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Maternal carriage of group B streptococci in developing countries


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The Pediatric Infectious Disease Journal: June 1998 - Volume 17 - Issue 6 - p 499-503
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The global burden of neonatal disease caused by the group B streptococcus (GBS) is difficult to estimate because the importance of GBS varies around the world.1-4 Although GBS continues to be an important pathogen associated with neonatal sepsis in many developed countries,4-8 studies from developing countries suggest that GBS is a much less important cause of neonatal sepsis.1-4 In a review of 36 hospital-based studies of bacterial pathogens associated with neonatal sepsis in various geographic regions of the world, Stoll1 reported that the proportion of sepsis caused by GBS detected in hospitalized newborns ranged from 0 to 5% for India/Pakistan/Southeast Asia, 0 to 24% for North Africa/Middle East, 0 to 30% for Sub-Saharan Africa and 2 to 35% for the Americas/Caribbean. Gramnegative organisms were isolated more frequently than Gram-positive organisms in the majority of studies reviewed. Most studies made no distinction between early and late onset sepsis. In the United States important differences in colonization rates have been identified among women of different ethnic groups that appear to correlate with infection rates in newborns.5 In an attempt to understand the lower rates of invasive GBS disease among neonates in many developing countries, we reviewed 34 studies that evaluated GBS colonization rates in pregnant women.


Studies evaluated for this paper were identified by computer searches of the scientific literature published between 1980 and 1996. Electronic databases used included Medline Express, 1980 to 1996 (National Library of Medicine, National Institutes of Health) and Abstracts on Tropical Agriculture and Rural Development in the Tropics, 1975 to 1995 (Royal Tropical Institute, Amsterdam, the Netherlands). Additional references were found by reviewing the references cited in all relevant articles. Studies included in the review were performed in developing countries but were published in English, Chinese or French (all abstracts in English).

Specimen collection and laboratory methods were noted for each study. Methods were classified as adequate if specimen collection sites included the vagina and if samples were inoculated into selective broth media. Proportions were compared using the chi square test.


We reviewed the data on female genital colonization with GBS in 34 reports (Table 1).9-43 These studies present data on 7730 women from 23 countries. The majority of women cultured were pregnant. Only 7 of the studies presented data on nonpregnant women.9,20,21,28,32,38,43 Studies varied in the detail with which culture methods were presented, particularly regarding the use of selective media and the number of sites cultured. Among all studies colonization rates ranged from 0 to 31%, with only 7 of the 34 studies reporting rates of 20% or greater (Table 1).


Analysis of data from all studies (regardless of methods) showed the regional carriage rates as follows: India/Pakistan, 9% (97 of 1114); Asia/Pacific, 8% (143 of 1867); Sub-Saharan Africa, 18% (249 of 1400); Middle East/North Africa, 17% (298 of 1787); Americas, 12% (196 of 1562). The overall carriage rate estimated from these studies was 12.7% (average of all data). However, analysis of data from only those studies that used selective broth media and cultured the vagina (among other sites) showed regional rates of: India/Pakistan, 12% (86 of 727); Asia/Pacific, 19% (32 of 168); Sub-Saharan Africa, 19% (219 of 1144); Middle East/North Africa, 22% (251 of 1144); Americas, 14% (87 of 618). The estimated overall carriage rate for these studies was 17.8%. A comparison of studies that did and did not use selective broth media revealed that the GBS carriage rate was significantly increased by the use of selective media (675 of 3801, 17.8% vs. 308 of 3929, 7.8%; relative risk, 2.3; 95% confidence interval, 2.0 to 2.6; P < 0.001; Fig. 1).

Fig. 1
Fig. 1

Thirteen studies (from nine countries) presented the serotype distribution of GBS isolates (Table 2). Although relatively few isolates were studied, serotype distribution appeared to vary among studies. In 7 of 13 studies serotype III was the most frequently identified serotype. In the recent Gambian26 and Peruvian studies,43 which used appropriate culture and serotyping methods, serotype V, a relatively newly recognized invasive serotype, was reported for 38% and 18% of isolates, respectively.



