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.