Neonatal B streptococcal infection

Introduction to neonatal B streptococcal infection In the neonatal period, the disease caused by infection with group Bstreptococci (GBS) is neonatal B streptococcal infection. Streptococcus B is closely related to perinatal infection and has been shown to be an important cause of neonatal sepsis and meningitis in the 1970s. basic knowledge The proportion of illness: 0.012% Susceptible people: children Mode of infection: non-infectious Complications: pleurisy pulmonary edema meningitis osteomyelitis

Causes of neonatal B streptococcal infection

(1) Causes of the disease

Streptococcus is classified into (incomplete hemolysis), (complete hemolysis), and (insoluble hemolysis) according to hemolysis. Lance-field classifies B hemolytic streptococcus into 18 families according to different antigen structures, of which A Family (GAS) causes pharyngitis, scarlet fever, skin infections, and is associated with rheumatic fever and nephritis; GBS is associated with pregnancy, maternal and neonatal infections, and GBS is classified according to type-specific capsular polysaccharide antigen (S substance). At least 6 serotypes: Ia, Ib, Ic, II, III, IV, untyped are not associated with neonatal disease, early neonatal infection can be caused by any serotype, 90% of late infections are type III To.

(two) pathogenesis

Early-onset infection due to immature defense mechanism in low birth weight infants, mother with more bacteria, GBS caused local amnion, amniotic membrane rupture from this location and induced premature delivery, the incidence of premature rupture of amniotic membrane <19h was 0.7, 30h was 18.3 The amnion intact fetus can also be infected. Amniotic fluid contains lower levels of type-specific GBS antibodies, complement, phagocytic cells and other non-specific defense components. It is a good GBS medium, and the fetus inhales infected amniotic fluid, which can lead to Pneumonia, bacteremia and septic shock in the fetus and later neonates.

Serum GBS specific capsular polysaccharide antibody IgG level > 2g / ml, can enhance leukocyte opsonophagocytosis, and can kill GBS, immature children lack the type-specific antibodies from the mother, prone to GBS infection, once it occurs, can not The defects of the existing conditioning phagocytosis in mature children are further affected.

Early-onset GBS infection is characterized by bacteremia, pneumonia and pulmonary hypertension. Peripheral blood neutropenia, pulmonary granulocyte infiltration, increased vascular permeability, myocardial dysfunction, blood pressure drop, center Increased venous pressure and DIC.

The onset of late-onset GBS infection is associated with early childhood carcinogenesis. When a respiratory infection occurs, the mucosal barrier is destroyed, GBS is vaginally propagated, and a large number of GBS type III capsular polysaccharide antigens are produced, or the mother's autoantibodies are reduced. GBS osteomyelitis The onset is due to early-onset GBS bacteremia, although asymptomatic, but the bacteria can be inoculated into the injured bone (tibia), and then cause localized osteomyelitis, the child may have no systemic symptoms, because the child has produced a small amount Antibodies, elevated levels of specific IgG antibodies in the blood, limit infection to the metaphysis.

Neonatal B streptococcal infection prevention

GBS type specific antigen is its capsular polysaccharide, purified type Ia, II, III can be used as vaccine. If pregnant women have no GBS antibody at 30 weeks of gestation, after injection of type III GBS vaccine, pregnant women and newborn umbilical cord Antibodies can be produced in blood, and antibodies in newborns can last for 1 to 2 months, but polysaccharide antigens have an immune response to only 54% of pregnant women.

It is not appropriate for neonates to be injected with penicillin at birth because 50% of the babies are infected in the uterus, and they have symptoms within or within 6 hours of birth. Controlled to prevent bacteremia and reduce death. Both are ineffective unless one of the twins is infected and used for another asymptomatic person.