It is unclear why invasive neonatal GBS disease is reported less frequently from developing countries. The most important risk factor for invasive GBS disease in the neonate is exposure to the organism via the mother's genital tract. Other known risk factors include young maternal age, preterm birth, prolonged rupture of the membranes, maternal chorioamnionitis, exposure to a high inoculum of a virulent GBS strain and a low maternal serum concentration of antibody to the capsular polysaccharide of the colonizing GBS strain.44

In an attempt to understand the low rates of invasive GBS disease reported among neonates in many developing countries, we reviewed 34 studies that evaluated GBS colonization rates in women. Because of poor specimen collection and suboptimal laboratory techniques, some of these studies may have underestimated the true rate of maternal GBS colonization. It is well-known that use of selective media and culturing multiple sites (particularly culturing both the lower vagina and rectum) increase GBS isolation rates.45, 46 This review suggests that the rates of maternal GBS colonization may be underreported in many studies because of poor culture techniques and use of nonselective media. Nonetheless estimated developing country colonization rates (a composite of all country data reviewed) were similar to those reported for women in the United States and Europe.2, 3 The largest evaluation of GBS colonization among pregnant women in the United States, the Vaginal Infections and Prematurity Study,47 found GBS colonization rates of 21.2% for blacks, 20.9% for Hispanics and 13.7% for whites, values similar to those found in the studies reviewed in this article.

The distribution of GBS serotypes varied among studies. GBS serotype III, the most frequently identified invasive serotype in the West, was also identified in all studies reviewed and was the most frequently identified serotype in one-half of the studies. Serotype V, which has only been recognized as a cause of invasive disease in developed countries since the early 1990s,48 was identified in recent studies from Peru and the Gambia. Monitoring serotype distribution is important as candidate GBS vaccines are considered for areas with high rates of disease.

With estimated colonization rates among women in developing countries as high as 18%, one would expect higher rates of invasive neonatal disease than have been reported.1 Low rates of invasive GBS disease in some developing countries may be explained by less virulent strains, by genetic differences in susceptibility to disease, by as yet unidentified beneficial cultural practices or by high concentrations of transplacentally acquired protective antibody in serum (i.e. mother colonized but has protective concentrations of type-specific GBS antibody).

Hospital-based surveillance in developing countries may be insensitive for detecting sepsis in very young infants. In the United States ∼80% of infants with early onset GBS disease become ill within 24 h of birth.5 In developing countries, where most deliveries occur at home, infants with early onset sepsis often get sick and die at home or are taken to local health facilities where a diagnosis of possible sepsis may be missed (i.e. underrecognition) or where blood cultures cannot be performed. In this setting there may be underdiagnosis of early onset pathogens, including GBS. Hospital-based studies, which present data on organisms associated with neonatal sepsis, may be reporting results for late onset, as well as early onset cases.1

Increasing evidence suggests that heavy colonization with GBS increases the risk of delivering a preterm low birth weight infant.49 Population differences in the prevalence of heavy GBS colonization have been reported in the United States, where African-Americans have a significantly higher risk of heavy colonization.50 However, studies reviewed from developing countries did not report quantitative maternal genital colonization. If heavy colonization is more prevalent among women in developing countries and results in an increase in preterm low birth weight infants, GBS-related morbidity may appear as illness and death related to prematurity and neonatal GBS disease may be masked. By contrast heavy colonization could increase maternal type-specific GBS antibody concentrations, resulting in lower risk of neonatal disease. Further studies in developing countries are needed to explore these important issues.


