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Bacterial Sepsis & Meningitis 6 Bacterial Sepsis and Meningitis VICTOR NIZET and JEROME O. KLEIN CHAPTER OUTLINE Bacteriology Gastrointestinal Signs Group B Streptococci Skin Lesions Group A Streptococci Neurologic Signs Streptococcus Pneumoniae Diagnosis Other Streptococci Maternal History Enterococcus Species Microbiologic Techniques Staphylococcus Aureus and Coagulase- Laboratory Aids Negative Staphylococci Management Listeria Monocytogenes Choice of Antimicrobial Agents Escherichia Coli Current Practice Klebsiella Species Continuation of Therapy when Results of Enterobacter and Cronobacter Species Cultures are Available Citrobacter Species Management of the Infant whose Mother Serratia Marcescens Received Intrapartum Antimicrobial Pseudomonas Aeruginosa Agents Salmonella Species Treatment of the Infant whose Bacterial Culture Results are Negative Neisseria Meningitidis Management of the Infant with Catheter- Haemophilus Influenzae Associated Infection Anaerobic Bacteria Treatment of Neonatal Meningitis Neonatal Tetanus Management of the Infant with a Brain Mixed Infections Abscess Uncommon Bacterial Pathogens Treatment of the Infant with Meningitis Epidemiology whose Bacterial Culture Results are Incidence of Sepsis and Meningitis Negative Characteristics of Infants who Develop Treatment of Anaerobic Infections Sepsis Adjunctive Therapies for Treatment of Nursery Outbreaks or Epidemics Neonatal Sepsis Pathogenesis Prognosis Host Factors Predisposing to Neonatal Prevention Bacterial Sepsis Obstetric Factors Infection in Twins Chemoprophylaxis The Umbilical Cord as a Focus of Infection Maternal Factors Administration of Drugs to the Mother Immunoprophylaxis Before Delivery Decontamination of Fomites Administration of Drugs other than Epidemiologic Surveillance Antibiotics to the Neonate Sepsis in the Newborn Recently Pathology Discharged From the Hospital Clinical Manifestations Congenital Infection Fever and Hypothermia Late-Onset Disease Respiratory Distress Infections in the Household Jaundice Fever in the First Month of Life Organomegaly 217 218 SECTION II • Bacterial Infections Bacterial sepsis in the neonate is a clinical syndrome Table 6-1 Characteristics of Early-Onset and Late-Onset characterized by systemic signs of infection and accom- Neonatal Sepsis panied by bacteremia in the first month of life. Menin- † gitis in the neonate usually is a sequela of bacteremia Characteristic Early Onset* Late Onset and is discussed in this chapter because meningitis and Time of onset (days) 0-6 7-90 sepsis typically share a common cause and pathogen- Complications of + ± esis. Infections of the bones, joints, and soft tissues and pregnancy or of the respiratory, genitourinary, and gastrointestinal delivery tracts can be accompanied by bacteremia, but the cause, Source of organism Mother’s genital tract Mother’s genital clinical features, diagnosis, and management of these tract; postnatal infections are sufficiently different to warrant separate environment discussions. Bloodstream and central nervous system Usual clinical Fulminant Slowly progressive or (CNS) infections caused by group B streptococci (GBS), presentation fulminant Staphylococcus aureus, and coagulase-negative staphy- Multisystem Focal lococci (CoNS), Neisseria gonorrhoeae, Listeria monocyto- Pneumonia frequent Meningitis frequent genes, Salmonella spp., and Mycobacterium tuberculosis are Mortality rate (%) 3-50‡ 2-40‡ described in detail in other individual chapters. Chapter 2 *Many studies define early-onset sepsis as that which occurs in the first describes the features of neonatal sepsis and meningitis 72 hours of life; others in the first 5 or 6 days of life. in developing regions. †Very small premature infants may have late-onset sepsis beyond 90 days The two patterns of disease, early-onset and late-onset, of life. have been associated with systemic bacterial infections ‡Higher mortality rates in earlier studies. during the first month of life (Table 6-1). Early-onset disease typically presents as a fulminant, systemic ill- has been accompanied by increased risk for nosocomial ness during the first 24 hours of life (median age of onset or hospital-associated infections and for very-late-onset approximately 6 hours), with the large majority of other disease1 (see Chapter 35). cases presenting on the second day of life. Infants with early-onset disease can have a history of one or more obstetric complications, including premature or pro- Bacteriology longed rupture of maternal membranes, preterm onset of labor, chorioamnionitis, and peripartum maternal The changing pattern of organisms responsible for neo- fever, and many of the infants are premature or of low natal sepsis is well illustrated in a series of reports by birth weight (LBW). Bacteria responsible for