Streptococcus agalactiae (also known as
group-B streptococcus or beta-strep) is
a Gram-positive coccus, non-motile,
non-spore-forming, catalase-negative, spherical
or ovoid, and less than 2 µm (micrometres) in
diameter; it is usually β-haemolytic and can
grow in pairs or short chains (Figure
1). S. agalactiae causes invasive
disease primarily in newborns and in women in
the postpartum period. Adults with severe
infections unrelated to pregnancy are usually
elderly and have underlying illness such as
diabetes mellitus, liver failure, malignancy,
acquired immunodeficiency syndrome, or renal
failure. In non-pregnant adults, skin or
infection, and pneumonia are the most common
manifestations of disease.
Figure 1. A
micrograph depicting Streptococcus
Colonial morphology of S.
agalactiae in culture is typically gray to
whitish-gray in colour when grown on sheep blood
agar. As mentioned, most strains of this
organism are beta-hemolytic, suggesting that
they are able to lyse red blood cells and grow
on blood agar medium. In addition, the
CAMP test is
an important test for its identification (Figure
2). Mainly Streptococcus agalactiae
bacteria are screened through this test. It is
characterized by the presence of group B
Lancefield antigen and by its ability to
hydrolyze sodium hippurate. It is also sensitive
to bile and will lyse in its presence.
Figure 2. If
the laboratory is not able to identify group-B
streptococci by the Lancefield grouping
procedure, there are other microbiologic tests
that can be used to identify group-B
streptococci. This picture shows one of these
tests. It is called the CAMP test.
infection is diagnosed using samples collected
from blood, urine or spinal fluid. To identify
this pathogen, vaginal and rectal swabs are
typically culture on sheep blood agar medium and
are identified using the CAMP test (Figure
2). This test allows microbiologists to
distinguish between the different
Streptococcus groups; for instance,
Streptococcus pyogenes is CAMP-negative.
Similarly, many other hemolytic streptococci
species also do not produce this particular CAMP
factor. During the test, the CAMP reacts with
the partially lysed area on the sheep blood agar
to enhance the hemolytic activity. There should
be an arrowhead-like shape of the zone with
enhanced hemolytic activity by the S.
agalactiae near the Staphylococcus streak (Figure
S. agalactiae possesses two
major virulence factors that account for its
pathogenicity, namely, pore-forming toxins and a
sialic acid-rich, antiphagocytic capsular
polysaccharide. Pore-forming toxins are a
critical component of pathogenesis in many
disease causing bacteria. These toxins promote
entry of the pathogen into host cells and
facilitate their intracellular survival and
systemic dissemination. The virulence of
pathogens defective in expression of
pore-forming toxins is severely attenuated.
S. agalactiae encodes at least two
pore-forming toxins, namely,
β-hemolysin/cytolysin (β-H/C) and CAMP factor.
β-H/C is a surface-associated, pluripotent toxin
that is crucial for various facets of S.
agalactiae disease involving both the
pathogen and the host. β-H/C promotes S.
agalactiae invasion of host cell barriers
such as the epithelial and endothelial cells of
the lung and the blood–brain barrier.
Furthermore, β-H/C impairs cardiac function,
promotes liver failure and induces host
inflammatory responses that contribute to
neurological sequelae. CAMP factor is an
extracellular cytolysin (cytolytic protein) 25
kDa in size (kiloDaltons) that binds the Fc
fragments of immunoglobulin G (IgG), similar to
protein A of
Staphylococcus aureus. Overall, both
these pore-forming toxins disrupt target cell
membrane structures, leading to cell lysis and
red blood cell damage. The polysaccharide
capsule, on the other hand, helps to inhibit
phagocytosis of the bacterium by host immune
cells (Rajagopal, 2009).
S. agalactiae is the leading cause of
newborns in the United States and Europe.
Infection of this disease usually occurs in the
first week of life; however, infants can get a
slightly less serious form of Group B strep that
develops a week to a few months after birth. The
increase risk of S. agalactiae is
associated with the colonization of this
bacterium in the maternal genital tract.
Vertical transmission from mothers to their
newborns may occur before or during the birth.
The reservoir for this pathogen is in the
gastrointestinal tract, which is the source of
vaginal colonization. Other reservoirs can
include cattle, horses, dogs, rabbits, guinea
pigs, and mice. S. agalactiae is also a
normal part of the rectal and vaginal flora (Domelier et al., 2008).
The most active antibiotics in treating S.
agalactiae are penicillin G,
third-generation cephalosporins, and meropenem.
Penicillin G is an excellent antibiotic for the
treatment of S. agalactiae peritonitis
because of its lower cost, proven safety,
efficacy, and narrow spectrum of antimicrobial
activity. Its extensive use for intrapartum
chemoprophylaxis may lead to chemoresistance;
however, ceftriazone, cefamandole, cefotaxime,
and meropenem are as effective as penicillin G
and more effective than cephalothin, rifampicin,
and vancomycin. The use of second- and
third-generation cephalosporins and meropenem is
recommended in case of penicillin G allergy.
Domelier, A., van der
Mee-Marguet, N., Arnault, L., Mereghetti, L.,
Lanotte, P., Rosenau, A., Lartigue, M., &
Quentin R. (2008). Molecular characterization of
Streptococcus agalactiae strains.
Journal of Antimicrobial Chemotherapy, 1-7.
Rajagopal, L. (2009).
Understanding the regulation of Group B
Streptococcal virulence factors. Future
Microbiology, 4(2): 201-221.
Scanziani, R., Dozio., B.,
et al. (1999). Vaginal colonization
with group B Streptococcus (Streptococcus
agalactiae) and peritonitis in a woman on CAPD.
Nephrology Dialysis Transplantation,