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Neonatal & maternal group B streptococcal infections:
A comprehensive review
Anita Shet & Patricia Ferrieri*
Departments of Paediatrics & *Laboratory Medicine & Pathology,University of Minnesota
Medical School, Minnesota, USA
Received September 19, 2003
Group B Streptococcus is an important cause of maternal and neonatal morbidity and mortality
in many parts of the world. The last two decades have seen intensified efforts in the Western
hemisphere in the prevention of this devastating infection by identifying and treating pregnant
women who carry group B streptococci or who are at highest risk of transmitting the organism
to newborns. The intrapartum use of antibiotics in these women has led unequivocally to a
decrease in the rate of neonatal group B streptococcal disease. Although studies in India show a
predominance of Gram negative bacterial sepsis among infants, contributing to infant mortality,
it is possible that the role of group B Streptococcushas been underestimated. This review discusses
its epidemiology in India, and summarizes current concepts of microbiology, pathogenesis, clinical
management and preventative issues regarding group B streptococcal disease.
Review Article
Indian J Med Res 120, September 2004, pp 141-150
141
Group B Streptococcus(GBS) is a leading cause
of neonatal infection in the Western hemisphere. The
recognition that maternal colonization with the
organism is a key factor in the occurrence of GBS-
associated neonatal morbidity and mortality was a
milestone in the history of perinatal health 1. A
nationwide change in health practices helped diminish
mortality and morbidity associated with the disease.
In India, however, the spectrum of group B
streptococcal disease remains a largely under-
recognized problem.
Puerperal sepsis has been described for centuries,
and ancient Indian texts in 1500 BC have recorded
that good hygiene leads to a reduction in perinatal
disease 2. In 1879 Louis Pasteur identified the
streptococcus as the causative organism for puerperal
sepsis3. Since the early 1930s when Rebecca
Lancefield reported her grouping system for
haemolytic streptococci, group A Streptococcus
(Streptococcus pyogenes) was widely acknowledged
as the major pathogen associated with puerperal
sepsis4. GBS was initially thought to be a commensal,
until 1937, when Fry reported seven cases of GBS-
associated puerperal fever with 3 deaths5.
Epidemiology and transmission
During the 1970s and 1980s, GBS emerged as a
significant neonatal and maternal pathogen in the
United States (US) and Western Europe with reported
mortality rates of 15 to 50 per cent 6,7. In the US, 10
Key words Chemoprophylaxis - colonization - group B Streptococcus- neonatal mortality - perinatal transmission - sepsis
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142 INDIAN J MED RES, SEPTEMBER 2004
to 35 per cent of pregnant women are asymptomatic
carriers of GBS in the genital and gastrointestinal tract
at the time of delivery8. The prevalence of GBS
colonization during pregnancy is variable; in one
study, among women who had positive GBS cultures
between 26 and 28 wk gestation, only 65 per centremained colonized at term, while 8 per cent of those
with negative prenatal cultures were positive for GBS
at term9. Treatment of these colonized mothers
succeeded in temporarily eradicating the organism, but
most of the women were re-colonized within
6 wk. At birth, 50 to 65 per cent of infants who are
born to colonized mothers have positive GBS cultures
from mucus membranes and skin (external ear canal,
throat, umbilicus, anorectal sites)1,10. Approximately
98 per cent of colonized newborns remain healthy, but
1 to 2 per cent develop invasive GBS infection7
. Theoverall incidence of neonatal GBS infection was
approximately 2 per 1000 live births in the United
States prior to the introduction of intrapartum
prophylaxis7.
Epidemiological studies in India have shown lower
colonization and infection rates in general 11-15.
However on closer analysis, taking into consideration
use of adequate culture techniques and microbiological
media, some of the GBS colonization rates reported
from India and other developing countries are similarto those reported in the United States11. In a study
done in 507 pregnant Indian women, 12 per cent were
reported to have GBS isolated from the throat and
vagina, and 10 per cent had positive vaginal cultures
alone12. Similarly, another study showed the overall
carriage rate in pregnant women to be 16 per cent13.
Although both these studies used selective broth media,
culture sites did not include the anorectum and this
might have lowered the yield of positive cultures.
