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GROUP B STREPTO COCCI : CLINICAL ASPECTS
The clinical findings are nonspecific and similar to those found in other serious infections in the neonatal period . Respiratory distress, fever, lethargy, irritability, apnea, and hypotension are common. Fever is sometimes absent, and infants may even be hypothermic. Pneumonia is common, and meningitis is present in 5 to 10% of cases, but most infections have GBS circulating in the bloodstream without localizing findings. The onset is typically in the first few days of life, and signs of infection are present at birth in almost 50% of cases. The late-onset (1 to 3 month) cases have similar findings but are more likely to have meningitis and focal infections in the bones and joints. Even with appropriate and prompt treatment, the mortality rate for early onset GBS infection ap-proaches 20%.
GBS infections in adults are uncommon and fall in two groups. The first are peripar-tum chorioamnionitis and bacteremia, the mother’s side of the neonatal syndrome. Other infections include pneumonia and a variety of skin and soft tissue infections similar to those produced by other pyogenic streptococci. Although adult GBS infections may be serious, they are usually not fatal unless patients are immunocompromised. GBS are not associated with rheumatic fever or acute glomerulonephritis.
The laboratory diagnosis of GBS infection is by culture of blood, cerebrospinal fluid, or other appropriate specimen. Definitive identification involves serologic determination of the Lancefield group by the same methods used for group A streptococci. Methods for di-rect detection of GBS antigen in vaginal specimens have been evaluated, but their sensi- tivity is far too low for use in the diagnosis of neonatal infection.
GBS are susceptible to the same antimicrobics as group A organisms. Although penicillin is the treatment of choice, GBS are slightly less susceptible toβ-lactams than other strep-tococci. For this reason neonatal infections are often initially treated with combinations of penicillin (or ampicillin) and an aminoglycoside. These combinations have been shown to accelerate killing of GBS in vitro.
Current strategies for prevention of neonatal GBS disease are focused on reducing contact of the infant with the organism. In colonized women, attempts to eradicate the carrier state have not been successful, but intrapartum antimicrobial prophylaxis with penicillin or ampicillin has been shown to reduce transmission and disease in high-risk populations. It is now recommended by expert obstetric and perinatology groups that all newborns at risk receive such prophylaxis, but there is debate about the practical aspects of determining risk. One approach is to screen all expectant mothers for vaginal GBS colonization in the third trimester and administer prophylaxis during labor to all found to be culture positive. This safe but expensive approach can be applied only to those who seek regular prenatal care. A second approach is to assign risk on clinical grounds (eg, prematurity, prolonged membrane rupture, fever), which is less expensive but will miss some colonized babies. There is evidence that prophylaxis is working. The incidence of early-onset neonatal GBS disease dropped 65% over a 5-year period when these strategies were being implemented. Prevention by immunization with purified GBS capsular polysaccharide has been shown to be feasible, and considerable effort is now being directed at development of a vaccine.
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