RESEARCH DISSERTATION

ON

THE PREVALENCE OF GROUP B STREPTOCOCCUS

IN PREGNANT WOMEN WITH PRETERM

PRELABOUR RUPTURE OF MEMBRANES

SUBMITTED IN PART FULFILLMENT OF THE

REQUIREMENTS FOR THE FMCOG PART II

EXAMINATION OF THE NATIONAL

POSTGRADUATE MEDICAL COLLEGE OF NIGERIA

BY

DR EDE-EDOKPOLOR OSAHON

MAY, 2013

THE PREVALENCE OF GROUP B STREPTOCOCCUS

IN PREGNANT WOMEN WITH PRETERM

PRELABOUR RUPTURE OF MEMBRANES

BY

DR. EDE-EDOKPOLOR OSAHON

DEPARTMENT OF OBSTETRICS AND GYNNECOLOGY

LAGOS UNIVERSITY TEACHING HOSPITAL (LUTH)

P.M.B. 12003, LAGOS

DISSERTATION FOR FMCOG PART II

PROJECT TITLE

THE PREVALENCE OF GROUP B STREPTOCOCCUS IN

PREGNANT WOMEN WITH PRETERM PRELABOUR

RUPTURE OF MEMBRANES

NAME OF CANDIDATE

DR. EDE-EDOKPOLOR OSAHON

NAME OF SUPERVISORS

DR. J.A OLAMIJULO

FMCOG,FWACS, FRCOG,DFFP.

INSTITUTION

DEPARTMENT OF OBSTETRICS AND GYNAECOLOGY,

LAGOS UNIVERSITY TEACHING HOSPITAL (LUTH)

P.M.B 12003, LAGOS, NIGERIA

ATTESTATION

This dissertation by Dr. Ede-Edokpolor Osahon in part fulfillment of

the requirements for the FMCOG II of The National Postgraduate

Medical College of Nigeria was supervised by me.

_____________________

Dr. J.A Olamijulo FMCOG, FWACS, FRCOG, DFFP

_______________________________

Prof. B.A. Oye-Adeniran FMCOG, FWACS, mni.

Head of Department

ACKNOWLEDGEMENT

I thank all my consultants for the knowledge they impacted on me and for their constructive

criticism during the course of my training. Special thanks to thanks to Professor B.O

Oyeadeniran, Professor R.I Anorlu, Dr. Olamijulo, Dr. Adegbesan-Omilabu in enhancing my

academic and professional up liftment.

I am primarily indebted to my wife Dr. Mrs. Precious Ede-Edekpolor, my children

Osahenrumwen, Nosazena, Osadebamwen; my parents, Elder Pius Edokpolor and Deaconess

Grace Edokpolor for their love, support and inspiring encouragement over the years. I also

thank my siblings for their love and persistent motivation.

I am grateful to my colleagues for sharing their knowledge and experience with me and for

their support and encouragements so far.

I thank all members of the Obstetrics and Gynaecology department, LUTH for their warm

and approachable character and willingness to be of assistance to me whenever the need

arises.

I am grateful to everyone who has contributed in one way or the other in making me what I

am today.

Above all, my gratitude goes to God who has been my sustenance.

TABLE OF CONTENTS

Content Page

Title Page … … … … … … … … … … … … i

Title Project… … … … … … … … … … … iii

Attestation Page… … … … … … … … … … … iv

Acknowledgement… … … … … … … … … … … v

Table of Content… … … … … … … … … … … vi

List of Abbreviation … … … … … … … … … … vii

Abstract… … … … … … … … … … … … 1

Introduction… … … … … … … … … … … 3

Relevance of the Study… … … … … … … … … … 6

Literature Review… … … … … … … … … … … 9

Statement of Objectives… … … … … … … … … … 19

Methodology… … … … … … … … … … … 20

Result… … … … … … … … … … … … 25

Discussion… … … … … … … … … … … … 38

Limitation of Study… … … … … … … … … … 43

Recommendation… … … … … … … … … … … 44

References… … … … … … … … … … … … 45

Appendix A – Consent Form… … … … … … … … … 52

B – Performa… … … … … … … … … 54

LIST OF ABBREVIATIONS

The following are the full meanings of some abbreviations used in this book:

AIDS - Acquired Immune Deficiency Syndrome

CI - Confidence interval

CLSI - Clinical Laboratory Standards institute.

ECS - Endocervical swab

HIV - Human Immunodeficiency Virus

HVS - High Vaginal Swab

LUTH - Lagos University Teaching Hospital

M/C/S - Microbiology, culture and sensitivity

OR - Odds Ratio

RR - Relative risk

UNFPA - United Nations Population Fund.

UNICEF - United Nations children Fund

WHO - World Health Organization

% - Percentage

ABSTRACT

Background. Group B streptococcus and premature rupture of membranes are independent

risk factor for the development of both maternal and perinatal morbidity and mortality.

Objective. To determine the prevalence of group B streptococcus, pregnancy outcome,

antibiotics sensitivity and resistance pattern among pregnant women with preterm prelabour

rupture of membrane.

Design. A Case-control study comprising 50 cases of PPROM and 50 control. The control

group comprised pregnant women similar in age, parity and gestational age without PPROM.

Methods. Using a proforma, information on the socio-demographic data and obstetric profile

were obtained from both cases and control. High vaginal swabs were done for both cases and

control. Buccal, umbilical and skin swabs were also obtained from the neonates at birth.

Results. The overall prevalence of GBS from the study was 7%. GBS was only isolated in 7

of 50 pregnant women with PPROM. The women studied ages from 22 to 42 years with

mean age of 32.92 years for the test group and 32.46 years in the control group. The women

with GBS have mean age of 35years while those with PPROM without GBS have mean age

of 32.58 (p value =0.078). Also, the overall mean parity was 0.86 for the test group and 1.32

in the control group. Women with GBS have mean parity of 3.57 while GBS negative

PPROM have mean parity of 0.95 ( p value = 0.0003). The mean gestational age of rupture of

fetal membranes was 31.86 weeks in GBS positive women and 31.16 weeks in GBS negative

PPROM and there was statistically significant difference in their latency period (p value of

0.042). The Apgar score at 5 minutes was also found to be significantly different ( p value of

0.0113). Six babies had neonatal sepsis but only one tested positive for GBS. The odds ratio

for neonatal sepsis, stillbirth, chorioamnionitis and puerperal sepsis in subjects positive for

GBS were 1.27, 2.22, 3.42 and 8.20 respectively. GBS was sensitive to most of the

commonly prescribed antibiotics including Ampicillin (100%), Cefuroxime (100%), Amoxyl-

clavulinic acid (85.71%), Erythromycin (85.71%), Benzathin penicillin (85.71%),

Ceftriaxone (71.43%) and Tetracycline (42.86%).

Conclusion

Group B streptococcus infection is commoner in pregnant women with PPROM. It is

associated with shorter latency period and increased risk of maternal infection. It is also

associated with lower five minute APGAR score but a rare cause of neonatal sepsis.

INTRODUCTION

Prelabour rupture of fetal membrane is an important obstetric complication. It is a potentially

lethal threat to the mother and fetus1. It remains a major contributor to both perinatal and

maternal morbidity and mortality worldwide2. It is defined as the spontaneous rupture of fetal

membranes prior to the onset of labour at any gestational age2. It is preterm prelabour rupture

of membrane when it occurs after age of viability but before the completion of 37weeks2.

Preterm prelabour rupture of membranes is estimated to complicate about 1-3% of all

pregnancies and account for 25-30% of all cases of prelabour rupture of membranes2,3. It is

thus a leading identifiable cause of preterm delivery and its associated complications

including respiratory distress syndrome, neonatal infection and intraventicular haemorrhage4.

The success in preventing preterm prelabour rupture of membranes and preterm birth is

hampered by our limited knowledge of its etiology.

The aetiology is uncertain though probably multifactorial. It has been linked to several risk

factors including history of previous prelabour rupture of membrane, polyhydramnios,

socioeconomic status, antepartum hemorrhage, multifetal pregnancies and previous abortions.