Other studies have reported colonization rates of 5 to
6 per cent, but no selective broth media were used inthese cases14,15. Colonization rates in infants born to
asymptomatic maternal carriers of GBS are 53 to 56
per cent and are consistent with rates reported in other
parts of the world13,15. Despite significant GBS
colonization rates, reports of invasive neonatal GBS
disease in India are infrequent. During a 10-yr study
between 1988 and 1997 in Vellore, only 10 cases of
neonatal GBS infection were identified, giving an
incidence of 0.17 per 1000 live births16. However, this
number represents only the cases occurring among
deliveries in a tertiary care hospital located in a
predominantly rural community. In India where 65 per
cent of women give birth at home, the true incidenceof invasive GBS disease in the newborn is largely
unknown17. In addition, blood cultures from ill
neonates are not always done in many rural primary
health care centres, which may contribute to the
underestimation of the number of GBS cases. Preterm
births and stillbirths are also usually not investigated,
and thus the total burden of perinatal GBS disease
remains unrecognized.
The estimated incidence of neonatal GBS infection
in India can be calculated from Indian epidemiologicaldata reporting maternal and infant GBS colonization
rates as 10 and 50 per cent respectively12,13,15. Since
about 2 per cent of colonized neonates develop true
infection6, the attack rate of neonatal GBS infection
in India may be calculated as approximately 1 per
1000 live births. Bearing in mind the above estimated
attack rate and current Indian demographic data
(midyear population count in the year 2001 was
approximately 1027 million, and birth rate was 26
births per 1000 population per year)18, the projected
total number of GBS infection in newborn infants inIndia may be as high as 26,700 cases per year.
GBS serotypes and pathogenesis
Group B streptococci (also called Streptococcus
agalactiae) are Gram positive cocci belonging to
Lancefield group B. There are 9 antigenically distinct
serotypes based on their capsular polysaccharide
structure (types Ia, Ib, II - VIII) identified to date. In
the US and Western Europe, types Ia, II, and III
accounted for 85 per cent of the isolates frominfants19,20. Recent studies in the US have
demonstrated that serotypes Ia, III, and V (in
descending frequency) accounted for 78-87 per cent
of early-onset (less than seven days after birth)
invasive disease in newborn infants and parturient
women21,22. Late-onset GBS disease in infants 7-90
days of age is dominated by serotype III, followed by
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143
serotypes Ia and V22. Studies from the state of
Minnesota from January 1993 through December 1999
reflected the above national trends in the US (Fig.),
(Ferrieri P. unpublished data). Studies from India show
a variable distribution of serotypes, but the most
common isolates belong to types III, II and Ib
13-15,23
.
The most important risk factor for early-onset GBS
infection in the neonate is the presence of the organism
in the maternal genitourinary tract at delivery.
Ascending bacteria from the maternal genital tract
reach the amniotic fluid, usually after rupture of the
amniotic membranes1,24. Alternatively, the newborn
can come into contact with GBS during passage
through the birth canal. When the foetus aspirates
contaminated amniotic fluid, group B streptococci
reach the lower respiratory tract and damage
pulmonary epithelial cells, resulting in pneumonia and
respiratory distress usually within the first few hours
after birth. Severe GBS sepsis occurs with
intravascular invasion of bacteria and failure of the
host to eliminate the pathogen25,26
. Ascending infectioncan also occur through intact chorioamniotic
membranes, with subsequent events occurring in utero,
resulting in stillbirths or death within hours after
birth24. The pathogenesis in late-onset disease is less
clear. Horizontal transmission plays a major role: close
contact with the mother, breast-feeding and
nosocomial transmission.
The polysaccharide capsule is the most important
virulence factor26. However, the role of surface
Fig. Distribution of GBS serotypes isolated from patients with invasive disease from January, 1993 through December, 1999. The
pie diagrams are for early-onset (left), late-onset (right) and non pregnant adults (center). (Ferrieri P, unpublished data).
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144 INDIAN J MED RES, SEPTEMBER 2004
localized GBS proteins in pathogenesis and protection
is under intensive investigation26. The presence of
maternal serum antibodies to specific capsular
polysaccharides of GBS serotypes appears to be
protective against acquisition of neonatal GBS disease
as colonized pregnant women with high levels of serum
antibodies were less likely to have neonates with
invasive GBS infection27,28. Moreover, infected infants
had low levels of specific antibody to the infective
serotype29. In a recent cross-sectional study, it was
shown that pregnant women colonized with GBS
serotypes Ia, II, III or V (the most common serotypes)
had significantly higher serum concentrations at
delivery of IgG specific for the capsular
polysaccharide of their colonizing GBS strain than
did noncolonized women30.