early-onset pediatricians at the Yale–New Haven Hospital covering disease are acquired hours before delivery from the birth the period 1928 to 20032-8 (Table 6-2). Before develop- canal during delivery after overt or occult rupture of ment of the sulfonamides, gram-positive cocci, including membranes. The mortality rate varies from 3% to as high S. aureus and β-hemolytic streptococci, caused most cases as 50% in some series, especially with gram-negative of neonatal sepsis. With the introduction of antimicro- pathogens. Late-onset disease has been variably defined bial agents, gram-negative enteric bacilli, particularly for epidemiologic purposes as occurring after 72 hours E. coli, became the predominant cause of serious infec- to 6 days (e.g., GBS) of life. Very-late-onset infection tion in the newborn. Reports for the periods of 1966 to caused by GBS (disease in infants older than 3 months) 1978 and 1979 to 1988 document the rise to impor- is discussed in Chapter 12. Term infants with late-onset tance of GBS and E. coli as agents of neonatal sepsis. In infections can have a history of obstetric complications, the most recent analysis from 1989 to 2003, CoNS spe- but these are less characteristic than in early-onset sep- cies, predominantly Staphylococcus epidermidis, emerged sis or meningitis. Bacteria responsible for late-onset sep- as the single most commonly identified agent of neo- sis (LOS) and meningitis include those acquired from natal sepsis, with GBS, E. coli, Enterococcus faecalis, S. the maternal genital tract and organisms acquired aureus, and Klebsiella spp. also occurring at substantial after birth from human contacts or, infrequently, from frequency. The latest reports also document the prob- contaminated hospital equipment or materials, where lem of sepsis in very premature and LBW infants who prolonged intensive care is needed for a neonate. The have survived with the aid of sophisticated life-support mortality rate usually is lower than that for early-onset equipment and advances in neonatal intensive care; it is sepsis but can vary between 2% and 40%, with the latter these infants for whom CoNS are particularly threaten- figure typically for very-low-birth-weight (VLBW) infants ing. Emerging data from the same center indicate that with gram-negative sepsis. Because different microor- intrapartum antibiotic prophylaxis protocols, although ganisms are responsible for disease according to age at reducing the overall incidence of early-onset sepsis, may onset, the choice of antimicrobial agents also differs. be influencing a higher proportion of septicemia attribut- Some organisms, such as Escherichia coli, groups A and able to ampicillin-resistant E. coli.9 B streptococci, and L. monocytogenes, can be responsible The etiologic pattern of microbial infection observed at for early- and late-onset infections, whereas others, such Yale Medical Center also has been reported in studies of as S. aureus, CoNS, and Pseudomonas aeruginosa, rarely neonatal sepsis carried out at other centers during the same cause early-onset and typically are associated with late- intervals. Studies indicate that GBS and gram-negative onset disease. The survival of VLBW infants with pro- enteric bacilli, predominantly E. coli, were the most frequent longed stays in the neonatal intensive care unit (NICU) pathogens for sepsis, but other organisms were prominent 6 • Bacterial Sepsis and Meningitis 219 Table 6-2 Bacteria Causing Neonatal Sepsis at Yale–New Haven Hospital, 1928-2003 NO. OF CASES Organism 1928-1932* 1933-1943† 1944-1957† 1958-1965‡ 1966-1978§ 1979-1988ǁ 1999-2003¶ β-Hemolytic streptococci 15 18 11 8 86 83 155 Group A 16 5 0 0 0 0 Group B 2 4 1 76 64 86 Group D (Enterococcus) 0 1 7 9 19 65 Viridans streptococci 11 10 Staphylococcus aureus 11 4 8 2 12 14 70 Staphylococcus epidermidis 36 248 Streptococcus pneumoniae 2 5 3 2 2 2 0 Haemophilus spp. 1 9 9 5 Escherichia coli 10 11 23 33 76 46 106 Pseudomonas aeruginosa 1 0 13 11 5 6 33 Klebsiella and Enterobacter spp. 0 0 0 8 28 25 97 Others 0 6 4 9 21 38 54 Total no. of cases 39 44 62 73 239 270 784 Mortality rate for years 87% 90% 67% 45% 26% 16% 3% *Data from Dunham EC: Septicemia in the newborn, Am J Dis Child 45:229, 1933. †Data from Nyhan WL, Fousek MD: Septicemia of the newborn, Pediatrics 22:268, 1958. ‡Data from Gluck L, Wood HF, Fousek MD: Septicemia of the newborn, Pediatr Clin North Am 13:1131, 1966. §Data from Freedman RM, Ingram DL, Cross I, et al: A half century of neonatal sepsis at Yale, Am J Dis Child 35:140, 1981. ǁData from Gladstone IM, Ehrenkranz RA, Edberg SC, Baltimore RS: A ten-year review of neonatal sepsis and comparison with the previous fifty-year experience, Pediatr Infect Dis J 9:819, 1990. ¶Data from Bizzarro MJ, Raskind C, Baltimore RS, Gallagher PG:
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