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PREVALENCE OF ASYMPTOMATIC

BACTERIURIA IN PRETERM LABOUR:


A CASE- CONTROL STUDY

Thesis submitted to the


National Board of Examinations, New Delhi,
In partial fulfilment of the requirement for the Award of Diplomate of
National Board in the speciality of
Obstetrics and Gynaecology

by

DR. RAMADOSS KABILAN VIDHYALAKSHMI

Provisional Reg.No: 125-28122-131-107161

DEPARTMENT OF OBSTETRICS AND GYNAECOLOGY

JUBILEE MISSION HOSPITAL

THRISSUR, KERALA

2013-2016

1
CERTIFICATE

This is to certify that the work in the thesis entitled,

PREVALENCE OF ASYMPTOMATIC BACTERIURIA IN

PRETERM LABOUR: A CASE-CONTROL STUDY has been carried

out by, Dr. Ramadoss Kabilan Vidhyalakshmi under my supervision

and guidance during the academic years January 2013-2016. This thesis,

submitted by the candidate, in partial fulfilment of the requirements for

the award of Diplomate of National Board in the speciality of Obstetrics

and Gynaecology, has not previously formed the basis of award of any

Degree or Diploma.

Head of the Department


Dr.Sareena Gilvaz
Professor
Dept. of Obstetrics and Gynaecology
Jubilee Mission Hospital, Thrissur

Guide Co-Guide
Dr. Annie V Thadicaren Dr. Neetha George
Additional Professor Associate Professor
Dept. of Obstetrics and Dept. of Obstetrics and
Gynaecology Gynaecology
Jubilee Mission Hospital, Thrissur Jubilee Mission Hospital, Thrissur

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DECLARATION

I, Dr. R. K. Vidhyalakshmi, hereby declare that, the present dissertation

entitled, PREVALENCE OF ASYMPTOMATIC BACTERIURIA IN

PRETERM LABOR: A CASE-CONTROL STUDY, was performed by

me, at Jubilee Mission Hospital, Thrissur. I also declare that, this is an

original work and no part of this study has been previously submitted for

the award of any degree or diploma in any university.

Place: Thrissur

Date: Dr. R. K. Vidhyalakshmi

3
ACKNOWLEDGEMENT

I express my sincere gratitude to my Head of the Department Dr.Sareena

Gilvaz, my guide Dr. Annie Thadicaren and my co-guide Dr. Neetha

George, for their valuable guidance, constant encouragement and critical

approach which have both stimulated my thinking and spurred me on to

do my best in this endeavour.

I gratefully acknowledge the help given by Dr. K.P. Suresh, scientist

(Biostatistics), NIVEDI, Bangalore and other consultants Dr.Lola,

Dr.Saley, Dr.Aswath, Dr.Alice Kuzhinjalil and Dr. Bindu for their

guidance and support.

I thank all the staff of Department of Obstetrics and Gynaecology for

providing the necessary help.

Words cannot express my thanks to parents, colleagues and friends, who

have been a constant source of love, encouragement and support to me.

For whatever I have achieved in my life, I am indebted to them.

Last but not the least; I thank all the patients who took part in the study,

hopefully for a better cause.

Dr. R. K. Vidhyalakshmi

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ENDORSEMENT

1. Head of the Department


Dr.Sareena Gilvaz
Professor
Dept. of Obstetrics and Gynaecology
Jubilee Mission Hospital, Thrissur

2. Guide
Dr. Annie V Thadicaren
Additional Professor
Dept. of Obstetrics and Gynaecology
Jubilee Mission Hospital, Thrissur

3. Co-Guide
Dr. Neetha George
Associate Professor
Dept. of Obstetrics and Gynaecology
Jubilee Mission Hospital, Thrissur

4. Head of the Institution


Fr. Francis Pallikunnath
Director
Jubilee Mission Hospital
Thrissur, Kerala 680 005.

5
CONTENTS

Sr. No. PARTICULARS Page No.

1 INTRODUCTION 7

2 AIMS AND OBJECTIVES 8

3 REVIEW OF LITERATURE 9

4 MATERIAL AND METHODS 24

5 RESULTS AND ANALYSIS 30

6 DISCUSSION 52

7 LIMITATIONS 56

8 SUMMARY 57

9 CONCLUSION 58

10 REFERENCES 59

11 INFORMED CONSENT DOCUMENT 70

12 STUDY PROFORMA 71

13 ABBREVIATIONS 73

14 MASTER CHART 74

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1. INTRODUCTION

Urinary tract infection (UTI) is one of the most frequent bacterial


infections1. It is also one of the most common bacterial infections seen during
pregnancy2. It could be either symptomatic or asymptomatic.

The symptomatic urinary tract infection may be complicated or


uncomplicated. Uncomplicated urinary tract infection is also symptomatic
urinary infection characterized by dysuria, urgency, frequency or suprapubic
pain with a normal genitourinary tract3. Complicated urinary tract infection is
symptomatic urinary infection in women with structural or functional
abnormalities of genitourinary tract involving either bladder or kidney or both4.

Asymptomatic bacteriuria is defined as persistently and actively


multiplying bacteria in significant numbers (more than 10 5 per ml) within the
urinary tract without any obvious symptom5. The pregnant women are two
times more commonly affected than age matched non-pregnant females6,7.
Asymptomatic bacteriuria is found in 2-10% of pregnant women8,126.

If asymptomatic bacteriuria is not treated approximately 25% of women


will subsequently develop acute symptoms of an infection during pregnancy9.
Asymptomatic bacteriuria is an entity with serious consequences in the form of
maternal and fetal morbidity10. It can cause maternal anemia, pyelonephritis,
recurrent infection, preterm labour11, septicemia and even death of the mother12.
It can cause Intra Uterine Growth restriction (IUGR)13, prematurity, low birth
weight of the fetus14 and the fetal mortality12. Out of these preterm labour pain
and pyelonephritis are the most common adverse effects11.

The association between ASB and preterm delivery (<37 weeks of


gestation) and that between asymptomatic bacteruria and low birth weight
(<2500 gram) were unknown until 1962 when Kass observed an increased risk
among untreated bacteruric women of the delivery of low birth weight. The
mean duration of pregnancy among untreated bacteriuric women was found to
be reduced by one week on average15. Also ASB in pregnant women as a risk
factor for preterm birth and antibiotic therapy has been found to significantly
reduce the risk.16,17

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2. AIMS & OBJECTIVES

1) To find out the prevalence of asymptomatic bacteriuria (ASB) in pregnant


women presenting with preterm labour pain.

2) To determine the common pathogenic micro organisms associated with


Asymptomatic Bacteriuria (ASB).

3) To determine their antibiotic sensitivity.

8
3. REVIEW OF LITERATURE

Definition

Delzell JE et al18 defined Asymptomatic bacteriuria (ASB) as persistent


and actively multiplying bacteria of more than or equal to 1,00,000 colony
forming units per ml of urine without any urinary tract symptoms including
lower abdominal pain, burning micturition, fever, frequency, urgency, dysuria,
supra pubic discomfort, offensive smelling urine, urge incontinence and
nocturia.

Antony J et al19 stated that Asymptomatic Bacteriuria is a microbiological


diagnosis based on the isolation of a specified quantitative count of bacteria in a
clean catch midstream urine from persons without signs or symptoms.

Prevalence

Gayathree et al20 studied 900 pregnant women who attended the Hassan
District hospital, Hassan to study the prevalence of asymptomatic bacteriuria.
They found that ASB was prevalent in 6.2% in 900. There was a higher
prevalence in 3rd trimester (61.77%) than in the 2nd trimester(32.35%) and the 1st
trimester (5.88%) and concluded that screening for ASB in all the three
trimesters is necessary to prevent the dangerous complications which are
associated with ASB in pregnancy.

Ullah et al21 did a cross-sectional followed by cohort type of study


conducted among the pregnant mothers of second trimester in the rural areas of
Rajshahi district, Bangladesh. A total of 1800 pregnant mothers of second
trimester were selected from 18 unions applying 2- stage random sampling. A
total 216 pregnant mothers with asymptomatic bacteriuria were paired among
the rest of the healthy pregnant mothers (withoy bacteriuria) on the basis of age,
gravida and economic status for cohort study to relate asymptomatic bacteriuria,
hypertensive disorders in pregnancy and pre-term delivery. The prevalence of
asymptomatic bacteriuria was 12% among the pregnant mothers in Rajshahi.

In a study carried out by Gulfareen Haider et al22 ten out of 111, (9%)
women had bacteriuria. Amongst them 10% were below 20 years and 90% were
between 20-30 years of age.

Masindei A et al23 studied 247 pregnant women, out of whom 78 (31.5%)


were symptomatic and 169 (68.4%) were asymptomatic. Prevalence of

9
bacteriuria among symptomatic and asymptomatic were 17.9% and 13.0%
respectively.

Turpin et al24 studied 220 pregnant women, out of them 16 had


significant bacteriuria and the prevalence rate was 7.3%. The highest age-
specific prevalence was found in the 35-39 year old age group (13%) and the
lowest in the 15-19 year old age group (0%).

RISK FACTORS

Pregnancy:
Stenqvist et al25 found that the frequency of bacteriuria increases
by about 1% during pregnancy. He also confirmed that the reisk of
acquiring bacteriuria increases with the duration of pregnancy from 0.8%
of bacteriuric women in the 12th gestational week to 2% at the end of
pregancy. But Kutley et al 26 stated that the prevalence of asymptomatic
bacteriuria in pregnancy varies from 4-7% (range 2-11%) and it is similar
to that observed in non-pregnant women.

Socio economic status:


Wesley WE et al27 in 2002 found that the prevalence is higher
among lower socio economic classes. Kiningham R et al 28 in 1993
reported that low socio-economic status, sickle cell trait, diabetes and
grand multiparity predispose to urinary tract infection and each is
associated with 2 fold increase in the bacteriuria.

Maternal age:
Nicolle LE et al29 found that high prevalence of ASB in patients
with advanced maternal age is due to increasing incidence of co morbid
conditions, which are associated with neurogenic bladder and increased
residual urine volume or urinary reflux.

Anemia:
Lavanya and Jogalakshmi D et al30 found that bacteriuria in
pregnancy is associated with maternal anemia. But Fatima et al31 didnt
find any association between bacteriuria and anemia.

10
Diabetes:
Renko et al 32 conducted a systematic review and meta-analysis of
published data since 1966 to evaluate whether ASB is more common in
patients with diabetes than among control subjects. Out of 22 studies
which fulfilled the inclusion criteria, they found that ASB was present in
439 out of 3,579 (12.2%) patients with diabetes and in 121 out of 2,702
(4.5%) healthy control subjects. ASB was more common in patients with
both T1DM and T2DM than in control subjects. The prevalence of ASB
was higher in both men and women as well as in children and adolescents
with diabetes than in healthy control subjects.

Sexual activity:
Scholes et al33 in 2000 found that women who have been sexually
active within the past month are 6 times more likely to present with
infection compared with women who are not sexually active. Scholes D
et al34 in 2005 found that women with a new sexual partner also have
increased risk of infection.

Contraception:
Gupta K et al35 in 2005 found that women who use spermicides
for birth control have an increased vaginal pH and increased colonization
with potential uropathogens particularly E. Coli.

Other factors:
London WB et al36 in 1999 showed that patients with
abnormalities of urinary tract, stones in the urinary tarct,
immunosuppression and past history of UTI had increased risk of ASB
Raz R et al37 in 2000 showed that there is genetic predisposition to
ASB.

11
PHYSIOLOGICAL CHANGES OF URINARY TRACT

Renal blood flow and glomerular filtration rate (GFR) increase by 10-
20% before menstrual cycle begins.38 If pregnancy occurs, these changes
continue to occur till delivery.39 By 16 weeks, GFR is 55% more than non-
pregnant levels.40 Renal blood flow is 70-80% above the non-pregnant levels by
2nd trimester and 45% above the non-pregnant level by term.41

The pelvicalyceal system and the ureter dilate, particulary on right side
which may appear like an obstruction.42 The right pelvi calyceal system
dilates0.5mm/week from 6-32 weeks, maximum upto 20 mm, which is
maintained till term. The left pelvi calyceal system dilates upto 8 mm till 20
weeks and maintained till term.43 Increased bladder volume and decreased
bladder and ureteral tone, contribute to increased urinary stasis and uretero
vesical reflux.44

The female urethra is relatively short and is anatomically proximal to


the vagina, which is colonized with organisms from the GIT. Normal
phsiological changes in pregnancy, place women at risk for pyelonephritis.
There is also relative obstruction of the ureters, because the enlarging uterus
physically blocks them and the hormonal milieu of pregnancy leads to
relaxation of the smooth muscle of the ureters and the bladders.45,46,47

Pregnancy increases the risk of urinary tract infections. At around 6th


week of pregnancy ureters begin to dilate physiologically. This is known as
Hydronephrosis of Pregnancy, which peaks at 22-26 weeks and continues
to persist until delivery.

Both progesterone and estrogen levels increase during pregnancy and


these will lead to decreased ureteral and bladder tone. Increased plasma volume
during pregnancy leads to decreased urine concentration and increased bladder
volume. The combination of all theses factors lead to urinary satsis and uretero-
vesical reflux.18

Sobel et al48 found that the glycosuria and aminoaciduria of pregnancy


provide an excellent medium for bacterial proliferation.

12
PATHOGENESIS

Uropathogenic E.coli is responsible for most of ampicillin resistant UTI.


E.coli has adhesins such as P and S fimbria. They increase the virulence of the
organism. They bind to vaginal and uroepithelial cells by expression of pap G
gene, that encodes the tip of P fimbria and also by the production of hemolysin.

The expression of DRA gene cluster is associated with ampicillin


resistant E.coli. Adhesins bind to specific glycoprotein receptors on the surface
of epithelial cells, which will increase the virulence of the organism.