Clinical features
Neonatal morbidity : Two distinct clinical syndromes
are recognized, early-and late-onset disease. Early-
onset GBS disease occurs within the first 7 days of
life, although most cases are evident in the first 24 h
after birth. As can be demonstrated by serotyping GBS
isolates from colonized mothers and infants,
transmission of early-onset disease is vertical9.
Infection may be acquired by the intraamniotic route,
or directly during passage through the birth canal. The
initial presentation is respiratory distress in more than80 per cent of neonates. Pneumonia and septicaemia
are the most common manifestations, and 5 to 10 per
cent neonates will also have meningitis. The incidence
of early-onset disease is about 10 times higher in
premature than in term neonates31. Late-onset disease
develops in infants after 7 days and up to 3 months of
age, the median age of onset being 1 month.
Transmission can be either horizontal (from other
infected infants or health care workers) or vertical
(from the mother due to close proximity). These infants
almost always have an unremarkable early neonatalhistory, and later present with meningitis or sepsis.
Osteoarticular infections and cellulitis can also occur.
The initial signs usually are fever, lethargy, irritability,
poor feeding and tachypnoea. Respiratory distress as
a presenting feature is less common. Over 20 per cent
of survivors of GBS meningitis have permanent
neurological sequelae, including sensorineural hearing
loss, mental retardation, cortical blindness and
seizures32. Table I lists the differences between early-
onset and late-onset GBS disease. The case fatality
ratio in the US has dramatically decreased over the
last 3 decades: from up to 50 per cent in the 1970s to
6 per cent in the early 1990s33. The most recent report
from the CDC reports a 2002 mortality rate of 0.7
per 100,000 population34. Case series from India also
report high mortality: in a 1975 study where 8 cases
of neonatal GBS infection were followed over a period
of 18 months, 6 infants died within the first week of
diagnosis35. A more recent study published in 1999
reported 10 infants with GBS infection, of which 1
died on the second day of life16. However, there is
insufficient data presented to calculate the actual
mortality rate.
Table I. Neonatal manifestations of group B streptococcal
disease
Early-onset Late-onset
disease disease
Onset First week One week to
of life 3 months
(usually within of age
the first 24 h)
Clinical presentation Respiratory distress Sepsis
Pneumonia Meningitis
Sepsis Osteoarthritis
Incidence of Increased No change
prematurity
Maternal obstet rical Frequent (70%) Uncommon
complications
Transmission Vertical: acquired Usually
in uteroor horizontal
intrapartum transmission;
can also beintrapartum
Predominant Ia, III, V III, Ia, V
serotypes*
Mortality (%) 10-15 2-6
*In descending order of prevalence
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Perinatal morbidity: Group B streptococcal genital
colonization has been considered a possible cause of
premature deliveries and premature rupture of
membranes36, although definite evidence of a causal
relationship is still lacking. Several prospective studies
have also suggested that GBS colonization may play
a causal role in the occurrence of intrauterine deaths,late abortions and low birth weight infants19,37,38. In a
prospective study of 325 pregnant women in Vellore,
31 per cent of the GBS-colonized mothers reported a
history of foetal losses and neonatal deaths as opposed
to only 18per cent of non-colonized mothers16. Among
the group of colonized mothers, the birth weights of
their infants were lower, the duration of rupture
membranes before delivery was longer and the
incidence of peripartum fever was more frequent.
Although these numbers were too small for statistical
significance, there were clear trends of the association
between GBS colonization and perinatal morbidity.
Maternal infect ions : GBS can cause significant
morbidity in pregnant women. Manifestations of
symptomatic maternal infection include
chorioamnionitis, endometritis, cystitis, pyelonephritis
and febrile GBS bacteraemia19. Caesarian delivery
appears to be a prominent risk factor for postpartum
endomyometritis39. GBS is also a common cause of
fever in postpartum patients. Colonization with GBS
was significantly associated with prolonged labour,
premature rupture of membranes and preterm
delivery36. Less commonly, GBS is isolated in cases
of post-operative wound infection, pelvic abscess,
septic pelvic thrombophlebitis and osteomyelitis. The
current maternal mortality rate in India is 408 per
100,000 live births17. Maternal sepsis is responsible
for over 35per cent of these deaths40. The aetiological
agents have been inadequately studied, but group B
Streptococcus likely plays a major role in maternal
mortality as well as morbidity41.
