neonatal infection: Risk factor,clinical manifestation,and treatment plus congenital Infections(TORCH)

1. Neonatal Infection
Dr. Abinet Takele

2. Outline
• Objective
• Neonatal sepsis
• Neonatal Infection
• Work Up
• Management principle
• Congenital infection
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3. Neonatal Infection
Objective:
At the end of this session students able to:-
• Describe definition and pathogenesis of neonatal sepsis and
Meningitis
• List etiologies
• Describe risk factors
• Discuss the clinical manifestations, diagnosis and Principles of
management
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4. Causes of Neonatal Mortality (Ethiopia)
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5. Neonatal sepsis
• Neonatal sepsis is a clinical syndrome of systemic illness accompanied
by bacteremia occurring in the first month of life.
• SIRS + suspected(confirmed) bacteremia
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6. SIRS: manifested by 2 or more of the following conditions:
• Temperature instability <35°C (95°F) or >38.5°C (101.3°F)
• Respiratory dysfunction: Tachypnea Hypoxemia,
• Cardiac dysfunction: Tachycardia, Delayed capillary refill,
Hypotension,
• Perfusion abnormalities: Oliguria, Lactic acidosis, Altered mental
status
Sepsis: The systemic inflammatory response to an infectious process
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7. Pathophysiology
Two clinical situations:
• early-onset, and
• late-onset disease.
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8. Early-onset
• Presents in the first 7 days of life.
• The infant has acquired the organism during the intrapartum period
from the maternal genital tract.
• Characterized by a sudden onset and fulminant course
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9. Late-onset
• Occurs 7-28 days of age.
• Bacteria responsible for late-onset sepsis include those acquired after
birth from the maternal genital tract as well as organisms acquired
after birth from human contact or from contaminated equipment.
• The possibility of meningitis is very high 70%
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10. Etiology
• Prenatal (Congenital) infections: TORCH
• Toxoplasmosis,
• Other
• Rubella
• Cytomegalovirus
• Herpes simplex virus
• Perinatal: GBS, E.coli HSV, HIV
• Postnatal: E.coli, Staph aureus
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11. Cnt
• Group B streptococci (GBS): most common,
• Gram-negative enteric organisms, especially E.coli.
• Other Listeria monocytogenes, Staphylococcus, other streptococci
(including the enterococci), anaerobes, and Haemophilus influenzae
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12. Risk factors
• Prematurity and low birth weight.
• Prolonged (>18 h) rupture of membranes.
• Maternal peripartum fever or infection.
• Chorioamnionitis
• Prolonged labor(>24h).
• Meconium-stained or foul-smelling, cloudy amniotic fluid.
• Resuscitation at birth.
• Multiple gestation.
• Others
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13. Clinical presentation
• Hypo- or hyperthermia.
• Lethargy, irritability, or change in tone.
• Poor peripheral perfusion, cyanosis, mottling, pallor, petechiae,
rashes, or jaundice.
• Tachypnea, respiratory distress, apnea, tachycardia, or hypotension.
• Hypo- or hyperglycemia or metabolic acidosis.
• Feeding intolerance, vomiting, diarrhea, or abdominal distention with
or without visible bowel loops.
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14. Diagnosis
Laboratory studies
• Cultures
• Gram's stain of various fluids
• CBC
• Acute-phase reactants(CRP,ESR)
• Abnormal values for bilirubin, glucose, and sodium.
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15. Management
• Supportive: O2, Feeding, Seizure control
• Definitive: Emperic therapy
• Ampicillin 50mg/kg iv bid
• Gentamycine 5mg/kg iv daily
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16. Neonatal Meningitis
Definition.
• Neonatal meningitis is infection of the meninges and CNS in the first
month of life.
Incidence.
• More common in late onset sepsis.
• The mortality rate is 20-50%, and there is a high incidence (50%) of
neurodevelopmental sequelae in survivors.
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17. Pathophysiology
• Infection occurs because of hematogenous seeding of the meninges
and CNS.
• Accompanied by ventriculitis, which makes resolution of infection
more difficult.
• Organisms implicated in neonatal sepsis also cause neonatal
meningitis
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18. Risk factors
• Similar to sepsis
Clinical presentation
• lethargy, reluctance to feed, emesis, respiratory distress, irritability,
and temperature instability.
• Signs suggestive of a CNS involvement convulsion, bulged fontanel,
nuchal rigidity, signs of increased intracranial pressure.
.
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19. Diagnosis
Laboratory studies:
• Culture(CSF /Blood),
• CSF analysis,
• CBC with diff.
Radiologic studies:
• Cranial ultrasound examination,
• CT scan.
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20. CSF analysis suggestive of meningitis:
• Identification of organism on gram stain or culture
• WBC count greater than or equal to 20 cells/mm3
• Low glucose (less than two third of serum value) and
• Protein greater than 150 mg/dl
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21. Management
• Empiric therapy: Ampicillin and gentamicin are usually started as
empiric therapy for suspected sepsis or meningitis.
• Gram-positive meningitis: Penicillin or ampicillin for 14-21 days
• Gram-negative meningitis: Treatment should continue until 14 days
after cultures are negative or for 21 days, whichever is longer.
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22. Complications
Neonatal Sepsis
• DIC
• Endocarditis, septic emboli, abscess formation
Meningitis
• Immediate Cx: ventriculitis, cerebritis, and brain abscess
• Late Cx – occurs in 40–50% of survivor
• hearing loss, abnormal behavior, developmental delay, cerebral palsy,
focal motor disability, seizure disorders, and hydrocephalus.
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23. CONGENITAL INFECTION
TORCH INFECTION