Lower levels of interleukin-6 in pregnancy has been associated with


increased incidence of ASB in pregnancy.49 Virulence factor of E.coli is fimH, a
surface adhesin which binds to uroplakin on the bladder surface.50

ORGANISMS:

The organisms that cause UTI are those which are normally present in the
anal area. E.coli, Klebsiella and Enterobactericia account for 90% of UTI.51,52,53
Proteus, Coagulase negative Staphylococcus and Pseudomonas also cause
UTI.54

The organisms colonize the perineum, introitus, urethra, bladder, ureter


and kidney. When the immunity is less as in pregnancy, they cause infection.
Enterococci, Gardenella vaginalis and Ureaplasma urealyticum can also cause
UTI.55,56,57

Sevki Celen et al58 did a study between December 2009 and May 2010,
outpatient clinical setting in Zekai Tahir Burak Womens Health Education and
Research Hospital in Ankara, Turkey. Of the 2011 pregnant women included,
171 had ASB (8.5%). E.coli was the most frequently isolated microorganism
(76.6%) followed by Klebsiella pneumonia (14.7%)

13
IMPORTANCE OF SCREENING

Reshmani et al59 in 2004 found that urinalysis is the commonly used test
for evaluation of patients with potential urinary tract infections. UTI are one of
the commonest infections to occur during pregnancy. Their frequency and
seriousness have been well recognised for more than a century. The early
detection and treatment of asymptomatic bacteriuria is of greta potential value
for pregnant women.

The American College of Obstetrics and Gynaecology60 strongly


recommends that the urine culture to be obtained in the first prenatal visit itself.

The American Academy of Family Physicians61 also recommends screening


for ASB at 12-16 wks of gestation or at the first visit by culture method.

The Infectious Disease Society of America62 recommends screening with a


urine culture at least once in early pregnancy.

The American Academy of Paediatrics63 recommend screening for ASB


early in pregnancy, as appropriate

The United State Preventive Service Task Force (USPSTF)64 recommends


screening for ASB with urine culture for pregnant women at 12-16 wks or at the
1st prenatal visit if later. This is Grade A recommendation. The USPSTF
recommends against screening for ASB in men and non pregnant women. This
is Grade D recommendation.

The National Institute for Clinical Excellence65, The European Association


of Urology66, The Canadian Task Force on Preventive Care67 and The
Scottish Inter College Guidelines Network68 also recommend screening for
ASB in pregnancy.

Delzell et al18 stated that the Gold standard for detection of bacteriuria is
urine culture. Faster screening methods like leukocytes esterase dipstick, nitrite
dipstick, urinalysis and gram staining are not useful in the screening for
ASB69,70,71

14
VARIOUS TESTS FOR DETECTING BACTERIURIA

Pyuria:

Pyuria is the presence of increased number of polymorphonuclear


leukocytes in the urine. It is evidence of an inflammatory response to the
bacteria.72

Mortazavi M et al 73 conducted a study to evaluate the sensitivity and


specificity of pyuria and its relationship with urinary tract infection. In that
clean-catch midstream urine samples of 90 patients (34 women and 56 men)
were obtained and divided into two parts for examination fo urine sediment and
urine culture. Forty five participants had pyuria and only 16 (35.5%) of them
had a positive urine culture for infection. Pyuria and urinary tract infection were
present in 52.9% and 29.4% of the women and 48.2% and 10.7% of the men
respectively. The sensitivity and specificity of pyuria screening for UTI was
100% and 61.8% respectively. The positive and negative predictive values were
35.5% and 100% respectively. And they concluded that because of the low
specificity and positive predictive values, samples with positive pyuria should
be cultured to confirm urinary tract infections.

Gram Satining:

Kass74 in 1956 found that gram stained smears of centrifuged urine were
positive for 80% of the patients whose colony counts were more than or equal to
105. And whose colony counts less than 105 were also positive for gram
staining. He concluded that gram staining is not as effective as urine culture to
detect significant bacteriuria.

Dip Stick:

Tinceloo D.G75 did a preospective study to evaluate the performance of


reagent strips in screening pregnant women for asymptomatic bacteriuria at
their first visit to an antenatal clinic. Sensitivity was low with a maximum of
33% when all the four tests were used in combination. Specificity was high with
typical values of 99% or more. Positive predictive value reached a maximum of
69% and negative predictive value was typically 95% or more. They concluded
that reagent strips are not sufficiently sensitive to be of use in the screening of
asymptomatic bacteriuria

15
Griess test:

The Griess test is one of the chemical tests used for screening ASB.
Griess, a german scientist in 1879 developed a reagent for the detection of
nitrites in solutions. The reagent is an acid solution of sulfanilic acid and
naphthylamine and it undergoes a diazotization reaction with nitrites to form a
red azo dye. The Griess test utilies the principle that nearly all of the bacterial
species which cause ASB reduce the nitrate that is normally present in the urine
to nitrite if given sufficient time. The test is easy to perform, easy to read and
seems very accurate in detecting significant bacteriuria.76

Khattak A.M et al77 in 2001 studied 290 cases examines for bacteriuria
with Griess test. Out of 290 cases, 18 were positive for bacteriuria with Griess
test and 24 were culture positive cases. Out of the culture positive cases, 6 were
found to have mixed growth and out of rest of them only 18 had pure growth
giving 75% sensitivity and 97.79% specificity for the test.

PREVENTION:

General measures:

Plenty of water intake, increasing the ascorbic acid (Vitamin-C)


consumption, wiping from front to back after defecation, avoiding vaginal
douches, spermicides and foams. Regular and complete bladder emptying and
utilizing double micturition technique in patients with residual urine is
helpful.78,79

Many other behavioural factors have been said to contribute to recurrent


urinary infection including taking baths rather than showers, type of underwear,
perineal wiping habits after voiding and tpe of menstrual protection. Case-
control studies have explored these putative risk factors, however consistently
found no association with urinary infection.80,81,82

Similarly no scientific evidence suggests that women with cystitis should


increase their fluid intake and some doctors speculate that increased fluid may
be detrimental becuase it may decrease the urinary concentration of
antimicrobial agents.83

16
Cranberry Juice:

The use of cranberry juice to treat or prevent urinary infection has been a
popular recommendation for many years. Proposed mechanisms of efficacy
include an antiseptic effect of hippuric acid, blocking of urithelial E.coli
receptors or decreased bacterial fimbrial production.84 In two studies of women
with frquent recurrent urinary infection, cranberry products as juice or tablets
decreased the frequency of recurrent infection by about 30%).85,86

Vaccination:

Vaccine strategies to prevent recurrnt urinary tract infection in women.


They are whole-cell heat-killed mixture of ten uropathogens administered as a
vaginal suppository (Urovac),87 oral immunostimulating fractions of 18
uropathogenic E.coli88 and fimH vaccine.89

TREATMENT

Aymptomatic bacteriuria other than pregnancy is said not to require any


treatment. Smail F et al90 in 2002 stated in a cochrane systematic revies of
randomised controlled trials that antibiotic treatment reduced persistent
bacteriuria during pregnancy, reduced preterm delivery or lowbirthweight
babies and rduced the development of pyelonephritis.

Nitrofurantoin:

It is the drug of choice in pregnancy.91 But it should be avoided after the


onset of labour in G6PD deficiency, since it may cause hemolysis in neonates
due to immature erythrocyte enzyme systems (Glutathione instability).92 It
cannot be used in cases of pyelonephriris since it does not achieve adequate
tissue penetration.93

Trimethoprim:

It should be avoided in first trimester, because it is folic acid antagonist


and it is associated with increased risk of neural tube defects.93

17
Sulfonamides:

Sulfanamides can be used in first and second trimester but is best avoided
in third trimester because it competes for bilirubin-binding sites on albumin in
the fetus and causes severe juandice and kernicterus especially in preterm
babies.94 Quinolones and Tetracyclines have possible toxic effects on the fetus
and are contraindicated in pregnancy.94

Ampicillin:

Historically, ampicillin has been the drog of choice, but in recent years
E.coli has become increasingly resistant to ampicillin. Ampicillin resistance is
found in 20-30% of E.coli cultured from urine in the outpatient setting.
Currently 30-50% of E.coli are ampicillin resistant and 20-30% are
Cephalosporin resistant.95

Amoxicillin:

All penicillins are safe to use in pregnancy. Since there are lots of
reisitance to amoxicillin, it is not suitable for emperical therapy.96 It can be used
when the urine culture shows suscptibility.93

Fosfomycin:

Fosfomycin trometamol is a derivative of phosphonic acid. It can be


taken as a single dose 3 gram sachet orally which is equally effective as 7-10
days course of nitrofurantoin, norfloxacin or cotrimoxazole.97 This drug is
active against E.coli, Enterococci, Citrobacter, Enterobacter, Klebsiella and
Serratia species.

18
MATERNAL COMPLICATIONS

Symptomatic Infection:

Pregnancy is a provocation for the asymptomatic bacteriuria to become


symptomatic bacteriuria.98 One of the biggest risk factors for symptomatic
infection is asymptomatic bacteriuria.

Mcfadyen IR et al99 in 1973 found that detection of all women with


asymptomatic bacteriuria is important as 25% to 30% will develop symptomatic
urinary tract infection while pregnant. He concluded that treatment of
asymptomatic bacteriuria neither decreases the frequency nor prevents further
episodes of asymptomatic bacteriuria.

Recurrent Infection:

Recurrent urinary tract infection is defined as three episodes of infection


with three positive urine cultures in the previous 12 months or two episodes in
the last 6 months.100 UTI recur in 4-5% of pregnancies especially when the
initial infection is inadequately treated. Pregnant females with urinary tract
calculi, diabetes mellitus and a past history od UTI are prone to recurrence.
Even after adequate antimicrobial therapy the risk of recurrence is 16-26%.101

Dwyer et al102 in 2002 found that the patients may experience recurrent
infection from rectal reservoir.

Recurrent urinary infection may be either relapse or reinfection. Relapse


is a recurrent infection caused by an organism which has persisted within the
genitourinary tract and emerges following antimicrobial therapy. Relapse is
charcterised by isolation of the same strain prior to and following therapy,
whereas reinfection is generally charcterized by isolation of distinct strains.3

Reinfection is a recurrent infection with an infecting organism ascended


into the bladder from the normal flora of genito urinary mucosa.3

Ikaheime R et al103 in 1996 followed 179 women from17-82 years old


who initially presented to a family physician with acute cystitis; 88(43%) had
atleast one episode of urinary infection during 12 months follow-up, 13% of
subjects had 2 episodes and 5% had threee or more episodes.

19
Preeclampsia:

Abyad et al104 in 1991 found that asymptomatic bacteriuria is associated


with hypertension and pre eclampsia. It can occur due to chronic subclinical
infection, which increases maternal cytokines level sufficient enough to affect
vascular endothelial finction and prime individuals for subsequent development
of preeclampsia. There is no compelling evidence of an association of
asymptomatic bacteriuria in pregnancy with hypertension in pregnancy or of
long-term renal damage in the antibiotic era.105

Maternal Anemia:

Mc gladdery et al106 in 1992 found that asymptomatic bacteriuria during


pregnancy is associated with anemia of the mother, especially after 32 weeks of
gestation. Pyelonephritis causes bone marrow suppression, increased
erythrocyte destruction and decreased red cell production. Fathima N et al31
found bacteriuria was associated with maternal anemia.

But Gulfareen Haider et al22 did not find any association between
bacteriuria in pregnancy and maternal anemia.

Chorioamniotis:

Mc gladdery et al106 in 1992 found that bacteriuria in pregnancy may


cause infection in the amniotic cavity. But in the study conducted by JA Ives et
al107 on 20 women showed no infection in the amniotic cavity, which do not
support the results that ASB may lead to chorioamnionitis.

Preterm labour & PPROM:

Cox SM et al108 in 1987 found that bacterial enzymes such as collagenase


may weaken the fetal membranes which can result in preterm premature rupture
of membrane.

There is evidence that when there is no symptom, untreated bacteriuria


in pregnancy may lead to less favourable pregnancy outcomes and
complications like preterm delivery, low birth weight, pre-eclampsia and
anemia of pregnancy. Prematurity is one of the leading causes of perinatal
mortality. Uterine contractions may be induced by cytokines and
prostaglandins, which are released by microorganisms.142,143

20
Kass144 reported that severe uterine contractions occur within moments
after endotoxin injection in an animal model, thus linking bacteriuria with early
delivery. Furthermore, Apitz145 reported that endotoxin causes a generalized
Shwartzman reaction in the pregnant rabbit.

Zahl and Bjerknes146 used the same substance to induce decidual -


placental hemorrhage in the female mouse. Also, as gestation lengthens, the
uterus was shown to be progressively more susceptible to endotoxin, and some,
but not all, rabbit wombs primed with estrogen and progesterone exhibited
uterine hyperirritability. Conversely, the uterus of the nonpregnant rabbit did
not react at all. Thus, gestation somehow sensitizes the uterus to these powerful
oxytocics, and, when the situation is complicated by bacteriuria due to
gramnegative organisms, the endotoxins elaborated by the organisms causing
infection could theoretically precipitate preterm labor.

Patterson et al109 in 1987 found that subclinical chorioamnionitis


associated with bacteriuria. Phospholipid A2 production by the bacteria may be
the proposed cause for initiation of preterm labour. It may be also due to release
of pro inflammatory cytokines, secreted by maternal and fetal monocytes in
response to bacterial products.

Fathima N et al31 in 2006 studied 590 women. 6 out 28 women with


bacteriuria and 27 out of 552 women without bacteriuria went into preterm
labour, which is statistically significant.

But findings from Cardiff Birth Survey110 in 1995 which prospectively


studied 25,844 births, reported that asymptomatic bacteriuria adjusted for
demographic and social factors was not associated with preterm delivery.

However, when preterm births were categorised into medically


indicated or spontaneous preterm births, there was a significant association
between bacteriuria and medically indicated preterm births but not for
spontaneous preterm births and the authors concluded that if asymptomatic
bacteriuria does not progress to pyelonephritis, it is not associated with preterm
birth.