Infection in nonpregnant adults: Invasive group B
streptococcal infections cause substantial morbidity
and mortality in nonpregnant adults, especially those
who are elderly and those who have serious underlying
diseases42-44. Skin or soft tissue infections,
osteomyelitis, bacteraemia, urosepsis, pneumonia and
peritonitis were the most common clinical
manifestations. The GBS serotype distribution is quite
different in non-pregnant adults, compared to mothers
and infants (Fig.). Serotype V accounts for 30-45 per
cent of invasive infections in this nonpregnant
population22.
Detection of GBS colonization and diagnosis of
infection
Important factors that influence the accuracy of
detecting GBS maternalcolonization are the choice
of bacteriological media, the body sites sampled, and
the timing of the sampling. GBS resides in the
genitourinary and gastrointestinal tracts where large
numbers of Gram negative bacteria are also present.
The use of a selective broth medium that inhibits the
growth of Gram negative enteric bacilli and other
normal flora can increase culture sensitivity for GBS
to over 90 per cent12,45. The most widely used selective
medium is Todd-Hewitt broth with gentamicin (8 g/
ml) or colistin (10 g/ml) and nalidixic acid (15 g/ml)46. The highest culture yield is obtained when both
the lower vaginal area and anorectal sites are
sampled47. The optimal time for performing antenatal
cultures is between 35 to 37 wks gestation 46.
Rapid diagnostic tests are based on identification
of the GBS group-specific polysaccharide antigen
from swab specimens and use latex agglutination or
enzyme linked immunosorbent (ELISA) technology48.
Although they have good specificities (95%), they tend
to have low sensitivities (33 - 65%) which increase
only with heavy colonization; hence a negative test
cannot rule out GBS colonization. Some investigators
have attempted to increase sensitivity by using
enrichment media prior to antigen testing49. Recent
development of real-time PCR and fluorescence
labeling technologies has provided new detection
platforms for bacterial identification50, however cost-
effectiveness of these new methods is yet to be
established.
The diagnosis of invasive GBS infection is
established by isolation of the organism from culture
of blood, cerebrospinal fluid, amniotic fluid or specific
site of infection (i.e., bone or joint fluid)7. Further
identification of GBS may be done by the CAMP test
and specific group B antigen detection tests. ( i.e.,
commercial latex agglutination kits)7. The only
limitation of culture as a method is the time (24 to
48 h) required for a result, making it less useful when
the patient presents in labour.
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146 INDIAN J MED RES, SEPTEMBER 2004
Chemoprophylaxis and therapeutic considerations
Prevention is of paramount importance in areas of
high incidence of invasive group B streptococcal
disease. It is impractical to administer
chemoprophylaxis to all parturient mothers and
neonates. The challenge therefore is to identifycorrectly high risk infants before they are born. The
most effective way to prevent neonatal early-onset
infection is maternal antibiotic administration during
labour. However, there is no evidence that
chemoprophylaxis prevents late-onset disease. The
Centers for Disease Control and Prevention (CDC)
consensus recommendations for group B streptococcal
prophylaxis were originally put into practice in 1996,
and by the end of 1999, the incidence of early-onset
GBS disease in the US decreased by a remarkable 70
per cent51. Two preventative approaches were used: a
culture screening-based and a risk-based approach.The first approach involved universal screening for
GBS colonization of all pregnant women between 35
and 37 wk gestation using vaginal and rectal cultures
to detect GBS colonization. As discussed earlier,
properly obtained and processed antenatal cultures
correctly identified most women colonized at the time
of labour. Intrapartum antibiotics are administered to
all those with a positive GBS culture regardless of
risk factors. The risk-based approach involved
administration of antibiotics based solely on the
presence of antenatal or intrapartum risk factors.
