Streptococci

Streptococci
Streptococci are Gram-positive, nonmotile, catalase-negative, facultativelyanaerobic cocci that occur in chains or pairs. They are classified basedon their hemolytic capacity (a-, b-, c-hemolysis) and the antigenicity of acarbohydrate occurring in their cell walls (Lancefield antigen).b-hemolytic group A streptococci (S. pyogenes) cause infections of theupper respiratory tract and invasive infections of the skin and subcutaneous connective tissue. Depending on the status of the immune defenses and the genetic disposition, this may lead to scarlet fever and severe infections suchas necrotizing fasciitis, sepsis, or septic shock. Sequelae such as acute rheumatic fever and glomerulonephritis have an autoimmune pathogenesis. pneumococci (S. pneumoniae) cause infections of the respiratory tract. Penicillins are the antibiotics of choice. Resistance to penicillins is Persons at high risk can be protected from pneumococcal infections with an active prophylactic vaccine containing purified capsular polysaccharides. Certain oral streptococci are responsible for dental caries. Oral streptococci also cause half of all cases of endocarditis.
Although enterococci show only low levels of pathogenicity, they frequently cause nosocomial infections in immunocompromised patients
(usually as elements of a mixed flora)

General characteristics
Streptococci are round to oval, Gram-positive, nonmotile, nonsporing bacteria that form winding chains or diplococci. They do not produce catalase. Most are components of the normal flora of the mucosa. Some can cause infections in humans and animals

Classification
According to the
1- Haemolysis of red blood cell types
a-, b-, c-hemolysis.
a-hemolysis. Colonies on blood agar are surrounded by a green zone. This “greening” is caused by H2O2, which converts hemoglobin into methemoglobin.
b-hemolysis. Colonies on blood agar are surrounded by a large, yellowish
hemolytic zone in which no more intact erythrocytes are present and the
hemoglobin is decomposed
c-hemolysis. This (illogical) term indicates the absence of macroscopically visible hemolytic zones
2-Lancefield groups. Many streptococci and enterococci have a polymeric carbohydrate (C substance) in their cell walls called the Lancefield antigen.
They are classified in Lancefield groups A-H, K-U based on variations in the antigenicity which retune to the variation in the types of amino sugar
of this antigen.
Specific characteristics of enterococci that differentiate them from streptococci include their ability to proliferate in the presence of 6.5% NaCl, at 45 8C and at a pH level of 9.6.

Streptococcus pyogenes (A Streptococci)
Morphology and culturing. Gram-positive cocci with a diameter of 1 lm
that form chains Colonies on blood agar show b-hemolysis
caused by streptolysins
Fine structure. The murein layer of the cell wall is followed by the serogroup A carbohydrate layer, which consists of C substance and is covalently bound to the murein. M proteinis a Long, twisted protein threads that extend outward are anchored in the cell wall murein it appears as hair-like projections of the cell wall streptococci :it is a major virulence factor of goup A (S.pyogens). A streptococci are classified in serovars with characteristic M protein chemistry. Like the hyaluronic acid capsules seen in some strains, the M protein has an antiphagocytic




Gram positive cocci in twisted chains.


Culture characters: small, whitish-gray colonies surrounded by large b-hemolysis zones; a 5% CO2 atmosphere provides optimum conditions for b-hemolysis.