21
Postpartum Endometritis:

Monif GRG et al111 in 1991 found that 40% of women with bacteriuria at
delivery had developed postpartum endometritis in their poetpartum period
where as only 2.2% of women without bacteriuria at delivery developed the
same. Romero et al112 in 1989 also found that bacteriuria can result in
postpartum endometritis.

Pyelonephritis:

Pyelonephritis is an inflammation of the renal parenchyma. It is a clinical


syndrome characterized by chills and fever, flank pain and constitutional
symptoms like nausea and vomiting caused by bacterial invasion of the kidney.
Joseph KS et al113 in 1988 found that if the bacteriuria is not treated, 30-40%
develop pyelonephritis in the late pregnancy.

Turner AN et al114 in 2002 also found that bacteriuria if not treated led
to Pyelonephritis in 30-40%mof patients. Hill JB et al115 in 2005 found that it
can also result in septicemia (17%), transient renal dysfunction (2%) and
pulmonary insufficiency (7%). Cook DJ et al116 in 1989 found that
emphysematous pyelonephritis can result as a complication of pyelonephritis.

Thorley et al117 in 1974 found that pyelonephritis results in renal and


perinephric abscess. Jerkeman M et al118 in 1992 found that bacteremia can
occur due to pyelonephritis.

Cunningham FG et al 119 in 1987 found that about one in five pregnant


women with pyelonephritis will dvelop multiple system derangement from
endotoxinemia and sepsis.

Towers CV et al 120 found that sepsis manifests mostly as acute


respiratory distress syndrome, which had been reported in approximately 1 in 50
women with acute pyelonephritis.

Maternal mortality:

Tayo Ao et al12 studied 352 patients, 36 patients (11.2%) had significant


growth. They had that proper screening for asymptomatic bacteriuria reduces
maternal mortality and morbidity.

22
FETAL COMPLICATIONS

Prematurity:

Asymptomatic bacteriuria in pregnancy causes prematurity as it causes


preterm delivery. Nicolle et al121 found that incidence of prematurity is 2.4
times greater than those without urinary infection. The mechanism for an
association between preterm labour and asymptomatic bacteriuria is the
production of phopholipase A2 by microorganisms which then can initiate
labour through the activation of prostaglandin.

Low birth weight:

In a meta-analysis of 19 studies, Romero et al112 in 1989 reported that


women with asymptomatic bacteriuria had a 54% higher risk of low birth
weight infant. He also proved that antibiotic treatment of asymptomatic
bacteriuria reduces incidence of low birth weight. Antibiotic therapy eradicates
organisms from the cervix and vagina which may associated with sublinical
chorioamnionitis rather than a direct effect of treatment of urinary infection.

Intra Uterine Growth Restriction:

Harris RE et al122 in 1976 found 70 cases (5%) of asymptomatic


bacteriuria out of a,400 pregnant women. He found that there was an association
between presence of asymptomatic bacteriuria and intra uterine growth
retardation. Romero et al112 also stated that ASB was associated with IUGR.

Neonatal group B streptococcal infection:

Car J et al123 in 2006 found that even when treated group B streptococcal
infection is associated with heavy colonization of vagina and therefore an
increased risk of neonatal group B strptococcus disease.

Perinatal mortality:

Jayalakshmi et al124 in 2008 showed that asymptomatic bacteriuria can


cause still birth. Bacteriuria during pregnancy can even cause sudden
unexpected infant death. Nicolle LE et al121 in 1994 showed that bacteriuria in
pregnancy is associated with fetal mortality. Gardner et al125 in 1985 also
found that asymptomatic bacteriuria is associated with sudden unexpected
infant death.

23
4. MATERIALS AND METHODS

Study Area- Obstetrics & Gynaecology and Microbiology, Jubilee Mission


Hospital, Thrissur.

Study Method:

A prospective case-control study.


This study was carried out in 50 pregnant women with preterm (24-
37wks) labour pain admitted in the labour room (Case) and 50 preterm
(24-37wks) pregnant women who were not in labour in the out-patient
department (Control) of Jubilee Mission Hospital.
Case:
Primigravida or multigravida, singleton pregnancy who presented
with preterm labour pain after 24 weeks and before 37 completed weeks
of gestation who were admitted in the labour room.
Control:
Primigravida or multigravida, singleton pregnancy who did not
present with preterm labour pain after 24 weeks and before 37 completed
weeks of gestation in the out-patient department.
Type of study- A prospective case-control clinical study.
Sample size- Around 100 pregnant women (50+50)
Period Of Study- From Oct 2013 to March 2015.
A predesigned proforma was used to record relevant information (patient
data, finding, inv report) from individual patients selected with inclusion
and exclusion criteria.
Informed written consent.

INCLUSION CRITERIA:

1) For preterm group in labour (Case): Primigravida or multigravida,


singleton pregnancy who presented with preterm labour pain after 24
weeks and before 37 completed weeks of gestation.
2) For preterm group not in labour (Control): Primigravida or multigravida,
singleton pregnancy who did not present with preterm labour pain after
24 weeks and before 37 completed weeks of gestation.

24
EXCLUSION CRITERIA:

1) Women with present history of UTI or any clinical presentation of UTI


(frequency of micturition, burning micturition, loin pain, etc) in the
present pregnancy or in the past 1 yr.
2) Women known to be diabetic, chronic hypertensive, and women who are
immune compromised, as in long-term corticosteroid therapy.
3) Women already on any antibiotic therapy in the past 1 month.
4) Multiple pregnancy.
5) Women initially asymptomatic and became symptomatic during the
course of pregnancy.

METHODOLOGY

Clean catch method

Patients and labour room staff were instructed to take clean catch mid
stream urine sample for urine culture and also for quantitative and
microscopic examination.

They were instructed to clean the periurethral are with soap and water,
next to spread the labia and then to collect 30 ml of mid stream urine
specimen in a sterile bottle.

The samples were immediately transported to the laboratory and were


processed within one hour and maximum within 2 hours.

In case of delay, the samples were refrigerated at 40 C.


Firstly, 0.02 ml of potassium nitrate was added to 1 ml of urine sample
and incubated. After culturing the urine specimen for quantative bacterial
count, microscopic examination was carried out for the detection of
leucocytes (pus cells).

25
Microscopic examination for pus cells:

Unspun urine is examined directly under the microscope and pus cells per
high power field were calculated. A count of 10 or more pus cells per high
power field is an indication of urinary tract infection.

QUANTITATIVE BACTERIOLOGY

Calibrated loop direct streak method:

In this method a flame sterilised and cooled 4 mm platinum loop,


delivering 0.01 ml of urine is used. One biconvex loop full of well mixed
uncentrifuged urine specimen was deposited on blood agar plate and Mac
conkeys agar plate.

Both plates were streaked by passing the loop through the inoculum
downwards to the lower edge of the plate in a T pattern from the inoculums site.
Both plates were incubated overnight at 350C and red next morning.

Colonies were examined and counted on both plates. Total counts were
estimated from blood agar plate and Mac conkeys agar plate. In each case
colonies were multiplied by 100 to give an estimate of the number of colonies
per millilitre of urine. 105 colonies per ml were taken as significant bacteriuria.

After determining the plate count, organisms were identified and


susceptibility to antibiotics was determined by Disc-Diffusion method. Mixed
growth of two or more organisms was considered as contamination and the
sample was repeated. If there is no growth, the specimens were held in
incubator for another 1 day and if still negative reported as no growth after 48
hours.

26
Identification of Organisms:

A smear was prepared from the culture, selecting a single colony and
stained by gram staining method. In case if gram positive cocci were found in
clusters, a coagulase test was performed by tube method to differentiate
between pathogenic and non pathogenic staphylococci

. When gram positive cocci in pairs were isolated from Mac conkeys agar
plate, bile solubility heat resistance and mannitol fermentation tests were carried
out to confirm enterococci.

When pink coloured or pale colonies on Mac conkeys agar plate were seen,
Gram staining was done. Similarly a set of biological investigations were
carried out to identify various Gram negative bacteria.

27
Antibiotic sensitivity:

This is done by Disc-Diffusion method of Kirby Bauer. In case of urinary


infection the suitable antibiotic drug was found out by the sensitivity of
organisms in vitro.

The organisms were grown on nutrient broth for 18 hours. Mueller


Hinton Agar plates were then inoculated uniformly by flooding the surface
with 2 ml of broth cultures. The excess removed and the discs were then
placed at suitable distance from each other and incubated overnight at 370C.

Antibiotic sensitivity zones were read in the zone reader and compared to
a standard chart with specified zone diameters for each antimicrobial disc to
determine either sensitivity or resistance of the bacterium in question.

28
TREATMENT & FOLLOW UP

After screening, women with bacteriuria were treated with 14 days course
of antimicrobial drugs as per the sensitivity of the organisms. Repeat cultures
were obtained 2 weeks after completion of the therapy. If culture was sterile,
periodic repeat cultures were done at 4 weeks interval till culture was sterile.

All the patients in both groups were followed up till delivery for any
evidence of complications like preeclampsia, anemia, preterm labour, fetal
growth restriction. Mode of delivery and period of gestation at the time of
delivery were assessed. Newborns were assessed for maturity, birth weight and
APGAR scores.

STATISTICAL METHODOLOGY: Descriptive and inferential statistical


analysis has been carried out in the present study. Results on continuous
measurements are presented on Mean SD (Min-Max) and results on
categorical measurements are presented in Number (%). Significance is
assessed at 5 % level of significance. The following assumptions on data is
made,

Assumptions: 1. Dependent variables should be normally distributed,

2. Samples drawn from the population should be random,


Cases of the samples should be independent.

Student t test (two tailed, independent) has been used to find the significance
of study parameters on continuous scale between two groups (Inter group
analysis) on metric parameters.

Chi-square/ Fisher Exact test has been used to find the significance of study
parameters on categorical scale between two or more groups.

Significant figures : + Suggestive significance (P value: 0.05<P<0.10)


* Moderately significant (P value: 0.01<P 0.05)
** Strongly significant (P value: P0.01)
Statistical software: The Statistical software namely SAS 9.2, SPSS 15.0, Stata
10.1, MedCalc 9.0.1 ,Systat 12.0 and R environment ver.2.11.1 were used for
the analysis of the data and Microsoft word and Excel have been used to
generate graphs, tables etc.

29
5. RESULTS AND ANALYSIS

Table 1: Age distribution of the patients studied

Age in Cases Controls


years No % No %
18-20 7 14.0 3 6.0
21-25 20 40.0 20 40.0
26-30 16 32.0 18 36.0
31-35 7 14.0 9 18.0
Total 50 100.0 50 100.0
Mean
25.024.23 26.104.05
SD
Samples were age matched with P=0.195

Cases
40
Controls
35
30
Percentage

25
20
15
10
5
0
18-20 21-25 26-30 31-35
Age in years

Out of 50 cases and 50 controls, 40% of the patients in each group were
in the age group 21-25 years with the mean age 25 years. The samples
were age matched with the p value of 0.195.

30
Table-2 Prevalence of asymptomatic bacteriuria in preterm labour

ASB PTL %
No 39 78.0
Yes 11 22.0

Total 50 100.0

22%

78%

No
Yes
ASB

Out of total 50 cases with preterm labour,

11 patients had asymptomatic bacteriuria (22%),


32 patients had no growth in culture (64%) and
7 patients had mixed growth (14%) which is suggestive of contamination
and those samples were repeated and treated accordingly.
In this study the prevalence of asymptomatic bacteriuria in preterm labour
is 22%.

31
Table 3: Diagnosis in two groups studied

Cases Controls
Diagnosis
No % No %
ANC 0 0.0 50 100.0
PTL 50 100.0 0 0.0
Total 50 100.0 50 100.0

0% 0%

100% 100%

ANC ANC
PTL PTL
Cases Controls

This table shows the diagnosis of the two groups studied.

All cases were admitted with the diagnosis of Preterm labour pain.
All controls were patients in the Antenatal clinic.
Cases and controls were numerically matched.

32
Table 4: Urine culture examination

Cases Controls
Urine examination (n=50) (n=50) P value
No % No %
Culture sensitivity
No Growth 32 64.0 44 88.0
Mixed
7 14.0 6 12.0 <0.001**
Growth
ASB 11 22.0 0 0.0

90 cases

80 controls
70
60
Percentage

50
40
30
20
10
0
No growth mixed growth ASB
Culture sensitivity

This table shows urine culture examination results in the patients studied.
11 out of 50 patients in the cases group had asymptomatic bacteriuria
(22%).
Patients in the control group are those who do not have asymptomatic
bacteriuria.
Both case and control groups had 14% and 12 % of mixed growth
respectively which can be ignored.
The P value is <0.001** which is statistically very significant.

33
Table 5: Organisms isolated

Organism Cases Controls


isolated No % No %
No Growth 32 64.0 44 88.0
Mixed
7 14.0 6 12.0
Growth
E coli 10 20.0 0 0.0
Klebsiella 1 2.0 0 0.0
Pseudomonas 0 0.0 0 0.0
Total 50 100.0 50 100.0
P<0.001**, Significant, Fisher Exact test

90 Cases
80
Controls
70
Percentage

60
50
40
30
20
10
0

Organism isolated

Out of 11 patients with asymptomatic bacteriuria in cases group, E.coli


was grown in 10 cultures and Klebsiella was grown in 1 culture.
The P value is <0.001** in Fischer Exact test which is statistically
significant.
The most common organism isolated in this study was E.coli followed by
Klebsiella.

34
Table 6: Past Obstetric History

Obstetric Cases Controls


History No % No %
Primi 36 76.0 22 44.0
Multi 14 28.0 28 56.0
Total 50 100.0 50 100.0

P=0.005**, Significant, Chi-Square test

Cases
80
Controls
70
60
Percentage

50
40
30
20
10
0
Primi Multi
Obstetric History

Out of 50 cases, 36 patients were primigravida (76%) and 14 patients


were mutigravida (28%).
Out of patients in control group, 22 patients (44%) were primigravida
and 28 patients (56%) were multigravida.
The presence of asymptomatic bacteriuria and preterm labour was more
in primigravida than in multigravida with the P value of 0.005** Chi-
Square test which is statistically significant.

