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Neonatal Infections

Neonatal Infections. Mesfin Woldesenbet, MD Jimma University, Jimma, Ethiopia Houston, Texas July, 2012. Questions?. Why are infants, especially premies, more susceptible to infections? What are the clinical manifestations of neonatal infections? Bacterial? HSV?

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Neonatal Infections

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  1. Neonatal Infections Mesfin Woldesenbet, MD Jimma University, Jimma, Ethiopia Houston, Texas July, 2012

  2. Questions? • Why are infants, especially premies, more susceptible to infections? • What are the clinical manifestations of neonatal infections? • Bacterial? • HSV? • How to prevent infections? • Antibiotics - indications, contraindications, cautions, resistance, etc. • How to interpret labs? • Any precautions with lines?

  3. Objectives • To briefly review neonatal immunology and why neonates are so susceptible to infections • To review the epidemiology, clinical presentation, diagnosis and treatment of the most common bacterial and HSV neonatal infections. • To review modes of infection prevention. • To differentiate between preterm and term infants in all these areas

  4. “Prematurity is an infectious disease.” - James Todd, M.D.

  5. Why are infants, especially premies, more susceptible to infections?

  6. Neonatal Immune System • All neonates relatively immunocompromised • Immature and Ineffective: • Antibodies • Complement • Neutrophils • Skin / mucosal barriers

  7. Antibody

  8. Antibodies  Infectious agent   Immunity Antibodies (anti- foreign bodies) are produced by host white cells on contact with the invading micro-organism which is acting as an antigen (e.g. generates antibodies). The individual may then be immune to further attacks. (Modified From: Roitt, I: Essential Immunology, 4th edition, Blackwell Scientific Publications, 1980)

  9. Antibodies  Infectious agent   Immunity x x No contact with infectious agents = no antibody production

  10. Maternal Transfer of Antibodies • Antibody transfer increases with GA • Most during 3rd trimester • No guarantee maternal antibodies present to the infecting organism Remington and Klein, Sixth Edition, 2006

  11. Complement

  12. Neutrophils

  13. Neonatal Neutrophils • Immature •  Chemotaxis •  Deformability •  Phagocytosis •  Storage pool • Adults 14-fold > circulating pool • Neonates only 2-fold

  14. Manroe et al, J Pediatr, 1979

  15. “Normal” VLBW neonates Mouzinho et al, Pediatr 94:76, 1994

  16. Neonatal Barriers to Infection

  17. Neonatal Anatomic Barriers • Immature skin and mucosal surfaces • layers • junctions between cells • secretory IgA • Umbilical cord • Breaches - catheters, tape

  18. Invasive Fungal Dermatitis in a VLBW infant JL Rowen, Sem Perinatal 27:406-413, 2003

  19. Epidemiology

  20. Incidence • Mortality • 13-69% world wide • 13-15% of all neonatal deaths (US) • Meningitis • 0.4-2.8/1000 live births (US 0.2-0.4/1000) • Mortality 13-59%; US 4% of all neonatal deaths • Sepsis • 1-21/1000 world wide; US1-8/1000 live births • Culture proven 2/1000 (3-8% of infants evaluated for sepsis) • Premature <1000 g 26/1000 1000- 2000 g 8-9/1000

  21. Neonatal Sepsis: Incidence • 2/1000 live births with culture proven sepsis • Bacterial / Viral / Fungal • 80% infants develop bacterial sepsis • 20% infants perinatally acquired viral infections • ~ 25% of infected infants have meningitis • Higher rate with preterm birth • 26/1000 preterm infants with BW < 1000g • 8-9/1000 preterm infants with BW 1000-2000g Remington and Klein, Sixth Edition, 2006

  22. Neonatal Bacterial Sepsis:Disease Patterns • Early Onset Neonatal Sepsis (EONS) • Fulminant, multi-system illness • < 7 days old • Obstetrical complications • Prematurity • Perinatal acquisition • High mortality, 5-50% • Late Onset Neonatal Sepsis (LONS) • Sepsis and/or meningitis • 7days to 3 months old • Perinatal or postnatal acquisition • Lower mortality, 2-6%

  23. Infection Timing • Onset • Early Onset 1st 24 hrs 85 % 24-48 hrs 5% • Late Onset 7-90 days

  24. Etiologic Agents of Neonatal Sepsis Frequency(%)  Group B Streptococci 40  Escherichia coli 17 Streptococcus viridans 7 Staphylococcus aureus 6 Enterococcus spp 6 Coagulase-negative staphylococci 5 Klebsiella pneumoniae 4 Pseudomonas spp 3 Serratia marcescans 2 Others 10 *Schuchat et al, Pediatrics 105: 21-26, 2000

  25. Etiologic Agents of Neonatal Meningitis Gram Positive Bacteria; Frequency (%)  Group B Streptococci 53 Listeria monocytogenes 7 Miscellaneous gram-positives 6 Gram Negative Bacteria:  Escherichia coli 19 Klebsiella species 8 Haemophilus influenzae 1 Miscellaneous gram-negatives 8 Anaerobes 3 Feigen & Cherry, Fifth Edition, 2004

  26. Incidence of Neonatal Group B Streptoccal Sepsis • 5-35% Pregnant women colonized • 1/100-200 colonized women • infant with early onset disease • 1-7/1000 live births in 1993 • 0.44/1000 live births in 1999 Remington and Klein, Sixth Edition, 2006

  27. Group B Strep Association formed 1st ACOG & AAP statements Rate of Early- and Late-onset GBS Disease in the 1990s, U.S. CDC draft guidelines published Consensus guidelines Schrag, New Engl J Med 2000 342: 15-20

  28. What do we know about trends in “other pathogens”? • Most studies: stable rates of ‘other’ sepsis • Concerns for increased rates of E. coli, all gram negatives, or amp-R infections • Population-based (multicenter) studies find stable rates of total non-GBS and E. coli • One multicenter study of very LBW infants found a decrease in GBS by 4.2 /1,000, but an increase in E coli rates of 3.6/1,000 (Stoll et al, NEJM, 2002, 347:240-7) • % of E. coli sepsis w/ amp resistance may be increasing • Increases restricted to low birth weight or preterm deliveries

  29. Ampicillin Susceptibility of E. coli from Early-Onset Sepsis Cases, Full-Term Infants, ABCs, Selected Counties CA and GA, 1998-2000 N=22, p=0.52, linear trend Hyde et al, Pediatrics 2002;110(4):690-5.

