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Streptococcal infections are caused by
species of the genus streptococcus, which includes Streptococcus
pyogenes (group A), S. agalactiae (Group B), S. faecalis (group D), S.
pneumoniae (pneumococcus) and the viridans streptococci group.
Although streptococci elicit
suppurative inflammatory responses, there are several nonsuppurative
complications that reflect immune responses and deposition of immune
complexes.
Streptococcal infections occur
throughout the world, even where antibiotics are readily available.
As in the case of many infections,
problems with streptococci are greatest among underprivileged
populations for whom penicillin and other antibiotics are not readily
available.
Streptococci
become nonvirulent on desiccation, and indirect spread rarely occurs.
To acquire
infection, an individual must usually be inoculated with millions of
streptococci, spread by close contact with a carrier or with some one
who has an active infection. But of those colonized with streptococci,
a few actually develop an overt infection. Whether or not infection by
a streptococcus becomes clinically apparent, patients are at risk from
the late, “nonsuppurative”, immune complications (Eg.
rheumatic
heart disease, acute glomerulonephritis, and
erythema nodosum
.
The streptococcus is gram-positive and
is demonstrated in cultures, smears, and tissue sections. The
organisms are spherical and very small (less than 2 micrometer
diameter), and the oil immersion lens must be used in searching for
them in tissue sections.
Cultural, biochemical, and immunologic
studies have identified many groups and subtypes of streptococci :
Group A
beta-hemolytic streptococci (for example S. pyogenes) cause
nasopharyngeal and cutaneous lesions, different strains infecting
these sites.
Group B streptococci
produce infections of the new born.
Group C, G, and other streptococci
are responsible for
respiratory infections.
Alfa (green)
hemolytic streptococci (for instance S. viridans), are part of the
flora of the mouth and cause about one-half of all bacterial endocarditis.
Group D
streptococci (e.g. enterococci)
are an important cause of infections
of the urinary tract, endocarditis, postsurgical infections,
septicemia, and other infections.
Pneumococci
(Streptococcus pneumoniae) produce primary bacterial pneumonia,
septicemia, meningitis, and other infections.
ANTIGENS AND
EXOTOXINS:
The capsule of the streptococcus is a
polysaccharide that contains hyaluronic acid.
The cell wall contains antiphagocytic
“M protein” (closely linked to virulence), and lipoteichoic acid,
which is required for recognition of and adhesion to the host
epithelial cell membranes.
The structural backbone of the
cell wall is a peptidoglycan that has pyrogenic properties and weak
endotoxicity.
Group A streptococci produce several
exotoxins, including erythrogenic toxins (pyrogenic exotoxins) and cytolytic toxins (streptolysins S and O).
Erythrogenic toxins cause the rash of
scarlet fever (not directly but by enhancing acquired hypersensitivity
to diverse streptococcal products).
Most, but not all, group A streptococci
produce both streptolysin S and streptolysin O, which are not only
“hemolysins” (lysing red blood cells), but also cytolytic (that is,
they damage and lyse a broad spectrum of mammalian cells and cellular
components).
The surface hemolysis on blood
agar plates is largely caused by streptolysin S, which also lyses
bacterial protoplasts (L-forms) and probably destroys neutrophils
after they ingest group A streptococci.
This toxins influences T-lymphocytes to
a much greater extent than B-lymphocytes and has antitumor activity.
Because streptolysin S is not
immunogenic, its effect may be unimpeded even after repeated
streptococcal infections.
By contrast, streptolysin O induces a
persistently high antibody titer, an effect that provides a useful
marker for the diagnosis and epidemiologic studies of group A
streptococcal infections and the late nonsuppurative complications.
Streptolysin O also has
cardiotoxic properties, possibly playing a role in acute rheumatic
fever and
rheumatic
heart disease
.
PRIMARY STREPTOCOCCAL INFECTIONS:
Infections of the Upper Respiratory Tract :
Infections of the upper respiratory
tract are caused mainly by group A beta-hemolytic streptococcus and
present as pharyngitis, pneumonia, and pulmonary abscesses.
The pharyngitis varies in
intensity from mild lesions resembling the common cold, to more severe
lesions that involve the epiglottis and the tonsillar crypts.
These lesions commonly produce
vasodilatation, spreading edema, and an exudate composed mostly of neutrophils, often mixed with macrophages.
Streptococci may spread from the
pharyngitis to the airways, especially if there is a peritonsillar or
a retropharyngeal abscess.
Scarlet Fever :
Visit:
Scarlet Fever
Scarlet fever, which results from an
acute pharyngitis or tonsillitis caused by group A streptococci, is
characterized by a rash produced by the erythrogenic toxin.
The incubation period of 2 to 5 days is
followed by chills and fever, fiery red pharyngeal mucosa, small crypt
abscesses in enlarged tonsils, and a bright red tongue with edematous
papillae ("raspberry tongue").
Erysipelas :
Erysipelas, caused chiefly by
beta-hemolytic group A streptococci, is the classic cutaneous
streptococcal infection.
It is common in warm climates, but is
not often seen before the age of 20 years.
Erysipelas is an erythematous swelling
of the skin that usually begins on the face and spreads rapidly.
The map-like area of brawny erythema
has a sharp, well-demarcated, serpiginous border.
A diffuse, edematous, acute
inflammatory reaction in the dermis and epidermis extends into the
subcutaneous tissues.