35
Table 7: History of PTL in previous pregnancies in the two groups studied

History Cases Controls


of PTL No % No %
No 46 92.0 43 46.0
Yes 4 8.0 7 14.0
Total 50 100.0 50 100.0
P=0.338, Not significant, Chi-Square test

Cases
100
Controls
90
80
70
Percentage

60
50
40
30
20
10
0
No Yes
History of PTL

Out of 50 patients in the cases group with the diagnosis of PTL this
pregnancy, 46 patients (92%) had no history of preterm labour in
previous pregnancies and only 4 patients (8%) had history of preterm
labour in previous pregnancies.
This is statistically not significant P value is 0.338, Chi-Square test.
92% of cases had no history of preterm labour may be because 72% of
cases were primigravida.

36
Table 8: Associated co morbidities

Cases Controls
Co morbidities (n=50) (n=50)
No % No %
Not significant 32 64.0 47 94.0
Significant 20 40.0 3 6.0
PCOS 7 14.0 0 0.0
Hypothyroid 1 2.0 2 4.0
Treated for
1 2.0 1 2.0
infertility
Abruption 1 2.0 0 0.0
APH 1 2.0 0 0.0
Bicornuate
1 2.0 0 0.0
uterus
CIDP 1 2.0 0 0.0
GDM on diet
1 2.0 0 0.0
Breech
Hep-A + 1 2.0 0 0.0
Irregular mensus 1 2.0 0 0.0
ITP 1 2.0 0 0.0
Severe
1 2.0 0 0.0
Preeclampsia

37
Cases
100
Controls
90
80
70
Percentage

60
50
40
30
20
10
0
Not significant Significant
Co morbidities

10
Cases
Percentage

Controls
5

0
ITP
CIDP
PCOS

Abruption

APH

Hep-A +
B/L PCOS

Irregular mensus

IUGR
Hypothyroid

Anemia

Severe Preeclampsia
GDM on diet Breech
Treated for infertility

Bicornuate uterus

Co morbidities

Considering associated co morbid states, out of 50 cases with Preterm


labour, 7 patients (14%) had PCOS.
All other co morbid states were not significantly associated with Preterm
labour.
Even PCOS (14%) was not strongly associated with Preterm labour.
Severe preeclampsia was present in only 2% of cases which is
statistically not significant.

38
Table 9: Hemoglobin (mg/dl) levels in two groups studied

Cases Controls
Hemoglobin
(mg/dl) No % No %
<9 2 4.0 2 4.0

9-10 29 58.0 24 48.0

10-12 18 36.0 22 44.0

>12 1 2.0 2 4.0

Total 50 100.0 50 100.0

Mean SD 10.101.23 10.381.19


P=0.796 Not significant, Chi-Square test

60 Cases
Controls
50

40
Percentage

30

20

10

0
<9 9-10 10-12 >12
Hemoglobin (mg/dl)

Maternal anemia (Hemoglobin <10) was present in 62% of patients in the


cases group.
Maternal anemia was present in 90% of patients with asymptomatic
bacteriuria.
The mean hemoglobin level in the cases group was 10.101.23 mg/dl
The mean hemoglobin level in the control group was 10.381.19 mg/dl
The P value is 0.796 which is not significant, Chi-Square test.

39
Table 10: Preterm premature rupture of membrane

Preterm
premature No. of
%
rupture of patients
membrane
No 35 70.0
Yes 15 30.0
Total 50 100.0

30%

70%

No
Yes

Preterm premature rupture of


membrane

Out of 50 cases with preterm labour pain, only 15 patients (30%) had
Preterm premature rupture of membrane as well, during admission.
PPROM also may be the reason for Preterm labour pain also. This
association is not statistically significant.

40
Table 11: Gestational Age in weeks at the time of admission

Gestational Cases Controls


Age(wks) No % No %
28-32 21 42.0 0 0.0
33-37 29 58.0 0 0.0
38-40 0 0.0 50 100.0
Total 50 100.0 50 100.0

P<0.001**, Significant, Fisher Exact test

100 Cases
90 Controls
80
70
Percentage

60
50
40
30
20
10
0
28-32 33-36 37-40
Gestational Age(wks)

Out of 50 cases, 29 patients (58%) had preterm labour pain between 33-
37 weeks and 21 patients (42%) preterm labour pain between 28-32
weeks.
Patients in the control group are those who do not have preterm labour
pain and they got admitted at term either with spontaneous labour pain or
for safe confinement.
This is statistically significant P<0.001** Fischer Exact test.

41
Table 12: Comparison of Mode of Delivery

Cases Controls
Mode of Delivery
No % No %
PTVD 41 82.0 0 0.0
FTND 5 10.0 42 84.0
FT vacuum D 0 0.0 1 2.0
PT LSCS 4 8.0 0 0.0
FT LSCS 0 0.0 7 14.0
Total 50 100.0 50 100.0

100%
90%
80%
70%
60% cases
50% controls
40%
30%
20%
10%
0%
Vaginal delivery LSCS

Out of 50 cases that came with spontaneous preterm labour pain, 41


patients (82%) had preterm vaginal delivery and 4 patients (8%) had
preterm caesarean section for obstetric indications.
5 patients in the cases group responded to tocolysis and delivered
vaginally at term.
The number of caesarean sections is more in the control group (7
patients-14%) than in the cases (4 patients-8%) but not statistically
significant

42
Table 13: Urine examination

Cases Controls
Urine examination (n=50) (n=50) P value
No % No %
Routine- Pus cells
No 24 48.0 27 54.0
0.548
Yes 26 52.0 23 46.0
Microscopic
examination
NS 21 42.0 23 46.0
Bacteria 16 32.0 18 36.0
0.382
RBC 7 14.0 2 4.0
WBC 6 12.0 7 14.0

Cases
Controls
54

52

50
Percentage

48

46

44

42
NS Routine examination Yes

Presence of pus cells (pyuria) in urine routine examination was seen in 26


patients (52%) in the case group and 23 patients (46%) in the control
group which is not statistically significant with P value 0.548
All patients with pyuria in urine routine examination had asymptomatic
bacteriuria in urine culture examination which is significant.

43
50 Cases
45 Controls
40
35
Percentage

30
25
20
15
10
5
0
NS Bacteria RBC WBC
Microscopic examination

Presence of bacteria, RBC and WBC in urine microscopic examination


were not significantly related to asymptomatic bacteriuria and preterm
labour.

44
Table 14: Antenatal ultrasonogram in two groups studied

Cases Controls
Ultrasonogram (n=50) (n=50)
Antenatal
No % No %
Not significant 38 76.0 48 96.0
Significant 12 24.0 2 4.0
IUGR 5 10.0 0 0.0
AFI 0 0.0 2 4.0
Low lying
3 6.0 0 0.0
placenta
RPC 2 4.0 0 0.0
Breech 1 2.0 0 0.0
SGA 1 2.0 0 0.0
P=0.004**, Significant, Chi-Square test

Cases
100
Controls
90
80
70
Percentage

60
50
40
30
20
10
0
Not significant Significant
Ultrasonogram Antenatal

Comparing the features of ultrasonogram which was taken in the


antenatal period in both case and control groups, 12 patients (24%) in the
case group had significant features and only 2 patients (4%) in the control
group had significant features.
The P value is 0.004** which is statistically significant, Chi-Square test.
Out of 12 (24%) with significant features, 5 patients (10%) had IUGR
changes in the case group and none (0%) in the control group which is
statistically significant.

45
Table 15: Effectiveness of Tocolysis

No. of
Tocolysis %
patients
Failure 29 58.0
Not tried 16 32.0
Success 5 10.0
Total 50 100.0

60

50

40
Percentage

30

20

10

0
Failed Not tried Success
Tocolysis

Out of 50 cases with preterm labour pain, tocolysis was tried in 34


patients (68%) and was successful in only 5 patients (10%) and failed in
29 patients (58%).
Tocolysis was not tried in 16 patients (32%) as there was PPROM in 15
patients and 1 in advanced stage of preterm labour.
The result was statistically not significant.

46
Table 16: Term/Preterm births in two groups studied

Cases Controls
Term/Preterm
No % No %
Term 6 12.0 50 100.0
Preterm 44 88.0 0 0.0
Total 50 100.0 50 100.0
P<0.001**, Significant, Chi-Square test

Cases
100
Controls
90
80
70
Percentage

60
50
40
30
20
10
0
Term Preterm
Term/Preterm

Out of 50 cases, 44 patients (88%) delivered preterm and 6 patients


(12%) delivered term (after successful tocolysis).
All patients in the control group delivered at term (100%).
The P value is <0.001** which is statistically significant, Chi-Square test.

47
Table 17: Birth Weight (kg) distribution in two groups studied

Weight Cases Controls


(kg) No % No %
<1 4 8.0 0 0.0
1-2 21 42.0 0 0.0
2-3 20 40.0 25 50.0
3-4 5 10.0 25 50.0
Total 50 100.0 50 100.0
Mean
2.050.68 3.060.37
SD

P<0.001**, Significant, Student t test

50 Cases
45 Controls
40
35
Percentage

30
25
20
15
10
5
0
<1 1-2 2-3 3-4
Weight (kg)

The mean birth weight of the babies in the case group was 2.050.68 kg
The mean birth weight of the babies in the control group was 3.060.37
kg
This difference is due to prematurity and fetal growth restriction in the
cases.
None of the babies in the control group had prematurity.
This is statistically significant P value is <0.001**, student test.

48
Table 18: Apgar 1 min of neonates studied

Apgar 1 Cases Controls


min No % No %
0-6 5 10.0 0 0.0
>7 45 90.0 50 100.0
Total 50 100.0 50 100.0
P=0.056+, Significant, Fisher Exact test

120%

100%

80%

60% cases
controls

40%

20%

0%
0-6 >7

Apgar values in 1 minute

The number of low apgar scores in cases was 5 (10%) and 0 (0%) in
controls.
All neonates in the control group had normal apgar scores and it is
statistically significant with P value 0.056+, Fischer exact test.

49
Table 19: Neonatal intensive care unit admission in cases group

Neonatal
No. of
intensive care %
neonates
unit admission
No 38 76.0
Yes 7 14.0
Dead 5 10.0
Total 50 100.0

80
70
60
Percentage

50
40
30
20
10
0
No Yes Dead
Neonatal intensive care unit admission

Out of 50 babies in the cases, 12 babies (24%) were admitted in NICU.


Out of 12 babies (24%) who were admitted 5 babies (10%) expired.
None of the babies from the control group were admitted in NICU which
is significant.

50
Table 20: Nitrofurantoin sensitivity in cases with ASB

Cases with
Nitrofurantoin ASB
sensitivity
No %
No 7 63.64
Yes 4 36.36
Total 11 100.0

Cases Controls
Nitrofurantoin
No % No %
No 47 94.0 50 100.0

Yes 3 6.0 0 0.0

Total 50 100.0 50 100.0


P=0.242, Not significant, Fisher Exact test

Cases
100
Controls
90
80
70
Percentage

60
50
40
30
20
10
0
No Yes
Nitrofur

Out of 11 cases with asymptomatic bacteriuria, sensitivity to


nitrofurantoin was not present in 63.64% of asymptomatic bacteriuria and
sensitivity to nitrofurantoin was present in 36.36% of asymptomatic
bacteriuria.

51
6. DISCUSSION

Asymptomatic bacteriuria (ASB) occurs in 2-10% of all pregnancies8,126. The


majority of the most recent studies21,126-132, including observational studies from
developing countries found the prevalence of asymptomatic bacteriuria in
pregnant women ranged between 4-10%. Different studies have shown different
indices.

This variation in studies can be attributed to several factors such as the


geographical variation, socio-economic status, ethnicity of the subjects, setting
of the study (primary care, community based, or hospitals), and the variation in
the screening tests (urine dipstick, microscopy, and culture).

Prevalence:

Prevalence of ASB in preterm labour also varies with the above


mentioned factors. In the present study prevalence of asymptomatic bacteriuria
in preterm labour was 22% (Table-2)

Study Prevalence of ASB in PTL


Hazhir et al134 2007 36%
El-Sokkary et al133 2011 23.5 %
Present study 2015 22%

Study Prevalence of ASB in pregnancy


Al-Haddad AM135 2005 30%
Abdullah AA et al136 2005 4.8%
Aseel M et al132 2009 9.9%
Moghadas AJ et al137 2009 3.3-6.1%
Delzell JE18 2000 8%
Khatun et al138 1985 30%
Present study 2015 22%

52
Culture method:

The ASB diagnosed using urine culture examination was 22% in the
cases group with p vale <0.001** which is statistically significant. (Table-4).
Delzell et al18 stated that the Gold standard for detection of bacteriuria is urine
culture. Faster screening methods like leukocytes esterase dipstick, nitrite
dipstick, urinalysis and gram staining are not useful in the screening foe
ASB69,70,71

Organisms isolated:

The dominant isolates in the study was Escherichia coli which is 20%.
(Table-5). Others were Klebsiella and mixed growth. This is similar to the
findings of previous studies given in the following table.

Study Common organism


Keah SH et al139 E.coli
Gayathree et al20 E.coli
Masinde et al23 E.coli
Nerissa Isabel C et al140 E.coli
Jayalakshmi et al124 E.coli
Present study E.coli

Maternal age and ASB:

The highest age specific prevalence of ASB and Preterm labour was
found in the age group of 20-30 years and lowest more than 30 years (Table- 1).
This is probably because this comes under reproductive age group and most of
the patients had their pregnancy during this period. Mean age of 25 years was
noted by Gebre-Selassie141 in his study.

Primi or Multi- gravida and ASB:

The presence of asymptomatic bacteriuria was more in primigravida than


in multigravida with the P value of 0.005** Chi-Square test which is
statistically significant. (Table-6). But several authors have reported increasing
rise of symptomatic bacteriuria with age and parity. Mc Fadyen99 found no
relationship with age or parity.

