Nasreen Kirmani  ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )

Group B Streptococci (Strept agalactiae) are the etiologic agents of bovine mastitis, and until recently were not believed to cause serious human diseases. However it has been established that Group B Streptococci (GBS) are present in the vaginal flora of approximately 25% women and have also been frequently isolated from rectal swabs and less frequently from throat and male urethra¹. Colonies on sheep blood agar typically produce small zones of beta hemolysis. They are usually bacitrecin sensitive and give a positive response to CAMP test².
Lancofield Group B Streptococci cause skin infections, endocarditis, puerperal infections, neonatal septicemia and meningitis. Wound infections are most common in patients with diabetes mellitus and peripheral vascular disease. GBS are currently the commonest pathogen causing serious neonatal infections.³ These orga­nisms have special importance in female genital tract. They were present in 5 — 35% of cultures obtained from asymptomatic pregnant women⁴ and 2 — 14% of women with endometritis⁵.
Pasteur first observed those organisms in patients with puerperal fever and other investi­gators later reognized them as the commonest genital isolate in women with endocarditis⁶. The rate of harbouring this organism ranges from 4.6 — 9%^7,8. In addition GBS commonly cause intrapartum infection (chorio-amnionitis). Infec­tions with GBS also occur frequently in patients delivering preterm infants⁶.
Certain reports have emphasized the opportunistic nature of Group B Streptococcal infections with diseases like diabetes mellitus, immunosuppression and urinary tract infec­tions^7,9,10. The association between diabetes mellitus and Group B Streptococcal infection is well known^7,10 Patients with diabetes are at greater risk for colonization or infection by GBS than others without this disease 11. GBS. is also a potential pathogen of urinary tract during pre­gnancy. Group B Streptococcal isolates were identified from urine specimens of patients with asymptomatic bacteriuria, cyst itis, and pyelone­ phritis¹².
Lancofield Group B Streptococci is the most common gram’s positive bacterium causing neonatal meningitis and sepsis¹³. An increase in the incidence of neonatal Group B Streptococcal disease appeared in later 1950s and early 1960s¹⁴.
There are two ways in which neonatal Group B Streptococcal disease may present clinically 1 The early onset form of disease may either be bacterimic or meningitic and tends to affect premature and low birth weight infants, and is often associated with prolonged labour after rupture of membranes. Late onset form of disease affects otherwise healthy infants between 2 — 4 weeks of age and is largely meningitic¹⁴ .
Early onset Group B Streptococcal disease in the infants is acquired by vertical transmission from mothers colonized with GBS^15,16. The presen­tation of early onset disease is mainly that of respiratory distress and shock. Mortality rate varies from 50 — 90%. Approximately half of the survivors with meningitis will have neurologic sequelae. Attack rate of early onset disease vary from 1- per 1000 live births³. Serotype of GBS, isolated from infants with early onset disease are identical to those isolated from genital tract of their mothers¹⁶. Adults rarely get severe infections and meningitis’ due to GBS.
Majority of infants with late onset disease have meningitis and mortality rate is approxi­mately 20%. The route of infection of these infants is not clear; nosocomial acquisition of organisms is suggested¹⁸.
Antibiotic sensitivity pattern of GBS are generally similar to Group A Streptococci. Pene­cillin G is the drug of choice¹⁹. Majority of GBS strains are also sensitive to Erythromycin, Chlor­amphenicol, Cephalosporin,Lincomycin and Clin­damycin²⁰.
Ptevention of neonatal disease by prophy­lactic administration of penicillin or by immuni­zation is controversial²⁰. Seigel et al. showed that prophylaxis with benzl penicillin (which is highly sensitive against GBS, crosses the placenta and thus protects the fetus directly) given at birth reduced the incidence of both colonization and infection with GBS. It was also suggested that mass prophylaxis might lead to the emergence of neonatal disease resistant to penicillin² 1 Adminis­tration of penicillin during labour appears to be the most efficacious method of preventing neona­tal Group B Streptococcal Sepsis^21,22.
Yow et at achieved good results by using Ampidillin Sodium intravenously during labour arid delivery to women colonized with GBS. In­travenous administration is an effective method of preventing intrapartum transmission of GBS from mother to infant. Intravenous route is preferable to the oral route because of the rapid and reliable concentration of the drug in the serum, tissues and amniotic fluid. Treatment of colonized women by intravenous route at term is a suitable method of preventing GBS infections in neonates¹⁶.
Antibiotic therapy alone seems to be of only limited value in early onset disease. The infected baby may be deficient in compliment and phagocytic function, in other words it is an immunocompromised host. Overwhelming GBS bacterimia is often associated with neutropenia. The combination of chemotherapy and immuno­therapy (plasma and granulocyte transfusions ) has been used successfully in the management of some immunocompromised patients¹⁴.