Traditionally, rupture of fetal membranes was attributed to physical stress, particularly that

associated with labour, however fetal membrane rupture is now thought to be related to a

biochemical process including disruption of collagen within the extracellular matrix of the

amnion and the chorion5. It has been proposed that the fetal membranes and the maternal

uterine lining (decidua) respond to various stimuli including membrane stretching and

infection of the reproductive tract by producing mediators such as prostaglandins, cytokines

and protein hormones that govern the activity of matrix degrading enzymes5.

The identification of pathologic micro- organisms in human vaginal flora soon after

membrane rupture provides support for the concept that bacterial infection may have a role in

the pathogenesis of PPROM. In women with preterm prelabour rupture of membranes, about

one-third of pregnancies have positive amniotic fluid cultures5. Ascending bacterial infection

may therefore be responsible for the weakening of the membranes and consequently for their

rupture. It however remains unclear why in some of the patients with the same micro

organisms these do not lead to the rupture of their membranes.

Group B streptococcus is a normal commensal in about 10-30% of pregnant women6. It is

potentially harmful to both mother and the baby itself. It emerged as a leading infectious

cause of neonatal morbidity and mortality in the 1970s7. Its colonization of the birth canal

during labour or after membrane rupture has been noted to result in miscarriage, stillbirths,

prematurity and neonatal GB sepsis.7 There is clear evidence that intrapartum colonization is

strongly associated with early onset GBS neonatal sepsis with a case fatality of

approximately 4%8. It also accounts for other morbidities such as pneumonia, meningitis,

osteomyelitis or septic arthritis in the neonate. Because of this, much attention has been given

to the prevention of neonatal group B streptococcus. Group B streptococcus has also been

recognized as an important maternal pathogen. A variety of maternal GBS infections may

occur in the course of pregnancy and the postpartum period especially after preterm prelabour

rupture of membranes. Apart from cervicovaginal colonization which is usually

asymptomatic, GBS can cause urinary tract infections, chorioamnionitis, endometritis,

puerperal sepsis, bacteremia, meningitis and wound infections9.

Group B streptococcus and premature rupture of membrane are independent risk factor for

the development of both maternal and perinatal sepsis, hence a major contributor to maternal

and perinatal morbity and mortality. Intrapartum prophylaxis has been showed to reduce both

incidence of maternal and neonatal sepsis. Nevertheless, current centre for disease control

and prevention (CDC) guidelines call for intrapartum prophylaxis for early onset neonatal

group B streptococcus10.

This study is therefore designed to investigate the prevalence of Group B Streptococcus in

pregnant women with preterm prelabour rupture of membranes, its antimicrobial sensitivity

pattern and impact on fetal and maternal health. If the prevalence of GBS in PPROM is found

to be significantly high, it may scientifically justify the prescription of certain antimicrobial

routinely for all cases of PPROM.

RELEVANCE OF THE STUDY

Preterm prelabour rupture of fetal membranes is a distressful obstetric condition both to the

obstetrician and the mother. It affects both the mother and the fetus. Its gravest effects are

related to the inherent risks and consequences associated with premature delivery. It accounts

for approximately 40% of cases of preterm delivery with an estimated perinatal deaths of

10% either directly or indirectly2. It results in increased hospital costs and longer length of

stay for mother and infant2 . It has a tremendous socioeconomic impact on the society.

It is a major contributor to neonatal infection which is an important cause of morbidity and

mortality in the newborn. The risk of infection is high when prelabour rupture of membranes

is prolonged and when it is associated with maternal chorioamnionitis. Also expectant

management especially in cases of preterm prelabour rupture of membranes has been

associated with increased incidence of cord prolapse, pulmonary hypoplasia, fetal distress

and placenta abruption.

The relationship between Group B streptococcus and preterm rupture of membrane is not

clear in terms of aetiopathogenesis4. However patients with prelabour rupture of membrane

and prolonged rupture of fetal membranes of more than 18 hours are a high risk group for the

development of neonatal Group B streptococcus sepsis.7 Neonatal Group B streptococcus has

emerged as a major cause of neonatal morbidity and mortality prior to the advent of

implementation of preventive guidelines in the developed countries. There is clear evidence

that intrapartum colonization is strongly associated with early onset Group B streptococcus

sepsis which has a case fatality of approximately 4%8. Other serious morbidities include

sepsis, pneumonia, meningitis, osteomyelitis or septic arthritis. Also, Group B streptococcus

colonization after membrane rupture can lead to miscarriage, stillbirths and preterm

deliveries8.

Maternal group B streptococcus threatens not only the child but also the mother. Group B

streptococcus and preterm prelabour rupture of membranes are independent risk factors for

the development of puerperal sepsis. The maternal sequelae due to Group B streptococcus

sepsis do not differ from those related to other bacteria. Sepsis remains an important cause of

maternal morbidity and mortalities. In developing countries, puerperal sepsis is one of the

main factors leading to maternal mortality11. Also, maternal Group B streptococcus

colonization following rupture of fetal membranes can cause significant maternal morbidities

such as endometritis, chorioamnionitis and bacteremia. Also women with GBS colonization

are at increased risk of GBS colonization in a subsequent pregnancy.

The presence of GBS influences the choice of management in patients with preterm prelabour

rupture of membrane, since subclinical Group B streptococcus intrauterine infections has

been implicated as a major factor in the pathogenesis and consequential maternal and

neonatal morbidity. For patients with preterm prelabour rupture of membrane and a positive

or unknown Group B streptococcus culture antibiotics therapy is recommended to prevent or

treat ascending intrauterine infections10,12.

Consequently, since preterm prelabour rupture of fetal membrane is associated with

significant maternal and perinatal morbidity and mortality, early detection of offending

organisms will guide use of antibiotics prophylaxis based on the sensitivity pattern obtained

and hence greatly affect pregnancy outcome. This is why universal screening between 35-

37weeks is being advocated in some developed countries as part of routine antenatal care and

also in high risk patients such as patient with preterm prelabour rupture of membrane and

prelabour rupture of fetal membrane greater than18hrs10.

Intrauterine and perinatal infections remain an important cause of maternal and neonatal

morbididty and mortality worldwide but especially in the developing countries. One of the

bacterial species commonly responsible for these infections is Streptococcus agalactiae. Very

limited local data exist on the role of Group B Streptocccus as a cause of sepsis in particular

and mortality in general. Elsewhere, studies have demonstrated significant correlation

between Group B streptococcus, premature rupture of membrane and maternal and perinatal

sepsis10,12.

Screening for Group B streptococcus among pregnant woman with Preterm prelabour rupture

of membrane and intravenous administration of antibiotics when in labour is not routinely

done in our hospital in contrast to what is done in developed countries10,13,14.

Since published work on this subject is scarcely available, it is hoped that information

obtained from this study will assist to define the magnitude of the problem as well as

stimulate further research interest. This could help reshape the use of antibiotics in patient

with preterm prelabour rupture of membrane.

LITERATURE REVIEW

GROUP B STREPTOCOCCUS AS AETIOLOGICAL AGENT IN PRETERM

PRELABOUR RUPTURE OF FETAL MEMBRANES (PPROM).

Infection has been linked with PPROM, yet whether maternal GBS colonization is a predictor

of preterm prelabour rupture of membranes is unclear.

Group B streptococcus also known as Streptococcus agalactiae is the sole member of

Lancefield group B12. It is an encapsulated gram positive diplococcus bacteria that may

colonize the gastrointestinal and genital tracts in about 10% to 30% of pregnant women6. The

prevalence of maternal carriage of GBS in developing countries including Subsahara Africa

is similar to that identified in populations in the United States15,16. A maternal and infant

colonization rates of 22% and 23% was respectively quoted by Suara etal in a study from

Gambian16. Women with pregnancy complicated with preterm premature rupture of fetal

membranes have higher colonization rate compared to normal pregnancy17. GBS forms small

3 to 4mm, grey white colonies that have a narrow zone of beta haemolysis on blood agar18. It

is identified in the clinical laboratory by its characteristic narrow zone of beta haemolysis by

its elabouration of cAMP factor, which enhances the haemolysis caused by beta lysis of many

staphylococcus aureus stains and by biochemical characteristics including lack of hydrolysis

of bile esculin agar and hydrolysis of hippurite19.

