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The main characteristics of streptococci include the following.
- They are Gram-positive cocci arranged in pairs and chains.
- They are fastidious facultative anaerobes.
- They require rich blood-containing media.
- They may be cultured from the site of infection (throat, wound,
etc.) or in blood cultures.
- Colonies are distinguished by haemolysis: complete (ß) or
incomplete (a) and none (?).
is carried asymptomatically in the pharynx
of 5-30% of the population, more commonly in children. It is
transmitted by the aerosol route and by contact.
Streptococcus pyogenes is surrounded by the M protein antigen,
which reduces leucocyte phagocytosis. Antibodies to M proteins
are protective but only against infection with the same M type and
there are multiple M types. They adhere via fibronectin receptors.
Other features are:
- toxins are important in their pathogenicity:
- erythrogenic toxin associated with scarlet fever;
- pyrogenic exotoxins A, B and C associated with toxic shock;
- production of S. pyogenes cell envelope proteinase (SpyCEP),
which degrades IL-8 and other cytokines, thereby retarding neutrophil
- ability to invade and survive intracellularly making them difficult
to eradicate with penicillin;
- production of degrading enzymes (immunoglobulin proteases,
hyaluronidase and collagenases).
Streptococcus pyogenes, which is an important cause of mortality
worldwide, has the following associations:
1 Invasive disease
characterized by rapid onset, local tissue
destruction and rapid spread within the tissues. Systemic toxicity
is common and associated with toxin production. Syndromes
2 Postinfectious immune-mediated diseases
- pharyngitis - the most common bacterial cause (see Respiratory tract infections
- skin infection - erysipelas, impetigo, cellulitis, wound infections
and rarely, necrotizing fasciitis or pneumonia (see Infections of the skin and soft tissue);
- puerperal sepsis (see Congenital and perinatal infections
- complications such as septicaemia and metastatic infections (e.g.
- severe toxicity:
- erythrogenic toxin causes scarlet fever;
- pyrogenic toxin-producing strains are associated with streptococcal
shock and have a high mortality due to multiple organ
which include rheumatic
fever, glomerulonephritis and erythema nodosum, are
thought to be immune-mediated because antibodies to bacterial
structures cross-react with host tissues. Rheumatic fever, now
uncommon in developed countries, is a major cause of long-term
morbidity and mortality, particularly in areas of poverty and
Prevention and control
Streptococcus pyogenes can spread rapidly in surgical and obstetric
wards; infected or colonized patients should be isolated in a side
room until 48 h after initiation of effective antibiotics. Prompt
treatment prevents secondary immune disease (e.g. rheumatic
fever). Benzylpenicillin is the treatment of choice and resistance
has never been reported. Amoxicillin may be used for oral therapy
in less severe infections. Macrolides are an alternative for patients
Streptococcus agalactiae (group B streptococcus) is a commensal
in the gut and female genital tract. It causes:
- early perinatal pneumonia or septicaemia;
- later perinatal meningitis;
- puerperal sepsis.
The polysaccharide antiphagocytic capsule is the main pathogenicity
determinant. Prophylactic therapy to prevent neonatal
disease can be given to those mothers in labour who are febrile,
known to be colonized or who have previously had an affected
child. There is currently no vaccine available.
Clinical features and diagnosis
Infected neonates may initially lack the classical clinical signs of
sepsis, such as fever and the bulging fontanelle of meningitis. A
chest X-ray may demonstrate pneumonia, and specimens of blood,
CSF, amniotic fluid and gastric aspirate should be cultured.
Antigen detection tests are available and can be applied to body
fluids for rapid diagnosis.
Treatment and prevention
Neonatal group B streptococcal sepsis requires empirical therapy
that includes a penicillin and an aminoglycoside. Perinatal penicillin
can prevent invasive infection but should be targeted at babies
who are at high risk.
Enterococci possess a group D carbohydrate cell wall antigen and
can exhibit all three types of haemolysis (see above). They are
principally commensals of the bowel but may cause disease if they
become established at other sites. Of more than 12 species, Enterococcus
faecalis and E. faecium are the most common members
to act as human pathogens, causing urinary tract infection, wound
infection and endocarditis. Enterococci are emerging as hospital
pathogens, with some species (e.g. E. faecium) now resistant to
commonly used antibiotics. Most strains are sensitive to ampicillin/
amoxicillin; however, resistance levels are increasing. Some
enterococci have developed resistance to glycopeptides by the
acquisition of an alternative peptidoglycan transpeptidation
enzyme (the van A or van C system) that alters the usual Ala-DAla
cross-linkage so it is not glycopeptide susceptible. Such strains
may require therapy with drugs such as linezolid, daptomycin or