B grubu ß- hemolitik streptokoklar

Abstract

B grubu ß-hemolitik streptokoklar (BgrBHS) kadın genital yollarına kolonize olarak yenidoğanlarda sepsis ve menenjite, erişkinde çeşitli infeksiyonlara neden olmaktadır. Bu derlemede B grubu streptokokların önemli özellikleri, yaptığı infeksiyonlar, laboratuvar teşhis yöntemleri, infeksiyondan korunma ve tedavide bilinmesi gerekenler gözden geçirilmiştir.

Group B ß-hemolytic streptococci (GBS) are known as Streptococcus agalactiae. They typically are ß-hemolytic and produce zones of hemolysis that are only slightly larger than the colonies 1-2 mm in diameter. The group B streptococci hydrolyse sodium hippurate and give a positive response in the so-called CAMP (Christie, Atkins, Munch-Paterson). Several commercial kits are available for rapid detection of group B streptococcal antigen from vaginal, rectal, umbilical and throat swaps. These kits use enzymatic or chemical methods to extract the antigen from the swap, then use enzyme-linked immunosorbent assay (ELISA) or agglutination tests to demonstrate the presence of the antigen. The tests can be completed 1-4 hours after the specimen is obtained. They are 60-90% sensitive and 98-99% specific when compared to culture methods. Kit tests are more rapid than cultures. BGS are member of the female genital tract and a major cause of disease in the perinatal and neonatal periods. Females become colonized with the organism in the vagina, the rectum and the urethra, and asymptomatic vaginal colonization is found 2.3-43% of pregnant women. Among colonized pregnant women, 60% of their infants will acquire the identical group B strain either in utero or during delivery. In addition, the neonate may become colonized by nosocomial exposure to the organism after birth. Among colonized newborns, disease may occur in two to five newborns per 1000 live births. Neonatal disease with GBS follows two clinical syndromes. Early-onset disease is associated with in utero or perinatal acquisition of the organism and occurs during the first 5 days of life. The disease spectrum includes sepsis and pneumonia. Late onset disease occurs from 7 days to 3 months after birth and may result from perinatal or nosocomial acquisition of the organism. Bacteremia with accompanying meningitis is predominant clinical presentation. GBS can be serotyped into nine serotypes designed Ia, Ib, Ic, Ib/c, II, III, IV, X and R .. Septicemia and meningitis caused by GBS, especially early-onset disease, can involve any of the group B streptococal serotypes, but most cases of meningitis (late onset disease) are caused by serotype III organisms. In older children, this organism causes a variety of other clinical manifestations, including conjunctivitis, otitis media, osteomyelitis, arthritis, and omphalitis. Infections in adults usually involve the urinary tract and most occur in compromised hosts, such as those on chemotherapy or with underlying diseases such as diabetes. These organisms colonize the female genital tract and rarely causes endomethritis and other postpartum infections. GBS bacteremia may be seen in one third of the cases. Attempts to prevent neonatal dissease have met with limited success. GBS are uniformly susceptible to penicillin G, which is the drug of choice.