Group B streptococci are found in the digestive tract, urinary tract and genital area of the

adults. Several risk factors have been associated with cervicovaginal GBS colonization.

Regan and colleagues reported higher incidence with low parity, older maternal age, and

extreme increases in sexual activity including both frequent intercourse and multiple partners,

concurrent colonization with candida specie, higher education level, purulent vaginal

discharge and vaginal pH greater than 5 during antenatal period. However,

Liampongsabhudhi and colleagues reported older maternal age as the only significant risk

factor for natural colonization20. Method of contraception is another predisposing factor that

might be studied. Previous history of use of intrauterine contraceptive device was linked to

more GBS colonization9.

The bacterium adhere to a variety of human cells including vaginal epithelium, placental

membranes, respiratory tract epithelium and blood brain barrier endothelium. It has been

noted to efficiently bind the extracellular matrix components fibronectin which allows it to

compete with other microflora for a niche on the gastrointestinal and vaginal mucosa, the

ability of the organism to penetrate host cellular barriers is a first distinguishing feature of its

pathogenesis. In tissue culture, Winram and colleagues21 were able to demonstrate that GBS

are able to invade chorionic epithelial cells but not amniotic cells and induce cell death. β-

hemolysis appears to play the key role in GBS induced macrophage and epithelial death22. It

could be speculated that processes that lead to bacterial lysis and β- hemolysis release, such

as the antibiotic treatment of colonized women may potentially lead to trophoblast toxicity

and disruption of the placenta integrity23.

Also Clavellina and colleagues demonstrated that infection of fetal membranes with GBS is

followed by active secretion of metalloproteinase 9 and 2 and the choriodecidual is the

principal source of this extracellular matrix degradation24. Using a two- step process

beginning with placental circulatory leucocytes as a proxy for intrauterine leucocytes,

Guadalupe and colleagues found that co-incubation of amniochorion explants with plasma

from placental whole blood preincubated with Group B streptococci resulted in a significant

increase in tumor necrosis factor alpha (TNF-α) and matrix metalloproteinase 9 levels in

tissue25 . These data further demonstrated that Group B streptococci induced degradation of

the amniochorion as a result of mmp-9 production, probably via TNF-α.

GBS infection acquired from the colonized birth canal during labour or after membrane

rupture is a notable cause of miscarriage, stillbirth, prematurity or invasive neonatal disease7.

It is a recognized cause of a bacterial infection in neonates up to 3 months of age. Although

GBS can cause early or late neonatal disease, 80% of disease is of early onset occurring

within 48hours of delivery7. Because of this much attention has been given to the prevention

of neonatal GBS disease. Guidelines to prevent neonatal GBS disease were developed in the

1990s in United States. After the implementation of this preventive guideline, the incidence

of early onset disease decreased markedly from an estimated 1.8 cases per 1000 live birth in

1990 to 0.32cases per 1000 live births in 2003 in the U.S. Other countries showed a similar

decrease26. Despite the decrease in the incidence, GBS remains the number one cause of

infectious neonatal morbidity and mortality in the western world. Although 60-70% of

newborns born to maternal carriers will be colonized at birth,27 passively acquired immunity

derived from maternal antibodies protects the majority of healthy newborns. Thus only 1% of

colonized newborns will develop symptomatic disease. Also in developing countries,

including population in tropical Africa, recent studies suggested that GBS is emerging as an

important cause of neonatal sepsis. Katherine and colleagues in a study in Malawi reported

an incidence of early and late onset invasive GBS disease to be 0.92 and 0.92 per 1000 live

birth respectively with overall case fatality rate of 33%28. Also a study from Johannesburg

reported an early onset disease incidence rate of 1.16 per 1000 livebirth29.

Young infants with invasive GBS disease usually present with sepsis or pneumonia and less

often contact meningitis, osteomyelitis or septic arthritis. The proportion of infants with

meningitis is higher among those with late onset infections.

Certain factors further increase the incidence of neonatal sepsis. Infants born prematurely

have a risk of developing early-onset GBS sepsis. Neonatal sepsis is 8 times higher in

preterm birth than those born at term while those born 18hours or more after rupture of

membranes are 8.6 times more likely to develop GBS disease26,27.

In a study in Sagamu, Nigeria the prevalence of neonatal sepsis was associated with weight

less than 1.5kg, prolonged labour, prolonged rupture of membrane30. Neonates as a group are

at a risk for infections and this particularly so in preterm neonates31. When compared to older

children and adults, neonates have an intrinsic limitation in their capacity to produce

neutrophils and a subsequent susceptibility to exhaustion of marrow reserves during times of

increased utilization such as sepsis32. In addition, those neutrophils that are produced have

impairments of numerous functions important to the clearance of microbes including marrow

regress, adhesion to the microvascular endothelium, chemotaxis and bacteria function32.

Furthermore, studies have also shown that vernix caseosa which is sparse in the preterm

infant contains proteins important to host defence functions including antimicrobial peptides

and factors that promote opsonization and inhibit protease activity33.

Death from early onset sepsis is inversely related to gestational age and birth weight.

Surveillance data obtained before the release of the initial CDC consensus statement showed

an overall case fatality rate of 16% for infants with GBS early onset sepsis27. Approximately

65% of these deaths occurred in neonates weighing 2500g or less34.

MATERNAL HEALTH OUTCOME OF GBS COLONIZATION IN PREGNANT

WOMEN WITH PRETERM PRELABOUR RUPTURE OF MEMBRANE

Group B streptococcus and PPROM are independent risk factors for maternal morbidity.

GBS has been recognized as an important maternal pathogen. Apart from cervicovaginal

colonization which is usually asymptomatic, GBS has been implicated in urinary tract

infection, vulvovaginitis, intra-amniotic infection, endometritis and wound infection.

PPROM is an independent risk factor for intra-amniotic infection. It is a clinical syndrome of

infection of the placenta and membranes accompanied by signs and symptoms in the mother

and/or the fetus. Bacteria normally present in the vagina are the most common amniotic fluid

isolate in women with intra-amniotic infection35. The risk of intra-amniotic infection

increases with the duration of rupture of the membranes36.

Intra-amniotic infection increase maternal morbidity and mortality. Bacteremia occurs in 2-

6% of patients with intra-amniotic infection, however a higher incidence of 18% has been

linked with bacteremia when GBS is the causative agent37.

Furthermore, puerperal sepsis which is an important cause of maternal mortality in

developing countries is an important sequelae of GBS colonization in PPROM10. Among

cases of GBS puerperal infection, bacteremia occurred in 31% to 35%37. However the

maternal sequelae due to GBS sepsis do not differ from those related to other bacteria. Other

associated predisposing factors for puerperal sepsis are anaemia in pregnancy, prolonged

labour (at least 12hours), frequent vaginal examination during labour (more than 5 times),

manual removal of placenta, low socioeconomic status. In early postpartum endometritis i.e.

within the first 48 hours GBS is an important contributor as it is most frequently isolated38. In

studies of endometritis, GBS has been identified as the sole pathogen in 2-14% of cases38.

Strategies specifically aiming at GBS may be helpful in reducing the incidence of puerperal

sepsis. The incidence of GBS endometritis declined after the introduction of the GBS

prophylaxis39. In a longitudinal study Locksmith et al40 compared the infection rates

following three consecutive protocols for the prevention of GBS disease. In the selective

screening protocol, GBS cultures where obtained from women with PPROM or preterm

labour and intrapartum antibiotics were administered to all women with positive culture and a

risk factor for neonatal GBS disease. Under the universal screening protocol, a culture was

performed between the 35-37week of gestation and intrapartum antibiotic prophylaxis given

to all women with a positive GBS culture. In the risk-based protocol, intrapartum antibiotics

were given to all women with unknown colonization status and a risk factor for neonatal GBS

disease. Under all 3 protocols the postpartum endometritis rates were reduced40.

