Literature
review

Streptococcus
agalactiae, group
B streptococcus (GBS), is a Gram-positive encapsulated bacterium that belongs
to the group of pyogenic streptococci. It is the only Streptococcus species
harboring the Lancefield group B cell-wall-specific polysaccharide antigen that
is common to all GBS strains. In most cases, GBS is an asymptomatic colonizer
of the digestive and genitourinary tracts of healthy human adults. The
serotypes that cause human infections identified frequently in many parts of
the world are III, Ia, Ib, II and V (Dogan et al., 2005; Ippolito et al., 2010;
Madzivhandila et al., 2011; Edmond et al., 2012). Neonatal infections are most
commonly caused by serotypes Ia, III and V (Pettersson, 2007). Since the 1960s,
GBS has remained a leading cause of life-threatening neonatal infections,
including bacterial meningitis (Wilson, C. B., 2015).

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Meningitis is the acute inflammation of the
meninges, subarachnoid space, and brain vasculature resulting from infection (Barichello, Tatiana, et al., 2015). Bacterial meningitis is a devastating
infection associated with high mortality and morbidity in the neonatal
population. While overall incidence and mortality have declined over the last
several decades, morbidity associated with neonatal meningitis remains
virtually unchanged (Polin, R. A., & Harris, M. C., 2001; Heath, P.
T., Okike, I. O., & Oeser, C., 2012). Babies and young children are
particularly vulnerable to meningitis as they cannot easily fight infection
because their immune system is not yet fully developed. Babies, toddlers and
young children under five are the most at-risk group for meningitis, with over
50% of all cases occurring in this age group. Whilst most children will make a
good recovery, around 10% will die and 15 % will be left with life-long
disabilities (Mann, K., & Jackson, M. A., 2008)

For
years, GBS screening methods for pregnant woman followed by administration of
intrapartum antimicrobial prophylaxis
have been developed, resulting the
decline of early onset GBS infection by 85%–90% (Schrag, S. J., Zell, E.
R., Lynfield, R., Roome, A., Arnold, K. E., Craig, A. S., … & Gamble, M.,
2002). However, rapid and accurate
identification of GBS in children under 5 years old is still highly demanded
and essential for a good outcome, since in infants and children, clinical
presentation is vague, due to the immaturity of central nervous system. Until
today, according to Rosa-Fraile, M., & Spellerberg, B. (2017), many
clinical microbiology laboratories rely on more traditional phenotypic methods
for the identification of GBS. Rosa-Fraile, M., & Spellerberg, B. (2017) also
describe available techniques for GBS detection and points out their
limitations: chromogenic media’s lack of sensitivity, CAMP’s test lack of
specificity and MALDITOF – MS lack of ability to directly identify subject from
clinical specimen.

Moreover, the sensitivity of gram staining and culture is
less than 50 % in patients who are already on antibiotic treatment. Latex agglutination
test (LAT) alone, although efficient in detecting soluble bacterial antigens in
CSF of patients suspected with bacterial meningitis, lacks sensibility. Combination
of Gram staining, culture, and LAT can achieve 100% sensitivity and specificity
although the process is time
consuming (Carbonnelle, E., 2009).

In
2012, de Zoysa, Aruni, et al. conducted real-time PCR assay targeting the cylB
gene for detection GBS from clinical samples. The assay was able to detect GBS
positive samples among the culture-negative samples of blood and CSF,
suggesting real-time PCR assay was superior to culture methods. The method is
rapid, sensitive, specific, reproducible, thus make an attractive option to
supplement culture-based tests.

(1)  
Edwards
MS, Nizet V, Baker CJ. 2016. Group B streptococcal infections, p411–456. In
Wilson CB, Nizet V, Maldonado Y, Klein JO, Remington JS(ed), Remington and
Klein’s infectious diseases of the fetus and newborn infant. Elsevier Saunders,
Philadelphia, PA.
Hood M, Janney A, Dameron G. 1961. Beta hemolytic streptococcus group B
associated with problems of the perinatal period. Am J Obstet Gynecol
82:809–818. https://doi.org/10.1016/S0002-9378(16)36146-4.

(2)  
Pathophysiology
of neonatal acute bacterial meningitis. Barichello T, Fagundes GD, Generoso JS,
Elias SG, Simões LR, Teixeira AL J Med Microbiol. 2013 Dec; 62(Pt 12):1781-9.

(3)  
Neonatal
bacterial meningitis. Polin RA, Harris MC Semin Neonatol. 2001 Apr;
6(2):157-72.

(4)  
Neonatal
meningitis: can we do better? Heath PT, Okike IO, Oeser C Adv Exp Med Biol.
2011; 719():11-24.

(5)  
Meningitis.
Mann K, Jackson MA Pediatr Rev. 2008 Dec; 29(12):417-29; quiz 430.

(6)  
A
population-based comparison of strategies to prevent early-onset group B
streptococcal disease in neonates. Schrag SJ, Zell ER, Lynfield R, Roome A,
Arnold KE, Craig AS, Harrison LH, Reingold A, Stefonek K, Smith G, Gamble M,
Schuchat A, Active Bacterial Core Surveillance Team. N Engl J Med. 2002 Jul 25;
347(4):233-9.