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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).

SHET & FERRIERI: NEONATAL & MATERNAL GBS INFECTIONS

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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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145

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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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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147

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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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.

References

1. Ferrieri P, Cleary PP, Seeds AE. Epidemiology of group B

streptococcal carriage in pregnant women and newborn

infants. J Med Microbiol 1977; 10 : 103-14.

2. Kutumbiah P. Anc ien t Indian medicine . Madras: Orient

Longman; 1962.

3. Pasteur L. Septicemie puerperale. Bullet in de LAcademie

de Medecine (Paris) 2me serie- tome VIII1879 : 8256-60.

4. Lancefield R, Hare R. The serological differentiation of

pathogenic and non-pathogenic strains of hemolyticstreptococci from parturient women. J Exp Med1935; 61 :

335-49.

5. Fry RM. Fatal infections by haemolytic streptococcus group

B. Lancet1938; i:199-201.

6. Pass MA, Gray BM, Khare S, Dillon HC, Jr. Prospective

studies of group B streptococcal infections in infants.

J Pediatr1979; 95 : 437-43.

8/11/2019 0901 Jur Nal

9/10

149

7. Baker CJ, Edwards MS. Group B streptococcal infections. In:

Remington JS, Klein JO, editors.Infectious diseases of the fetus

and newborn infant. Philadelphia: W.B. Saunders; 2001 p. 1091-

156.

8. Regan JA, Klebanoff MA, Nugent RP. The epidemiology of

group B streptococcal colonization in pregnancy. Vaginal

Infections and Prematurity Study Group. Obstet Gynecol 1991;77 : 604-10.

9. Boyer KM, Gadzala CA, Kelly PD, Burd LI, Gotoff SP. Selective

intrapartum chemoprophylaxis of neonatal group B streptococcal

early-onset disease. II. Predictive value of prenatal cultures. J

Infect Dis1983; 148 : 802-9.

10. Hoogkamp-Korstanje JA, Gerards LJ, Cats BP. Maternal carriage

and neonatal acquisition of group B streptococci.

J Infect Dis1982; 145 : 800-3.

11. Stoll BJ, Schuchat A. Maternal carriage of group B streptococci

in developing countries. Pediatr Infect Dis J1998; 17 : 499-

503.

12. Dalal S, Lahiri A, Parel CC. Carriage rate of group B streptococci

in pregnant women and evaluation of different isolation media.

J Indian Med Assoc1998; 96 : 360-1, 366.

13. Chaudhary U, Sabherwal U, Chugh TD. Prevalence of group B

streptococci in obstetrical cases. Indian J Med Res1981; 73 :

710-4.

14. Lakshmi V, Das S, Shivananda PG, Savithri P, Rao K.

Incidence of group-B beta haemolytic streptococci in the vaginal

flora of pregnant women.Indian J Pathol Microbiol1988; 31 :

240-4.

15. Mani V, Jadhav M, Sivadasan K, Thangavelu CP, Rachel M,

Prabha J. Maternal and neonatal colonization with group BStreptococcusand neonatal outcome.Indian Pediatr1984; 21 :

357-63.

16. Kuruvilla KA, Thomas N, Jesudasan MV, Jana AK. Neonatal

group B Streptococcal bacteraemia in India: ten years

experience.Acta Paediatr1999; 88 : 1031-2.

17. Maternal and Reproductive Health: National Family Health

Survey (NFHS-2), 1998-1999. Vol. 2003. Mumbai, India:

International Institute for Population Sciences (IIPS), 2000:http:/

/www.nfhsindia.org/india.html accessed on September 26, 2003.

18. Census of India 2001.http://www.censusindia.net/2001.accessed

on January 23, 2003.

19. Dillon HC, Jr., Khare S, Gray BM. Group B streptococcalcarriage and disease: a 6-year prospective study.J Pediatr1987;

110 : 31-6.

20. Baker CJ, Barrett FF. Group B streptococcal infections in infants.

The importance of the various serotypes. JAMA1974; 230 :

1158-60.

21. Zaleznik DF, Rench MA, Hillier S, Krohn MA, Platt R,

Lee ML, et al. Invasive disease due to group B Streptococcus in

pregnant women and neonates from diverse population

groups. Clin Infect Dis2000; 30 : 276-81.