Infections in perineal and abdominal wounds after delivery can be caused by GBS. It is not

known to what extent GBS contributed to the incidence of wound infection. However,

abdominal wound infections after caesarean section may be caused by the same

microorganisms that can be isolated from the amniotic fluid. There is some evidence that

GBS prophylaxis is also beneficial in the prevention of wound infection39. Prevention of

endometritis is therefore important for the prevention of wound infection. It is unclear

whether this is a direct effect of the antibiotics or indirectly through a reduction in the

incidence of endometritis. General strategies to prevent wound infection and its extension are

straightforward and not specific for GBS. Most important is proper hygiene and proper

surgical technique.

PREVENTION STRATEGIES FOR GBS DURING PREGNANCY.

Therapeutic interventions to prevent transmission of early onset neonatal group B

Streptococcus infection and maternal morbidity remain an issue for debate. Three approaches

for preventing early onset neonatal GBS infections have generally been used: Universal

screening of all pregnant women for GBS colonization with intrapartum antibiotics given to

those with positive results; Universal screening of all pregnant women with intrapartum

antibiotics given only to those with positive results as well as other risk factors for GBS

transmission; and intrapartum antibiotics for all women with risk factors for GBS

transmission without prior screening.

While all three approaches for prevention of early-onset neonatal GBS infections have

previously been recommended, a 2002 landmark article by Schrang et al showed in a

retrospective cohort study that universal screening for GBS was statistically superior to risk

based approaches to prevention41. In light of these data, the U.S center for disease control and

prevention, the American college of obstetricians and Gynaecologists42 and the societies of

Obstetrician and Gynecologist of Canada43 narrowed their recommendations to universal

screening and intrapartum antibiotics for a GBS carriers to the exclusion of other strategies.

Professional organizations from other parts of the world however have questioned the

movement to universal prenatal GBS screening. In 2003, the Royal College of Obstetricians

and Gynaecologists in the United Kingdom recommended against offering antenatal GBS

screening and promoted patient discussion regarding intrapartum antibiotic prophylaxis based

on specific risk factors44. In 2004, the New Zealand GBS consensus working party

recommended a risk based prevention strategy over universal screening45.

Universal screening for maternal GBS infection and intrapartum antibiotic prophylaxis of all

colonized women might carry risks including unexplained maternal penicillin anaphylaxis, an

epidemiologic shift from gram positive to gram negative neonatal sepsis,7 changing resistance

patterns among GBS and other organisms and increased rates of other serious neonatal

infection46.

Intrapartum chemoprophylaxis (i.e. administration of antimicrobial agents after onset of

labour or membrane rupture but before delivery) is the most likely method of preventing both

early-onset disease and maternal illnesses resulting from GBS. Several antimicrobial

regimens have been used for intrapartum chemoprophylaxis.

Other studies also have documented the protective efficacy of intrapartum chemoprophylaxis

administered to GBS carriers in certain high risk groups (e.g. women with heavy genital

colonization)6,47 and with rupture of membranes at ≤ 34 weeks gestation and > 12 hours

before labour onset47.

Restricting antimicrobial agents to selected populations’ at increased risk for delivering a

newborn with GBS disease would decrease the likelihood of adverse reactions and

antimicrobial-resistant infections. Oral antimicrobial agents should not to be used to treat

women who are found to be colonized with GBS during prenatal screening. Such treatment is

not effective in eliminating carriage or preventing neonatal disease7.

For intrapartum chemoprophylaxis, intravenous penicillin G (5mU initially and then 2.mU

every 4 hours) should be administered until delivery. Intravenous ampicillin (2g initially and

then 1g every 4 hours until delivery) is an acceptable alternative to penicillin G, but penicillin

G is preferred because it has a narrow spectrum and this is less likely to select for antibiotic

resistant organisms. Clindamycin or erythromycin may be used for women allergic to

penicillin, although the efficacy of these drugs for GBS disease prevention has not been

measured in controlled trials7.

Also authors have evaluated the prevalence of antibiotic resistance among group B

streptococcus over the last 15 years48.

Joachin etal in Tazania found all isolates of group B streptococcus sensitive to vancomycin

and ampicillin and resistant to clindamycin, erythromycin and penicilline G in 17.6%, 13%

and 9.4% respectively49. Among retrovaginal samples, studies performed more than ten years

later have found clindamycin resistance ranging from 3% -21% and erythromycin resistance

ranging from 5% -29%48,49. In the Africa population, a study in Malawi found that all isolates

were susceptible to the B-lactam antimicrobial drugs and that about 96% were resistant to

tetracycline. However, 21% of isolates were resistant to erythromycin28.

The administration of prerequisite vaccines is the most promising approach to the prevention

of neonatal GBS disease50. A major rationale for the vaccination of women against GBS is

that the majority (85-90%) of pregnant women lack protective antibodies at the time of

delivery. In a decision analytical model, effective maternal vaccination in combination with a

screening approach was predicted to prevent 66% of peripartum GBS infection and 1 of 25

preterm births51. The goal of a universally effective vaccine and a successful immunization

strategy remains elusive. The development of efficacious vaccines with global relevance has

been hindered by changes in the prominence of various GBS serotypes and antigenicity

patterns over time as well as by regional variations in human populations52.

Alternative approaches to the eradication of GBS colonization have been considered

including the development of topical agents that can target GBS. One approach, involving the

use of chlorhexidine as a vaginal disinfectant. This has been favoured by some because of

low cost, lack of impact on the development of antibiotic resistance and its potential use in

undeveloped areas. While a systematic review of the literature was consistent with a decrease

in neonatal GBS colonization of neonates, this was not associated with a reduction in early

onset neonatal disease53. Also one novel agent, aqueous allicin, a substance derived from

garlic, has been shown to have potent bactericidal activity against GBS isolates in culture54.

Another consideration involves bacteriophage lysins, which are cell wall hydrolases that

render bacterial vulnerable to Lysis55. In vivo studies in neonatal mice have shown the

potent wide spectrum bacteriocidal activity of a bacteriophage lysine, PlyGBS, against

GBS colonization. Interesting possibilities of this approach include potential utility in

cases of antibiotic resistance, its rapid action and the apparent lack of toxicity.

STATEMENT OF OBJECTIVES

AIM

To evaluate the prevalence of Group B streptococcus among pregnant Nigeria women with

preterm prelabour rupture of membrane.

OBJECTIVES

1. To determine the prevalence of Group B streptococcus among pregnant Nigerian

population with preterm prelabour rupture of membranes.

2. Determine antimicrobial sensitivity and resistance pattern among pregnant women

with preterm prelabour rupture of membranes who tested positive to GBS.

3. To determine pregnancy outcome (maternal and neonatal sepsis) in pregnant women

with preterm prelabour rupture of membrane colonized with Group B streptococcus.

METHODOLOGY

STUDY DESIGN

This research was a case-control study.

SETTING

The study was conducted at the labour ward and the neonatal unit of the Lagos University

Teaching Hospital (LUTH), Lagos, Nigeria. LUTH is a tertiary institution located in the

mainland area of Lagos and set mainly as a referral centre for other hospitals in both public

and private sectors in Lagos. The parturient seen are the booked antenatal patients of LUTH

and unbooked patients referred from various maternity homes, private hospitals and other

government hospitals. Average of 160-200 deliveries are conducted monthly. The culture and

sensitivity pattern was done in collaboration with a microbiologist at the Lagos University

Teaching Hospital.

STUDY POPULATION

The participants were pregnant women admitted to the labour ward, who meet the

inclusion criteria.

INCLUSION CRITERIA

Patients with preterm prelabour rupture of membrane with gestational ages between

28 and 37 weeks.

Confirmed PPROM according to RCOG screening guidelines based on maternal

history and observation of fluid pooling in the vagina, or leaking from the cervical OS

on sterile speculum examination5 and positive nitrazine paper test (colour change of

yellow to blue).

EXCLUSION CRITERIA

PPROM with cord prolapse.

