Portal de Periódicos da CAPES

EARLY ONSET NEONATAL SEPSIS CAUSED BY SEROTYPE VIII GROUP B STREPTOCOCCI

2000; Lippincott Williams & Wilkins; Volume: 19; Issue: 4 Linguagem: Inglês

10.1097/00006454-200004000-00022

1532-0987

Kousaku Matsubara, Masako Sugiyama, Kiyoshi Hoshina, Hiroshige Mikamo, Kunizo Baba,

Kawasaki Disease and Coronary Complications

Prevalent capsular serotypes of group B streptococci (GBS) causing neonatal invasive infection have varied with time and among populations. Before the 1990s the major serotypes were types Ia, Ib, II and III throughout the world.1 Type V strains have emerged as a causative organism in the United States since the first report in 1993.2, 3 In Japan serotypes VI and VIII have been increasingly recognized among isolates from pregnant women since the early 1980s,4, 5 and currently serotype VIII is a leading isolate from pregnant women, accounting for 25 to 36%.5–7 The first neonate infected by this capsular type was noted in 1983.7 However, the incidence of type VIII neonatal infection is rare compared with the carriage rate among pregnant women. In a nationwide surveillance of neonatal GBS infection from 1988 to 1992, only 9 of 99 strains were type VIII among the serotypes examined.8 Because of the scarcity clinical profiles of neonates with this serotype infection are not yet fully known. We present the clinical features of four neonates with early onset sepsis caused by type VIII GBS. Methods and patients. GBS serotyping was determined with a commercially available kit (Denka Seiken, Tokyo). Type VIII GBS were isolated from blood on admission in all patients described below. Patient 1. This 3784-g male baby was born in August, 1986, from a 26-year-old woman by cesarean section because of fetal distress at a gestational age of 40 weeks and 4 days. Amniotic fluid was heavily stained with meconium. The Apgar score was 4 at 1 min and 8 at 5 min. Because respiratory distress did not resolve despite suctioning and oxygen administration, the baby was transferred to the regional neonatal center after intubation. On admission central cyanosis and respiratory retraction were seen. A chest radiograph showed the findings indicative of meconium aspiration syndrome. The blood count showed a white blood cell (WBC) count of 33 600/μl with 69% neutrophils. The patient had profound acidosis. Intensive therapy including artificial respiration with 100% oxygen, dopamine, diuretics and antibiotics (ampicillin and gentamicin) failed to improve the infant's condition. Eight hours after birth the patient died. Patient 2. This female baby weighing 3560 g was vaginally delivered in May, 1992, from a 30-year-old mother at 39 weeks and 2 days of gestation. Eight hours after birth the baby's body temperature was 38.4°C, and peripheral cyanosis was apparent. The laboratory findings showed a WBC count of 36 000/μl with 15% segmented and 67% band forms. Cerebrospinal fluid examination disclosed no abnormalities. We treated the patient with ampicillin (200 mg/kg/day) and amikacin (10 mg/kg/day) for 7 days. She became afebrile and appeared well on the day after admission. Patient 3. This male baby weighing 3482 g was born uneventfully in July, 1993, at 37 weeks and 3 days of gestation. The Apgar score was 10 at 1 and 5 min. Five hours after birth the patient became cyanotic and respiratory distress was noted. On admission to the neonatal center from a neighborhood obstetric ward, central cyanosis and tachycardia were noted. The WBC count was 22 900/μl with 72% neutrophils. A chest radiograph showed a diffuse reticular shadow mimicking respiratory distress syndrome. The patient received respiratory support for 11 days, antibiotics (ampicillin and cefotaxime of 100 mg/kg/day) for 12 days, gamma-globulin (200 mg/kg/day) for 3 days, diuretics for 3 days and dopamine for 5 days. The patient was discharged at 14 days of age without sequelae. Patient 4. A 2788-g girl was born in August, 1998, at 36 weeks and 5 days of gestation to a 31-year-old woman. Apgar scores were 9 and 9 at 1 and 5 min, respectively. The infant's mother was recognized as having vaginal colonization with GBS at 27 weeks of gestation. The mother was hospitalized at 31 weeks of gestation because of preterm contractions. She was treated with ritodrine hydrochloride and piperacillin at 2 weeks, at which time vaginal cultures were negative for GBS. At 4 h after birth the infant suddenly became apneic and cyanotic. The WBC count showed marked leukopenia of 1400/μl with 1.5% neutrophils. A chest radiograph was normal, as was the cerebrospinal fluid examination and culture. Artificial respiratory ventilation was started. We treated the infant with ampicillin (200 mg/kg/day) for 14 days and gamma-globulin (500 mg/kg) on the first day. Diuretics, dopamine and anticoagulant therapy were also administered because severe hypoxemia, renal failure and disseminated intravenous coagulopathy persisted. The infant recovered from multiple organ failure by the 7th day of intensive treatment. A magnetic resonance image of brain did not depict any abnormalities, but mental retardation has been observed with a development quotient of 75 at 12 months old. Discussion. Early studies indicated that GBS strains isolated from pregnant women and infected neonates were evenly divided among serotypes I, II and III,1 but new serotypes have emerged in the past decades: IV in Europe; V in the United States; and VI and VIII in Japan.2–8, 9, 10 In contrast to the epidemiologic studies5, 7, 8 little is known about the clinical features of neonates infected by the new serotypes in Japan. To our knowledge this is the first report describing the clinical course of type VIII GBS infection in neonates. Our patients typically developed a clinical course similar to that observed in other newborn patients with common GBS serotypes.1 Three of the four developed shock, respiratory failure and transient renal failure. There were no patients with meningitis. The time of onset was from 0 to 8 h after birth. Only one of the four mothers had risk factors. Approximately 60% of infants with early onset GBS infection in Japan have one or more maternal risk factors.8 Despite increased awareness of the disease and improvements in supportive therapy, GBS sepsis remains a serious infection with high morbidity and mortality in neonates.1, 11 A recent multicenter study in our nation revealed that the mortality and morbidity rates were 14.2% (43 of 302) and 7.7% (20 of 259), respectively.8 Of our four patients with type VIII GBS infection, one died and one had neurologic sequelae. Several risk factors associated with severity have been proposed.1, 11, 12 Payne et al.12 used multivariate analysis to identify six factors predicting a fatal outcome; birth weight <2500 g, absolute neutrophil count < 1500/μl, hypotension, apnea, pleural effusion on the initial chest radiographs and low blood pH (<7.25). The patient who died and the one with sequelae had scores predicting a fatal outcome. None of the patients received intrapartum chemoprophylaxis. The fourth patient's mother received antepartum antibiotic treatment. Reinfection by self-inoculation from the rectal reservoir or from a colonized partner could have occurred. In conclusion we have shown that type VIII GBS strains have virulence for human neonates with a clinical presentation similar to that of the previously described and more common serotypes. However, to more precisely know their prevalence and clinical conditions associated with this infection, prospective evaluation of type VIII GBS infections in neonates is necessary. Acknowledgments. We thank F. Hayakawa, M.D., Department of Pediatrics, Anjo Kosei Hospital, S. Ishigo, M.T., the Infection Control Center, Ogaki Municipal Hospital, and H. Inaba, M.D., Department of Pediatrics, National Mie Chuo Hospital, for providing the clinical records of the patients and their critical advice.