The successful treatment of GBS diseases needs early diagnosis and effective therapy, and it is especially important to screen all the pre­gnant, especially diabetic pregnant, women for GBS bacterimia to minimize adverse maternal and neonatal consequences of infection.

1. Volk, WA., Benjamin, D.C., Kadner, R.J. and Parsons, J.T. Essential of medical microbiology. 3rd ed. Philadelphia, Lippencott,, 1982, p. 369.
2. Jawetz, E., Melnick, J.L., Adelberg, E.A. Review of medical microbiology. 17th ed., Norwalk, Appleton and Lange, 1987,p. 225.
3. Baker, C.J. Summary of Workshop on perinatal infections due to group B Streptococcus. J. Infect, Dis., 1977; 136:. 137452.
4. Gilstrap, L.C. and Cunningham, F.C. Ten bacterial pathogenesis of infection following cesarean section. Obstet. Gynecol., 1979; 53:545.
5. Gibbs, R.S., Jones, P.M. and Wilder, C.J. Anti­biotic therapy of endometritis following cesarean section. Obstet. Gynecol., 1979; 52:31.
6. Gibbs, R.S. and Blanco, J.D. Streptococcal infections in pregnancy. Am. J. Obstet. Gynecol., 1981; 140:405.
7. Eickhoff, T.C., Klein, J.O., Daly, A.K. , Ingall, D., & Finland, M. Neonatal sepsis and other in­fections due to Group B Beta hemolytic Strep­tococci. N. Engl.J.Med., 1964; 271: 1221-1228.
8. Franciosi, RA., Knostman, J.D., Zimmerman, R.A. Group B Streptococcal neonatal and infant infections. J. Pediatr., 1973; 82: 707.
9. Mhalu, F.S. Streptococcus agalactiae in urinary tract infections. Post Grad. Med. J., 1977; 53:216.
10. Duma, Ri., Weinberg, A.N., Medrek, T.F., and Kunz, Li. Streptococcal infections; a bacterio­logical and clinical study of Streptococcal bac­terimia. Medicine, 1969;48:87.
11. Wood, E.G., Dillon, H.C. Jr. The prospective study of Group B Streptococcal bacteriuria in pregnancy. Am. J. Obstet. Gynecol., 1981; 140: 515.
12. Mead, P.J., Harris, R.E. The incidence of Group B Beta haemolytic Streptococci in ante­partum urinary tract infections. Obstet. Gynecol., 1978;51: 412.
13. Baker, Ci., Barrett, F.F., Gordon, R.C. and Yow, MD. Suppurative meningitis due to Streptococci of Lancefield group B. A study of 33 infants.J.Pediatr., 1973; 82: 724.
14. Editorial: Neonatal infections with Group B Streptococci. Lancet, 1:181.
15. Baker, C.J., and Barrett, F.F. Transmission of group B Streptococci among paturient women and their neonates. J. Pediatr, 1973; 83: 919.
16. Yow, MD., Masson, E.O., Leads, Li., Thom­pson, P.K, Clark, D.J. and Gardonor, S.E. Ampicillin prevents intrapartum transmission of group B Streptococcus. JAMA., 1979; 241:1245  1247.
17. Lazarus, J.M., Sellers, DY., Marine, W.M. Mening­itis due to group B beta hemolytic Streptococcus. N. Engi. J. Med., 1965; 272: 146447.
18. Aber, R.C., Allen, N., Howell, J.T., Wilkenson, H.W., and Facklam, R.R. Nosocomial transmission of group B Streptococci. Pediatrics, 1976; 58: 346.
19. Bayer, A.S., Chiow, A.W., Anthony, BF., Guze, L.B. Serious infection in adults due to group B Streptococci; Clinical and serotypic characteri­zation. Am. J. Med., 1976; 61: 498.
20. Joklik, W.K., Willett, H.P. and Amos, D. B. Zunsser microbiology, 1984, 18th ed. Apple­ton-Century Crofts, 1984, p.472.
21. Seigel, J.D., McCraker, G.H., Threlkeld, N., Milvenan, B and Rosenfeld, C.R. Single dose penecillin prophylaxis against neonatal group B Streptococcal infections. A controlled trial in 18, 738 new born infants. N. Engl. J. Med., 1980; 303:769.
22. Pyati, S.P., Pildes, R.S., Jacobs, N.M., Rama­murthy, R,S., Yeh, TY., Raval, D.S., Lilllen, LD., Amma, P., and Melzger, WJ. Peneciffin in infants weighing two kilograms or less with early onset group B Streptococcal disease. N. Engl.J.Med., 1983; 308: 1383.