Maternal risk factors for group B streptococcalneonatal sepsis are as follows46: preterm labour or
premature rupture of membranes (< 37 wks
gestation); prolonged rupture of membranes (18 h);
intrapartum fever 100.4 F (38.0 C); history of
a previous newborn with GBS disease; and group B
Streptococcusbacteruria during pregnancy. Revised
guidelines from CDC were published in 2002 46.
In India, universal culture screening for GBS maybe difficult to implement, from a logistic as well as
cost-effective viewpoint. However, a strategy based
on identifying maternal risk factors could potentially
be used, which, according to one source, would require
intrapartum antimicrobial prophylaxis in 18 per cent
of deliveries and would hypothetically prevent 70 per
cent of the cases of early-onset GBS disease52.
Intrapartum antibiotics
Group B Streptococcus remains exquisitely
sensitive to penicillin. Penicillin G is preferred because
of its narrow spectrum, and is expected to diminish
induction of resistant organisms and maternal yeast
infections. Clindamycin and erythromycin are
acceptable alternatives for women with an allergy to
penicillin, although there is increased resistance of
GBS to these two antibiotics46. Table II outlines the
most recent guidelines for intrapartum
chemoprophylaxis, in non-penicillin allergic women
and in penicillin-allergic women with a high or low
risk for anaphylaxis. These guidelines for maternal
prophylaxis will undoubtedly increase the use ofantibiotics during labour. There are many concerns
about adverse effects of increased use of antibiotics,
Table II. Regimens for intrapartum chemoprophylaxis of group B streptococcal infection
Recommended treatment Alternative treatment
No known allergy Penicillin G: 5 million units Ampicillin: 2 g given in an
as an iv load, then 2.5 iv load, then 1 g every 4 h
million units every 4 h until delivery
until delivery
Penicillin allergy First generation
(not high risk for anaphylaxis) cephalosporin, i.e.,
cefazolin, 2 g iv initial dose,
then 1 g every 8 h until delivery
Penicillin allergy (at high risk for Clindamycin: 900 mg iv every Erythromycin: 500 mg iv every 6 h
anaphylaxis)* 8 h until delivery until delivery
*If GBS resistance to clindamycin or erythromycin is known or suspected, the recommended treatment is vancomycin 1 g iv every
12 h until delivery. Source - Ref. 7
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such as severe anaphylactic reactions or possible
emergence of antimicrobial resistance in either group
B streptococci or other perinatal pathogens. Although
no penicillin-resistant isolates of GBS have been
detected so far, resistance to erythromycin and
clindamycin has been increasing53
.
Clinical management of the infant
A term asymptomatic infant whose mother has
received appropriate chemoprophylaxis (delivery four
or more hours after intrapartum antibiotics, administered
according to recommended dosage intervals) may be
observed during the immediate neonatal period46. For an
asymptomatic infant less than 35 wk gestation, or an
infant whose mother has received inadequate
chemoprophylaxis, a limited diagnostic evaluation (whitecell count with differential, blood culture, and chest
radiograph if respiratory abnormalities are present) may
be performed, and the infant observed without
antimicrobial therapy for at least 48 h. If signs of sepsis
develop, a complete diagnostic evaluation (including a
lumbar puncture) and empiric antibiotic therapy
should be initiated46. An alternative approach is to
consider those asymptomatic infants born to
mothers with chorioamnionitis and/or fever to be
at higher risk for infection than those born to
asymptomatic mothers with only a positive GBS
culture. This approach recommended performing afull diagnostic evaluation and empiric antibiotic
initiation on these high-risk infants54. Ampicillin
plus an aminoglycoside (e.g., gentamicin) is the
initial treatment of choice for a newborn infant with
presumptive, invasive GBS infection as these agents
are also active against other organisms that might
cause neonatal sepsis7,46. Such a combination is also
synergistic for killing GBS and may be continued
empirically for 48 to 72 h until definite infection
with GBS is ruled out
55
. When GBS sepsis with orwithout meningitis has been firmly established, the
combination may be continued for 10 to 14 days,
or the course of treatment can be completed with
penicillin G or ampicillin alone7. The suggested
doses and duration of therapy for different infection
types are summarized in Table III.
