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Neonatal sepsis (Sepsis neonatarum). Risk factors for neonatal sepsis:. 1. Vaginal colonization with group B streptococcus. 2. Prolonged rupture of membranes (>24hr). 3. Amnionitis. 4. Maternal fever or leukocytosis. 5. Fetal tachycardia. 6. Preterm delivery. 7. Black race and male sex.
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Risk factors for neonatal sepsis: 1. Vaginal colonization with group B streptococcus. 2. Prolonged rupture of membranes (>24hr). 3. Amnionitis. 4. Maternal fever or leukocytosis. 5. Fetal tachycardia. 6. Preterm delivery. 7. Black race and male sex. 8. Congenital immune deficiency or asplenia. 9. Presence of galactosemia (E.coli sepsis). 10. Congenital malformation e.g. obstructive uropathy.
Portal of entery : 1. Transplacental hematogenous spread (vertical transmission)of M.O. from the mother to her infant which might occur at different times during with manifestation of infection present at birth or delayed for months or years. 2. Ascending infectionsthrough the cervix, with or without rupture of membranes, which might results in amnionitis, funisitis (infection of umbilical cord), congenital pneumonia or sepsis.
3. Infection acquired from passage through an Infected birth canalor exposure to infected blood at delivery (e.g. herpes simplex, hepatitis B, bacterial infection) 4. Nosocomial infectionwhich occurs after birth due to neonatal exposure to various infectious agents in the nursery or in the community, especially in the presence of central vein catheter, umbilical vessels catheter, endotracheal tube, or electronic monitoring devices.
Types of neonatal sepsis: It's of 3 types according to the time of onset which are early-onset, late-onset and nosocomial sepsis. I. Early-onset sepsis: Its manifested at period from birth-7 days of life, the infection is usually begins in utero and usually is due to infection by bacteria in the mother GUT, which include group B streptococcus, E.coli, Klebsiella, L.monocytogenes, and nontypable H.influenzae.
II. Late-onset neonatal sepsis: In which the manifestations begin between 8-28 days of life, its usually occur in healthy full-term neonate who was discharged in good health from the normal newborn nursery. Causative microorganisms of late-onset sepsis are similar to those in early-onset sepsis, but late-onset sepsis may be caused by the pathogens usually found in older infants (H. influnzae type B, streptococcus pneumoniae, N. meningitides), in addition to viral agents (HSV, CMV).
III. Nosocomially acquired sepsis: (8days-discharge) Occurs predominantly in premature infants in the NICU, many of these infants have been infected with multidrug-resistant bacteria which present in NICU Risk factors: 1. Frequent treatment with broad spectrum antibiotics for sepsis in the NICU. 2. Presence of central venous catheters, endotracheal tubes, umbilical vessel catheters, and electronic monitoring devices.
Causative microorganisms: Commonly s. aureus (occasionally methicillin-resistant), S. epidermidis (usually methicillin-resistant), and gram negative pathogens.
Clinical features: 1. Early manifestations include grunting, poor feeding, pallor, apnea, lethargy, hypothermia or abnormal cry (which is non specific manifestations). 2. In preterm infants, it's often very difficult to differentiate sepsis from RDS, so that most preterm infants with RDS receive broad spectrum antibiotics. 3. Multiorgan system disease manifested by respiratory failure, shock, DIC, acute tubular necrosis and symmetric peripheral gangrene.
4. Hematogenous spread (especially in late-onset sepsis): may result in focal infection such as meningitis (75%of late-onset and 30% of early-onset sepsis cases), osteomylitis (group B streptococci, s.aureus), arthritis (gonococcus, s. aureus, Candida albicans), and UTI (gram negative bacteria). 5. Nosocomial sepsis might associated with omphalitis, eye discharge, diarrhea and bullous impetigo.
Investigations: 1. Blood culture and urine culture. 2. Cerebrospinal fluid (CSF) for gram stain, cells count, protein and culture. Normal newborn infants have elevated CSF protein (100-150 mg/dl), and as many as 25 WBC, 75% of which are lymphocytes in the absence of infection. 3. Detection of bacterial and viral antigens in blood, urine, or CSF by counterimmunoelectrophoresis or Latex agglutination test.
4. Serial CBC to identify neutropenia, an increased numbers of immature neutrophils (bands) and thrombocytopenia. 5. C-reactive protein levels which are elevated in bacterial sepsis. 6. Chest X-ray to detect pneumonia. 7. Arterial blood gases to detect hypoxia and metabolic acidosis. 8. Blood pressure, urine output and peripheral perfusion monitoring to determine the need to treat septic shock with fluids and vasopressor agents (dopamine, dobutamine).
Treatment: 1. Combination of ampicilline and gentamycin for 10-14 days is effective against most organisms responsible for early-onset sepsis. If meningitis is present, the treatment is extended to 21 days, or 14 days after a negative CSF culture. **If gram negative meningitis present or increase resistance rate to ampicillin, as in late-onset sepsis, most centers change to a third generation cephalosporines (cefotaxime or ceftazidine) plus ampicillin.
