Streptococcus agalactiae

Beta-hemolytic streptococci of serogroup B (GBS) bear the scientific name Streptococcus agalactiae. In clinical usage, however, they are referred to as B streptococci . B streptococci are aerobic, gram-positive chain cocci that are primarily animal pathogens. In cows, they cause "yellow galt", an inflammation of the udder. In humans, they occur as colonizers of the intestinal tract and vagina. However, only Streptococcus agalactiae is of human pathogenetic significance. These are identified by their common heat- and acid-stable, group-specific antigen B, according to Lancefield, a polysaccharide (Lancefield RC 1928).

Streptococcus agalactiae can be divided into serotypes Ia, Ib and II-VIII on the basis of polysaccharides in the outer cell wall.

In addition, there are the protein antigens c, R and X.

The natural location of GBS is the intestine of humans and animals. Human colonization is not at all uncommon, and it is then found in the mouth, genital area and on the skin.

Up to 30% of the normal population is colonized. Nosocomial infections by personnel are also possible.

The infections of the newborn: They generally arise by transmission from the mother's rectovaginal flora. Up to 30% of women - including pregnant women - are vaginally colonized. However, this condition is not stable. In practice, this means that the result of an examination during pregnancy does not necessarily indicate peripartum colonization.

Clinical symptoms in the newborn: There is no transplacental infection of the fetus. Aspiration of infected amniotic fluid leads to predominantly pulmonary infection with S. agalactiae in some infants, but this may progress from asymptomatic bacteremia to the early form of neonatal sepsis or even septic abortion. In immature neonates, sepsis manifests more frequently, whereas in mature neonates pneumonia usually develops, which is initially indistinguishable from respiratory distress syndrome.

Without treatment, such infection is sometimes dramatic and in many cases threatening. About 4% of children with sepsis/meningitis die. Depending on the time of onset of the disease, one speaks of "early" or "late" manifestation.

Early onsettype: The early disease occurs within a few hours (on average 20 hours) up to 3-4 days after birth. The pathogenic bacteria are probably acquired intra partum from the newborn. The early onset type occurs mainly in preterm infants with low birth weight. In addition to sepsis, meningitis is also feared, which is lethal in about 50% of cases after 24-48 h (Hof H 2019).

Late onset type: The rarer "late onset type" becomes apparent within 7 days to 3 months after birth . The bacteria are transmitted post partum from the mother, but also from the wider environment of the child. Such diseases can also occur as nosocomial infections, as 40% of children come from culture-negative mothers. Severe courses of infection can leave permanent damage to the infected organs.

Clear detection of the B-group antigen is sufficient for reliable identification. The best studied virulence factors of S. agalactiae are the type-specific polysaccharides of the outer capsule.

The C protein, a surface associated antigen, plays a role in the resistance of the bacteria to opsonization and phagocytosis. The ß antigen of the C protein binds the Fc portion of human IgA antibodies, protecting the bacterium against mucosal immune mechanisms. By binding human IgA antibodies on the cell surface, it prevents the binding of other opsonizing antibodies and thereby their phagocytosis. The C protein is expressed by most clinical S. agalactiae isolates of types Ia, Ib and II, but is rare in serotype III (Bevanger L.1983; Johnson D et al. 1984).

The cell wall of streptococci is also characterized by a high content of polysaccharide , which forms a very strong structure when combined with the C protein. The cell wall of most species is therefore very resistant to enzymatic degradation, e.g. by lysozyme (Lütticken R 1992).

Culture: The germ requires complex culture media (pH 7.2-7.8) with addition of native protein in the form of blood or serum. Glucose addition also promotes rapid multiplication. S. agalactiae is facultatively anaerobic and its optimum temperature is 37°C. After 18-24 hours of incubation, colorless to whitish colonies form that are larger than those of A streptococci, with a small halo of incomplete hemolysis that may occasionally be absent.

CAMP factor: Typical of B streptococci is also the CAMP factor. Typing is done by latex agglutination. PCR also has a high sensitivity.

Antigen B: Group B streptococci (GBS) identify themselves by their common heat- and acid-stable, group-specific antigen B, a polysaccharide.

Pregnant women should be checked 1-5 weeks before the planned birth to see whether the birth canal is colonised. If necessary, amoxicillin should be used for eradication.

1. Bevanger L. (1983) Ibc proteins as serotype markers of group B streptococci. Acta Pathol Microbiol Immunol Scand [B]. 91(4): 231-4.
2. Johnson D et al. (1984) Group B streptococcal Ibc protein antigen: distribution of two determinants of wild-type strains of common serotypes. J. Clin. Microbiol. 19: 506-510.
3. Lancefield RC (1928) The antigenic complex of Streptococcus hemolyticus. I Demonstration of a type-specific substance in extracts of Streptococcus hemolyticus. The Journal of Experimental Medicine 47:91-103.
4. Lütticken R (1992) Streptococcaceae. In: Microbiological diagnostics. Ed. F. Burkhardt, Stuttgart pp 51-67.