Table III. Antibiotic therapy for neonatal GBS infection
Infection type Antibiotic Dose per day (iv)* Duration
Suspected Ampicillin 300 mg/kg in 3-6 divided Until blood and cerebrospinal
bacteraemia or doses fluid cultures are sterile (48 to
meningitis plus + 72 h)
Gentamicin 7.5 mg/kg in 3 divided doses
Bacteraemia Ampicillin 150-200 mg/kg in 4 div. doses 10 days (range: 10 to 14 days)
without or
meningitis Penicillin G 200,000 units/kg in 4 div. doses
Meningitis Ampicillin** 300 mg/kg in 4-6 divided Minimum 14 days (range: 2 to
doses 3 wk)
or
Penicillin G 500,000 units/kg in 4-6
divided doses
plus + 7.5 mg/kg in 3 divided
Gentamicin doses
* Antibiotic dosages should be adjusted for preterm infants and postnatal age.
**For infants 7 days of age or younger, recommended dosages are: Ampicillin: 200-300 mg/kg/day in 3 divided doses;
Gentamicin: 5 mg/kg/day in 2 divided doses; Penicillin G: 250,000-450,000 units/kg/day in 3 divided doses. Source-Ref. 46
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148 INDIAN J MED RES, SEPTEMBER 2004
The future
While the different strategies for identification of
high risk mothers and infants and provision of
intrapartum prophylaxis may reduce the rate of
neonatal sepsis, they are unlikely to eliminate the
problem. Maternal immunization against GBS appearsto be a promising and potentially lasting approach for
preventing neonatal sepsis, preterm deliveries and low
birth weight infants. GBS capsular polysaccharide-
protein conjugate vaccines for types Ia, Ib and III have
been shown to be safe and efficient in inducing type-
specific antibody levels in healthy vaccinated
individuals56,57. Epidemiological surveillance of
serotype distribution in the population is critical for
vaccine studies. A vaccine formulation of GBS types
Ia, II, III and V would be expected to provide
protection against over 90 per cent of infections
21
. Thecost of developing and implementing a vaccine
strategy, although formidable, is considerably less than
that of treating these infections, and for some infants,
their life-long sequelae58. Among experts in this field,
there is considerable discussion regarding whom to
immunize - nonpregnant adolescents or pregnant
women in the first trimester. In addition, an argument
can be made for vaccinating 'at risk' nonpregnant
adults. Clinical trials are in progress and research is
ongoing for developing a safe and efficacious vaccine
against GBS disease.
Conclusion
The infant mortality rate in India has decreased
steadily over the last decade and is currently 68per
1000 live births according to the 2001 census 18. This
is mainly due to improvements in primary health care,
immunization coverage, health education and other
factors. Despite the progress, a large proportion of
deaths occur in the neonatal period. Sepsis is a major
cause of death in up to 30 to 45 per cent of cases 59.
Microbial colonization of the maternal genital tract
is a key factor in most cases of sepsis. Althoughprevalence studies report a predominance of Gram
negative bacilli among female genital colonizers and
Gram negative sepsis among their infants, it is possible
that the role of group B Streptococcus has been
underestimated due to inadequate culture techniques
and microbiological methods11,60. In addition, it must
be recognized that the spectrum of GBS disease in
infants is a continuum that includes intrauterine death,
preterm delivery, early-onset and late-onset disease.
Currently reported low rates of invasive GBS disease
in India may be due to one or several factors, such as
prevalence of less virulent strains, or high levels of
transplacentally acquired protective antibody in
serum, and unrecognized causes of early neonatal or
premature deaths and stillbirths. Maternal colonization
rates are comparable with those in other parts of the
world; hence neonatal exposure to the organism is
similar. A genetic difference in susceptibility to disease
is less likely to be responsible as seen in a study of
families of Indian origin living in South Africa where
the incidence of neonatal GBS sepsis was high at 2.6
per 1000 live births61. Continued surveillance and
more detailed studies are essential in the understanding
of the epidemiology and spectrum of disease caused
by the group B Streptococcus.
The dramatic decrease of the burden of group B
streptococcal disease in the United States did not result
from a major scientific breakthrough; it resulted from
provision of a simple well known antibiotic to a select
group of women during labour and to high risk infants.
An invaluable lesson that can be learned from the story
of the group B Streptococcus in the Western
hemisphere is that often what is needed to make a
major difference in public health is a decision that the
problem must be addressed.
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