**Because the nosocomial sepsis is caused by multidrug-resistance bacteria which present in the NICU, so it treated by combination of Vancomycin or naficillin with gentamycin. **The dose and intervals of all aminoglycosides, such as gentamycin, vary with postnatal age and birth weight. Treatment with aminoglycoside for more than 3 days needs monitoring of serum levels to avoid ototoxicity and nephrotoxicity. Persistent signs of infection despite antibiotics treatment should suggest candidal or viral sepsis.
2. Inhaled nitric oxide and/or ECMO for treatment of septic-related pulmonary hypertension. 3. Treatment of septic shock by I.V. fluid, plasma expanders, and vasopressor agents.
Congenital infections (STORCH)
Congenital syphilis: Its caused by spirochete Treponema pallidum. Newborn infants acquired infection transplacentally from an infected mother to her fetus and, less commonly, at birth, in postpartum period, or by infected blood.
Clinical features: Early manifestations: occurring between birth and 1st year of life, including: Fever, anemia, failure to thrive, irritability, mucocutaneous lesions (maculopapular rash on trunk, palms and soles, condylomata, bullous eruption), persistent rhinitis (snuffles), HSM, lymphadenopathy, and pseudoparalysis due to osteochondritis. Late manifestations: appears many years after birth and manifested as multiple bone signs (frontal bossing, saber shins), Hutchinson teeth (screw-like teeth), and saddle nose deformity.
saber shins Snuffles
Investigations: 1. Direct hyperbilirubinemia. 2. Elevated liver function tests. 3. Bone X-ray shows multiple sites of osteochondritis. 4. Thrombocytopenia. 5. Coombs test negative hemolytic anemia. 6. Leukocytosis.
Diagnosis: Its confirm by: 1. Western blot test or PCR to identify treponema antigens. 2. Dark field examination of mucocutaneous lesions which might show motile organisms. Treatment: Crystalline penicillin G 100,000 – 150,000 U/kg I.V. every 8 hr for 2-3 wk.
Congenital toxoplasmosis: It's caused by Toxoplasma gondii parasite, and congenital infection occur through transplacental transmission during acute infection of pregnant women.
Clinical features: Most infected mothers are asymptomatic, and if infection occur during pregnancy, 40-60% of infants will be infected. If mother infected latter in the pregnancy (3rd trimester), the fetus will be more likely to be infected, but with less sever illness than that if the infection occurs earlier in pregnancy. Severely infected fetus will be stillborn. Live infants have poor feeding, fever, rash, petichae, LAP, HSM, jaundice, hydrocephalus or microcephaly, microphthalmia, seizures, cerebral calcification and chorioretinitis.
Diagnosis: By detection of IgM anti-toxoplasma antibodies. Treatment:combination of oral pyrimethamine and sulfadiazine for 1 year. Doses: Pyrimethamine 1-2mg/kg/24hr for 2 days then 1mg/kg/24hr for 2 mo or 6mo, then 1mg/kg/24hr 3 days a week. Sulfadiazine 100mg/kg/24hr loading dose, then 10mg/kg/24hr in 2 divided doses
Congenital rubella syndrome: Its serious multisystemic syndrome, acquired from infected mother with rubella virus, characterized by wide spectrum of clinical manifestations and congenital defects. The risk of congenital defects and disease is greater with primary maternal infection during the first trimester, congenital defects occur in about 90% of infants if mother acquired infection during 1st trimester.
Clinical features: IUGR (most common), cataract, microphthalmia, myocarditis, and congenital heart diseases (PDA, or pulmonary artery stenosis), sensorineural deafness and meningoencephalitis. Persistent infection leads to pneumonia, hepatitis, thrombocytopenia, and anemia. Later sequale include motor and mental retardation.
Diagnosis: Is confirmed by finding rubella-specific IgM antibodies in the neonatal serum or by culturing rubella virus from infant (nosopharynx, urine or tissues). Virus can be shed in the urine for 1 yr or longer.
Congenital CMV infection: CMV transmitted from infected mother (primary or reactive diseases) transplacentally, during birth and by breast milk. Clinical features: Prematurity, respiratory distress, pallor, sepsis-like signs, HSM, thrombocytopenia, neutropenia, petechial rash, intracranial calcification, hearing loss and jaundice.
Diagnosis: 1. Detection of CMV in the urine, pharyngeal secretions or peripheral blood leukocytes during 1st week of life. 2. Serological tests to detect a positive CMV-IgM antibodies. Treatment: by antiviral drugs (acyclovir or fascarent).
Neonatal herpes simplex virus (HSV) infection: Majority of cases of neonatal HSV infections are caused by HSV-2 and are acquired when the infant pass through an infected birth canal. Most infected mothers are asymptomatic, and usually no history of maternal or paternal genital HSV infection.
Clinical features: Its caused disseminated (systemic) neonatal infection with initial symptoms occurs within 1 week of birth, these manifestations are: 1. Vesicular or pustular rash 2. Nonfocal meningoencephalitis syndrome. 3. Respiratory distress syndrome. 4. Generalized systemic infection involving several organs including CNS and liver. 5. Systemic infection progresses to acidosis, coagulopathy, shock, and death in majority of untreated cases.
Diagnosis: By PCR or tissue culture for virus. Treatment: by I.V. acyclovir. Thank you for your attention
