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Streptococci
Streptococcus is a genus of spherical Gram-positive bacteria, Cellular division
occurs along a single axis in these bacteria, and thus they grow in chains or pairs. Most
streptococci are oxidase- and catalase-negative, and many are facultative anaerobes.
Classification of Streptococcus:Species of Streptococcus are classified based on their:1- Hemolytic properties:Alpha hemolytic species cause oxidization of iron in hemoglobin molecules within
red blood cells, giving it a greenish color on blood agar. Beta hemolytic species cause
complete rupture of red blood cells. On blood agar, this appears as wide areas clear of
blood cells surrounding bacterial colonies. Gamma-hemolytic species cause no
hemolysis.
2- Rebecca Lancefield:Streptococci are further characterized via Lancefield serotyping, which describes
specific carbohydrates present on the bacterial cell wall. There are 20 described
serotypes, named Lancefield groups A to V (excluding I and J).
In the medical setting, the most important groups are: S. pyogenes (group A
streptococci) and S. pneumoniae (pneumococci). Some of the other medically
important streptococci are S agalactiae (group B), an etiologic agent of neonatal
disease. S. mutans and S. sanguis (viridians streptococci) are responsible for the
formation of dental plaque
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Streptococcus pyogenes :is a spherical, Gram-positive bacterium that is the cause of group A streptococcal
infections. S. pyogenes displays streptococcal group A antigen on its cell wall. S.
pyogenes typically produces large zones of beta-hemolysis (the complete disruption of
erythrocytes and the release of hemoglobin) when cultured on blood agar plates.
Antigenic Types: The cell wall of this bacteria is composed of repeating units of Nacetylglucosamine and N-acetylmuramic acid, the standard peptidoglycan. In group A
streptococci, the R and T proteins may serve as epidemiologic markers, but the M
proteins are clearly virulence factors associated with resistance to phagocytosis. The
capsule of S. pyogenes is composed of hyaluronic acid, which is chemically similar to
that of host connective tissue and is therefore non-antigenic. The cytoplasmic
membrane of S. pyogenes has antigens similar to those of human cardiac, skeletal, and
smooth muscle, heart valve fibroblasts, and neuronal tissues, resulting in a molecular
mimicry
Pathogenesis :Streptococcus pyogenes owes its major success as a pathogen to its ability to
colonize and rapidly multiply and spread in its host while evading phagocytosis and
confusing the immune system.
S. pyogenes has several virulence factors that enable it to attach to host tissues,
evade the immune response, and spread by penetrating host tissue layers. A
carbohydrate-based bacterial capsule composed of hyaluronic acid surrounds the
bacterium, protecting it from phagocytosis by neutrophils. In addition, the capsule and
several factors embedded in the cell wall, including M protein, lipoteichoic acid, and
protein F (SfbI) facilitate attachment to various host cells. M protein also inhibits
opsonization by the alternative complement pathway by binding to host complement
regulators. The hemolysin released by streptococci is of two types: Streptolysin-S
which is an oxygen-stable cytolysin and Streptolysin-O which is a reversibly oxygenlabile cytolysin. Both are leukotoxic. Hyaluronidase , Streptokinases participate in
fibrin lysis. Streptodornases possess deoxyribonuclease activity. Three pyrogenic
(erythrogenic) exotoxins of S. pyogenes (SPEs) are recognized: types A, B, C. These
toxins act as superantigens. This pyrogenic exotoxin is responsible for the rash of
scarlet fever and many of the symptoms of streptococcal toxic shock syndrome. They
stimulate T cells by binding class II MHC molecules directly and nonspecifically.
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Clinical Manifestations:
Group A Streptococcus (GAS), is the causative agent in a wide range of Group A
streptococcal infections. These infections may be non-invasive or invasive. The noninvasive infections tend to be more common and less severe. The most common of
these infections include streptococcal pharyngitis (strep throat) and impetigo(infection
of the superficial layers of the skin) or cellulitis (infection of the deep layers of the
skin), skin infection (pyoderma) and scarlet fever (rash). The invasive infections,
toxigenic infections cause by Group A β-hemolytic streptococcus tend to be more
severe and less common. This occurs when the bacterium is able to infect areas where
it is not usually found, such as the blood and the organs. The diseases that may be
caused as a result of this include streptococcal toxic shock syndrome (STSS),
destructive wound infections (necrotizing fasciitis NF) (the 'flesh-eating' bacterial
infections). Invasion of the upper or lower respiratory tracts results in infections of the
middle ear (otitis media), sinuses (sinusitis), or lungs (pneumonia). In addition,
meningitis can occur by direct infection from the middle ear or sinuses to the meninges
or by way of bloodstream invasion from the pulmonary focus. Bacteremia can also
result in infection of bones (osteomyelitis) or joints (arthritis).
Post streptococcal Sequelae: Infection with S. pyogenes (but not S pneumoniae) can
give rise to serious nonsuppurative sequelae: 1- acute rheumatic fever and 2- acute
glomerulonephritis. These sequelae begin 1-3 weeks after the acute illness, a latent
period consistent with an immune-mediated rather than pathogen-disseminated
etiology.
