure & death.

  2. Myositis: Infection from throat with bacteraemic spread to muscle.

  3. Toxic shock syndrome (TSS): Similar to Staphyloccoccal toxic shock syndrome. Patients may be bacteraemic & often have necrotising fascitis.

  4. Bacteraemia: In patients with TSS or NF.

10.Puerepral sepsis: Females following delivery.

11.Other infections: Lymphangitis or Pneumonia.

Complications/ Late or Non-suppurative sequelae.

  1. Rheumatic Fever:

  • After pharyngitis or scarlet fever (NOT skin infection).

  • Occurs 1-5 weeks later.

  • Characteristics: Inflamatory changes in the heart, joints, blood vessels and sub-cutaneous tissues.

  • Clinical signs: Fever, malaise and migrating arthritis.

  • Antigens in the heart resemble S.pyogenes antigens. Antibodies formed against S.pyogenes cross-react with antigens in heart. Produce cellular damage in heart. Described as immune complex disease or hypersensitivity reaction in individuals following repeated exposure to antigen.

  • Diagnosis. Rise in ASO titres.

2. Glomerulonephritis.

  • After skin infection usually (sometimes pharygitis).

  • About 1 week after infection with nephritogenic strains.

  • Characterised by acute inflamation of glomeruli with oedema, hypertension, haematuria and proteinuria.

  • Patients present with dark urine (tea/coffee colour), haematuria and puffiness / swelling due to fluid retention.

  • Diagnosis: anti-DNAase antibodies.

  • Immunogenic Reaction. Antibody mediated inflammatory disease in glomeruli of kidney. Antigens from nephritogenic streptococci induce antibody response. Resulting antigen antibody complexes travel to and are depositied in glomerular basement membrane. Leads to glomerular destruction in the kidney.

3. Erythema nodosum

  • Skin lesions may follow S.pyogenes infections.

  • Erythema nodosum may also follow tuberculosis or coccidiodiomycosis infection.

  • Suggested that the streptococcal cell wall might be the toxic agent responsible for this syndrome.

Laboratory diagnosis

  1. Specimen: Depends on site. (Throat / Skin swab, pus or blood).

  2. Microscopy: Detect Gram-positive cocci in chains.

  3. Culture: Blood agar. Small (1mm) β-haemolytic colonies.

  4. Confirmatory tests:

  • Catalase: Streptococci are catalase negative.

  • Bacitracin: Sensitive. Zone of inhibition around disc.

  • Antigen detection: Detect S.pyogenes antigen by latex agglutination.

  • Antibody detection for Complications: Antibodies to S.pyogenes. Anti-streptolysin O“ASO”(rheumatic fever) or anti-DNAase in glomerulonephritis.

Treatment and Prevention

  • Penicillin: First choice. Treatment for 3-5 days limits severity of attack & prevents complications.

  • Erythromycin, Azithromycin or cephalosporins (allergic patients).

  • Sulphonamides suppress growth but do not prevent complications.

  • Penicillin as prophylaxis in cases of rheumatic fever recommended, to avoid further damage to heart.

  • Vaccines against S.pyogenes NOT successful because of numerous types of M-protein.

  • Possibility of immunological cross-reactions of many antigens with host tissue components has also made it difficult to prepare vaccines.

Group B streptococci. S.agalactiae (β-haemolytic).

  1. Group characteristics.

  2. β-haemolytic. Difficult to distinguish Group A and Group B (Use Bacitracin disc tests).

  3. Frequently found in female genital tract & in colon.

  4. Virulence Factors:

  • Capsule.

  • Peptidoglycan cell wall.

  • Hydrolytic enzymes help spread of disease.

Clinical Infections.

  • Previous importance in Bovine mastitis. Human infections now known.

  1. Early-onset Neonatal Disease. Acquired prior to or at birth. Pneumonia, meningitis, or bacteraemia. Pulmonary manifestations most common.

  2. Late-onset Neonatal Disease. Older infants acquired from mother or other infant. Meningitis most common.

  3. Infections in Pregnant Women. Urinary tract infections in women during and soon after pregnancy.

  4. Infections in Men & Non-pregnant women. Usually older patients with other conditions. Present with bacteraemia, pneumonia, bone & joint infections or skin infections.

Other β-haemolytic streptococci sometimes producing human disease are Groups C, G and F.
Viridans Group Streptococci (α- haemolytic)

  • Heterogenous group of α-haemolytic streptoccocci.

  • Classification not based on Lancefield antigen.

  • Group name derived from “viridis” in Latin means green.

  • About 24 species known. Include; S.salivarius, S.sanguis, S.mitis, S.intermedius and S.mutans.

  • Normally found in oropharynx, gastrointestinal tract and genitourinary tract.

  • Can cause variety of infections but commonly associated with 3 main diseases: Endocarditis, dental infection, abscesses and malignancy.

Clinical Infections:
1. Endocarditis

  • After tooth manipulation, bacteria enter blood.

  • Specially in patients with a previously damaged heart valve (rheumatic fever, congenital heart disease or other heart disease).

  • Grow on endocardial surface of heart.

  • Bacteria produce material allowing them to cling to cardiac valves.

  • Results in sub-acute bacterial endocarditis.

  • Characterised by slow growth (sub-acute) and piling up of bacteria to produce long vegetative structures on heart which produce emboli.

  • Emboli are shed from time to time into blood.

  • Clinical symptoms - low grade fever, fatigue, anemia, heart murmur and valve destruction.

  • Diagnosis by blood culture.

  • Treated with long course of Penicillin.

  1. Dental Infections: Viridans Streptococci especially S.mutans produce dental caries. Bacteria adhere to teeth and use carbohydrates in diet to produce acid which destroys teeth producing cavities. Prevention of caries by; diet, hygeine, fluoride and restoration of caries.