22. Harrison LH, Elliott JA, Dwyer DM, Libonati JP, Ferrieri

P, Billmann L, et al. Serotype distribution of invasive

group B streptococcal isolates in Maryland: implications

for vaccine formulation. Maryland Emerging Infections

Program. J Infect Dis1998; 177 : 998-1002.23. Prakash K, Ravindran PC, Sharma KB. Group B beta

haemolytic streptococci and their serological types in human

infections. Indian J Med Res1976; 64 : 1001-7.

24. Galask RP, Varner MW, Petzold CR, Wilbur SL. Bacterial

attachment to the chorioamniotic membranes. Am J Obstet

Gynecol1984; 148 : 915-28.

25. Spellerberg B. Pathogenesis of neonatal Streptococcus

agalactiae infections. Microbes Infect2000; 2 : 1733-42.

26. Nizet V, Ferrieri P, Rubens CE. Molecular pathogenesis of

group B streptococcal disease in newborns. In: Stevens DL,

Kaplan EL, editors. Streptococcal infections: clinical

aspects, microbiology, and molecular pathogenesis . NewYork: Oxford University Press; 2000 p.180-221.

27. Baker CJ, Kasper DL. Correlation of maternal antibody

deficiency with susceptibility to neonatal group B

streptococcal infection. N Engl J Med1976; 294 : 753-6.

28. Baker CJ, Edwards MS, Kasper DL. Role of antibody to

native type III polysaccharide of group B streptococcus in

infant infection. Pediatrics1981; 68 : 544-9.

29. Gotoff SP, Papierniak CK, Klegerman ME, Boyer KM.

Quantitation of IgG antibody to the type-specific

polysaccharide of group B Streptococcustype 1b in pregnant

women and infected infants. J Pediatr1984; 105 : 628-30.

30. Campbell JR, Hillier SL, Krohn MA, Ferrieri P, ZaleznikDF, Baker CJ. Group B streptococcal colonization and

serotype-specific immunity in pregnant women at delivery.

Obstet Gynecol2000; 96: 498-503.

31. Yagupsky P, Menegus MA, Powell KR. The changing

spectrum of group B streptococcal disease in infants:

an eleven-year experience in a tertiary care hospital.

Pediatr Infect Dis J1991; 10 : 801-8.

32. Edwards MS, Rench MA, Haffar AA, Murphy MA,

Desmond MM, Baker CJ. Long-term sequelae of group B

streptococcal meningitis in infants. J Pediatr 1985; 106 :

717-22.

33. Schuchat A. Group B Streptococcus. Lancet 1999; 353 :

51-6.

34. Active Bacterial Core Surveillance (ABCs) Report: group

B Streptococcus. vol. 2003: Emerging Infections Program

Network, 2002:http://www.cdc.gov/ncidod/dbmd/abcs/

survreports/gbs02.pdf accessed on August 22, 2003.

35. Sharma KB, Prakash K, Ravindran PC, Narang P. Neonatal

septicemia due to group B beta hemolytic streptococci.

Indian J Med Res1975; 63 : 781-6.


8/11/2019 0901 Jur Nal

10/10


36. Regan JA, Chao S, James LS. Premature rupture of

membranes, preterm delivery, and group B streptococcal

colonization of mothers. Am J Obstet Gynecol1981; 141 :

184-6.

37. Joshi AK, Chen CI, Turnell RW. Prevalence and significance

of group B Streptococcus in a large obstetric population.

CMAJ1987; 137 : 209-11.

38. Bobitt JR, Damato JD, Sakakini J, Jr. Perinatal

complications in group B streptococcal carriers: a

longitudinal study of prenatal patients.Am J Obstet Gynecol

1985; 151 : 711-7.

39. Minkoff HL, Sierra MF, Pringle GF, Schwarz RH. Vaginal

colonization with Group B beta-hemolytic streptococcus as

a risk factor for post-cesarean section febrile morbidity.

Am J Obstet Gynecol1982; 142 : 992-5.

40. Anandalakshmy PN, Buckshee K. Maternal mortality in a

referral hospital of northern India: a sixteen-year review.

J Fam Welf1997; 43 : 1-4.

41. Walsh JA, Hutchins S. Group B streptococcal disease: its

importance in the developing world and prospect

for prevention with vaccines. Pediatr Infect Dis J1989; 8 :

271-7.