The inflammatory infiltrate
(mostly neutrophils) is more intense around vessels and adnexae of the
skin.
Cutaneous microabscesses and
small foci of necrosis are not uncommon.
Impetigo:
Visit:
Staphylococcal
Impetigo
Impetigo,
another infection of skin that may be caused by
streptococci, has increasingly been reported as a cause of
post-streptococcal complications in children.
Streptococcal
and staphylococcal impetigo have similar lesions, including
folliculitis, pyoderma, wound infection, lymphatic spread, and sepsis.
Streptococcal
impetigo more often induces lymphangitis (red streaks along the
draining lymphatics) than does staphylococcal impetigo, and less
frequently causes focal tissue necrosis or abscesses.
Apthous Ulcers :
Recurrent aphthous ulcers of the lip
(chancres) have been associated with and may be caused by
Streptococcus sanguis in those who are susceptible.
Puerperal Sepsis :
Puerperal sepsis, a result of infection
by group A streptococci from the contaminated hands of attendants at
delivery, was formerly common but with the acceptance of the “germ
theory” of disease and improved hygiene, is now rare in the developed
countries.
Group B streptococcus is an important
neonatal pathogen, causing pneumonia, sepsis, and meningitis. Infants
acquire the infection from their mothers during delivery, and
mortality rates are high (50% or more) if the onset on infection is
within 10 days of delivery.
SECONDARY STREPTOCOCCAL
INFECTIONS:
Streptococcal septicemia:
Streptococcal septicemia
with group A streptococci may spread
from the nasopharynx to the systemic circulation and seed the lungs,
meninges, or heart valves. Streptococcal septicemia can develop
quickly, may be life-threatening, and is a particular hazard for
splenectomized patients or those with abnormal splenic function.
Pneumococcal pneumonia and meningitis:
Pneumococcal pneumonia and
meningitis result from infection with S. pneumoniae (the pneumococcus),
an organism that is responsible for 80% of all bacterial pneumonias.
Pneumococci also spread from the nasopharynx through the systemic
circulation and seed the meninges. Some patients develop meningitis
from primary pneumococcal pneumonia . For example, in most parts of
Africa, a meningitis is more commonly caused by the pneumococcus than
by the meningococcus. The histologic features of pneumococcal
meningitis resemble those described for meningococcal meningitis.
Meningococcal Infection
Bacterial endocarditis :
Visit:
Infective Endocarditis
Bacterial endocarditis is a
complication of streptococcal septicemia in which the organisms spread
from a site of local infection through the circulation to colonize
heart valves. The alpha-hemolytic streptococci are a leading cause of
subacute bacterial endocarditis , where as Streptococcus pneumoniae
frequently produces acute bacterial endocarditis. Endocarditis
caused by group A streptococci is rare. Group D streptococci
(including enterococci) also cause endocarditis, but infection of the
valves with group A streptococci is rare.
NONSUPPURATIVE COMPLICATIONS:
Rheumatic Fever :
Rheumatic fever is an acute, recurrent,
systemic inflammatory process that usually follows a pharyngeal
infection by group A streptococci. Rheumatic fever probably results
from a reaction between antibodies to streptococcal antigens and
tissue antigens that takes place in many sites, but it is particularly
dangerous in the heart. The disease is characterized by pancarditis,
migratory polyarthritis of large joints, erythema marginatum of the
skin, subcutaneous nodules, and chorea (a neurologic
disorder with involuntary, purposeless movements).
Acute Glomerulonephritis :
Acute glomerulonephritis is an immune
complex-mediated disease that is caused only by certain nephritogenic
strains of group A streptococci. There is a latent period between the
infection and the onset of nephritis during which the titer of
antibodies (Eg: Antistreptolysin-O) increases. Granular deposits
in the glomeruli contain immunoglobulin and complement, a reflection
of antigen-antibody complexes.
Erythema Nodosum :
Visit:
Erythema Nodosum
Erythema nodosum is an inflammatory
reaction of the subcutaneous adipose tissue (panniculitis) that is
sometimes associated with infections, including those with group A
streptococci. The connective tissue septa of the fat are widened
by edema and an exudate of fibrin and neutrophils. Later the
inflammatory infiltrate contains lymphocytes, histiocytes, giant cells
and occasional eosinophils.
Abstracts:
Viridans group streptococcal infections
among children with cancer and the importance of emerging antibiotic
resistance.
Semin Pediatr
Infect Dis. 2006 Jul;17(3):153-60.
Transient encephalopathy complicating
poststreptococcal glomerulonephritis in an adult with diagnostic
findings consistent with cerebral vasculitis.Am J Kidney Dis. 2006 Sep;48(3):489-94.
Acute peritonitis and salpingitis
associated with streptococcal toxic shock syndrome caused by
Lancefield group G alpha-haemolytic Streptococcus dysgalactiae subsp.
equisimilis.J Med Microbiol.
2006 Jul;55(Pt 7):953-6.
A large food-borne outbreak of group A
streptococcal pharyngitis in an industrial plant: potential for
deliberate contamination.Isr Med
Assoc J. 2006 Sep;8(9):618-21.
Rapid antigen detection testing in
diagnosing group A beta-hemolytic streptococcal pharyngitis.Expert Rev Mol Diagn. 2006 Sep;6(5):761-6.
Acute group A streptococcal mastoiditis
complicated by pneumocephaly in a previously healthy adult.Scand
J Infect Dis. 2006;38(8):719-21.
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