For high-risk pregnant women with premature delivery, fever, premature water (more than 12h), or suspected chorioamnionitis, selective drug treatment, can effectively prevent early infection of newborns, check pregnant women at 26-28 weeks of pregnancy GBS carries bacteria, and intravenous treatment with ampicillin in the delivery (2 g for the first dose, 1 g for every 4 hours thereafter) can reduce the infection and infection of the newborn, and another method is to use the rapid antigen detection method during the labor. 5h out of the results) to check the birth canal GBS, the majority of carriers with ampicillin treatment.

Neonatal B streptococcal infection complications Complications pleurisy pulmonary edema meningitis osteomyelitis

Early onset can be seen asphyxia, continuous fetal circulation, pleurisy, pulmonary edema, meningitis ventriculitis, late onset can be complicated by osteomyelitis, urinary tract infection.

Symptoms of neonatal B streptococcal infection Common symptoms Edema, septicemia, bruises, bruising, convulsions, convulsions, meningitis, nasal discharge, sleepiness

1. Early-onset: Early onset can occur at birth, especially in premature infants, which occurs 6 to 12 hours after birth, and full-term infants are as late as 24 hours, with mild infection as asymptomatic bacteremia, pneumonia and lung Transparent membrane disease is not easy to identify. Severe symptoms are severe perinatal asphyxia (combined pneumonia, coma, shock), septic shock or continuous fetal circulation. Respiratory symptoms include cyanosis, apnea, shortness of breath, nasal fan, and three concave signs. Etc., chest radiographs have reticular granules (50%), lung spot infiltration (30%), rare pleural effusion, pulmonary edema, heart enlargement and increased pulmonary blood.

30% to 40% of patients with sepsis without lesions, 30% of meningitis (mostly type III), 30% to 40% of pneumonia, bacteremia in 3 manifestations, and meningeal involvement may have convulsions , lethargy, coma, refusal to milk, anterior convexity, etc., but can not be diagnosed according to the clinical, all suspected early or late neonatal sepsis should be worn by the waist.

2. Late-onset infection: 60% of meningitis, mainly type III, can not be differentiated from meningitis of other pathogens, and other localized lesions such as osteomyelitis and urinary tract infection.

Examination of neonatal B streptococcal infection

Determining the diagnosis depends on bacterial culture positive (from blood, cerebrospinal fluid, urine, local lesions), while positive skin and mucous membranes only indicate bacteria.

In recent years, the antigen diagnosis of bacteria has progressed rapidly. No matter whether antibiotics or antibiotics have been used, antigen detection methods can be used. Latex agglutination, synergistic agglutination, convective immunoelectrophoresis and enzyme-linked immunosorbent assay are commonly used to accurately convective immunoelectrophoresis. The sample is better, and the sample with less GBS content is superior to the antigen detection bacterial culture.

Elevated specific GBS antibodies may suggest a recent GBS infection, anti-streptolysin O (ASO) and anti-deoxyribonuclease B (DNAse B) only help the diagnosis of GAS, not applicable to GBS.

X-ray examination should be routinely performed to understand the heart, lung condition, electroencephalogram, electrocardiogram examination, brain CT examination if necessary, B-ultrasound and other examinations.

Diagnosis and identification of neonatal B streptococcal infection

diagnosis

According to the history and clinical manifestations, combined with laboratory tests to confirm the diagnosis.

Differential diagnosis

Differential diagnosis of early onset includes: hyaline membrane disease, amniotic fluid inhalation syndrome, continuous fetal circulation, sepsis (Escherichia coli through the birth canal, herpes simplex infection), metabolic disease (hypoglycemia, hyperammonemia), anatomy An abnormality (congenital heart disease, paralysis) or other causes of bruising and sepsis-like manifestations.

In some cases, GBS infection is difficult to distinguish from hyaline membrane disease, such as low Apgar score, shock and apnea on the first day after birth, early water break, heart, pleural effusion, rapid deterioration of the disease, etc. With hypoxia, hypotension, neutropenia, apnea, etc., continuous fetal circulation can occur.

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