1. Stoll BJ. The global impact of neonatal infection. Clin Perinatol 1997;24:1-21.
2. Schuchat A. Group B streptococcal disease in newborns: a global perspective on prevention. Biomed Pharmacother 1995;49:19-25.
3. Walsh JA, Hutchins S. Group B streptococcal disease: its importance in the developing world and prospect for prevention with vaccines. Pediatr Infect Dis J 1989;8:271-6.
4. Mayon-White RT. The incidence of GBS disease in neonates in different countries. Antibiot Chemother 1985;35:17-27.
5. Baker CJ, Edwards MS. Group B streptococcal infections. In: Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn. ed 4. Philadelphia: Saunders, 1995:980-1054.
6. Bennett R, Eriksson M, Melen B, et al. Changes in the incidence and spectrum of neonatal septicemia during a fifteen-year period. Acta Paediatr Scand 1985;74:687-90.
7. Gladstone IM, Ehrenkranz RA, Edberg SC, Baltimore RS. A ten-year review of neonatal sepsis and comparison with the previous fifty-year experience. Pediatr Infect Dis J 1990;9:819-25.
8. Weisman LE, Stoll BJ, Cruess DF, et al. Early-onset group B streptococcal sepsis: a current assessment. J Pediatr 1992;121:428-33.
9. Chaudhary U, Sabherwal U, Chugh TD. Prevalence of group B streptococci in obstetrical cases. Indian J Med Res 1981;73:710-14.
10. Mani V, Jadhav M, Sivadasan K, Thangavelu CP, Rachel M, Prabha J. Maternal and neonatal colonization with group B Streptococcus and neonatal outcome. Indian Pediatr 1984;21:357-63.
11. Kishore K, Deorari AK, Singh M, Bhujwala RA. Early onset neonatal sepsis: vertical transmission from maternal genital tract. Indian Pediatr 1987;24:45-8.
12. Akhtar T, Zai S, Khatoon J, Zohra A, Taj Roghani M, Ahmad A. A study of group B streptococcal colonization and infection in newborns in Pakistan. J Trop Pediatr 1987;33:302-4.
13. Lakshmi V, Das S, Shivananda PG, Savitri P, Rao K. Incidence of group-B beta haemolytic streptococci in the vaginal flora of pregnant women. Indian J Pathol Microbiol 1988;31:240-4.
14. Kirmani N, Hassen TJ, Jafarey SN, Hafiz S. Carriage of group B streptococci in rectum and urogenital tract of pregnant women. JPMA J Pak Med Assoc 1991;41:42-4.
15. Chan SH, Murai T, Liang ST, Kaneko Y, Fok TF, Lau SP. Group B streptococcal carriage in Chinese females of Hong Kong. In: Kimura Y, Kotami S, Shiokawa Y, eds. Recent advances in streptococci and streptococcal diseases. Japan: Reedbooks, 1984:46-7.
16. Pengsa K, Puapermpoonsiri S, Taksaphan S, et al. Group B streptococcal colonization in mothers and their neonates. Ramathibodi Med J 1984;7:83-90.
17. Liang ST, Lau SP, Chan SH, Fok TF, Murai T, Kaneko Y. Perinatal colonization of group B Streptococcus: an epidemiological study in a Chinese population. Aust NZ J Obstet Gynaecol 1986;26:138-41.
18. Gyaneshwar R, Nsanze H, Singh KP, Pillay S, Seruvatu I. The prevalence of sexually transmitted disease agents in pregnant women in Suva. Aust NZ J Obstet Gynaecol 1987;27:213-5.
19. Zhang JH, Yuan L, Yang YH. Perinatal colonization of group B Streptococcus: a study in 600 cases in Beijing Tiantan Hospital. Chung-Hua Liu Hsing Ping Hsueh Tsa Chih 1995;16:36-9.
20. Zhu YZ, Yang YH, Zhang XL. Vaginal colonization of group B Streptococcus: a study in 267 cases of factory women [in Chinese]. Chung-Hua Liu Hsing Ping Hsueh Tsa Chih Chinese J Epidemiol 1996;17:17-9.
21. Onile BA. Group streptococcal carriage in Nigeria. Trans Roy Soc Trop Med Hyg 1980;74:367-70.
22. Dawodu AH, Damole IO, Onile BA. Epidemiology of group B streptococcal carriage among pregnant women and their neonates: an African experience. Trop Geogr Med 1983;35:145-50.
23. Nathoo KJ, Mason PR, Chimbira THK, and the Puerperal Sepsis Study Group. Neonatal septicaemia in Harare Hospital: aetiology and risk factors. Cent Afr J Med 1990;36:150-6.
24. Faye-Kette-Achi H, Dosso M, Kacou A, et al. Portage genital du streptocoque du groupe B chez la femme enceinte a Abidjan (Cote-d'Ivoire). Bull Soc Pathol Exot 1991;85:532-9.
25. David-Prince PM, Ategbo S, deSouza AE, et al. Portage du streptocoque B dans le couple mere-enfant a la naissance: a propos de 106 cas. Bull Soc Pathol Exp 1991;84:522-31.
