Aetiology
Infection results either from direct spread from a colonised site or by bacteraemic seeding of a distant site. This normally only occurs in patients with identifiable risk factors (i.e., extremes of age, pregnancy, diabetes, immunocompromised, or presence of intravascular device or urinary catheter).[14]
Early-onset neonatal infection is due to infection of the amniotic fluid before birth, and involves serotypes Ia, II, III, and V.[15] This is more likely in prematurity, if the mother is heavily colonised, if the membranes rupture prematurely, if there is an intrapartum maternal fever, or if there are low levels of serotype-specific antibody in the mother and infant.[16][17] Neonatal aspiration of the amniotic fluid results in respiratory infection. The most common infections in this group are meningitis, sepsis, urinary tract infection (UTI), and pneumonia.
Late-onset neonatal infection is due to colonisation after birth; obstetric complications are therefore not a risk factor. The most common infections in this group are sepsis of unknown focus and meningitis. The proportion of cases of meningitis in late-onset disease is greater than that in early-onset disease (19% versus 6%), reflecting the greater proportion of disease caused by serotype III (71% versus 30%).[18][19]
Infections in children are the least well studied. In children aged 90 days through to 1 year, underlying conditions (excluding preterm birth) are uncommon, and were present in only 11% of cases.[7] In children aged 1 to 14 years underlying conditions were present in 44% of cases.[7] Neurological disorders (25%), immunosuppression (23%), asthma (23%), malignancy (15%), and renal disease (13%) were the most common causes. The most common infections in this group are sepsis with unknown focus, meningitis, pneumonia, septic arthritis, and peritonitis.[7]
In adults, infection is normally associated with pregnancy, or with comorbidities that predispose to infection, such as diabetes, neurological impairment, and cirrhosis.[14] Healthcare-associated infections (i.e., acquired >72 hours after admission) are frequently associated with other comorbidities, cannulation, catheterisation, and impaired levels of consciousness.[20][21] Infections in pregnant women in this group may present as UTI, chorioamnionitis, postnatal sepsis, endometritis, and wound infection.[7] In non-pregnant adults in this group the most common infections are sepsis with unknown focus, skin and soft-tissue infection, meningitis, and UTI. Less common infections in non-pregnant adults include septic arthritis, pneumonia, conjunctivitis, sinusitis, otitis media, and intra-abdominal infection.
Pathophysiology
Group B streptococci (GBS) are normal commensals of the gastrointestinal tract, female genitourinary tract, and perineum. Colonisation of the respiratory tract and mucous membranes can occur in neonates. GBS has also been isolated from the pharynx in adults.
Colonisation is facilitated by several different adhesion factors that permit colonisation in many tissue types.[15] Infection follows colonisation in all forms of GBS disease. Tissue invasion is facilitated by several toxins (e.g., haemolysin), enzymes (e.g., C5a peptidase), proteins (C proteins), and carbohydrates (capsular polysaccharides) that produce tissue damage and inhibit the immune response. The exact mechanism of action of many of these proposed virulence factors is not completely understood. Haemolysin is a pore-forming cytolysin implicated in cell invasion. The capsule of GBS, composed of capsular polysaccharides and sialic acid, is able to inhibit phagocytosis through complement inhibition. C5a peptidase cleaves complement factor C5 and thereby inhibits opsonisation.[15]
Classification
Morphological classification of group B streptococci (GBS)
GBS are beta-haemolytic, gram-positive cocci, arranged in chains. They are catalase-negative and express the Lancefield group B antigen, a capsular polysaccharide that is detected by latex agglutination tests, on their surface. Other groups (i.e., A to G) also exist but are beyond the scope of this topic. Streptococcus agalactiae is the only species in group B. Between 1% and 2% of group B streptococci are non-haemolytic.[1]
GBS are further classified into 10 serotypes according to the expression of other carbohydrate and surface protein antigens.
Classification scheme for neonatal infection[2]
Early-onset: 0 to 6 days after delivery, usually first 12 hours.
Late-onset: 7 to 89 days after delivery, usually first 4 weeks.
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