INTRODUCTION

Many pelvic infection are caused by  bacteria present in the cervical and vaginal epithelium¹. Invasions of membranes near the cervical os by bacteria appear to be a common event particularly in the late gestation. This often results in local chorioamnionitis². When the bacteria spread to the amniotic cavity and grow in the amniotic fluid, the fetus often aspirates the infected fluid, which commonly leads to congenital pneumonia and the initiation of the labour^2-5.Human normal term labour is thought to be initiated by the chorionic phospholipase. A2, an enzyme that liberates arachidonic acid esters from the phopholipids of these membranes leading to synthesis of prostaglandin by the placental membranes⁶-¹⁰. 

The most common bacteria found in the cervix and vagina, with the exception of G.vaginalis, are Bacteroides fragilis, Peptostreptococcus, Fusobacterium, S.viridans. They have the highest phospholipase A2 activity, on the other hand Lactobacillus, Peptococcus, M.homines and Staph.epidermis, Strep.faecalis, Beta hemolytic streptococcus A & B, E.Coli, Klebsiella sp and Pneumococcus have low specific activities^{8, 11,12.} The specific activities from these organisms are several times higher than that of the membrane phospholipase A2 of the amnion and chorion^8-9.  If these organisms infect the endocervix the proteolytic enzyes may penetrate the chorion and amnion and thus initiate labour⁸. It is therefore, postulated that premature labour may be initiated by these organism and cause preterm deliveries and low birth weights.

Since vaginal infection are known to cause premature rupture of membranes preterm labour and delivery low birth weight and also other serious complications ^13-16  ,it is important that recognition of infections be achieved at an early stage so that proper treatment measures may be adopted.

PATIENTS AND METHODS

The study was conducted over a period of one year. Pregnant women at the time of labour and delivery were selected by convenient sampling from JPMC, irrespective of age, parity, excluding diabetic patients, those taking antibiotics during last 14 days and patients with any obstetric complications. At the time of registration a questionnaire was filled with complete present and past obstetrics history and physical examination of the patients. Birth weight of the new born was taken immediately after birth.

From each patient three high vaginal swabs were collected during labour and transferred to Stuart transport media. From set-I, Trichomonas vaginatis were studied from wet smear by direct microscopic examinations. Set-II of swabs for dry smear were stained by Gram’s method for bacteria, yeast and clue cells stained (for Gardeneralla.vaginalis). Set-III of swabs were cultured at 37⁰ C for 24-48 hours into blood agar, Islam's agar, chocolate agar and Islam's, chocolate agar, MacConkey's agar and Sabauroud's dextrose agar plates. Blood agar were incubated under aerobic and anaerobic conditions and chocolate agar under carbondioxide.

Colonies isolated were identified by colony morphology, Grams staining, biochemical tests and other specific confirmatory tests¹⁷ and isolates were further tested against antibiotic sensitivity for Penicillin, Ampicillin, Erythromycin, Septran, Fosformycin, Metronidazole, Velosef, Tetracycline, Augmentin, Tarivid, Cefotaxine and Nebcin.

Data was analysed using SPSS version 8 and effect of vaginal infection on initiative of labour and birth weight was determined, using Fisher exact test for significance between infected and non infected mothers.

RESULTS

During a period of one year 149 mothers and their new borns were studied from the Department of OB/GYN, of JPMC. Their age in years was 25± 5.5 (Mean ± SD) range 17-45 yrs. Primi paras  were 63, those with parity 1 to 2 were 55 and in rest (31) parity ranged from 3 to 8.

Among 149 mothers infection was present in 144 (96.6%). Main isolates were Trichomonas vaginalis among bacteria staph.aureus E.Coli, Gardenella vaginalis and in yeast candida Albicans and Candida species. Bacteria were isolated in 144 (96.6%), yeasts that is candida albicans and candida species in 10 (6.7%) and 26 (17.4%) respectively and Trichomonas vaginitis in 13 (8.7%) as seen in (Table-1).

Among study population (149 mothers) the frequency of low birth weight was 32.2% ( Table-2). Considering only infected mothers the proportion of low birth was more 36% (Table-3). In infected mothers Pre-term delivery was higher (65%) as compared to non-infected mothers (Table-4). Single infection was present in 121 of 144 infected mothers (84%) and multiple infection in 23(16%). Pre-term delivery was more common among mothers with multiple infection (78%) as compared to those with single infection (63% Table-5).  