53
Preterm birth/labour and ASB:

Preterm births in the current study were 100% in patients with


asymptomatic bacteriuria. Preterm births in the cases group were 88% which is
statistically significant. (Table-16). Asymptomatic bacteriuria in pregnancy
causes prematurity as it causes preterm delivery.

Fathima N et al31 in 2006 studied 590 women. 6 out 28 women with


bacteriuria and 27 out of 552 women without bacteriuria went into preterm
labour, which is statistically significant. Nicolle et al121 found that incidence of
prematurity is 2.4 times greater than those without urinary infection.

But findings from Cardiff Birth Survey110 in 1995 which prospectively


studied 25,844 births, reported that asymptomatic bacteriuria is not associated
with preterm delivery. The authors concluded that if ASB did not progress to
pyelonephritis, it would not be associated with preterm births.

Low hemoglobin level and ASB:

In the present study, low Hemoglobin (<10 Hb) was seen in 62 % of


patients with preterm labour and 90% of patients with maternal anemia had
asymptomatic bacteriuria (Table- 9)

Lavanya and Jogalakshmi D et al30 found that bacteriuria in pregnancy


is associated with maternal anemia. But Fatima et al31 didnt find any
association between bacteriuria and anemia.

PPROM and ASB:

PPROM was present in 15 patients (30%) in the cases group in the


present study. PPROM may also be the reason for preterm labour pain. (Table-
10).

Cox SM et al108 in 1987 found that bacterial enzymes such as collagenase


may weaken the fetal membranes which can result in preterm premature rupture
of membrane.

54
Severe Preeclampsia and ASB

Severe preeclampsia was present in only 1 patient with Preterm labour


and had no asymptomatic bacteriuria in the present study.( Table -8).

Abyad et al104 in 1991 found that asymptomatic bacteriuria is associated


with hypertension and pre eclampsia. But, there is no compelling evidence of an
association of asymptomatic bacteriuria in pregnancy with hypertension in
pregnancy or of long-term renal damage in this antibiotic era.105

Low birth weight and ASB:

The mean birth weight of the babies in the case group was 2.050.68 kg
in the present study with P<0.001**, Significant, Student t test. (Table-17). This
comes under low birth weight category.

Romero et al112 in 1989 reported that women with asymptomatic


bacteriuria had a 54% higher risk of low birth weight infant.

Intra uterine growth restriction and ASB:

IUGR was seen in 10 % of the patients with preterm labour pain in USG
which is statistically significant when compared none in the control group.
(Table- 14)

Harris RE et al122 found that there was an association between presence


of asymptomatic bacteriuria and intra uterine growth retardation. Romero et
al112 also stated that ASB was associated with IUGR.

Nitrofurantoin sensitivity:

This study found that out of 11 cases with asymptomatic bacteriuria, 7


patients (63.64%) were not sensitive to nitrofurantoin and 4 patients (36.36%)
were sensitive to nitrofurantoin. This result is different from other studies done
on nitrofurantoin sensitivity ( Table-20).

Gupta et al35 proved that prevalence of resistance by urinary isolates to


nitrofurantoin was only 0%-2%. He stated that nitrofurantoin is relatively safe
in pregnancy and is effective in most UTI, except that it can cause hemolysis in
G6PD deficiency baby if used near term.

55
7. LIMITATIONS

As with any prospective studies, our study also had limitations.

1. There were mixed growth which is suggestive of contamination found in


the urine culture. But this can be ignored as the number of mixed growth
was almost equally distributed.
2. Patients in the control group, who became symptomatic during the course
of the pregnancy were excluded from the study and new patients were
added to attain the sample size.
3. The patients in the control group had no asymptomatic bacteriuria which
may be due to strict following of exclusion criteria, because the patients
initially who had asymptomatic bacteriuria became symptomatic during
the course of pregnancy.

56
8. SUMMARY

The study was conducted on 50 pregnant women with preterm (24-


37wks) labour pain admitted in the labour room (Case) and 50 preterm (24-
37wks) pregnant women who are not in labour and in the out-patient department
(Control).

Urine culture and sensitivity was done to find out the prevalence of
asymptomatic bacteriuria (ASB) in pregnant women presenting with preterm
labour pain, to determine the common pathogenic micro organisms associated
with asymptomatic bacteriuria (ASB) and to determine their antibiotic
sensitivity. Both maternal and fetal adverse outcomes were noted.

The prevalence of asymptomatic bacteriuria in the study population was


22 %. Common pathogen was E.coli occurring in 20% of the patients in the
cases group. Sensitivity to nitrofurantoin was seen in 36.36% of the patients
with ASB.

Significant maternal morbidities were presence of preterm premature


rupture of membrane and maternal anemia. Preterm premature rupture of
membrane was present in 30% of the patients in the cases group. But PPROM
was not present in all the patients with asymptomatic bacteriuria.

Maternal anemia (Hemoglobin <10) was present in 62% of patients in


the cases group 90% of patients with asymptomatic bacteriuria. Severe
preeclampsia was seen in only 1 patient in the cases group and not associated
with asymptomatic bacteriuria.

Significant neonatal outcomes were prematurity and low birth weight.


Preterm birth was present in 88% of the patients in the cases group. The mean
birth weight of the babies in the case group was 2.050.68 kg.

Fetal mortality was observed in 5 cases (10%) and cause of the death was
prematurity.

57
9. CONCLUSION

Asymptomatic bacteriuria is a common infection. Pregnant women with


asymptomatic bacteriuria are at an increased risk for adverse maternal and fetal
outcomes which could be prevented by antimicrobial therapy.

In this study, out of 50 randomly selected women with preterm labour


pain, 11 were found to have asymptomatic bacteriuria which gives a prevalence
rate of 22%.

Organisms isolated were E.coli, Klebsiella pneumonia and mixed growth.


E.coli was the most common organism in the cases group (20%). Sensitivity to
nitrofurantoin was seen in 36.36% of the patients with ASB.

Maternal morbidities including low haemoglobin levels, PPROM and


severe preeclampsia were present in the patients in the cases group.

Significant fetal morbidities including preterm birth, IUGR and low birth
weight were seen in the patients in the cases group

. Hence pregnant women should be screened for bacteriuria and treated


with appropriate antibiotics according to the sensitivity if results are positive.

58
10. REFERENCES

1. Satmm WE, Hootan TM- Management of Urinary tract infection in adults


N Eng J medicine 1993;329;1328-34
2. Sampson JE, Gravett MG, Other infectious conditions in pregnancy:
James DK, Steer PJ, Weiner CP, Govik B eds. High Risk Pregnancy,
management options 2nd Edition, London WB Saunders, 1999:559-598
3. Hootan TM, Satmm WE. Diagnosis and treatment of uncomplicated
urinary tarct infection. Infect Dis Clin North Am 1997; 11:551-82
4. Nicolle LE. A practical approach to the management of complicated
urinary tract infection. Drug Aging 2001; 18:243
5. Uncu Y, Uncu G, Esner A et al. Should asymptomatic bacteriuria be
screened in pregnancy? Clinic Exp Obstet Gynaecol 2002;29:281-5
6. Nath G, Chaudhary M, Prakash J et al. Urinary tract infection during
pregnancy and fetal outcome. Indian J Microbiol 1996:14:158-60
7. Chandel LR, Kanga A, Thakur K et al. Prevalence of pregnancy
associated Bacteriuria: A study done in a tertiary care hospital. J Obstet
Gynaecol India 2012:62:511-4
8. Enayat K, Fariba F, Bahram N. Asymptomatic bacteriuria among
pregnant women referred to out patient clinics in Sanandaj. Iran. Int Braz
J Urol 2008:34:699-707
9. Rubenstein JN, Schaeffer AJ. Managing complicated urinary tract
infections: The urologic view. Infect Dis Clin North Am 2003: 17;333-
351
10.Patterson TF, Andriole VT. Detection, significance and therapy of
bacteriuria in pregnancy. Infect dis Clin North Am 1997;1:593-608
11.Kremery S, Hromec J, Demesova D. Treatment of lower urinary tract
infection in pregnancy. Int J Antimicrobe Agents. 2001;17(4):279-82
12.Tayo AO, OI Akinola, TA Ottum, JAA Anakoya, AO Ogunsanya.
Appraisal of asymptomatic bacteriuria in pregnancy: Nigerian Journal of
clinical medicine 2010: vol3 no2
13. Sharma JB., Sharma S, Gulai N et al. prevalence of significant
bacteriuria in preterm labour. J Obstet Gynaecol India 1900;40:336-8
14.Meis PG, Michielutte R, peters TJ et al. Factors associated with preterm
birth in cardiff, Wales. Am J Obstet Gynaecol 1995;173:597-602
15.Hazhir S. Asymptomatic bacteriuria in pregnant women. Urol.J..4(1):24-
27,2000

59
16.Smail F: Antibiotics for asymptomatic bacteriuria in pregnancy.
Cochrane database Syste. Rev.. 2: CD000490.2001
17.Cypher R L: Reducing recurrent preterm births: Best evidence for
transitioning to predictive and preventive strategies. J. Perinat.
Naeonatal. Nurs..26(3):220-9,2012
18. Delzell JE, Lefevre ML. Urinary tract infections during pregnancy. Am
Fam Physician. 2000;61(3):713-21
19.Antony J, Schaeffer & Edward. Campbell-Walsh Urology 9th Ed, Wein,
Kavoussi, Novick, partin, Peters Vol I, Saunders Publications,2007;677-
690
20.Gayathree L.,Shetty S.,Deshpande S.R.,Venkatesha D.T. Screening for
asymptomatic bacteriuria in pregnancy: An evaluation of various
screening tests in Hassan District Hospital, India. 2010;4(4):2702-6
21.Ullah A.M., Barman A.,Siddique M.A., and Haque A.K.M.E Prevalence
of asymptomatic bacteriuria and its consequences in pregnancy in a rural
community of Bangladesh. Bangladesh med Res Conc Bull 2007;33:60-
64
22.Gulfareen Haider. Gulfareen haider, Shazia Rani, Saima Ghaffar,
Ambreen Haider 2009;5:
23.Masindei A. Prevalence of urinary tract infection among pregnant women
at Bugando Medical Centre, Mwanza, Tanzania. Tanzania Journal of
health research, Vol.11, No.3,July 2009. 154-161
24.C.A. Turpin, Bridget Minkah, KA Danso and EH Frimpong. Ghana med
J.2007 March;41(1):26-29
25.Stenqvist K, Dahlen-Nilsson I, Lichin-Janson G, et al. Bacteiuria in
pregnancy. Frequency and Rsik Acquisition. Am J Epidemiol
1989;29(2):372-79
26.Kutlay S, Kutlay B, Karaahmetoglu O, AKC, Erkayas; Prevalence,
detection and treatment of asymptomatic bacteriuria in a Turkish obstetric
population: J Reprod Med.2003 Aug;48(8):627-30
27.Wesley WE. Urinary tract infection, females. Med J 2002;3:33-41
28.Kinningham R. Asymptomatic bacteriuria in pregnancy. Am FAM
Physician 1993;47(5):1232-1238
29.Nicolle LE. Management of asymptomatic UTIs in women. Medscape
Womens Health 1996;1(3)
30.Lavanya SV, Jogalakshmi D. Asymptomatic bacteriuria in antenatal
women. Indian J Med Microbiol 2002;20:105-6

60
31.Fathima N, Yasmin S, Ishrat et al: prevalence and complications of
asymptomatic bacteriuria during pregnancy: Professional med J Mar
2002;13(1):108-112
32.Renko M., Tapanaminen P., Pokka T., Uhari M. Diabetes care
2011;34:230-5
33.Scholes D, Hooton TM, Roberts PL, Stapleton AE, Gupta K, Stamm WE:
Risk factors for recurrent urinary tract infection in young women. J.
Infect. Dis. 182, 1177-1182 (2000)
34.Scholes D, Hooton TM, Roberts PL, Gupta K, Stapleton AE, Stamm WE:
Risk factors associated with acute pyelonephritis in healthy women. Ann.
Intern. Med. 142, 20-27(2005)
35.Gupta K, Hillier SL, Hooton TM, Roberts PL, Stamm WE: Effects of
contraceptive method on the vaginal microbial flora: a prospective
evaluation. J. Infect. Dis. 181,595-601 (2000)
36.London; WB Saunders, 1999; 559: 559-98
37.Raz R, Gennesin Y, Wasser J et al: Recurrent urinary tract infections in
post-menopausal women. Clin. Infect. Dis. 30, 152-156 (2000)
38.Van Beek E, Houben AJHM, van ES P N, et al: Peripheral
hemodynamics and renal function in relation to the menstrual cycle. Clin
sci 1996;91:163-168
39.Chapman AB, Zamudio S, Woodmansee W et al: Systemic and renal
hemodynamic changes in luteal phase of menstrual cycle mimic early
pregnancy. Am J Physiol (renal physio) 1997;273;777-782
40.Chapman AB, Abraham WT, Zamuido S et al: Temporal relationships
between hormonal and hemodynamic changes in early human pregnancy.
Kidney int 1998;54;2056-2063
41.Sturgiss SN, Dunlop w, Davidson JM: Renal hemodynamics and tubular
in human pregnancy. Baillieres clin obstet Gynecol 1994;8;2:209-234
42.Hertzberg BS, Carroll BA, Bowie JD et al: Doppler assessment of
maternal kidneys: Analysis of intra renal resistivity indexes in normal
pregnancy and physiological pelvicaliectasis. Radiology 1993;186:689-
692
43.Faundes A, Bricola-Filho M, Pinto e silva Lc: Dilatation of urinary tract
during pregnancy: proposal of a curve of maximal caliceal diameter by
gestational age. Am J Obstet Gynecol 1998;178:1082-1086
44.Patterson TF, Anriole VT. Bacteriuria in pregnancy. Infect Dis Clin North
Am 1987;1:807-22

