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Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students Medical Microbiology Dr. Saleh M.Y. Tuesday; 12/10/2010 Bacteriology Review and Overview Gram +ve cocci: (1) Streptococci, (2) Staphylococci, (3) Sites of infection (4) Toxins, (5) Pathogenicity, (6) Diagnosis (clinical and laboratory diagnosis) and (7) Treatment Definitions: additional to the previous words; define: Acute, Chronic, severe Streptococcus Organism: Genus: Streptococcus, Enterococcus Species: S. pyogenes (Group A), S. agalactiae (Group B), S. mutans (viridans), S. pneumoniae, E. faecalis (Group D) General Concepts: 1

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Page 1: Bacteriology1 strept-phse ii-12-10-2010 -

Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

Medical Microbiology

Dr. Saleh M.Y.

Tuesday; 12/10/2010

Bacteriology

Review and Overview

Gram +ve cocci:

(1) Streptococci,

(2) Staphylococci,

(3) Sites of infection

(4) Toxins,

(5) Pathogenicity,

(6) Diagnosis (clinical and laboratory diagnosis) and

(7) Treatment

Definitions: additional to the previous words; define: Acute, Chronic, severe

Streptococcus

Organism:

Genus: Streptococcus, Enterococcus

Species: S. pyogenes (Group A), S. agalactiae (Group B), S. mutans (viridans), S.

pneumoniae, E. faecalis (Group D)

General Concepts:

The streptococci are a very heterogeneous group of bacteria. Some members are a

part of our normal flora while others are potent pathogens.

The primary pathogens are S. pyogenes and S. pneumoniae but other species can be

opportunistic.

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Group B streptococcus (S.agalactiae)Neonatal septicemia/meningitis CAMP testHippurate hydrolysis testGroup D streptococcusUrinary tract infection/ endocarditis Bile-esculin testEnterococci Non-enterococciLarge colonyMinute colony Viridans streptococciDental caries/endocarditis

Group A streptococcus (S. pyogenes)Lancefield groupsHemolysis (alpha, beta, gamma)Bacitracin susceptibility test M, T, R proteinsStreptolysins O and SF protein/lipoteichoic acidRheumatic fever/carditis/arthritisGlomerulonephritisScarlet feverToxic shock-like syndrome/bacteremia“Flesh-eating bacteria”Pyrogenic toxinErythrogenic toxin

Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

Streptococcus pneumoniae and its infection site

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Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

Streptococcus pyogenes and its infection site

For example:

1. S. agalactiae can produce severe neonatal disease including:

meningitis, pneumonia and bacteremia in infants aged 7 days up to 3 months

2. S. faecalis (E. faecalis) may be implicated in endocarditis and urinary tract

infections.

3. S. mutans is an important contributor to dental caries.

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Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

The streptococci are generally delineated into groups according to the Lancefield

method.

As important as the acute diseases produced by these microorganisms are the later

sequelae of Group A streptococci. These sequelae include i) rheumatic fever

following respiratory infections and ii) glomerulonephritis following skin infections.

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Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

Distinctive Properties:

Streptococci are Gram-positive, non-motile cocci that divide in one plane, producing

chains of cells. S. pneumoniae is a lancet-shaped diplococcus (formerly genus

Diplococcus).

The streptococci are catalase negative (unlike Staphylococcus) and may be either

facultative or obligate anaerobes.

Hemolysis (alpha, beta) on blood agar is an important differential characteristic.

Lancefield groupings are based on the serology of cell wall polysaccharides (18

groups were originally established by Rebecca Lancefield).

The M proteins of group A serve as important virulence factors that help the organism

resist phagocytosis.

Lipoteichoic acids (LTA) mediate attachment to epithelial cells.

Many antigenic moieties on the streptococcal cell surface resemble human muscle

and connective tissue and these similarities may be responsible for the late sequelae.

For example, S. pyogenes membrane Ags resemble cardiac, skeletal, smooth muscle,

heart valve fibroblasts and neuronal tissue.

The capsule of S. pyogenes is composed of hyaluronic acid (like host connective

tissue) so it is non-antigenic while the capsule of S. pneumoniae is very antigenic and

is its sole virulence factor.

Toxins produced by streptococci include: streptolysins (S & O), NADase,

hyaluronidase, streptokinase, DNAses, erythrogenic toxin (causes scarlet fever rash

by producing damage to blood vessels; requires cell to be lysogenized by phage that

encodes toxin).

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Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

Pathogenesis:

S. pyogenes is the leading cause of bacterial pharyngitis and tonsillitis. It may also

produce sinusitis, otitis, arthritis and bone infections. Some strains prefer skin,

producing either superficial (impetigo) or deep (cellulitis) infections.

S. pneumoniae is the major cause of bacterial pneumonia in adults. Its virulence is

dictated by its capsule.

Post-infection sequelae of S. pyogenes occur 1-3 weeks after acute disease. These

sequelae include i) acute rheumatic fever (following pharyngeal infections) and ii)

glomerulonephritis (following either pharyngeal or skin infections). These sequelae

may be due to an altered immune response (autoantibodies). Glomerulonephritis

results from deposition of Ag:Ab complexes on basement membrane of kidney

glomeruli.

Other species/groups include:

Group B strep (e.g. S. agalactiae) most often produce disease in animals but

are also the leading cause of neonatal septicemia and meningitis.

Group D strep (e.g. E. faecalis) produce urinary tract infections and

endocarditis.

Viridans species (e.g. S. mutans) are responsible for oral caries and subacute

bacterial endocarditis following dental surgery.

Anaerobic streptococci may cause genital, brain or abdominal infections.

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Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

Host Defenses:

The normal host resists streptococcal infection; they are often secondary invaders.

The capsule of S. pyogenes is poorly immunogenic; anti-M protein Abs are important

in host defense.

The capsule of S. pneumoniae is very immunogenic; anti-capsule Abs are opsonizing,

enhancing phagocytosis.

Pneumococcal infections occur most often in debilitated persons (alcoholics, elderly,

those with underlying disease).

Epidemiology:

These organisms are widely distributed in nature.

Five to 15% of normal healthy individuals carry S. pyogenes.

Carriage of S. pneumoniae (a solely human organism) is age dependent:

Age % Carriage

Less than 5 40%

5 to 9 30%

10 to 15 17%

adults 6%

adults with children 25%

Streptococci are labile organisms that require close personal contact for

transmission; S. pyogenes respiratory disease peaks at 6 and 13 years old, showing

a seasonal pattern (late winter, early spring).

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Medical Microbiology Dr. Saleh M.Y. Phase II – MBBS Medical Students

Diagnosis:

Clinical: Diagnosis based solely upon symptomology is often not possible.

Laboratory: To confirm the presense of S. pyogenes, throat swabs are used. For S.

pneumoniae, sputum or blood samples are taken. The specimens may then be plated

on blood agar for isolation of Gram-positive, catalase-negative cocci. Useful

characteristics for differentiation include the pattern of hemolysis, bacitracin

resistance or sensitivity and optochin resistance or sensitivity. Immunologically-based

rapid test kits are often employed.

Control:

Sanitary: Since Streptococcus is a labile organism, close contact is required for

spread; hence, avoiding contagious contacts can prevent disease.

Immunological: Pneumococcal vaccines are available for persons at high risk,

particularly the elderly.

Chemotherapeutic: Penicillin is the drug of choice for S. pyogenes and S.

pneumoniae, when the organisms are susceptible. Chemotherapy is given over a 10

and 7-145 days regimen, respectively. Group D streptococci are resistant to many

antibiotics. Life long prophylaxis (low dose penicillin) is recommended for rheumatic

fever patients.

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