Late-onset sepsis (8 to 28 days) usually occurs in a healthy full-term infant who was discharged in good health from the normal newborn nursery. Clinical manifestations may include lethargy, poor feeding, hypotonia, apathy, seizures, bulging fontanelle, fever, and direct-reacting hyperbilirubinemia. In addition to bacteremia, hematogenous seeding may result in focal infections, such as meningitis (in 75% of cases), osteomyelitis (group B streptococci, Staphylococcus aureus), arthritis (gonococcus, S. aureus, Candida albicans, gram-negative bacteria), and urinary tract infection (gram-negative bacteria).
The evaluation of infants with late-onset sepsis is similar to that for infants with early-onset sepsis, with special attention given to a careful physical examination of the bones (infants with osteomyelitis may exhibit pseudoparalysis) and to the laboratory examination and culture of urine obtained by sterile suprapubic aspiration or urethral catheterization. Late-onset sepsis may be caused by the same pathogens as early-onset sepsis, but infants exhibiting sepsis late in the neonatal period also may have infections caused by the pathogens usually found in older infants (H. influenzae, S. pneumoniae, and Neisseria meningitidis). In addition, viral agents (HSV, cytomegalovirus, or enteroviruses) may manifest with a late-onset, sepsis-like picture.
Because of the increased rate of resistance of H. influenzae and pneumococcus to ampicillin, some centers begin treatment withampicillin and a third-generation cephalosporin (and vancomycin if meningitis is present) when sepsis occurs in the last week ofthe first month of life. The treatment of late-onset neonatal sepsisand meningitis is the same as that for early-onset sepsis.
An infection acquired transplacentally during gestation is a congenital infection. Numerous pathogens that produce mild or subclinical disease in older infants and children can cause severe disease in neonates who acquire such infections prenatally or perinatally. Sepsis, meningitis, pneumonia, and other infections caused by numerous perinatally acquired pathogens are the cause of significant neonatal morbidity and mortality. Congenital infections include a well-known group of fungal, bacterial, and viral pathogens: toxoplasmosis, rubella, cytomegalovirus (CMV), herpes simplex virus (HSV), varicella-zoster virus, congenital syphilis, parvovirus, human immunodeficiency virus (HIV), hepatitis B, Neisseria gonorrhoeae, Chlamydia, and Mycobacterium tuberculosis.
Many of the clinical manifestations of congenital infections aresimilar, including intrauterine growth restriction, nonimmunehydrops, anemia, thrombocytopenia, jaundice, hepatosplenomegaly, chorioretinitis, and congenital malformations. Some unique manifestations and epidemiologic characteristics of theseinfections are listed in Table 66-1. Evaluation of patients thoughtto have a congenital infection should include attempts to isolatethe organism by culture (for rubella, CMV, HSV, gonorrhea, and
M. tuberculosis), to identify the antigen of the pathogen (for hepatitis B and Chlamydia trachomatis), to identify the pathogen’sgenome with polymerase chain reaction (PCR), and to identifyspecific fetal production of antibodies (IgM or increasing titer ofIgG for Toxoplasma, syphilis, parvovirus, HIV, or Borrelia).