  2. Abscesses: By micro-aerophilic strains of this group. Often found in GIT. Produce abscesses in abdominal organs and sometimes brain.

  3. Malignancy:

Enterococcus faecalis. Group D (Previously S.faecalis

γ or α-haemolytic)

  1. Enterococci: Independent genus, with many species. E.faecalis most important.

  • Often found in GIT as normal bowel flora.

  • Grow well in 40% bile or 6.5% NaCl (Grow on MacConkey)

  • Clinical diseases: UTI, bile duct infections, bacteraemia and Sub-acute bacterial endocarditis (SBE). Often associated with debilitated patients and in nosocomial infections.

  • Resistant to many antibiotics including vancomycin. New drugs “Pritinomycins” used. May have side effects.

  • Laboratory diagnosis uses a bile esculin agar test. Produce black colonies.

Anaerobic Streptococci. Peptococcus & Peptostreptococcus.

  • Strict anaerobes, (Peptococcus and Peptostreptococcus).

  • Normally found in female genital tract and gastrointestinal tract.

  • Clinical infections: Intra-abdominal abscesses, brain abscesses, empyema, aspiration pneumonia, hepatic abscesses, infections of the female genital tract or infections following surgery in debilated patients.

  • Anaerobic bacteria generally sensitive to metronidazole and penicillin.

Streptococcus pneumonia. (Pneumococcus, Diplococcus).

α- haemolytic.

  • Major pathogen.

  • Encapsulated, Gram-positive, oval or lancet shaped arranged in pairs (Diplococci) or short chains.

  • Colonies α -haemolytic. Encapsulated strains produce larger mucoid colonies.

  • Produce autolytic enzyme.

  • Is fastidious. Requires enriched media.

  • Requires choline for growth.

  • Catalase negative (like other streptococci).

  • C-carbohydrate present but not used for Lancefield grouping.

  • Colonises oropharynx but can produce infection.

Virulence factors

  1. Capsule: Very Important. Anti-phagocytic in absence of type specific antibodies. More than 90 capsular serotypes. Infections involve 23 common serotypes.

  2. IgA1 protease: Extra-cellular protease cleaves human IgA 1. (Produced by other bacteria that cause meningitis). Helps bacteria overcome protective functions of IgA in URT.

  3. Pneumolysin: Intracellular membrane damaging toxin released by autolysis. Immunogenic overcomes host defense mechanisms.

  4. Autolysin: Activated autolysin lyses the bacteria. Releases pneumolysin & large amounts of cell wall fragments which result in large inflamatory response.

  5. Teichoic acid: Activates immune system.

Clinical infections

  1. Most frequent cause of pneumonia.

  2. Onset sudden, chills, rigors, high temperature 39 –41°C, cough with sputum and pleural pain.

  3. Predisposing factors:

  • Viral infection (flu or measles).

  • Natural defense mechanisms of respiratory tract are affected.

  • Drug addicts or alcoholics.

  • Circulatory defects (heart failure)

  1. Usually in lower lobes of lungs (Lobar pneumonia).

  2. Rapid recovery with suitable antibiotics (2-3 wks for Radiological resolution).

  3. Mortality: 5 % (depends on serotype & host factors).


  • Leading cause of bacterial meningtis.

  • Invasion from pharynx to meninges via bloodstream (bacteraemia co-exists).

  • Can follow lung, ear or sinus infection. Or after head injury.

  • Affects adults most often.

  • Classic signs of meningitis with neck rigidity present.

  • Risk of mortality or severe neurological defects higher with S.pneumoniae meningitis than other bacteria.

Otitis Media: Accounts for 50% of ear infections in children.
Sinusitis and Conjunctivitis.
Bacteremia: Occurs in 25 - 30% of pneumococcal pneumonia and 80% meningitis cases. Bacteria are generally not present in blood stream of patients with sinusitis or otitis media.
Laboratory Diagnosis

  1. Specimen: According to site. Sputum, blood, CSF, aspirate from ears or sinuses.

  2. Microscopy:

  • Detect Gram-positive lancet shaped diplococci.

  • Quellung test using anti-capsular antibodies aids detection of capsule.

  • India ink; black dye aids detection of capsule.

  1. Culture / Isolation: On enriched media (with blood). Fastidious organism difficult to isolate. May be overgrown with other respiratory flora in respiratory specimens. Need to distinguish it from Viridans Streptococci (Both are alpha-haemolytic).

  1. Confirmatory / Identification Tests.

  • Optochin: S.pneumoniae sensitive. Culture on blood agar and place othochin disc. Zone of inhibition seen around the disc. NOT observed with other α-haemolytic streptococci of viridans group.

  • Bile solubility test: S.pneumoniae colonies easily dissolved other α-haemolytic colonies remain unchanged.

  • Inulin fermentation: S.pneumoniae breakdown the carbohydrate inulin. Other α-haemolytic streptococci DO NOT ferment inulin.

  • Virulence in mice: Lethal for experimental animals.

Treatment & Control

  • Penicillin first drug of choice.

  • Cephalosporins / Erythromycin (azithromycin) for allergic patients.

  • Chloramphenicol for cases with meningitis.

  • Resistance to penicillin now documented and strains with multiple resistance known.


  • Pneumovax (first vaccine). 23 most common capsular antigens. In patients at high risk (e.g. immune-compromised and elderly). Low immunogenicity and efficacy in children.

  • Heptavalent (new) vaccine. 7 capsular antigens. Conjugated with non-toxic diphtheria protein, it increases immunogenicity. Almost 100% effective.


Dr. Razina/ Streptmed/2009/

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