61
45.J.D.Sobel and D. Kaye, Host factors in the pathogenesis of urinary tract
infections, American Journal of Medicine, vol.76, no.5, pp. 122-130,
1984
46.T. A. Stamey, The role of introital enterobacteria in recurrent urinary
infections, Journal of urolgy, vol.109, no.3, pp. 467-472, 1973
47.F. Himman Jr., Bacterial elimination Journal of Urology, vol.99, no.6,
pp. 811-825,1968
48.J.D.Sobel and D. Kaye, Host factors in the pathogenesis of urinary tract
infections, American Journal of Medicine, vol.76, n0.5,pp. 122-
130,1984
49.Fitzgerald MA. Urinary tract infection: providing the best care.
Medscape,2002
50.Mccarthy JM, Richard G, Huck W et al ; Randomised trial of short course
of ciprofloxacin or ofloxacin or trimethoprim/sulfamethoxazole for the
treatment of acute UTI in women. Am J. Med.106, 292-299(1999)
51.Perdue BE, Plaisance KI. Treatment of community acquired UTI, Am.
Pharm.1995;35-37
52.Gilstrap LC, Faro S. Urinary tract infections in pregnancy. Infections in
pregnancy, 2nd ed. New York Wiley-Lics, 1997;21
53.Lucas MJ, Cunningham FG. Urinary tract infections in pregnancy. Clin
Obstet Gynecol. 1993;36:855
54.Davidson J & Bayles C: Medical disorder in Obstetric Practce. Ed by
Michael de Swiet 4th edition: Blackwell Publishing. Pg 198-267, 2002
55.McDowall DR, Buchanan JD, Fairley KF, Gilbert GL. Anarobic and
other fastidious microorganisms in asymptomatic bacteriuria in pregnant
women. J Infect Dis 1981;144:114-22
56.Barr JG, Ritchie JW, Henry O, el Sheikh, el Deeb K.
Microaerophilic/anaerobic bacteria as a cause of urinary tract infection in
pregnancy. Br J Obstet Gynaecol 1985;92:506-10
57.McDowall DR, Buchanan JD, Fairley KF, Gilbert GL. Anarobic and
other fastidious microorganisms in asymptomatic bacteriuria in pregnant
women. J Infect Dis 1981;144:114-22
58.Sevki Celen, Ayla Sargin Oruc, Rana Kaayalcin, Sibel Saygan, Serpil
Unlu, Belgin S Polat and Nuri Danisman. Aysmptomatic Bacteriuria and
Antibacterial Susceptibility Patterns in an Obstetric Population. ISRN
Obstetrics nd Gynaecology Volume 2011, Article ID 721872, 4 pages

62
59.Reshmani R. Accuracy of urine dipstick to predict urinary tract infections
in an emergency department. J Ayub Med Coll Abbottabad 2004;16(1):4-
7
60.Antimicrobial therapy for obstetric patients. ACOG educational bulletin
no.245. Washington, D.C. American College of Obstetricians and
Gynaecologists, March 1998;245:8-10
61.American Academy of Family Physicians. Summary of recommendations
for clinical preventive services. Revision 6.4. August 2007
62.Nicolle LE, Bradley S, Colgan R, Rice JC, Schaeffer A, Hooton TM et al.
Infectious diseases Society of American guidelines for the diagnosis and
treatment of asymptomatic bacteriuria in adults. Clin Infect Dis.
2005;40:643-54 (PMID:15714408)
63.American Academy of Paediatrics, ACOG. Guidelines for Perinatal care.
6th ed. Elk Grove Village, IL, and Washington, DC: American Academy
of Pediatrics and American College of Obstetrics and Gynaecologists;
2007:100-1
64.DiGuiseppi C. Screening for Asymptomatic Bacteriuria In: Guide to
Clinical Preventive Services. US Preventive Services Task Force.
Department of Health and Human Services,1996
65.National Collaborating Centre for Womens And Childrens Health.
Clinical Guideline 6. Antenatal care. Routine care for healthy pregnant
women. Londan: National Institute for Clinical Excellence, October 2003
66.Naber KG, Bergman B, Bishop MC et al. EAU guidelines for the
management of urinary and male genital tract infections. Urinary tract
Infection (UTI) Working Group of the Health Care Office (HCO) of the
European Association of Urology (EAU). Eur Urol 2001;40:576-588
67.Nicolle LE. Screening for asymptomatic bacteriuria in pregnancy. In
Canadian guide to clinical preventive health care. Ottawa: Health
Canada,1994, pp. 100-106
68.Scottish Intercollegiate Guideline network. Management of suspected
bacterial urinart tract infection in adults. A national clinical guideline.
Edinburgh: Scottish Intercollegiate Guidelines Network, July 2006
69.Bachman JW, Heise RH, Naessens JM and Timmerman MG. A study of
various tests to detect asymptomatic urinary tract infections in an
obstetrics population. JAMA 1993; 270(16):1971-1974

63
70.Lenke RR and VanDorsten JP. The efficacy of the nitrite test and
microscopic analysis in predicting urine culture results. Am. J. Obstet.
Gynecol 1981; 140:427
71.Kattak am, Hussain I, Khan HU, Muhammad D. Evaluating the
microscopic Pyuria for screening covert bacteriuria during pregnancy.
72. Stamm WE. Measuremnt of pyuria and its relation to bacteriuria. Am J
Med 1983; 75 (Suppl 1B):53-58
73.Mojgan Mortazavi, Shiva Seyrafian, Shahrzad Shahidi, Zahra Abadpour,
Foroud Shahbazi. Pyuria as a screening test for detection of Urinary tract
Infection in patients on Long-term Hemodialysis, Iranian Journal of
Kidney Diseases 2011;5(1): 50-52
74.Kass E.H Asymptomatic infections in urinary tract. Trans Assoc Am
Physicians 1956;69:56-64
75.Dougles G Tincello, David H Richmond Evaluation of reagent strips in
detecting asymptomatic bacteriuria in early pregnancy: prospective case
series BMJ 1998;316:435-7
76. http://www.microbelibrary.org/library/laboratory-test/3660-nitrate-and-
nitrite-reduction-test-protocols
77.Aziz marjan Khattak, Habbibullah khan, Wasin Akhtar, Ihsamullah
Mahsud and Bushra Ashiq. Accuracy of griess Test to predict ASB
during pregnancy. Gomal Journal of Medical Sciences Jan-June 2004,
Vol.2 No.1 20-23
78.Stapleton A. Stamm WE. Prevention of urinary tract infections. Infect Dis
Clin north Am. 1997;11(3):719-33
79.Kontiokari T, Sundqvist K, Nuntiment M et al. Randomised trial of
cranberry-lingonberry juice and lactobacillus GG drink for the prevention
of UTI in women. BMJ. 2001;322(7302):1571
80.Foxman B, Gillespie B, Koopman J et al: Risk factors for second urinary
tract infection among college women. Am. J. Epidemiol. 2001;151,1194-
1205 (2000)
81.Foxman B, Frericks RR: Epidemiology of UTI: II. Diet, clothing and
urinary habits. Am. J. Public Health. 75,1314-1317 (1985)
82.Remis RS, Gurwith D, Hargrett-Bean NT, Layde PM: Risk factors for
urinary tract infection. Am. J. Epidemiol. 126, 685-694 (1987)
83.Naber KG. Treatment options for acute uncomplicated cyctitis in adults. J
Antimicrob Chemother 2000;46(suppl 1):S23-7

64
84.Raz R, Colodner R, Rohana Y, Rottensterich E, Wasser I, Stamm W:
Effectiveness of estriol containing vaginal pessaries and nitrofurantoin
macrocystal therapy in the prevention of recurrent urinary tract infection
in postmenopausal women. Clin. North Am 1, 793-806 (1987)
85.Nicolle LE, Ronald AR. Recurrent urinary tract infection in adult women:
Diagnosis and treatment. Infect. Dis. Clin. North Am. 1, 793-806 !1987)
86.Harding GKM, Roland AR, Nicolle LE, Thomson MJ, Gray GJ. Long-
term antimicrobial prophykaxis for recurrent urinary infection in females.
Rev. Infect. Dis. 4, 438-443 (1982)
87.Erikson BC: A randomised, open, parallel group study on the preventive
effect of an estradiol- releasing vaginal ring on recurrent urinary tract
infections in postmenopausal women. Am. J. Obstet. Gynecol. 180,1072-
1079 (1999)
88.Brown JW, Vittimghoff, Kanaga AM, Agarwal SK, Hulley S, Foxman B:
Urinary tract infections in postmenopausal women: Effect of hormone
therapy and risk factors. Obstet. Gynecol. 98,1045-1052 (2001)
89.Ouslander JG, Greendale GA, Uman G, Lee C, Paul W, Schenelle J:
Effects of oral estrogen and progestin on the lower urinary tract among
nursing home residents. J. Am. Geriatr. Soc. 49, 803-807 (2001)
90. Antibiotic treatment for asymptomatic bacteriuria: Antibiotic Vs no
treatment for asymptomatic bacteriuria in pregnancy. Cochrane Database
of Systematic Reviews 2002;(3):1-5
91.Australian Medicines Handbook. Adelaide: Australian Medicines
Handbook Pvt Ltd, 2004
92.WM Bamford & Company Limited. Nifuran. Medicine safety Data Sheet.
2004
93.Macejko AM, Schaeffer AJ. Asymptomatic bacteriuria and symptomatic
urinary tract infections during pregnancy. Urol Clin North Am
2001;34(1):35-42
94.ODonnell JA, Gelone SP, Abrutyn E. Selecting drug regimens for
urinary tract infections: Current recommendation. Infections in Medicine.
2002;19(1):14-22
95.Johnson JR, Russo TA: Extra intestinal pathogenic E.coli: The other bad
E.coli.J. lab. Clin. Med.139,155-162 (2002)
96.Clinical Knowledge Summaries (CKS). Urinary tact infection (lower)-
women. CKS, 2009

65
97.Stein G.E (1998) single dose of acute cystitis with fosfomycin
tromethamine. Annals of pharmacotherapy 32, 215-9
98.Donald I. Practical obstetric problems. 5th ed. London, Lloyd-luke
Ltd.,1979
99.McFadyen IR, Eykyn SJ, Gardner NHN, Vanier TM, Bennett AE, mayo
ME et al. Bacteriuria in pregnancy. J Obstet Gynaecol Br Commonwealth
1973;80:385-405
100. Albert X, Huertas I, Pereiro I, Sanfelix J, Gosalbes V, Perrotta C.
Antibiotics for preventing recurrent UTI in non-pregnant women.
Cochrane Database Review 2004, Issue 3, Art. No: CD001209.DOI.
101. Uncuy: Uncuy G; Esmer A; Bilgel N. Clinical Exp Obstet Gynecol
2002:29(4):281-5
102. Dwyer PL, OReily M. Recurrent urinary tract infection in the
female. Curr Opin obstet Gynecol. 2002; 14(5): 537-43
103. Ikaheimo R. SiitonenA, Heiskanen T et al: Recurrence of urinary
tract infection in a primary care setting: Analysis of a 1 year follow-up of
179 women. Clin. Infect. Dis. 22,91-99 (1996)
104. Abyad A. Screening for asymptomatic bacteriuria in pregnancy
urinalysis vs urine culture. J Fam Prac.1991;33(5):471-4
105. Patterson TF, Andriole VT: Bacteriuria in pregnancy. Infect Dis
Clin North AM 1987;1:807-822
106. McGladdery SL, Aparicio S, Verrier-Jones K, Roberts R.
Outcome of pregnancy in an Oxford-Cardiff cohort of women with
previous bacteriuria. QJM. 1992;83(303):533-9
107. Andriole V, Patterson TF. Epidemiology, natural history and
management of urinary tract infection in pregnancy. Med Clin North Am.
1991;75(2):359-371
108. Cox SM. Infection-induced preterm labor. Infections in pregnancy.
Gilstrap LC, Faro S (eds). Newyork, Alz Rliss Inc, 1990: 247-53
109. Patterson TF, Andriole VT. Bacteriuria in pregnancy. Infect Dis
Clin North Am 1987;1:807-822
110. Meis PJ, Michielutte R, Peter TJ et al. Factors associated with
preterm birth in Cardiff, Wales. I. Univariable and multivariable analysis.
Am J Obstet Gynecol 1995;173:590-596
111. Monif GRG: Intrapartum bacteriuria and postpartum endometritis.
Obstet Gynecol 1991;78:245-248

66
112. Romero R., Oyarzane E., Mazor M., Sirtori M., Hobbins,JC.,
Braken M (1989) Metaanalysis of relationship between asymptomatic
bacteriuria and preterm delivery/low birth weight. Obstetrics and
Gynaecology 73, 576-82
113. Joseph KS, Brahmadathan KN, Abraham S, Joseph A. Detecting
bacteriuria in a primary maternal and child health care program. Bri Med
J.1998;296:906-7
114. Turner AN, Savill J, Stewart LH, Cumming A. Kidney and
genitourinary disease. In: Davidsons principles and practice of medicine.
Haslett C, Chilvers ER, Boon NA, Colledge NR (eds). 19th ed.
Edinburgh, Churchill Livingstone, 2002, pp 575-639
115. Hill JB, Sheffield JS, McIntire DD et al (2005) Acute
pyelonephritis in pregnancy. Obstet Gynecol 10:18-23
116. Cook DJ, Achong MR, Dobranowski J. Emphysematous
pyelonephritis: complicated urinary tract infection in diabetes. Diabetes
Care 1989;12:229-32
117. Thorley JD, Jones SR, Sanford JP. Perinephric abscess. Medicine
(Balti-more) 1974;53:441-51
118. Jerkeman M, Braconier JR. Bacteremic and non-bacteremic febrile
urinary tract infection- A review of 168 hospital treated patients. Infection
1992;20:143-5
119. Cunningham FG, Lucas MJ, Hankins GD (1987) Pulmonary
injuiry complicating antepartum pyelonephritis. Am J Obstet Gynecol
156:797-807
120. Towers CV, Kaminskas CM, Garite TJ et al (1991) Pulmonary
injuiry associated with antepartum pyelonephritis: Can patients at risk be
identified? Am J Obstet Gynecol 164:974-978
121. Nicolle L.E. Screening for asymptomatic bacteriuria in pregnancy.
In: Ottawa: Health Canada 1994;100-110
122. Harris RE, Thomas VL Sheokov A. Amj Obstet gynaecology 1976
Sep1;126(1):20-5
123. Car J. Urinary tract infections in women: diagnosis and
management in primary care. BMJ 2006;332:94-7
124. Jayalakshmi J, Jayaram VS; Evaluation of various screening tests
to detect asymptomatic bacteriuria in pregnant women. IJPM:
51(3),2008;379-81