42. Munoz P, Llancaqueo A, Rodriguez-Creixems M, Pelaez T,

Martin L, Bouza E. Group B Streptococcus bacteremia in

nonpregnant adults. Arch Intern Med1997; 157 : 213-6.

43. Dhawan B, Khan U, Das BK, Mathur P, Pandhi RK,

Kapil A. Group B streptococcal bacteremia in an adult:

a case report from India. Southeast Asian J Trop Med Public

Health 2001; 32 : 867-8.

44. Mathur P, Kapil A, Das B, Dhawan B, Dwivedi SN. Invasive

beta-haemolytic streptococcal infections in a tertiary care

hospital in northern India.J Med Microbiol 2002; 51 : 791-2.

45. Persson KM, Forsgren A. Evaluation of culture methods

for isolation of group B streptococci.Diagn Microbiol Infect

Dis1987; 6 : 175-7.

46. Centers for Disease Control and Prevention. Prevention of

Perinatal Group B Streptococcal Disease. MMWR Morb

Mortal Wkly Rep2002; 51: 1-24.

47. Dillon HC, Jr., Gray E, Pass MA, Gray BM. Anorectal and

vaginal carriage of group B streptococci during pregnancy.

J Infect Dis1982; 145 : 794-9.

48. Walker CK, Crombleholme WR, Ohm-Smith MJ, Sweet RL.

Comparison of rapid tests for detection of group Bstreptococcal colonization.Am J Perinatol1992; 9 : 304-8.

49. Das A, Ray P, Sharma M, Gopalan S. Rapid diagnosis of

vaginal carriage of group B beta haemolytic streptococcus

by an enrichment-cum-antigen detection test. Indian J Med

Res2003; 117 : 247-52.

50. Ke D, Bergeron MG. Molecular methods for rapid detection

of group B streptococci. Expert Rev Mol Diagn 2001; 1 :

175-81.

51. Centers for Disease Control and Prevention. Prevention of

perinatal group B streptococcal disease: a public healthperspective. MMWR Morb Mortal Wkly Rep 1996; 45 : 1-

24.

52. Rouse DJ, Goldenberg RL, Cliver SP, Cutter GR,

Mennemeyer ST, Fargason CA, Jr. Strategies for the

prevention of early-onset neonatal group B streptococcal

sepsis: a decision analysis. Obstet Gynecol1994; 83 : 483-

94.

53. Lin FY, Azimi PH, Weisman LE, Philips JB, 3rd, Regan J,

Clark P, et al. Antibiotic susceptibility profiles for group

B streptococci isolated from neonates, 1995-1998.

Clin Infect Dis2000; 31 : 76-9.

54. Ferrieri P. Prevention of Group B Streptococcus infections.Semin Pediatr Infect Dis1997; 8 : 117-24.

55. Swingle HM, Bucciarelli RL, Ayoub EM. Synergy between

penicillins and low concentrations of gentamicin in the killing

of group B streptococci. J Infect Dis 1985; 152 : 515-20.

56. Kasper DL, Paoletti LC, Wessels MR, Guttormsen HK, Carey

VJ, Jennings HJ, et al. Immune response to type III group B

streptococcal polysaccharide-tetanus toxoid conjugate

vaccine. J Clin Invest1996; 98 : 2308-14.

57. Baker CJ, Paoletti LC, Wessels MR, Guttormsen HK,

Rench MA, Hickman ME, et al. Safety and immunogenicity

of capsular polysaccharide-tetanus toxoid conjugate vaccines

for group B streptococcal types Ia and Ib. J Infect Dis 1999;179 : 142-50.

58. Mohle-Boetani JC, Schuchat A, Plikaytis BD, Smith JD,

Broome CV. Comparison of prevention strategies for neonatal

group B streptococcal infection. A population-based economic

analysis. JAMA1993; 270 : 1442-8.

59. The World Health Report: Causes of neonatal deaths, 1995.

Geneva: The World Health Organisation; 1998 : http://www.

who.int/whr 2001/2001/archives/1998/index.htm.

60. Kishore K, Deorari AK, Singh M, Bhujwala RA. Early

onset neonatal sepsis: Vertical transmission from maternal

genital tract. Indian Pediatr1987; 24 : 45-8.

61. Haffejee IE, Bhana RH, Coovadia YM, Hoosen AA,

Marajh AV, Gouws E. Neonatal group B streptococcal

infections in Indian (Asian) babies in South Africa. J Infect

1991;22 : 225-31.

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