Extracellular toxins and enzymes. The most important in the context of
pathogenicity are:
Streptolysin O, streptolysin S. Destroy the membranes of erythrocytes
and other cells. Streptolysin O acts as an antigen. Past infections can be detected by measuring the antibodies to this toxin (antistreptolysin titer).
Pyrogenic streptococcal exotoxins (PSE) A, B, C. They esponsible for fever, scarlet fever exanthem and enanthem, sepsis, and septic shock. The pyrogenic exotoxins are superantigens and therefore induce production of large amounts of cytokines
Streptokinase. Dissolves fibrin; facilitates spread of streptococci in tissues.
Hyaluronidase. Breaks down a substance that cements tissues together.
DNases. Breakdown of DNA, producing runny pus.
Pathogenesis and clinical pictures. Streptococcal diseases can be classified as either acute, invasive infections or sequelae to them.
Invasive infections. The pathogens enter through traumas or microtraumas in the skin or mucosa and cause invasive local or generalized infections . The rare cases of severe septic infection and necrotizing fasciitis
PSE superantigens (especially PSEA) induce large amounts of cytokine by . The excess cytokines thus produced are the cause of the symptoms.
Sequelae. Glomerulonephritis is an immune complex disease and acute rheumatic fever may be a type II immune disease (p. 109).
Diagnosis. What is involved in diagnosis is detection of the pathogen by
means of microscopy and culturing. Group A antigen can be detected using particles coated with antibodies that precipitate agglutination (latex agglutination, coagglutination). Using these methods, direct detection of A streptococci in tonsillitis is feasible in the medical practice. However, this direct detection method is not as sensitive as the culture. Differentiation of A streptococci from other b-hemolytic streptococci can be realized in the laboratory with the bacitracin disk test, because A streptococci are more sensitive to bacitracin than the other types.
Streptococcus pneumoniae (Pneumococci)
Morphology and culturing. Pneumococci are Gram-positive, oval to lancets haped cocci that usually occur in pairs or short chains The cells are surrounded by a thick capsule.
When cultured on blood agar, S. pneumoniae develop a-hemolytic colonies with a mucoid (smooth, shiny) appearance (hence “S” form,
Mutants without capsules produce colonies with a rough surface (“R” form). Antigen structure. Pneumococci are classified in 90 different serovars based on the fine chemical structure of the capsule polysaccharides acting as antigens. This capsule antigen can be identified using specific antisera in a reaction known as capsular swelling.
Pathogenesis and clinical pictures. The capsule protects the pathogens from phagocytosis and is the most important determinant of pneumococcal virulence. Unencapsulated variants are not capable of causing disease. Other potential virulence factors include pneumolysin with its effects on membranes and an IgA1 protease. The natural habitat of pneumococci is provided by the mucosa of the upper respiratory tract. About 40–70% of healthy adults are carriers. Pneumococcal infections usually arise from this normal flora (endogenous infections). Predisposing factors include primary cardiopulmonary diseases, previous
infections (e.g., influenza), and extirpation of the spleen or complement
system defects. The most important pneumococcal infections are lobar pneumonia and bronchopneumonia. Other infections include acute exacerbation of chronic bronchitis, otitis media, sinusitis, meningitis, and corneal ulcer. Severe pneumococcal infections frequently involve sepsis.


gram-positive, round-oval, encapsulated cocci; clinical diagnosis: otitis media.

Culture on blood agar: gray coloniesoften mucoid (due to capsules); a zone of greening is often observed around the colonies, caused by a-hemolysis; the shiny appearance of the colonies is caused by light reflections from their mucoid

Diagnosis. The laboratory diagnosis includes detection of the pathogen in
appropriate test samples by means of microscopy and culturing. Pneumococci can be differentiated from other a-hemolytic streptococci based on their greater sensitivity to optochin (ethyl hydrocuprein hydrochloride) in the disk test or their bile solubility. Bile salts increase autolysis in pneumococci.

Streptococcus agalactiae (B Streptococci)
B streptococci occasionally cause infections of the skin and connective tissues, sepsis, urinary tract infections, pneumonia, and peritonitis in immunocompromised individuals. About one in 1000 neonates suffers from a sepsis with or without meningitis. These infections manifest in the first days of life (early onset type) or in the first weeks of life (late onset type). In the early onset form, the infection is caused intra partum by B streptococci colonizing the vagina. Potential predisposing factors include birth complications, premature birth, and a lack of antibodies to the capsule in mother and neonate

Oral Streptococci
Most of the oral streptococci of the type often known as the viridans group have no group antigen. They usually cause a-hemolysis, some c-hemolysis as well.
Oral streptococci are responsible for 50–70% of all cases of bacterial endocarditis, overall incidence of which is one to two cases per 100 000 annually. The origins of endocarditis lie in invasion of the vascular system through lesions in the oral mucosa. A transitory bacteremia results. The heart are colonized and a biofilm is formed by the organism. Predisposing factors include congenital heart defects, acute rheumatic fever, cardiac surgery,
and scarred heart valves. Laboratory diagnosis of endocarditis involves
isolation of the pathogen from blood cultures. Drug therapy of endocarditis is carried out with either penicillin G alone or combined with an aminoglycoside (mostly gentamicin). Bactericidal activity is the decisive parame

Enterococcus (Enterococci)
Enterococci are a widespread bacterial genus (p. 220) normally found in the intestines of humans and other animals. They are nonmotile, catalase-negative, and characterized by group antigen D. They are able to proliferate at 45 8C, in the presence of 6.5% NaCl and at pH 9, qualities that differentiate them from streptococci. As classic opportunists, enterococci show only low levels of pathogenicity. However, they are frequently isolated as components of a mixed flora in nosocomial infections .Ninety percent of such isolates are identified as E. faecalis, 5–10% as E. faecium. Among the most dangerous enterococcal infections is endocarditis, which must be treated with a combination of an aminopenicillin and streptomycin or gentamicin.