67
125. Gardner A. UTI in pregnancy and sudden unexpected infant death.
Lancet 1985;11:495
126. Tugrul S, Oral O, Kumru P, Kose D, Alkan A, Yildirim G.
Evaluation and importance of asymptomatic bacteriuria in pregnancy.
Clin Exp Obstet Gynecol 2005; 32(4): 237-240.
127. Abdullah AA, Al-Moslih MI. Prevalence of asymptomatic
bacteruria in pregnant women in Sharjah, United Arab Emirates. East
Mediterr Health J 2005; 11(5-6): 1045-1052.
128. Al-Haddad AM. Urinary tract infection among pregnant women in
Al-Mukalla district, Yemen. East Mediterr Health J 2005; 11(3): 505-
510.
129. Fatima N, Ishrat S. Frequency and risk factors of asymptomatic
bacteriuria during pregnancy. J Coll Physicians Surg Pak 2006; 16(4):
273-275.
130. Akinloye O, Ogbolu DO, Akinloye OM, Terry Alli OA.
Asymptomatic bacteriuria of pregnancy in Ibadan, Nigeria: a re-
assessment. Br J Biomed Sci 2006; 63(3): 109-112.
131. Hazhir S. Asymptomatic bacteriuria in pregnant women. Urol J
2007; 4(1): 24-27.
132. Aseel M, Al-Meer F, Al-Kuwari, Ismail M. Prevalence and
predictors of asymptomatic bacteriuria among pregnant women attending
primary health care in Qatar. Middle East J Fam Med 2009; 7(4): 10-13.
133. [El-Sokkary M. Prevalence of Asymptomatic Bacteriuria in
Antenatal Women with Preterm Labor at an Egyptian Tertiary Center.
Journal of American Science 2011;7(4):605-610]. (ISSN: 1545-1003).
134. Hazhir S. Asymptomatic bacteriuria in pregnant women. Urol J
2007; 4(1): 24-27.
135. Al-Haddad AM. Urinary tract infection among pregnant women in
Al-Mukalla district, Yemen. East Mediterr Health J 2005; 11(3): 505-
510.
136. Abdullah AA, Al-Moslih MI. Prevalence of asymptomatic
bacteruria in pregnant women in Sharjah, United Arab Emirates. East
Mediterr Health J. 2005; 11(5-6): 1045-1052.
137. Moghadas AJ, Irajian G. Asymptomatic urinary tract infection in
pregnant women. Iran J Pathol 2009; 4(3): 105-108.
138. Khatun AK, Rashid H, Chowdhury TA. Prevalence of urinary tract
infection in pregnancy. J Bangladesh Coll Phys Surg. 1985;2:6-10

68
139. Keah SH, Wee EC., Chng KS, Keah KC Antimicrobial
susceptibility of community-acquired uropathogens in general practice
Malaysian Family Physician 2007; Volume 2, Number 2 64-69
140. Nerissa Isabel C. Season, M.D.,Felice D.Garingalao-Molina,MD.,
Carla Elena J. Ycasiano, M.D., Mediadora C. Saniel, M.D., and Ricardo
M. Manalastas, M.D. Prevalence of asymptomatic bacteriuria and
associated risk factors in pregnant women. Phil J Microbiol Infect Dis
2003;32(2):63-69
141. Gebre Selassie S. Asymptomatic bacteriuria in pregnancy:
Epidemiological, clinical and microbiological approach. Ehiop Med J
1998 Jul; 36(3):185-92
142. Joseph KS, Brahmadathan KN, Abraham S, Joseph A.Detecting
bacteriuria ia a primary maternal and child health care program. Bri Med
J. 1988; 296: 906-7.
143. Roony C. Antenatal care and maternal health: How effective is it?
Maternal Health and Safe Motherhood Programme, Division of Family
Health, World Health Organization, 1992.
144. Kass EH. Hormones and host resistance to infection. Bacteriol Rev
1960;24:177 85.
145. Apitz K. A study of the generalized Shwartzman reaction
phenomenon. J Immunol 1935;29:255- 66.
146. Zahl PA, Bjerknes C. Induction of deciduaplacental hemorrhage in
mice by endotoxins of certain gram-negative bacteria. Proc Soc Exp Biol
Med 1943;54:329-32.

69
11. INFORMED CONSENT FORM

Subject identification number for this trial __________________________________

Title of the Project: Prevalence of asymptomatic bacteriuria in preterm labour: A


case-control study

Name of the Principal Investigator: R. K. Vidhyalakshmi Tel. No: 9633986153

I have received the information sheet on the above study and have read and / or

understood the written information.

I have been given the chance to discuss the study and ask questions.

I consent to take part in the study and I am aware that my participation is

voluntary.

I understand that I may withdraw at any time without this affecting my future care.

I understand that the information collected about me from my participation in this

research and sections of any of my medical notes may be looked at by responsible

persons (ethics committee members / regulatory authorities). I give access to these

individuals to have access to my records.

I understand I will receive a copy of the patient information sheet and the informed

consent form.

___________________________ __________________

Signature / Thumb Impression of subject Date of signature

______________________________

Printed name of the subject in capitals

___________________________ __________________

70
Signature / Thumb Impression of legally Date of signature

accepted representative

<<The legally acceptable representative signature should be added if the subject is a

minor or is unable to sign for themselves. The relationship between the subject and

the legally acceptable representative should be stated. The impartial witness signature
should be added if the subject / legally acceptable representative is unable

to read or write and consent should be obtained in his presence.>>

_______________________________________________

Printed name of legally acceptable representative in capitals

______________________________________________________

Relationship of legally accepted representative to subject in capitals

_______________________________________ __________________

Signature of the person conducting the Date of Signature

informed consent discussion

_________________________________________

Printed name of the person conducting the

Informed consent discussion in capitals

________________________________________ __________________

Signature of impartial witness Date of signature

________________________________________

Printed name of the impartial witness in capitals

71
12. STUDY PROFORMA

NAME: AGE: HOS NO:

ADDRESS: SES: PHONE NO:

SYMPTOMS: Abd pain leaking bleeding pv decreased fm


Urinary symptoms- present absent

PAST MEDICAL AND SURGICAL HISTORY:

MENSTRUAL HISTORY: Cycle-

MARITAL HISTORY: Married- Contraception- Sexual


acticity-

OBS/H: Antenatal: LMP- EDC-

Intrapartum- Mode of delivery- Postpartum-

FAMILY HISTORY:

PERSONAL HISTORY: Addictions Sleep Appetite Bowel & bladder

GENERAL EXAMINATION: Built- Nutrition-

Temp Pulse BP CVS RS CNS


Abd-

INV: Urine R/E- M/E- Hb-

Urine C/S- Usg A/N-

INCLUSION CRITERIA: Primi Multi Singleton PoG

MATERNAL OUTCOME: Term Preterm

FETAL OUTCOME:

72
13. ABBREVIATIONS
ASB- Asymptomatic bacteriuria
PTL- Preterm Labour
PPROM- Preterm premature rupture of membrane
LMP- Last menstrual period
EDC- Expected date of confinement
OBS/H- Obstetric history
Urine R/E- urine routine examination
Urine M/E- Urine microscopic examination
Urine C/S- Urine culture and sensitivity
Hb- Hemoglobin
BP- Blood pressure
CVS- Cardiovascular system
USG- ultrasonogram
PoG- Period of gestation
CNS- Central nervous system
Abd- Abdomen
Primi- Primigravida
Multi- Multigravida
E.coli- Escherichia coli
IUGR- Intra Uterine Growth Restriction
Nitrofur- Nitrofurantoin
NICU-Neonatal Intensive Care Unit
AFI- Amniotic Fluid Index
RPC- Retro Placental Clot
SGA- Small for Gestational Age
RBC- Red Blood Cells
WBC- White Blood Cells
NS- Nothing significant
PTVD- Pre Term Vaginal Delivery
FTND- Full Term Normal Delivery
FT vacuum D- Full Term vacuum Delivery
PT LSCS- Preterm Lower Segment Caesarean section
FT LSCS- Full Term Lower Segment Caesarean Section
ANC- Ante Natal Checkup
Wks- Weeks
GFR- Glomerular Filtration Rate
PCOS- Poly Cystic Ovarian Syndrome
APH Ante Partum Haemorrhage
CIDP- Chronic Inflammatory Demyelinating Polyneuropathy
GDM Gestational Diabetes Mellitus
ITP- Idiopthic Thrombocytopenic Purpura
Hep- A + Hepatitis A positive

73
14. MASTER CHART
CASES

SL Name Age Diagnosis PPROM Comorbidities O/H H/O Delivery


No PTL GA
1 Vincy 1 26 PTL NO B/L PCOS Primi No 36 PTVD
wks
2 Sanitha 1 31 PTL NO NS G3P2L2 No 32 PTVD
wks
3 Sheharban 1 20 PTL and NO Hep-A +, Primi No 33 PTVD
Jaundice Dengue Ig M +, wks
LFT-Abn
4 Savitha 1 20 PTL NO NS Primi No 29 PTVD
wks
5 Nithya 1 27 PTL NO B/L PCOS Primi No 36 PTVD
wks
6 Faseela 1 19 PTL NO NS Primi No 36wks Emer PT
LSCS
Ind-Fetal
Brady
7 Ramya 1 27 PTL NO NS G2A1 No 31wks PTVD

8 Niviya 1 24 PTL NO NS G2P1L1 Yes 33wks PTVD

9 Chandrika 1 22 PTL + YES NS Primi No 34wks PTVD


PPROM
10 Swathi 1 22 PTL NO NS Primi No 29 FTND
wks
11 Radhika 1 32 PTL NO APH G2P1L1 No 34 PTVD
wks
12 Sajitha 1 21 PTL + YES NS Primi No 33 PTVD
PPROM wks
13 Steffy 1 19 PTL NO NS Primi No 36 FTND
wks
14 Jessy 1 24 PTL NO IUGR Primi No 34 PTVD
wks
15 Kripa 1 23 PTL NO Irregular Primi No 34 PTVD
mensus wks
16 Lakshmi 1 22 PTL + YES NS Primi No 35 PTVD
PPROM wks
17 Renjini 1 21 PTL NO PCOS Primi No 29 PTVD
wks
18 Santha 1 32 PTL NO NS G2P1L1 Yes 35 PTVD
wks

74
19 Masitha 1 28 PTL NO NS Primi No 32 PTVD
wks
20 Diviya 1 22 PTL + YES PCOS Primi No 28 PTVD
PPROM wks
21 Jincy 1 21 PTL NO NS G2P1L1 No 32 FTND
wks
22 Rishmy 1 19 PTL + YES CIDP Primi No 35 PTVD
PPROM wks
23 Anitha 1 28 PTL NO NS Primi No 28 PTVD
wks
24 Rahila 1 22 PTL NO Treated for Primi No 31 PTVD
infertility wks
25 Muhasina 1 26 PTL NO NS G2E1 No 30 PTVD
wks
26 Sindhu 1 27 PTL + YES NS Primi No 30 PTVD
PPROM wks
27 Sakeela 1 25 PTL + YES NS Primi No 33 PTVD
PPROM wks
28 Nithya 1 18 PTL NO NS Primi No 30 PTVD
wks
29 Mubeena 1 25 PTL + NO Abruptio Primi No 33 PTVD
Bleeding wks
30 Jacklin 1 28 PTL NO GDM on diet G3P2L1 No 30 PTVD
Breech wks
31 Resmina 1 22 PTL NO NS Primi No 35 PTVD
wks
32 Aswathy 1 29 PTL NO ITP G2A1 No 35 PTVD
wks
33 Lisha 1 25 PTL + YES NS Primi No 34 PTVD
PPROM wks
34 Jinu 1 31 PTL NO NS Primi No 35 PTVD
wks

35 Nisha 1 28 PTL + YES Hypothyroidism Primi No 34 PTVD


PPROM wks
36 Sibitha 1 19 PTL NO NS G2P1L1 No 34 FTND
wks
37 Sruthy 1 21 PTL NO NS Primi No 28 PTVD
wks
38 Sajini 1 30 PTL + YES PCOS, Primi No 32 PTVD
PPROM Ovulation wks
induction /IUI
39 Rekha 1 32 PTL + YES Bicornuate G2P1Lo Yes 32 PTVD
PPROM uterus, wks
Cerclage done
40 Fousiya 1 23 PTL NO PCOS, Treated Primi No 29 PTVD
for infertility wks

75
41 Amina 1 29 PTL + YES Severe G3P2L1 No 34 Emer PT
PPROM Preeclampsia wks LSCS
Ind-Prev
LSCS in
labor
42 Sofiya 1 22 PTL NO NS Primi No 29 PTVD
wks
43 Meenu 1 28 PTL NO PCOS, Treated Primi No 34 Em PT LS
for infertility wks Ind-
Distress
44 Simja 1 21 PTL NO NS Primi No 33 FTND
wks
45 Shibina 1 33 PTL NO NS G3P2L2 No 35 PTVD
wks
46 Vimala 1 29 PTL + YES Anemia Primi No 35 Em PT LS
PPROM wks Ind- MSL
47 Sowmya 1 27 PTL + YES NS G2P1L1 No 34 PTVD
PPROM wks

48 Shaiji 1 22 PTL NO NS G2P1L1 No 34 PTVD


wks
49 Madhu 1 27 PTL + YES NS G2P1L1 No 32 PTVD
PPROM wks
50 Neenu 1 32 PTL NO NS G2P1L1 Yes 31 PTVD
wks

