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General ConceptsStreptococcus pyogenes, other Streptococci, and Enterococcus
Lecture StreptococcusProf . Dr. Abbas Hayat Lecture 2 ( Bacteriology) Class of 2011
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Pyogenic Cocci
• Gram Positive Cocci : 1.Staphylococci
2.Streptococci
3.Streptococci pneumoniae • Gram Negative cocci :
1.Niesseria Species
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Structure
Streptococci are
Gram-positive, Non motile, Non spore forming, Catalase-negative cocci that occur in pairs or chains
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Classification and Antigenic Types
Streptococci are classified on the basis of “
• A. Colony morphology, • B. Hemolysis, • C. Biochemical reactions,
and most definitively by :
D. Serologic specificity.
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• They are divided into three groups by the type of hemolysis on blood agar:
• b-hemolytic (clear, complete lysis of red cells). Lancfield group Streptococcus A-V.
• a hemolytic (incomplete, green hemolysis), • g hemolytic (no hemolysis).
• Serologic grouping is based on antigenic differences in cell wall carbohydrates (groups A to V), in cell wall pili-associated protein, and in the polysaccharide capsule in group B streptococci.
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LANCEFIELD BETA HEMOLYTIC GROUP
• Group A - S. pyogenes • Group B - S. agalactiae• Group C - S. equiniss zooepidemicus• Group D - S. suis • Group E - S. porcinus
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ANTIGENIC TYPES The cell wall structure of group A streptococci is among the most studied of any bacteria .
• The cell wall is composed of repeating units of N-acetylglucosamine and N-acetylmuramic acid, the standard peptidoglycan.
Rebecca Lancefield (1895-1981)
in 1922 while working for her PhD thesis.
• Eighteen group-specific antigens were established on basis C Carbohydrate.
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First Miss India 1929
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Vagaries of age 2009
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Host Defenses
Antibody to M protein gives type-specific immunity to group A streptococci.
• Antibody to Erythrogenic toxin, prevents the rash of scarlet fever.
• Immune mechanisms are important in the pathogenesis of Acute Rheumatic Fever.
• Maternal IgG protects the neonate against group B streptococci.
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Epidemiology• Group A ß-hemolytic streptococci spread by
respiratory secretions and fomites. • The incidence of both infections peaks in
childhood. Infection can be transmitted by asymptomatic carriers.
• Acute rheumatic fever was previously common among the poor; susceptibility may be partly genetic.
• Group B streptococci are common in the normal vaginal flora and occasionally cause invasive neonatal infection.
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• Clinical Manifestations• Disease occur chiefly in the Respiratory tract,
Bloodstream, or as Skin infections.
• Human disease most commonly associated with Group A streptococci.
• Acute group A streptococcal disease is most often a respiratory infection (pharyngitis or tonsillitis) or a skin infection (pyoderma).
• Also medically significant are the late immunologic sequelae, (rheumatic fever following respiratory infection and glomerulonephritis following respiratory or skin infection) which remain a major worldwide health concern.
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Scarlet Fever and Toxic-Shock-Like-Syndrome (TSLS)
• Scarlet Fever: childhood disease, diffuse rash, fever
• 1800s: Late outbreaks of highly virulent form, high death rate
• 1900 - 1950: milder form most common
• 1950: virtually disappeared (use of penicillin?)
• 1980: appearance of streptococcal toxic shock-like disease followed recognition of Toxic Shock Syndrome TSS (S. aureus).
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TOXIC SHOCK SYNDROME- begin frequently as skin or wound infection- developed into septicemia- death rate sometimes over 30% some disabled, some healthy- high fatality rate due to rapid development of shock, multiple organ failure
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Etiological agent: Streptococcus pyogenes • Clinical forms:
–a) Erysipelas. A cutaneous
infection. It results in the formation of a raised, welt-like, large spreading lesion, usually on the face. It is accompanied by a fever and a stinging sensation. It occurs in older persons.
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Etiological agent: Streptococcus pyogenes
• Clinical forms: a) Erysipelas.
A cutaneous infection. It results in the formation of a raised, welt-like, large spreading lesion, usually on the face. It is accompanied by a fever and a stinging sensation. It occurs in older persons.