Evidence of fetal distress.

PPROM with multiple gestation.

History suggestive of cervical incompetence.

History of bleeding in index pregnancy (Antepartum haemorrhage).

PPROM with established chorioamnionitis.

DATA COLLECTION

Selection of cases

The cases were parturients admitted into the labour ward with Preterm prelabour

rupture of membranes that fulfill the inclusion criteria above.

Neonates of parturients with preterm prelabour rupture of membrane.

Selection of controls

For every case, a control was recruited from the same study population similar in age, parity,

gestational age that does not have PPROM.

Evaluation of Cases and Controls

Data was collected with the aid of a structured proforma (appendix 1) designed based on the

study objectives. Content areas of the proforma included socio-demographic data such as age

and parity, last menstrual period, estimated gestational age, previous history of PROM/Birth.

Detailed review of antenatal delivery, postnatal records was done. The samples were

collected by sterile cotton tip swab after cleaning the perineum with sterile swab soaked with

saline. Each recruited subject had a high vaginal swab during a speculum examination to

confirm PPROM. Any abnormal discharge noted during speculum examination was recorded.

All patients recruited into the study were followed up till delivery noting presence of

chorioamnionitis, latency period, pyrexia during labour, mode of delivery, and puerperal

sepsis. Puerperal sepsis was defined using the World Health Organization diagnostic criteria,

which is infection of the genital tract occurring at any time between labour and the 42nd day

postpartum in which fever and one or more of the following are present; pelvic pain,

abnormal vaginal discharge for example presence of pus, abnormal smell and delay in the

rate of reduction of size of the uterus56.

Neonatal outcomes were reviewed and they included birth weight, mode of delivery, APGAR

score at one and five minutes and presence of neonatal sepsis. Buccal, umbilical and skin

swab were obtained from the neonate. Samples were collected by senior residents on call and

there were regular meetings of all members to ensure standardization of the collection

procedure.

LABORATORY METHODS

Samples were taken from subjects and transported to the medical Microbiology unit.

On arrival the swabs were removed from the transport medium and inoculated into selective broth

medium –Todd-Hewitt broth supplemented with either colistin and nalidixic acid or with gentamicin

and nalidixic acid.

This was incubated for 18-24 hours. This is in turn sub-cultured into blood agar plates. The

sheep blood agar plate was inspected to identify organisms suggestive of GBS (beta

hemolytic or non hemolytic, gram positive or catalase negative). The antimicrobial sensitivity

and resistance pattern was also determined for both the parturient and the neonate.

DETERMINATION OF SAMPLE SIZE

Using a prevalence rate of 3%2,3, the sample size was approximately 45 using the formula

n = Z2pq

d2

Where

n = the desired sample size

z = the standard normal deviation (usually 1.96) which corresponds to the 95% confidence

level

p = the proportion of the target population estimated to have a particular characteristic

q = 1.0 - p

d = the degree of accuracy desired (usually 0.05)

n = (1.96)2 × 0.03 × 0.97

(0.05)2

n = 45

However a total of 100 women were studied of which 50 were cases and 50 controls.

STATISTICAL ANALYSIS

The data obtained were analyzed using Epi-info 6.04 version. Categorical

variables were compared. Analysis included chi-square, Fisher exact and odd ratio where

appropriate.

A p value of <0.05 was considered significant.

ETHICS

The study was carried out after obtaining approval from the Health Research and Ethics

Committee of The Lagos University Teaching Hospital. Written consent was obtained

from the patients prior to recruitment. Investigation results obtained were treated with

confidentiality. Laboratory tests were carried out at no cost to the patients.

RESULTS

A case-control study of the prevalence of group B streptococcus in pregnant women with

preterm prelabour rupture of membranes was carried out at the labour ward of the Lagos

University Teaching Hospital (LUTH) from February 1 and December 31st 2012.

The study population comprised 50 cases of prelabour rupture of membranes and 50

control. The control group comprised pregnant women similar in age, parity, gestational

age to the cases without PPROM. High vaginal swabs were taken for both cases and

control.

TABLE 1: SOCIO-DEMOGRAPHIC VARIABLES BETWEEN THE CASES AND

CONTROL

VARIABLES PPROM CONTROL

AGES (YEARS)

20-25 4 (8%) 3(6%)

26-30 16(32%) 16(32%)

31-35 11 (22%) 15(30%)

36-40 16 (32%) 15(24%)

>40 3(6%) 1(2%)

Mean age 32.92 5.09 32.46 4.36

PARITY

Nulliparity 20 (40%) 23(46%)

1 12 (24%) 14(28%)

2 10 (20%) 10(20%)

3-5 7 (14%) 3(6%)

>5 1 (2%) -

Mean parity 0.86 0.94 1.32 1.53

LEVEL OF EDUCATION

No formal education 3(6%) 2(4%)

Primary 11(22%) 12(24%)

Secondary 20(40%) 21(42%)

Tertiary 16(32%) 15(30%)

The mean age of the study population was 32.92 years while the mean age of the control

group was 32.46 years. Also the mean parity of the both the study population and the control

group were 0.86 and 1.32 respectively. Majority of the patients were nulliparous in both the

cases 20 (40%) and 23 (46%) in the control group respectively. Forty seven (94%) of the

study population and 48 (96%) of the control group had formal education.

TABLE 2: OBSTETRIC VARIABLES OF CASES AND CONTROL.

VARIABLES PPROM CONTROL

Estimated gestational age

at delivery

28 < 32 16 (32.00%) - -

> 32 <34 27 (54%) -

>34< 37 7(14%) -

>37 - 50 (100%) X2=8.84

Mean gestational age at

delivery

32.68 1.74

39.22 1.13

P value= 0.003.

Average duration of stay in

postnatal ward (days).

4.32 2.23

2.38 0.53

X2= 30.02

P value= 0.00.

Puerperal sepsis 4(8%) - Fisher exact =0.059

Delivery occurs at a mean gestational age of 32.68 weeks in the PPROM group compared to

39.22 weeks in the control group. There was statistically significant difference between the

cases and control. (x2= 8.84, p value= 0.003). The average duration of stay in the postnatal

ward was shorter in the control group (2.38days) compared to the PPROM group (4.32 days)

( x2=30.02, p value= 0.00). Four of the patient with PPROM had puerperal sepsis but none in

the control group had puerperal sepsis (Fisher exact=0.059).

TABLE 3: FETAL OUTCOME BETWEEN THE CASES AND CONTROL.

VARIABLES PPROM CONTROL

APGAR score at 1 minute

<3 3 (6%) 1 (2%)

4-6 32 (64%) 5 (10%) X2=40.80

>7 11 (22%) 44 (88%) P value=0.58.

Mean APGAR score of 1

minute

5.67 1.43

8.04 1.55

APGAR score at 5 minutes

<3 - - -

4-6 6 (12%) 4 (8%) X2=34.63

>7 40 (80%) 46 (92%) P value= 0.77

Mean APGAR score of 5

minutes

7.87 1.31

9.36 1.37

Average birth weight (kg)

2.19 0.53

3.28 0.40

X2=84.4, p

value=0.0001.

Stillbirth 4 (8%) - Fisher exact=0.059

Neonatal sepsis 6 (12%) - Fisher exact= 0.013

The mean Apgar score at one minute was 5.67 for the cases and 8.04 for the control

(x2=40.80, p value =0.58). Also the mean Apgar score at five minutes was 7.87 for the cases

and 9.36 for the control. (x2=34.63 and p value =0.77). There was no statistically significant

difference between the cases and control. The average birth weight in the control group

(3.28kg) was larger than the birth weight in the cases (2.19kg) (x2=84.8, p value=0.0001).

Six (12%) of the neonates in women with PPROM developed neonatal sepsis but none in the

control group. (Fisher exact =0.013).