  30. Ampicillin Susceptibility of E. coli from Early-Onset Sepsis Cases Preterm Infants, ABCs, Selected Counties CA and GA, 1998-2000 N=37, p=0.02, linear trend Hyde et al, Pediatrics 2002;110(4):690-5.

  31. Susceptibility of GBS: ABC/EIP Isolates, 1995-2000 • 1280 isolates from MN, GA, NY, OR (1173 invasive, 107 colonizing): • All susceptible to penicillin, ampicillin, cefotaxime and vancomycin • 19% erythromycin resistance • 11% clindamycin resistance

  32. Risk Factors for Early Onset Neonatal Sepsis • Primary (significant) • Prematurity or low birth weight • Preterm labor • Premature or prolonged rupture of membranes • Maternal fever / chorioamnionitis • Fetal hypoxia • Traumatic delivery • Secondary • Male • Lower socioeconomic status • African-American race Remington and Klein, Sixth Edition, 2006

  33. Factors associated with early-onset GBS disease: multivariable analysis Schrag et al, NEJM 2002, 347:233-9

  34. Predisposing Factors Overall sepsis rate 8/1000 Maternal Fever 4/1000 PROM 10-13/1000 Fever & PROM 87/1000

  35. Early Onset Neonatal Sepsis:Risk Factors - Maternal Fever • Maternal fever is a significant risk factor for EONS and may add in the identification of infected but initially asymptomatic infant. • 5.36 = adjusted RR • 25% of asymptomatic infants, with culture positive sepsis, had maternal fever as the ONLY criteria for evaluation. Chen et al, J of Perinatal, 2002, 22:653-657

  36. Early Onset Neonatal Sepsis:Presentation and Diagnosis

  37. Early Onset Neonatal Sepsis:Signs/Symptoms ?

  38. Early Onset Neonatal Sepsis:Signs/Symptoms Strongly suggestive hypoglycemia / hyperglycemia hypotension metabolic acidosis apnea shock DIC hepatosplenomegaly bulging fontanelle seizures petechiae hematochezia respiratory distress

  39. Early Onset Neonatal Sepsis:Signs/Symptoms Nonspecific lethargy, irritability temperature instability -- hypothermiaor fever poor feeding cyanosis tachycardia abdominal distention jaundice tachypnea

  40. Early Onset Neonatal Sepsis:Signs/Symptoms - Fever • The infant with sepsis may have an elevated, depressed or normal temperature. • Fever is seen in up to 50% of infected infants. • Fever is more common in term infants, while hypothermia is more common in preterm infants • A single elevated temperature reading or fever as an isolated finding is infrequently associated with sepsis. • Persistent fever for greater than 1 hour is more frequently associated with infection. • Fever occurs more frequently with LONS or with viral, rather than bacterial, sepsis. Klein, Sem in Perinat, 5:3-8

  41. Early Onset Neonatal Sepsis:Laboratory Evaluation •  Cultures  • Chest Radiograph • Complete Blood Cell Count • Glucose • Bilirubin • Liver Function Tests • Coagulation studies • C-reactive Protein (CRP)

  42. RDS vs. GBS pneumonia???

  43. Early Onset Neonatal Sepsis:Cultures -- Who and Which? • Blood culture -- indicated in ALL infants with suspected sepsis. Repeat cultures indicated if initial culture positive. • Urine culture -- low yield in EONS • + in 1.6% EONS compared to 7.47% LONS Klein, Sem in Perinat, 5:3-8

  44. Early Onset Neonatal Sepsis:Cultures -- Who and Which? • CSF culture -- should always be considered Meningitis frequently accompanies sepsis • 50-85% meningitis cases have + blood culture • Yield reportedly low if respiratory distress is the only major sign of infection • Specific signs & symptoms occur in less than 50% of infants with meningitis • Using “selective criteria” for obtaining CSF may result in missed or delayed diagnosis in up to 37% of infants with meningitis Wiswell et al, Pediatrics, 1995

  45. Laboratory Diagnosis of Neonatal Meningitis CSF - - > 32 WBC/mm3 > 60% PMN glucose < 50% - 75% of serum protein > 150 mg/dl organisms on gram stain

  46. Early Onset Neonatal Sepsis:Complete Blood Cell Counts • Is the CBC helpful as an indicator of early onset neonatal sepsis? • Thrombocytopenia frequently associated with sepsis • WBC may be high, low or “normal • Persistent low WBC more predictive of sepsis than elevated WBC (ANC < 1200) • I:T quotient unreliable

  47. Early Onset Neonatal Sepsis:Complete Blood Cell Counts

  48. Early Onset Neonatal Sepsis:Complete Blood Cell Counts • Single or serial neutrophil values DO NOT assist in the diagnosis of EONS or determining the duration of therapy • 99% of asymptomatic, culture-negative neonates > 35 weeks GA had 1 or more “abnormal” WBC values

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