CASES CONTD
Urine Urine UrineC/S Organism USG Tocolysis T/PT Wt in Apgar 1 NICU
R//E M/E Hb A/N KG min admn
NS Bacteria ASB E Coli 9 gms NS Failed PT 2.92 9/10 No
+
NS PC 2-4, No No 11 Low Failed PT 1.35 7/10 No
EC+, Bac growth growth gms lying
+ placenta
NS WBC-10 No No 8 gms NS Not PT 1.8 9/10 Yes
growth growth tried

NS NS No No 12gms NS Failed Term 3.7 9/10 No


growth growth
NS RBC 1-3 No No 10 NS Failed PT 2.9 9/10 No
growth growth gms
20-30 PC RBC 28, ASB E Coli 9gms low Failed PT 2.3 9/10 No
WBC 53, lying
SqC 39, placenta
B+
NS RBC 3, No No 13gms SGA Failed PT 1.3 7/10 Yes
WBC 12, growth growth
Bact +

76
10-30 PC RBC 1, Mixed Mixed 9 gms RPC Failed PT 2 8/10 Yes
Bact + growth growth
NS NS No No 11 NS Not PT 1.9 9/10 Yes
growth growth gms tried
2-4 PC NS No No 10gms NS Success Term 2.8 9/10 No
growth growth
NS NS No No 11 NS Failed PT 2.3 9/10 No
growth growth gms
NS NS No No 10 NS Not PT 2.1 9/10 No
growth growth gms tried
10-30 PC Bact + Mixed Mixed 11 NS Success Term 3.2 9/10 No
growth growtth gms
36 PC Bact + ASB E Coli 9 gms IUGR Failed PT 2.2 9/10 Yes
10-30 PC WBC- 51 ASB E Coli 12 NS Failed PT 2.3 9/10 No
gms
NS Ns No No 11 NS Not PT 2.3 9/10 No
growth growth gms tried
12-30 PC Bact + Mixed Mixed 12 IUGR Failed PT 1.74 8/10 No
EC 3 growth growth gms
12 PC NS No No 9 gms NS Failed PT 2 7/10 No
growth growth
1-5 PC Bact + ASB E Coli 9 gms IUGR Failed PT 1.75 7/10 No
1-2 PC NS No No 12 NS Not PT 0.96 5/10 Dead
growth growth gms tried
12 PC Bact + Mixed Mixed 10 NS Success Term 3.2 9/10 No
growth growth gms
NS NS No No 10 NS Not PT 2.8 9/10 No
growth growth gms tried
25 PC 2-3 Wbc-75 Mixed Mixed 9 gms Breech Not PT 0.75 5/10 Dead
EC growth growth tried
2-3 PC WBC 5- No No 11 NS Failed PT 2.1 9/10 No
10 growth growth gms
20-25 PC WBC 30 ASB E Coli 9 gms IUGR Failed PT 1.39 8/10 Yes
Bact +
1-2 PC NS No No 11 Ns Not PT 1.8 8/10 No
growth growth gms tried
NS NS No No 9 gms NS Not PT 2 9/10 No
growth growth tried
7-10 PC Bact + ASB E Coli 9 gms NS Failed PT 1.4 7/10 No
30 PC Bact ASB Klebsiella 7 gms RPC Failed PT 1.2 0/10 Dead
++++
WBC 75
NS NS No No 10 NS Failed PT 1.5 9/10 No
growth growth gms
NS NS No No 10 NS Failed PT 2 9/10 No
growth growth gms

77
5 PC 10 WBC No No 9 gms NS Failed PT 2 9/10 No
growth growth
NS NS No No 10 NS Not PT 2.1 9/10 No
growth growth gms tried
10-15 PC RBC 28, ASB E Coli 9 gms NS Failed PT 1.8 9/10 No
WBC 53,
SqC 39,
B+
5-10 PC RBC 25 No No 10 NS Not PT 2.1 9/10 No
growth growth gms tried
NS NS No No 11 NS Success Term 3.2 9/10 No
growth growth gms
NS NS No No 10 NS Failed PT 0.88 0/10 Dead
growth growth gms
NS Bact+ No No 9 gms NS Not PT 1.6 7/10 Yes
growth growth tried

NS Bact + No No 11 NS Failed PT 1.9 9/10 No


growth growth gms

25 PC 2-3 RBC 23 ASB E Coli 10 NS Failed PT 1.2 9/10 No


EC Bact+ gms
NS NS No No 12 NS Not PT 2.3 9/10 No
growth growth gms tried

NS NS No No 11 NS Failed PT 0.75 5/10 Dead


growth growth gms
8-10 PC Bact 4 + Mixed Mixed 9 gms NS Failed PT 2.3 9/10 No
growth growth
NS NS No No 12 NS Success Term 3.5 9/10 No
growth growth gms
30 PC 5 Bact + ASB E Coli 9 gms IUGR Failed PT 2.1 9/10 No
EC RBC76
23 PC Bact + Mixed Mixed 9 gms NS Not PT 2.5 9/10 No
growth growth tried
NS NS No No 11 Low Not PT 2.5 9/10 No
growth growth gms lying tried
placenta
NS NS No No 11 NS Failed PT 2.1 9/10 No
growth growth gms
40-45 PC Bact + No No 10 NS Not PT 2.1 9/10 No
growth growth gms tried
25 PC 2-3 Bact+ No No 9 gms NS Failed PT 1.5 9/10 No
EC growth growth
NS NS No No 11 NS T 3.3 9/10
growth growth gms

78
CONTROLS

1 Raghi 2 23 ANC NS G2P1L1 No 40 FTND


wks
2 Niji 2 30 ANC NS G3P2L2 Yes 40 FTND
wks
3 Prema 2 35 ANC NS G2P1L1 Yes 38 FTVD
wks
4 Sangeetha 2 26 ANC NS Primi No 39 Em FT
wks LSCS.
Ind-CPD
5 Riya 2 21 ANC NS Primi No 38 Em FT
wks LSCS.
Ind-CPD
6 Athira 2 24 ANC- NS G3P1L1 No 39 FTND
spotting wks
PV
7 Ancy Lijoy 2 26 ANC NS G3P2L2 No 38 FTND
wks
8 Sanila 2 30 ANC NS G2P1L1 No 40 FTVD
wks
9 Babitha 2 32 ANC Hypothyroid G3P2L2 No 39 Elective
PCOS wks LSCS
10 Sona 2 24 ANC NS G2P1L1 No 39 FTND
wks
11 Ummu 2 21 ANC- NS Primi No 40 FTND
spotting wks
PV
12 Swetha 2 27 ANC Hypothyroid G2P1L1 No 39 FTVD
wks
13 Jini 2 25 ANC NS G2A1 No 39 FTVD
wks
14 Varsha 2 22 ANC NS Primi No 40 FTVD
wks
15 Hafsath 2 29 ANC NS Primi No 38 FTND
wks
16 Safana 2 32 ANC NS Primi No 38 FTVD
wks
17 Lasitha 2 31 ANC Treated for G2A1 No 38 FTVD
infertility wks
18 Reka 2 29 ANC NS Primi No 38 Em FT
wks LSCS.
Ind- CPD
19 Vanitha 2 26 ANC NS G2P1L1 Yes 38 FTVD
wks
20 Varsha 2 2 23 ANC NS Primi No 39 FTND
wks

79
21 Vani 2 25 ANC NS G2P1L1, No 38 FTVD
Prev FTVD wks

22 Glitty 2 28 ANC NS Primi No 38 FTND


wks
23 Sangeetha 2 30 ANC NS G3P2L2 No 38 FTVD
wks
24 dinisha 2 31 ANC NS G3P1Lo Yes 38 FTVD
wks
25 Sharmila 2 22 ANC NS Primi No 39 FTND
wks
26 Jamsheena 2 25 ANC NS G2P1L1 No 38 FTVD
wks
27 Ambika 2 26 ANC NS Primi No 38 FTND
wks
28 Sheethal 2 28 ANC NS G3P2L2 No 39 FTVD
wks
29 Amrutha 2 22 ANC NS Primi No 39 FTND
wks
30 Divya 2 21 ANC NS G3A1P1Lo No 38 FTVD
wks
31 Raseena 2 20 ANC NS Primi No 40 FTND
wks
32 Akhila 2 20 ANC NS G2P1L1 No 38 FTVD
wks
33 Saleena 2 32 ANC NS Primi No 40 FTND
wks
34 Shilna 2 25 ANC NS G3P1L1 No 39 FTND
wks
35 Akshaya 2 24 ANC NS G3P2L2 No 38 FTVD
wks
36 Nahiya 2 26 ANC NS G2P1L1 No 38 FTVD
wks
37 Nasriya 2 29 ANC NS G3P2L2 No 38 Elective
wks LSCS
38 Riya 2 31 ANC NS G2P1L1 No 40 FTND
wks
39 Ramsiya 2 22 ANC NS Primi No 38 FTND
wks
40 Saranya 2 21 ANC NS G2P1L1 No 38 FTVD
wks
41 Tilma 2 21 ANC NS G2A1 No 40 FTND
wks
42 Jumaila 2 19 ANC NS Primi No 40 FT
wks vacuum
D
43 Viji 2 27 ANC NS G2P1L1 Yes 38 FTVD
wks

80
44 Jiji 2 22 ANC NS G3P2L2 Yes 39 FTND
wks
45 Kavitha 2 28 ANC NS G2P1L1 No 38 FTND
wks
46 Bushara 2 32 ANC NS Primi No 39 Em FT
wks LSCS.
Ind-CPD
47 Shahana 2 32 ANC NS Primi No 38 Em FT
wks LSCS.
Ind-CPD
48 Anju 2 26 ANC NS G3P1L1 No 38 FTND

49 Zeenath 2 30 ANC NS Primi No 39 FTND


wks
50 Manisha 2 24 ANC NS G3P2L2 Yes 39 FTVD
wks
CONTROLS CONTD
NS NS No No growth 11 NS T 3.3 9/10
growth gms
NS Bac 2+, No No growth 11 NS T 2.7 9/10
EC growth gms
74/HPF
NS NS No No growth 12 NS T 2.5 9/10
growth gms
NS WBC 15- No No growth 13 NS T 3.41 9/10
20/HPF growth gms
10-15 PC Bact + Mixed Mixed 12 NS T 3.6 9/10
growth growth gms
2-3 PC Bact 4+ No No growth 11 NS T 3.1 9/10
wbc-1 growth gms

1-2PC Bact 3+ No No growth 9 NS T 2.8 8/10


1-2 EC growth gms
10-15 PC WBC-75 No No growth 12 NS T 2.9 8/10
Bact + growth gms
NS NS No No growth 11 NS T 3.2 9/10
growth gms
NS NS No No growth 10 g NS T 3.4 9/10
growth
NS RBC 2-3 No No growth 10 NS T 2.8 9/10
growth gms

10-15 PC WBC 15- No No growth 8 NS T 3.1 7/10


20/HPF growth gms
NS NS No No growth 10 NS T 3.2 9/10
growth gms
2-5 PC Bact + No No growth 11 NS T 3.6 9/10
growth gms

81
1-3 PC 1- NS No No growth 9 AFI-5 T 3.2 9/10
3EC growth gms cm
NS NS No No growth 11 NS T 2.5 7/10
growth gms
NS NS No No growth 9 NS T 3.5 9/10
growth gms
15 PC 5 EC WBC 54 Mixed Mixed 9 NS T 2.8 9/10
RBC 32 growth growth gms
NS NS No No growth 10 NS T 2.8 9/10
growth gms
NS NS No No growth 11 NS T 3.4 8/10
growth gms
2-3 PC Bact+ Mixed Mixed 9 NS T 2.9 9/10
growth growth gms

NS NS No No growth 10 NS T 3 9/10
growth gms
10-15 PC NS No No growth 9 NS T 2.2 9/10
growth gms
35 PC 15 Bact 4+ No No growth 10 NS T 2.8 9/10
EC wbc-1 growth gms
NS NS No No growth 11 NS T 3.4 9/10
growth gms
2-3 PC Bact+ Mixed Mixed 9 NS T 2.9 8/10
growth growth gms
NS NS No No growth 10 NS T 3 9/10
growth gms
10-15 PC Bact + No No growth 9 NS T 2.5 9/10
growth gms
NS NS No No growth 11 NS T 3.4 7/10
growth gms
35 PC 15 Bact 4+ No No growth 10 NS T 2.8 9/10
EC wbc-1 growth gms
NS NS No No growth 11 NS T 3.4 9/10
growth gms
2-3 PC Bact+ Mixed Mixed 9 NS T 2.9 9/10
growth growth gms
NS NS No No growth 10 NS T 3 7/10
growth gms
2-3 PC Bact 4+ No No growth 11 NS 3.4 9/10
wbc-1 growth gms
1-2PC Bact 3+ No No growth 9 NS T 2.8 9/10
1-2 EC growth gms
10-15 PC WBC-75 No No growth 12 NS T 2.9 9/10
Bact + growth gms
NS NS No No growth 11 NS T 3.2 8/10
growth gms
NS NS No No growth 10 NS T 3.4 6/10
growth gms

82
NS RBC 2-3 No No growth 10 NS T 3.8 9/10
growth gms
10-15 PC WBC 15- No No growth 8 NS T 2.6 9/10
20/HPF growth gms
NS NS No No growth 10 NS T 3.5 9/10
growth gms
2-5 PC Bact + No No growth 11 NS T 3.6 9/10
growth gms
NS NS No No growth 11 NS T 2.4 8/10
growth gms
NS Bac 2+, No No growth 11 NS T 3.1 9/10
EC growth gms
74/HPF
NS NS No No growth 12 AFI-7 T 2.6 9/10
growth gms cm
NS WBC 15- No No growth 13 NS T 3.41 7/10
20/HPF growth gms
10-15 PC Bact + Mixed Mixed 12 NS T 3.6 9/10
growth gms
2-3 PC Bact 4+ No No growth 11 NS T 3.2 9/10
wbc-1 growth gms
NS NS No No growth 10 NS T 3 9/10
growth gms
10-15 PC Bact + No No growth 9 NS T 2.6 8/10
growth gms

83
84