How
are streptococci differentiated? Discuss the diseases caused by each of these
groups and the mechanisms responsible for the cause of these diseases.
Outline:
·
Streptococcus pyogenes: pharyngitis, scarlet fever, cellulitis,
rheumatic fever, acute glomerulonephritis
·
Streptococcus agalactiae: neonatal meningitis and sepsis.
·
Viridans streptococci: endocarditis
·
Group D streptococci: urinary tract infection.
·
Streptococcus pneumoniae: pneumoniae, meningitis, sepsis.
Suggested
Answer:
The streptococci are divided into six groups by academic taxonomists. One
of the most important criteria for identification is the type of hemolysis.
Alpha-hemolytic streptococci form a green zone around their colonies as a result
of incomplete lysis of red blood cells in the agar. This group is loosely
described as ‘viridans streptococci’. Beta-hemolytic streptococci form a
clear zone around their colonies, since complete lysis of red cells occur. Some
streptococci are nonhemolytic (gamma-hemolysis).
The beta-hemolytic streptococci are arranged into groups A-U (known as
Lancefield groups) on the basis of antigenic differences in C carbohydrate. In
the clinical laboratory, the group is determined by precipitin tests with
specific antisera or by immunofluorescence.
Group A streptococci (Streptococcus pyogenes) are the most
frequent cause of pharyngitis. They adhere to pharyngeal epithelium via pili
covered with lipoteichoic acid and M protein. Many strains have a hyaluronic
acid capsule that is antiphagocytic. They produce a variety of exotoxins which
are responsible for the diseases they caused. Erythrogenic toxin causes the rash
of scarlet fever. Pyrogenic exotoxin A is a superantigen that causes the release
of large amounts of cytokines from helper T cells and macrophages, resulting in
toxic shock. Exotoxin B is a protease that rapidly destroys tissue and is
produced in large amounts by strains of S. pyogenes that cause
necrotizing fasciitis.
Poststreptococcal
diseases occur weeks later after local streptococcus infection and is
immune-mediated. Acute glomerulonephritis typically occurs 2-3 weeks after skin
infection by certain group A streptococcal types in children. The most striking
clinical features are hypertension, edema of the face and ankles, and
‘smoky’ urine. The disease is initiated by antigen-antibody complexes on the
glomerular basement membrane, and soluble antigens from streptococcal membranes
may be the inciting antigen. Rheumatic fever occurs approximately 2 weeks after
any type of group A streptococcal infection – usually pharyngitis, and is
characterized by fever, migratory polyarthritis and carditis. Rheumatic fever is
due to an immunologic reaction resulting from cross-reactions between
streptococcal antigens and antigens of joint and heart tissue.
Group
B streptococci (Streptococcus agalactiae) cause neonatal sepsis and
meningitis. They form part of the normal flora of the vaginal in many women. The
main predisposing factor is prolonged rupture of the membranes, ie, longer than
18 hours, in women who are colonized with the organism. Children born prior to
37 weeks’ gestation have a greatly increased risk of disease.
Group
D streptococci includes members of the genus Enterococcus and a few true
streptococci including Streptococcus bovis. Enterococci cause urinary
tract infections, especially in hospitalized patients. Indwelling urinary
catheters and urinary tract instrumentation are important predisposing factors.
Enterococci also cause endocarditis, especially in patients who have undergo
gastrointestinal or urinary tract surgery or instrumentation. They also cause
intra-abdominal and pelvic infections, especially in combination with anaerobes.
Streptococcus bovisi causes endocarditis, especially in patients with
carcinoma of the colon. Group C and group G streptococci can cause sore throat,
soft tissue infections, and other forms of invasive sepsis. Very occasionally
group C strains can cause acute glomerulonephritis and group G strains, scarlet
fever.
The most pathogenic member of the alpha haemolytic streptococci is Streptococcus
pneumoniae. It is distinguished from others as it is inhibited by a chemical
called optochin – the rest are resistant. The other members can be grouped as
the ‘viridans streptococci’. Streptococcus pneumoniae is not regarded
as part of the normal flora though it is frequently carried in the throat. Its
most important virulence factor is the anti-phagocytic capsule. Different
strains can produce many different types, which only confer type-specific
immunity after recovery. The main infections are pneumonia and meningitis.
Bacteraemia and septicaemia may occur. Pneumococcal pneumonia typically presents
with a lobar pattern of consolidation. Bacteraemia may result in seeding of
bacteria to other organs including joints and pericardium. Complications of
pneumonia include empyema and lung abscess. Other infections include upper
respiratory tract infections such as otitis media and sinusitis.
Infective
endocarditis is commonly caused by viridans streptococci that intermittently
enter the bloodstream from the oropharynx (as a result of poor dentition or
after dental surgery). Signs of endocarditis are fever, anemia, heart murmur,
and embolic events. It is 100% fatal unless effectively treated with
antimicrobial agents.
Members
of the Anginosus group of Streptococci used to be called Streptococcus
milleri but is now divided into three new species – S. anginosus, S.
constellatus and S. intermedius; members of this group are found in
the normal mouth and gut flora but are particularly associated with deep
abscesses.