TABLE 4: GROUP B STREPTOCOCCUS COLONIZATION IN BOTH CASES

AND CONTROL

GBS STATUS

Yes No

PPROM 7 (14%) 43 (86%)

Control 0 50 (100%)

Fisher’s exact = 0.0062

Of the pregnant women with PPROM 7(14%) had Group B streptococcus while the

remaining 43 (86%) had no group B streptococcus. Group B streptococcus was not cultured

in the control group. There was statistically significant difference in term of Group B

streptococcus colonization between the test and the control group (Fisher’s exact = 0.0062).

Therefore the prevalence of Group B streptococcus in the studied population was 7%.

TABLE 5: SOCIO-DEMOGRAPHIC VARIABLES BETWEEN THE GBS

NEGATIVE PPROM AND GBS POSITIVE PPROM

VARIABLES GBS NEGATIVE

PPROM

GBS POSITIVE

PPROM

Ages (Years)

20-25 3(6.98%) 1(14.29%)

26-30 16 (37.21%) -

31-35 8 (18.61%) 3(42.86%)

36-40. 14 (32.55%) 2(28.56%)

>40 2 (4.65%) 1(14.29%) X2=28.57

Mean age 32.58 4.97 35.00 5.74 P value=0.078

Parity

Nulliparity 20 (46.51%) -

1 11 (25.58%) 1 (14.29%)

2 8 (18.61%) 2 (28.57%)

3-5 4 (9.30%) 3 (42.86%)

>5 - 1(14.29%) X2=12.93

Mean parity 0.95 1.15 3.57 1.72 P value= 0.0003

Level of education

No formal education 2 (4.65%) 1 (14.29%)

Primary 9 (20.98%) 2 (28.56%)

Secondary 17 (39.54%) 3 (42.86%) X2=1.91

Tertiary 15 (34.88%) 1 (14.29%) P value = 0.59

The mean age of the study population was 32.58 years for group B negative PPROM and 35

years for group B positive PPROM (x2=28.54, p value=0.074). Also the mean parity of both

GBS negative PPROM and GBS positive PPROM were 0.95 and 3.57 respectively.

(x2=12.93, p value=0.0003). Twenty (46.51%) of the GBS negative PPPROM were

nulliparous while 4(57.15%) of GBS positive PPROM had parity of 3 and above.

There was a statistically significant difference in parity between the GBS negative PPROM

and GBS positive PPROM (X2=12.93, P value = 0.0003).

Majority of the patients had formal education. At least 41 (93.37%) and 6 (85.71%) had

minimum of primary education in the case and control group respectively. There was no

statistically significant difference between the GBS negative PPROM and GBS positive

PPROM (x2=1.91, p value= 0.59).

TABLE 6: OBSTETRIC VARIABLES OF THE GBS NEGATIVE PPROM AND

GBS POSITIVE PPROM.

VARIABLES GBS

NEGATIVE

PPROM

GBS POSITIVE

PPROM

Estimated gestational age

at rupture of membrane

28 < 32 25 (58.14%) 3 (42.86%) -

32 34 17 (39.53%) 4 (57.14%)

>34 1 (2.33%) - X2=3.78

Mean gestational age 31.16 31.86 P value =0.81

Estimated gestational age

at delivery

28 < 32 14 (32.56%) 2 (28.57%) -

>/ 32 \<34 23 (53.49%) 4 (57.14%) X2=1.40

>34 6 (13.95%) 1 (14.29%) P value= 0.98

Mean gestational age at

delivery

32.65

32.86

Average latency period 1.49 1 week X2= 4.12.

P value = 0.042.

Average duration of stay in

postnatal ward (days)

Vaginal delivery

3.52 days

4.33 days

X2=0.72.

P value= 0.39.

Caesarian section 5.71 days 8 days X2=2.62. p value = 0.11

Previous history of

PPROM

2(4.65%) 2 (28.57%) X2=4.68, p value = 0.089

Rupture of fetal membrane s occurs mainly at gestational age of 28< 32 weeks gestation (28

of the 50 cases of PPROM) while delivery occurs more at a gestational age of 32 34 (27

of the 50 cases of PPROM). The mean gestational age of rupture fetal membrane was 31.16

and 31.86 weeks while delivery occurs at mean gestational age of 32.65 and 32.86 in the

GBS negative and GBS positive PPROM respectively. There was no statistically significant

difference in the estimated gestational age of rupture of fetal membranes and the estimated

gestational age at delivery between the two groups of PPROM. (x2=3.76, p value= 0.81 and

x2=1.40, p value = 0.98).

The average latency period was 1.49 week and 1 week for GBS negative PPROM and GBS

positive PPROM respectively (x2 = 4.12, p= 0.042), and this was statistically significant.

There was no statistically significant difference between duration of stay in the postnatal

ward following vaginal delivery (x2 = 0.72, p value 0.39) and caesarian section (x2 =2.62, p

value 0.11) in the two groups of PPROM.

TABLE 7. FETAL OUTCOME BETWEEN THE GROUP B NEGATIVE PPROM

AND GROUP B POSITIVE PPROM.

VARIABLES GROUP B

NEGATIVE

PPROM

GROUP B POSITIVE

PPROM

APGAR score at 1 minute

<3 2 (5%) 1 (16.67%)

4-6 28 (70%) 4 (66.66%) X2=5.43

>7 10 (25%) 1 (16.67%) P value=0.0198.

Mean APGAR score of 1

minute

5.85 1.37 4.50 1.38

APGAR score at 5 minutes

<3 - - -

4-6 2 (5%) 4 (66.67%) X2=6.41

>7 38 (95%) 2 (33.33%) P value= 0.0113.

Mean APGAR score of 5

minutes

8.06 1.19

6.50 1.38

Stillbirth

3 (6.98%)

1 (14.29%)

OR =2.22

(CI=0.20-25.00).

Fisher exact=0.46.

Average birth weight

2.13 0.54

2.53 0.3817

X2=3.79

P value=0.051.

Neonatal GBS status None 2

Average duration of stay in

neonatal ward

10.71 9.73

10.67 days 4.41

X2=0.28

P value=0.60.

Neonatal sepsis

5 (10%)

1(2%)

OR =1.27,

CI=0.12-12.80.

Fisher exact=0.62.

The APGAR score at 5 minutes in the two groups with PPROM showed statistically

significant difference ( x2 = 6.41, p value= 0.011 at 5 minutes). The mean APGAR score at 1

minute were 5.85 and 4.50 while 5 minutes APGAR score were 8.06 and 6.50 for GBS

negative PPROM and GBS positive PPROM respectively.

Six cases of neonatal sepsis were recorded in the patients with PPROM. However, GBS was

cultured in only one of the neonates studied.

There was no statistically significant difference in the still birth rate, number of neonatal

sepsis and duration of stay in the neonatal unit for both group B positive PPROM and group

B negative PPROM.

TABLE 8: MATERNAL OUTCOME IN PATIENT WITH GBS NEGATIVE

PPROM AND GBS POSITIVE PPROM.

VARIABLES GBS NEGATIVE

PPROM

GBS POSITIVE

PPROM

Chorioamnionitis Fisher exact= 0.37.

Present 2 (4.65%) 1 (14.29%) OR= 3.42.

Absent 41 (95.35%) 6 (85.71%) CI= 0.27-43.71.

Pueperal sepsis Fisher exact=0.089

Present 2 (4.65%) 2 (28.57%) OR=8.2

Absent 41 (95.35%) 5 (71.43%) CI= 0.94-71.73.

Chorioamnionitis occurred in 2 (4.65%) of the patients with GBS negative PPROM and 1

(14.29%) of patients with GBS positive PPROM. The odds of chorioamnionitis in GBS

positive PPROM are 3.42 times compared to GBS negative PPROM. (Odd ratio = 3.42,

confidence interval = 0.27-43.71) and (Fisher’s exact = 0.37). However the numbers involved

were small.

Also 2 (28.57%) of the group B positive PPROM had puerperal sepsis while 2 (4.65%) of the

group B negative PPROM had puerperal sepsis (OR- 8.2 and 9.5% confidence interval 0.94-

71.73) (Fisher’s exact = 0.089).

TABLE 9: ANTIBIOTIC SENSITIVITY AND RESISTANCE PATTERN IN

PATIENTS WITH GBS POSITIVE PPROM.