Table I: Ecting organisms 

Table-2 Birth weight of neonates

Table-3 Infection and Birth Weight 

KEY: NS = Not Significant

Birth weight different between infected & non infected were not significant

Using Chi- square & Fisher exact test were used for comparison

Table-4 Infection and Pre-term delivery 

KEY: NS = Not Significant

Table-5 Multiple Infection and Pre-term Delivery

KEY: NS = Not Significant

DISCUSSION

Vaginal infection as seen in this study and also reported earlier ¹⁸ have an important bearing on fetal outcome. It may lead to premature rupture of membranes, premature delivery with its complication^20-23 low birth weights associated with intrauterine infection chorioamnionitis, urinary tract infection and early neonatal sepsis ^3-6.  Among the study population proportion of infected mother was high 98.7%(Table-1) which may be the cause of relatively high frequency of low birth weight neonates among them (Table-2), when compared to that reported among normal pregnancies ¹⁹ preterm delivery was more frequent among infected mothers when compared to non infected mothers (Table-4).The neonates born were low birth weight (£ 2.5 Kg), among infected mothers even if the pregnancy was continued to full term, Pregnancies associated with multiple infection resulted in higher proportion of preterm delivery (78%) as compared to those with single infection (Table-5). These differences were not statistically significant probably because the number of cases in each group was small.

CONCLUSION & RECOMMENDATION

This study shows a high vaginal infection in the local population 98.7% (Table-1). This necessitates proper detection and management of these infections during pregnancy. Proper control of vaginal infection will help reduce both maternal and neonatal mortality and morbidity especially low birth weight. Reduction in low birth weight neonates will lead to proper child development.

ACKNOWLEDGEMENT

The authors are highly gratefull to Syeed Ejaz Alam Senior statistical officer of PMRC Research centre at JPMC Karachi for statistical analysis.

REFERENCESS

Naeye, R. Causes and consequences of chorioamnionitis. N Engl J Med 1975; 293: 40.

Neaye R, Dellinger W, Blanca W. Fetal and neonatal features of antenatal bacterial infections. J.Pediatr 1971; 29: 733.

Shurin PA, Alpert S, Rosner B. Chorioamnionitis and colonization of the new born with genital mcoplasma.  N Engl J Med 1975; 293-5.

Naeye RL, Blanc W A. Relation of poverty and race to antenatal infection. N Engl J Med 1970; 283:555.

Beuirshe K. Routes and types of infection in the fetus and the newborn. Am J Dis Child 1960; 99:741.

Schultz F M, Schwarz B E, MacDonald P C. Initation of human partarerion II, identification of Pospholipase A2 in fetal chorioamnion and uterine deciduas. Am J Obstet  Gynecol 1995; 123: 650.

Schwarz B E, Shultz F M, MacDonald PC. Initiation of human parturition II, fetal membrane content of prostaglandin E2 and F2x precursors. Obstet Gynecol 1975; 46:546.

Schwarz B E, Shultz F M, Macdonald P C. Initiation of human parturition, Iv Demonstration of phospholipase A2 in the lysozymes of human fetal membranes. Am J Obstet Gynecol 1976; 125:1089.

Okazake T, Okita J, Macdonald PC. Initiation of human parturition, X, Substrate specificity of phospholipase A2 in the human fetal membranes. Am J Obstet Gynecol 1948; 130:432.

Greivy S., Liggins, G., Phospholipase A2 activity in human and ovine uterine tissue. Prostaglandins 1976; 12:229.

Goplerud, G., Ohm, M. Galask, R., Aerobic and anaerobic flora of the cervix during pregnancy and puerperium. Am J Obstet Gynecol 1976; 126:858.

Bejar R, Curbelo V, Davis C, Gluck L. Premature labour-II, Bacterial sources of phospholipase. Obstet Gynecol 1981; 57:459.

Hassan TJ, Baqai R, Alam SE. Maternal morbidity in the Department of Obstetric & Gynaecology. J Pakistan Med Assoc 1991; 41:223.

Bobitt JR, Ledger WJ. Amniotic fluid analysis. Its role in maternal neonatal infection. Obstet Gynecol 1978; 51(1): 56-62.

Bobitt JR, Ledger WJ. Unrecognized amnionitis and prematurity: a preliminary report. J Reprod Med 1977; 19(1): 8-12.

Naeye R, Peter E. Amniotic fluid infections with intact membrane, leading to prenatal death: A prospective study. Paediatrics 1978; 61:171.

Bailey W R, Baron EJ, Peterson LR, Fingold SM, eds. Bailey and Scott's diagnostic microbiology. St.Louis: Mosby, 1994; 355-421, 753.

Kirmani N, Hafiz S, Jafarey SN. Frequency of chlamydia, trachomatis in pregnant women. J Pakistan Med Assoc 1994; 44:73-4.

Hassan TJ, Ibrahim K, Haque M. Maternal factors affecting birth weight of uncomplicated pregnancy. J Pakistan Med Assoc 1991,41:164.

Gomella TC. Neonatology. 4^th edition. New Jersey: Appleton and Lange. 1999,503.

Tariq P, Kundi Z. Determinants of neonatal mortality. J Pakistan Med Assoc 1999; 49:56-60

O’Connor AR, Stephenson  T, Johonson A, Tobion MJ, Ratib S. Long term opthalinic outcome of low birth weight with and without retinopathy of prematurity. Pediatrics 2002;109 (1): 12-8.

Pal DK, Manadhar DS, Raj BandariS, Land JM, Patel N, De-L Costello AM . Neonatal hypoglycemia in Nepal prevalence and risk factor. Arch Dis Child Fetal Neonatal ED 2000; 82 (1): 46-51.