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• b) Puerperal Fever: - an infection of the uterine muscle tissue which usually occurs during childbirth when there is tearing of the tissue. – (Also called childbed fever). Often, the
organism spreads to the blood from the uterine muscle tissue, causing a fatal septicemia. (Puerperal Fever was very devastating with high fatality rate before antibiotics, and especially before antiseptic procedure was accepted)
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Shah Jahan and Mumtaz Mahal
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• c) Streptococcal Pharyngitis: - An infection of the throat; it is characterized by a reddened, highly inflamed, swollen area with a 103oF. fever.
• In itself, S. Sore throat is not life threatening. The most dangerous aspect of the disease is the possibility of it spreading and causing other sequel clinical forms. That is why S. sore throat is closely monitored
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• d) Glomerulonephritis: - A disease of the kidneys. It is called a Type III mediated immune response or an autoimmune disease because the organism (Strept. pyogenes from a previous infection) produced metabolites which become allergenic. The humoral immune system produces antibodies which combine with these allergens to form an immune complex. These immune complexes lodge in the glomeruli to cause inflammation of the kidneys.
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– e) Rheumatic Fever: A sequel disease to Scarlet Fever or from S. sore throat. It is also a Type III allergic disease or autoimmune diseases. Antigens during streptococcal infection, combine with the IgG antibodies, formed during sensitization.
• The IgG-allergen complex lodges in the joints and endocardium, including the heart valves. This is similar to Glomerulonephritis but different tissues are involved.
• With Rheumatic Fever, the tissue damage, especially to heart valves, can be very pronounced; often causes severe irreversible damage to the heart valves.
It is a very dangerous disease.
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f) Scarlet Fever.• It is characterized by a high fever (103- 104 F)
and by a red rash, usually on the roof of the mouth and on the skin. Usually arises from strep throat.
• These skin lesions (not open lesions, but a rash) tend to feel dry (sand paperish).
• Scarlet fever is not only a severe infection in itself, it may progress to Rheumatic Fever.
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h) Necrotizing Fascilitis (flesh eating strept):
Involves Gp A, strains M-1 & M-3.
Usually results when injury occurs, with these strains present, where the organism secretes SPE exotoxin (Streptococcal pyrogenic exotoxins).
Acts as a "super antigen", which stimulates T cells to produce large amounts of cytokines (MAF), attracting macrophages and leucocytes into the area, degranulate and secrete tissue damaging compounds .
Greatest damage done to blood vessel endothelium, causing fluid loss, shock, rapid tissue necrosis since the cells cannot get oxygen, and often death.
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Diagnosis• Based on cultures from
clinical specimens. Serologic methods can detect group A or B antigen; definitive antigen identification is by the precipitin test.
• Bacitracin sensitivity presumptively differentiates group A from other b-hemolytic streptococci (B, C, G);
• Group B streptococci typically show hippurate hydrolysis;
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• Group D is differentiated from other viridans streptococci by bile solubility and optochin sensitivity.
• Acute glomerulonephritis and acute rheumatic fever are identified by anti-streptococcal antibody titers ASO. In addition, acute rheumatic fever is diagnosed by clinical criteria.
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• Methods of Diagnosis of Group A Streptococcal Diseases: – a) Symptoms – b) The isolation of Streptococcus
species from the infected tissue. – c) ASO Titer (Anti-Streptolysin O
antibody) – d) Strep throat is now most often
diagnosed quickly by a serological diagnostic test. One of the most common types is a latex particle agglutination test, where the latex particles are coated with specific Ab. against the prevailing Ag types of Group A Streptococcus. The swab from your throat is tested for the presence of these Ags by swirling in the tube of latex particles with specific
Ab clumping being positive.
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• ASO TITER greater than 1 in 180 Todd units is helpful in diagnosis of Rheumatic fever.
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• GROUP B STREPTOCOCCI • 25% of all women have this organism as a
vaginal resident. It is an opportunistic pathogen. It causes postpartum endometriosis in a small percentage of women. Also, especially in neonates, a small percentage develops septicemia and pneumonia with a 50% to 70% fatality rate in the first 5 days of life. Meningitis may also occur in babies born to mothers with Group B, in 10th to 60th day of life. Often is fatal.
• Prevention is I.V. administration of ampicillin to expectant mothers who have Group B in vagina. Strept. agalactiae is positive for CAMP test named after Christie Anderson Munch Peterson.
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• GROUP D STREPTOCOCCI • Enterococcus faecalis (GI tract/feces).
Often causes UTI's and wound infection in fecal-contaminated wound and is particularly resistant to antibiotics.
• Non- Lancefield Streptococci (lack the C- carbohydrate group-specific antigen):
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