ANTIBODIES SENSITIVITY

PATTERN (%)

RESISTANCE PATTERN

(%)

Ampicillin 7 (100) -

Cefuroxime 7 (100) -

Amoxyl-clavulinic acid 6 (85.71) 1 (14.29)

Erythromycin 6 (85.71) 1 (14.29)

Benzathin penicillin 6 (85.71) 1 (14.29)

Ceftriaxone 5 (71.43) 2 (28.57)

Tetracycline 3 (42.86) 4 (57.14)

Out of the seven women from which GBS was isolated, all were sensitive to Ampicillin 7

(100%), Cefuroxime 7 (100%), Amoxyl-clavulinic acid 6 (85.71%), Erythromycin 6

(85.71%), Benzathin penicillin 6 (85.71%), Ceftriaxone 5(71.43%) but only 3(42.86%) to

tetracycline.

DISCUSSION

Group B Streptococcus and premature rupture of fetal membranes are independent risk

factors for the development of both maternal and perinatal infections, hence a major

contributor to maternal and perinatal morbidity and mortality. It is a leading cause of neonatal

infection in developed countries, but less appreciated is the fact that it causes maternal

infection also.

The overall prevalence of GBS from this study was 7%. This is relatively low compared to

most studies that quoted colonization rate of 10-30%6,15,16. GBS colonization was confirmed

in 23% of pregnant women in Tanzania49. However, low incidence of 6.6% was quoted in a

study from Greece56 while a culture positivity rate of 4.77% was isolated in patients with

preterm labour and pregnant women in india57.

Several risk factors have been associated with cervicovaginal GBS colonization. From this

study, the mean age in GBS positive PPROM was 35 years in comparison to 32.58 and 32.46

years for GBS negative PPROM and the control group respectively. Also the mean parity was

3.57 in GBS positive group compared to 0.95 and 1.32 in the GBS negative PPROM and the

control group respectively. There was a statistically significant difference in parity between

the GBS positive PPROM and the GBS negative PPROM (X2=12.93, p value =0.0003). One

may be justified to say from the study that GBS colonization occurs more in women with

higher parity. However Regan and colleagues reported higher incidence with low parity and

older maternal age58.These women were found to be living alone, with extreme increase in

sexual activity with multiple sexual partners during the previous year58. Liampongsabhudhi

and colleagues also reported older maternal age as the only significant risk factor for natural

colonization20. But no relationship was found between maternal age and colonization rate in a

study from Greece56 as there was also no association between GBS colonization and previous

history of GBS colonization, marital status and nationality. But GBS colonization was higher

among middle class women followed privately who had more prenatal visits. Therefore the

risk factors of maternal GBS colonization vary in different communities.

From the study, the mean gestational age of fetal membranes rupture was 31.16weeks and

31.86 weeks in the GBS negative PPROM and GBS positive PPROM respectively while

delivery occurs at mean gestational age of 32.65 and 32.86 weeks respectively. Delivery

occurs at a mean gestational age of 39.22weeks in the control group. However, there was

statistically significant difference in the latency period in the two groups of PPROM

(X2=4.12, p value =0.042). The mean latency period was approximately 1.5 weeks in the

GBS negative PPROM and 1.0 week in the GBS positive PPROM. These organisms might

have triggered the release of pro-inflammatory cytokines which in turn led to the release of

prostaglandins, metalloproteases and other inactive substances which are mediators of

labour24. This is however similar to a study in Iran where the mean gestational age of delivery

was 32.8 weeks15. However association between GBS colonization and rupture of fetal

membranes in terms of stimulation of labour, is still disputed in the literature. The researchers

in a study in the Netherlands to determine the relationship between maternal colonization

with GBS and preterm delivery reported that the combined estimate from random effect

metanalysis of 11 cohort studies was 1.06 (95% CI, 0.91-1.19) and for five cross-sectional

studies was 1.75 (95% CI, 1.43- 2.14). Also for the case control studies, the pooled odd ratio

was 1.59 (95% CI, 1.03- 2.44). However this systematic review did not show an association

between maternal GBS colonization during pregnancy and preterm delivery59.

GBS infection acquired from the colonized birth canal during labour or after membranes

rupture is a notable cause of stillbirth and early onset neonatal disease in developed

countries7,10. In this study, GBS was cultured in two of the neonates after birth and one of the

infants developed neonatal sepsis. However a total of six cases of neonatal sepsis were

recorded among the patients with PPROM with five of them in the GBS negative group.

There was no statistically significant difference in the groups. (Fisher exact=0.62, which is

greater than p value of 0.05). These neonatal sepsis might have been due to other organisms

such as Escherichia coli, Klebsiella and staphylococcus. A study done by Ogunlesi and

colleagues at Sagamu identified Staphylococcus aureus (31.0%), Klebsiella (23.0%),

coagulase-negative Staphylococcus (12.6%) and Escherichia coli (11.0%) as the leading

pathogens in neonatal sepsis30. Also in Mulagho hospital in Uganda, Staphylococcus aureus

and Eschericia coli dominated isolates in early and late onset sepsis60. GBS septicaemia may

not be a common cause of neonatal sepsis in our environment.

However from the study, the APGAR score at one and five minutes were statistically

different between the GBS positive PPROM and the GBS negative PPROM (X2= 5.43, p

value = 0.0198 at 1 minute and X2 = 6.41, p value of 0.011 at 5 minutes). But there was no

statistically significant difference between the birth weight, stillbirth rate and average

duration of stay in the neonatal ward in the two groups of PPROM.

Apart from the asymptomatic cervicovaginal colonization in pregnant women, GBS has been

associated with urinary tract infection, vulvovaginitis, chorioamnionitis, mastitis, sepsis,

endometritis and wound infection61. Also prolonged rupture of fetal membrane is an

independent risk factor for chorioamnionitis and puerperal sepsis. Dare and colleagues

reported that premature rupture of membrane and non-adherence to aseptic conditions during

delivery was the major predisposing factors for puerperal sepsis62.

From this study, 1 (14.2%) of the group B positive PPROM and 2 (4.65%) of the group B

negative PPROM developed chorioamnionitis. The risk of chorioamnionitis in PPROM

positive for GBS was higher than in GBS negative PPROM, (OR 3.42, CI 0.27-43.71). A

study by Krohn63 on maternal peripartum complications associated with vaginal group B

streptococci colonization revealed that the risk of chorioamnionitis was higher for women

with heavy GBS colonization (odds ratio OR : 2.05, 95% confidence interval 1.1-3.7) than for

those with light colonization (OR, 1.8; 95 CI , 1.3-2.7). These findings provide further

evidence that GBS is associated with maternal intrapartum complications. Unfortunately this

study was unable to analyze data with respect to the degree of GBS colonization as vaginal

swabs were directly inoculated into an enrichment broth and sub cultured onto a selective

medium without making any quantitative assessments. Bacteria normally present in the

vagina are the most common amniotic fluid isolates in women with chorioamnionitis and in

puerperal sepsis. GBS was found in 15.4% of the amniotic fluid isolates in women with

chorioamnionitis64.

Puerperal sepsis occurred in 2 (28.57%) of the patients with group B streptococcus positive

PPROM and 2 (4.65%) of GBS negative PPROM, respectively (OR 8.2 and 95% confidence

interval 0.94- 71.73 Fisher exact = 0.089). The role of GBS in puerperal sepsis cannot be

underestimated. Interestingly, the latest report of confidential enquiries into maternal deaths

for the United Kingdom shows that sepsis was the leading direct cause of maternal mortality

in the 2006-2008 triennim65 and the report shows that Streptococcus sprecies were the

leading identified microbial agent. Also puerperal sepsis was the leading cause of maternal

death (17.9%) in a recent study at the Lagos University Teaching Hospital 66.