26. Suara RO, Adegbola RA, Baker CJ, Secka O, Mulholland EK, Greenwood BM. Carriage of group B streptococci in pregnant Gambian mothers and their infants. J Infect Dis 1994;70:1316-9.
27. Osman NB, Folgosa E, Bergström S. An incident casereferent study of threatening preterm birth and genital infection. J Trop Pediatr 1995;41:267-72.
28. Benbachir M, El-Mdaghri N, Lahlou D, Mesbahi M. Etude du portage de Streptococcus agalactiae et de Listeria monocytogenes chez la femme marocaine. Med Mal Infect (Marocco) 1983;13:793-7.
29. Gosling PJ, Morgoso FW. Group B streptococci: colonization of women in labour and neonatal acquisition in the western region of Saudi Arabia. J Hosp Infect 1983;4:324.
30. Elzouki AY, Vesikari T. First international conference on infections in children in Arab countries. Pediatr Infect Dis 1985;4:527-31.
31. Uduman SA, Chatterjee TK, Al-Mouzan MI, Al-Suleiman S. Group B streptococci colonization among Saudi women in labor and neonatal acquisition. Int J Gynaecol Obstet 1985;23:21-4.
32. Farrag OA, Gawad AA, Antar S. Group B-beta haemolytic streptococcal colonization in women using intrauterine contraceptive devices. Contraception 1985;31:595-603.
33. Gökalp A, Oğuz A, Bakici Z, et al. Neonatal group B streptococcal colonization and maternal urogenital or anorectal carriage. Turk J Pediatr 1988;30:17-23.
34. Sunna E, El-Daher N, Bustami K, Nawas T. A study of group B streptococcal carrier state during late pregnancy. Trop Geogr Med 1991;43:161-4.
35. Ayata A, Ghven HH, Felek S, Denizmen Ayghn A, Kocabay K, Bektas S. Maternal carriage and neonatal colonisation of group B streptococci in labour are uncommon in Turkey. Paediatr Perinatol Epidemiol 1994;8:188-92.
36. Chaaya A, Chacar HR, Daoud M, et al. Screening of Streptococcus agalactiae (group B) in the perinatal period. J Med Liban 1996;44:203-8.
37. Benchetrit LC. Perinatal group B streptococcal infections. An Microbiol Rio J 1981;26:67-89.
38. Benchetrit LC, Fracalanzza SE, Peregrino H, Camelo AA, Sanches LA. Carriage of Streptococcus agalactiae in women and neonates and distribution of serological types: a study in Brazil. J Clin Microbiol 1982;15:787-90.
39. de Lourdes-Collado M, Kretschmer RR, Becker I, Guzman A, Gallardo L, Lepe CM. Colonization of Mexican pregnant women with group B streptococcus [Letter]. J Infect Dis 1981;143:134.
40. Solorzano-Santos F, Echaniz-Aviles G, Conde-Glez CJ, et al. Cervicovaginal infection with group B streptococci among pregnant Mexican women. J Infect Dis 1989;159:1003-4.
41. Trujillo H. Group B streptococcal colonization in Medellin, Colombia [Letter]. Pediatr Infect Dis J 1990;9:224-5.
42. Orrett FA, Olagundoye V. Prevalence of group B streptococcal colonization in pregnant third trimester women in Trinidad. J Hosp Infect 1994;27:43-8.
43. Collins TS, Calderon M, Gilman RH, et al. Group B streptococcal colonization in a developing country: its association with sexually transmitted disease and socioeconomic factors. Am J Trop Med (in press).
44. Baker CJ. Group B streptococcal infections. Clin Perinatol 1997;24:59-70.
45. Ferrieri P, Cleary PP, Seeds AE. Epidemiology of group B streptococcal carriage in pregnant women and newborn infants. J Med Microbiol 1977;10:103-14.
46. Badri MS, Zaweneh S, Cruz AC, et al. Rectal colonization with group B Streptococcus: relation to vaginal colonization in pregnant women. J Infect Dis 1977;135:308-12.
47. Regan JA, Klebanoff MA, Nugent RP for the Vaginal Infections and Prematurity Study Group. The epidemiology of group B streptococcal colonization in pregnancy. Obstet Gynecol 1991;77:604-10.
48. Blumberg HM, Stephens DS, Modansky M, et al. Invasive group B streptococcal disease: the emergence of serotype V. J Infect Dis 1996;173:365-73.
49. Regan JA, Klebanoff MA, Nugent RP, et al. for the VIP Study Group. Colonization with group B streptococci in pregnancy and adverse outcome. Am J Obstet Gynecol 1996;174:1354-60.
50. Newton ER, Butler MC, Shain RN. Sexual behavior and vaginal colonization by group B Streptococcus among minority women. Obstet Gynecol 1996;88:577-82.

Group B Streptococcus; maternal colonization; neonatal sepsis

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