2002/06/01 by Jürgen Dinger, Diane Müller, Nils Pargac +2
Medicine · #Neonatal and Maternal Infections #Streptococcal Infections and Treatments #Pneumonia and Respiratory Infections
paper · doi:10.1097/00006454-200206000-00017
A term female infant developed late onset group B streptococcal disease on Day 12 of life. The source of the organism appeared to be expressed maternal breast milk in the absence of clinical mastitis. Asymptomatic excretion of group B Streptococcus in breast milk may be an underrecognized cause of neonatal infection. Group B Streptococcus (GBS) is the most common cause of neonatal meningitis and septicemia in the first week of life (early onset streptococcal disease) and is related to vaginal carriage in the mother. Late onset streptococcal disease (>7 days after birth) is less common and usually attributed to cross-infection from the hands of health care workers. 1, 2 Alternatively it may reflect delayed manifestation after early colonization. There are only a few reports of late onset or recurrent disease associated with ingestion of infected mother’s milk. 3–7 We report a case of severe meningitis and septicemia in which the source of infection appeared to be the mother’s expressed breast milk, a route of transmission that may not be widely recognized. Case report. The female infant (gestational age, 39 weeks; birth weight, 2600 g) was born by spontaneous vaginal delivery without complications. Two vaginal and anal swabs of the mother 4 and 2 weeks before delivery were negative for GBS. There was no premature rupture of membranes; therefore skin swabs of the baby were not taken after delivery. The mother and her child were discharged home on Day 4 after delivery without problems. On Day 12 of life the girl developed muscular hypotonia, poor sucking, hyperexcitability and irritability on being touched. Clinical signs of bacterial infection when the infant was admitted to our neonatal intensive care unit were grayish skin color, muscular hypotonia, poor perfusion (capillary refill >3 s), arterial hypotension, tachycardia, lethargy, neck stiffness and tachypnea followed by apnea. The infant was intubated and mechanical ventilation was started. Blood cultures, skin swabs and culture from gastric juice were taken before initiation of antibiotic therapy. Blood and gastric juice cultures of the baby were positive for GBS. Three repeated samples of expressed breast milk during the next 3 days were positive for GBS. The samples of freshly expressed breast milk yielded >106 colony-forming units/ml, but there was no clinical evidence of mastitis. During this period the baby was weaned from breast-feeding, so that repeated transmission from child to mother can be excluded. Also enteral feeding of freshly expressed breast milk was not reintroduced to prevent further transmission of GBS from the mother to the child via breast milk. The GBS strains of mother and child were not serotyped. Antibiotic treatment of the baby was started immediately with penicillin, ampicillin and amikacin for 19 days. Arterial blood pressure of the infant improved after volume resuscitation and inotropic support. After correction of disseminated intravascular coagulation and thrombocytopenia 26 h after starting antibiotic treatment, lumbar puncture was performed and meningitis was diagnosed. The cerebrospinal fluid contained 1084 mg/dl protein, 26 mg/dl glucose and 24 320 leukocytes/mm3 with neutrophilic predominance (90%). The culture of the cerebrospinal fluid was negative for GBS. The infant developed hydrocephalus, and ventriculoperitoneal shunts were placed 4 weeks after starting treatment. The infant survived with severe neurologic handicaps. The mother was treated with oral amoxicillin for 10 days. Repeated cultures of breast milk after treatment were negative, but breast-feeding was not reintroduced for other reasons. Discussion. Early onset GBS infections are normally acquired from the mother’s genital tract. Late onset disease is believed to reflect delayed infection after early colonization, or cross-infection. 1 Early colonization is less likely in our case because there was no maternal carriage of GBS before delivery. Vaginal swabs were negative in the mother, and there was no reason to treat her prophylactically with antibiotics. The current recommendation is to screen pregnant women by culture of combined vaginal and anal secretions 4 and 2 weeks before delivery and to treat those with positive cultures. Polymerase chain reactions have been developed that provide results within 45 min. 8 Furthermore there were no other cases of GBS infection during the stay of the mother and her child in the maternity hospital and no evidence of cross-infection. Therefore it seems probable that the source of infection in this infant was the mother’s breast milk. However, superficial or rectal swabs were not taken from the infant at delivery so that an early colonization cannot be completely excluded. GBS is a well-recognized cause of mastitis in cattle, causing loss of milk production. This is the source of its original name, Streptococcus agalactiae.9 Although GBS has been recognized as a major cause of epidemic mastitis in herds, it has not been associated with human mastitis. Epidemiologic studies of human breast infections have shown that the same type of Streptococcus isolated from the mother’s breast is nearly always found in the nose and/or throat of a nursing infant. 3 Infection of the maternal breast follows colonization of the infant during the first few days of life and is thought to occur as a result of aspiration of organisms into the mammary ducts when negative pressure is created by sucking. 3 We suggest that GBS could also multiply in breast milk, be returned to the infant in massive numbers and produce severe disease in the nursing infant. Only a few cases of transmission of GBS from mother to baby through breast milk are reported in the literature. 3–7 Because of the fact that the colony counts of GBS remained high in mother’s milk until oral amoxicillin was introduced, it is tempting to postulate mother-to-child transmission of GBS in our case and the reported cases in the literature. 4 Further studies of bacterial growth in mother’s milk as it relates to colonization or disease of mothers and infants with GBS might be of interest. To our knowledge only one study has examined the breast carriage rate in humans, finding an incidence of 3.5% in 1132 samples from healthy lactating mothers. 10 We believe that cases of transmission of GBS in breast milk may be underreported. As seen in our case GBS may be present in breast milk without causing clinical mastitis. 4 Rifampin and amoxicillin have been successfully used to eradicate carriage of the organism in mother and neonate when there was GBS infection, but these are isolated reports. 4, 11 Fernandez et al. 12 reported that rifampin failed to reliably eradicate GBS colonization in infants. We treated our mother with amoxicillin. Repeated negative cultures of breast milk gave evidence of successful suppression or eradication of GBS in the mother’s milk. We conclude that transmission of group B streptococci via breast milk is unusual but should be considered in cases of late onset or recurrent GBS disease.