Reassuringly, this study found Group B streptococcus sensitive to most of the commonly

prescribed antibiotics. Out of the seven GBS isolated, none was resistant to cefuroxime and

ampicillin. However, resistance was found in Benzathin penicillin 1 (14.29%), erythromycin

1 (14.29%), amoxyl-clavulinic acid 1(14.29%), ceftriaxone 2(28.59%) and tetracycline 4

(57.14%). The resistance to tetracycline is not a major disadvantage as it is not recommended

in pregnancy. Erythromycin is widely used in the management of PPROM as recommended

by the ORACLE one randomized trial4. In the study by Heelen et al, all GBS were found

susceptible to penicillin and vancomycin, but resistance was found in 44 (22%) of the isolates

to erythromycin67. Also other studies have also quoted erythromycin resistance to range from

5% - 29% 48,49. Joachim et al in Tanzania found all isolates of group B streptococcus sensitive

to vancomycin and ampicillin and resistant to clindamycin, erythromycin and penicillin G in

17.6%, 13% and 9.4% respectively49. In an African population, a study in Malawi found all

isolates susceptible to the B-lactam antimicrobial drugs with 96% resistant to tetracycline and

21% resistant to erythromycin28.

In conclusion, the prevalence of Group B streptococcus was low in women with no additional

risk, however was relatively high in women with PPROM and hence should be tested for

GBS. It is associated with low five minute APGAR score, shorter latency period and maternal

infection but it is a rare cause of neonatal sepsis. GBS is sensitive to most commonly

prescribed antibiotics in the management of PPROM.

LIMITATIONS OF THE STUDY

1. The diagnosis of PPROM was not be clear cut, as nitrazine paper also turn blue in the

presence of contaminating fluids such as blood, semen, alkaline urine, alkaline

antiseptics and vaginal discharge in cases of bacterial vaginosis or trichomonas

infection, hence increasing the false positive results.

2. This study was a hospital-based study. Majority of participants were referred and may

have had different treatments including antibiotic therapy before presentation in

LUTH without their knowing. The results obtained may therefore not be truly

representative of prevalence of group B streptococcus in pregnant women.

3. The most sensitive tests for group B streptococcus antigens are the nucleic acid

amplification techniques (NAAT) for example with PCR. The cost of these however

makes them inappropriate as a screening tool in our environment. The possibility of a

few false negative results can therefore be expected because of the lower sensitivity of

the culture technique.

4. The number of patients tested for GBS was small. Larger study is required to

determine the risk factors, maternal and neonatal complication associated with GBS

colonization.

5. Historical evidence was used in the diagnosis of PPROM and this may affect the

latency period.

RECOMMENDATIONS

1. Reducing the burden of maternal infection and poor neonatal outcome demands

adequate focus on preventable causes like group B streptococcus colonization in

pregnant women with PPROM. Effective preventive strategies should focus on

detection and eradication through use of appropriate antibiotics in women with

PPROM.

2. This study has not found any significant need for routine screening of GBS in

pregnant women. More work (larger sample sizes) is needed to determine the risk

factors, fetal and maternal outcome associated with GBS colonization.

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CONSENT FORM

THE PREVALENCE OF GROUP B STREPTOCOCCUS IN PREGNANT WOMEN

WITH PRETERM PRELABOUR RUPTURE OF MEMBRANES.

INTRODUCTION

This consent form contains information about the research named above. To ensure you are

well informed about your participation in this research, kindly read this consent form. In case

there are words that you do not understand, please ask us to explain. If you choose to be in

this study, we will like you to sign this consent form.

REASON FOR THE RESEARCH

Preterm prelabour rupture of fetal membranes refers to the sudden gush of fluid from the

vaginal after 28weeks but before 37weeks of gestation. Group B Streptococcus are bacteria

(small organisms) present in the vaginal which can affect both the mother and baby. The

rupture of fetal membranes exposes the mother and baby to infection and this can affect both

the mother and baby.

We therefore want to identify how common is this small organism in pregnant women, the

factors associated with it, and the type of infection it can cause with the aim of preventing its

occurrence.

WHAT YOU NEED TO DO:

If you agree to be in this study, you will need to:

- Sign this consent form

- Answer some question

- Have a speculum examination while a swab will be taken.

PROCEDURE

We will use a sterile speculum to hold the vagina open and look at the cervix (neck of the

womb). We will take a swab using swab stick.

POSSIBLE RISKS

- You may experience some discomfort or embarrassment during the speculum

examination.

POSSIBLE BENEFIT

- All the texts are free of charge.

CONFIDENTIALITY

We will protect information about you and your participation in this research to be best of our

ability. Your name or any personal information about you will not be made public or be in

any research report. To ensure this, we will give you a unique identification number which

will be on the questionnaire and your samples. This will be recorded against your name and

phone number in a special log book that will be kept confidential. If you refuse any part of

this examination, it will not affect care that we give you in the future.

QUESTIONS OR ENQUIRIES

You can direct all your questions and further enquires to Dr. Osahon Ede-Edokpolor

(08065671353), Department of Obstetrics and Gynaecology, Lagos University Teaching

Hospitals Lagos.

VOLUNTEER AGREEMENT

I understand what I need to do to be part of this study titled “The Prevalence of Group B

Streptococcus in pregnant women with preterm prelabour rupture of membranes” and all

questions that I asked have been answered. I also understand that I can pull out of the study at

anytime without affecting any of the medical benefits I require.

I therefore agree to participate in the study.

…………………………………….. ………………………………….

Name of Participant Signature/Thumbprint of Participant

………………………………..

Date

……………………………….. ………………………………………

Name of Witness Signature of Witness and date

PROFORMA

The prevalence of Group B Streptococcus in pregnant women with preterm prelabour

rupture of membrane

SECTION A: BIODATA

1. Initial of Patient _____________________

2. Hospital number_________________________

3. Age (years)________________________

4. Occupation__________________________

5. Parity_________________________

6. Religion. Christain ( ) Muslim( ) others( ).

7. Marital status Married ( ) Single ( ) Others ( ).

8. Educational Level. 1o ( ) 2o ( ) 3o ( ) Nil ( )

9. LMP ____________ EDD _________________ EGA at presentation-------------

EGA at Delivery-----------------------

SECTION B: RISK FACTORS FOR PPROM

a) Previous history of PPROM. Yes/No

b) Genital tract infection in index pregnancy. Yes/No/not sure.

SECTION C: RISK FACTORS FOR GBS COLONIZATION

- History of STI/UTI in index pregnancy. Yes/No/not sure

- Previous history of contraceptive usage and type. Yes/No/not sure

- History of cigarette smoking before. Yes/No and in index pregnancy. Yes/No

- Prior antibiotics use in index pregnancy. Yes/No and type ________________

and duration of use ________

SECTION D: GBS CULTURE RESULT. Positive ( ) Negative ( ).

GBS Sensitivity pattern. Benzathin penicillin ( ), Erythromycin ( )

Cefuroxime ( ), Tetracycline ( ), Amoxyl-clavulanic acid ( )

Ceftriaxone ( ), others ( )………………………………………………..

GBS Resistance pattern. Benzathin penicillin ( ), Erythromycin ( )

Cefuroxime ( ), Tetracycline ( ), Amoxyl-clavulanic acid ( )

Ceftriaxone ( ), others ( )………………………………………………..

SECTION E: INDEX PREGNANCY/MATERNAL EFFECT

a) Duration of latency period (period of time between ROM and delivery)

__________________

b) Features suggestive of chorioamnionitis (fever,hyperthermia,tachycardia,increase

WBC.) Yes/No

c) History of perineal/ wound/Episiotomy infections.

d) History of postpartum endometritis. Yes/No

e) History suggestive of puerperal sepsis.Yes/No

f) Duration of stay in postnatal ward.-----------------

SECTION E: FETAL EFFECT OF GBS COLONIZATION

a) Estimated gestational age at delivery________________________

b) Mode of delivery ________________________________

c) APGAR score at birth____________________________

d) Duration of stay in neonatal ward __________________________

e) Stillbirth Yes/No or early neonatal death Yes/No A and date of death

____________________

f) Neonatal colonization. Yes ( ) No( ).

g) GBS disease. Yes( ) No( ).