1-Acute rheumatic fever:- is a sequela only of pharyngeal infections, Rheumatic
fever, a disease that affects the joints, kidneys, and heart valves, is a consequence of
untreated strep A infection caused not by the bacterium itself. Rheumatic fever is
caused by the antibodies created by the immune system to fight off the infection crossreacting with other proteins in the body. This "cross-reaction" causes the body to
essentially attack itself and leads to the damage above. Acute rheumatic fever can
result in permanent damage to the heart valves. however, recurrences are common, and
life-long antibiotic prophylaxis is recommended following a single case.
2- Acute glomerulonephritis:- acute glomerulonephritis can follow infections of the
pharynx or the skin. Acute glomerulonephritis results from deposition of antigenantibody-complement complexes on the basement membrane of kidney glomeruli. The
antigen may be streptococcal in origin or it may be a host tissue species with antigenic
determinants similar to those of streptococcal antigen (cross-reactive epitopes for
endocardium, sarcolemma, vascular smooth muscle). The incidence of acute
glomerulonephritis is more variable, perhaps due to cycling of nephritogenic strains,
but appears to be decreasing; recurrences are uncommon, and prophylaxis following an
initial attack is unnecessary.
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Diagnosis:
Clinical: It is not usually possible to diagnose streptococcal pharyngitis or tonsillitis
on clinical grounds alone. Accurate differentiation from viral pharyngitis is difficult
even for the experienced clinician, and therefore the use of bacteriologic methods is
essential. When documented streptococcal pharyngitis is accompanied by an
erythematous punctiform rash, the diagnosis of scarlet fever can be made. With
streptococcal toxic shock syndrome, unlike staphylococcal toxic shock syndrome
where the organism is elusive, there is often a focal infection or bacteremia. Criteria
for diagnosis of streptococcal toxic shock syndrome include hypotension and shock,
Isolation of S. pyogenes, as well as 2 or more of the following: renal impairment, liver
abnormality, coagulopathy, rash with desquamating soft tissue necrosis.
Rheumatic fever is a late sequela of pharyngitis and is marked by fever, polyarthritis,
and carditis. A combination of clinical and laboratory criteria is used in the diagnosis
of acute rheumatic fever. The other late sequela, acute glomerulonephritis, is preceded
by pharyngitis or pyoderma; is characterized by fever, blood in the urine (hematuria),
and edema; and is sometimes accompanied by hypertension and elevated blood urea
nitrogen (azotemia).
Identification:
Bacitracin susceptibility is a widely used method for identification of S. pyogenes.
Some of the group B-streptococci also may be bacitracin sensitive, but are
presumptively identified by their properties of hippurate hydrolysis and CAMP test
positivity.
Serologic Titers:
Antibodies to some of the extracellular growth products of the streptococci are not
protective but can be used in diagnosis. The antistreptolysin O (ASO) titer which
peak 2-4 wks after acute infection and anti-NADase titers (which peaks 6-8 weeks
after acute infection) are more commonly elevated after pharyngeal infections. Titers
observed during late sequelae (acute rheumatic fever and acute glomerulonephritis)
reflect the site of primary infection.
Control:
Antibiotic Treatment: Penicillin remains the drug of choice for S. pyogenes. It is
safe, inexpensive, and of narrow spectrum, and there is no direct or indirect evidence
of loss of efficacy. If penicillin allergy occurs, an alternative drug for treating
pharyngitis is erythromycin, although sporadic erythromycin and tetracycline
resistance has been reported, leaving clindamycin or the newer macrolides as
possible treatments. The most important goal of therapy in acute streptococcal
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pharyngitis is still to prevent rheumatic fever. Lifelong prophylaxis against
recurrences of rheumatic fever is achieved with long-acting penicillin or erythromycin.
Additional prophylactic coverage before some dental and surgical procedures is
necessary in the presence of rheumatic heart disease or prosthetic heart valves.
S. agalactiae, or GBS:causes pneumonia and meningitis in neonates and the elderly, with occasional
systemic bacteremia. They can also colonize the intestines and the female reproductive
tract, increasing the risk for premature rupture of membranes during pregnancy, and
transmission of the organism to the infant
S. pneumoniae:
S pneumoniae are Gram-positive bacteria in the shape of a slightly pointed cocci.
They are usually found in pairs (diplococci), but are also found singly and in short
chains. Streptococcus pneumoniae is known to cause bacteremia, otitis media, and
meningitis in humans, though it is best known for causing pneumonia, a disease of the
upper respiratory tract that causes illness and death all over the world. (5) Symptoms
of pneumonia include a cough accompanied by greenish or yellow mucous, fever,
chills, shortness of breath, and chest pain. The bacteria enter the body most commonly
via inhalation of small water droplets. Very young children and the elderly are the
most prone to catching pneumonia. S. pneumoniae can be separated from other αhemolytic streptococci on the basis of sensitivity to bile salt and optochin. S
pneumoniae is also identified by the Quellung reaction (capsular swelling test) that
employs type-specific anticapsular antibody.
Viridans Streptococci:
S mutans and S sanguis are responsible for the formation of dental plaque, the
dense adhesive microbial mass that colonizes teeth and is linked to caries and other
human oral disease.
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