24. Toxoplasmosis
• caused by the protozoa toxoplasma gondii.
• Infection transmitted from the mother to the fetus transplacentally or
during vaginal delivery.
• Overall risk of transmission 50%
• The most severe involvement results from maternal infection that
occurs during the first and second trimesters

25. • Manifestations include IUGR (intrauterine growth retardation),
prematurity, hepatosplenomegaly, jaundice and thrombocytopenia.
• The classical triad consists of hydrocephalus, chorioretinitis and
cerebral calcification.

26. Diagnosis
• Toxoplasma dye test
• Immunofluorescent IgG toxoplasma antibody test or
• IgM antibody test.
Treatment A combination of pyrimethamine and sulfonamide (sulfadiazine
or triple sulfonamides) should be given for one year.
Prevention
• The best way to prevent congenital toxoplasmosis is by preventing acute
maternal infection in pregnancy.

27. Rubella
• Between 50 and 80% are infected if maternal infection occurs prior
to the 8th week of gestation,
• fetal infection is uncommon if maternal infection is in the third
trimester.
Clinical manifestations
• Transient neonatal manifestations,
• Permanent organ malformations and tissue injury
• Delayed late onset disease.

28. Manifestations include:
• IUGR, microcephaly, microphthalmia, cataract, thrombocytopenia,
congenital heart disease (patent ductus arteriosus and peripheral
pulmonary artery stenosis), linear bone lesions, retinitis, convulsions and
sensorineural deafness
Late manifestation
• Hearing loss (87%)
• Congenital heart disease (46%)
• Mental retardation (39%) and
• Cataract and glaucoma (34%)

29.  Diagnosis
• Viral isolation from nasopharygeal secretions, urine or CSF
• Detection of rubella specific IgM
Treatment There is no specific treatment for rubella infection.
• Prevention includes: Rubella vaccine for all nonimmune individuals 12
months of age and older and child bearing age mothers.

30. Cytomegalovirus (CMV)
Mode of transmission include:
• transplacentally
• through genital secretions
• breast milk and
• blood transfusion

31. Clinical manifestations
• In about 40% of primary infections of the mother, the fetus will be
infected
• the majority of neonatal infections are asymptomatic.
• IUGR, jaundice, hepatosplenomegaly, petechial rash, chorioretinitis,
pneumonia, periventricular calcifications and microcephaly

32. Diagnosis :
• Isolation of the virus from the urine or saliva
• Demonstration of CMV specific IgM antibodies
• Treatment There is no specific therapy.

33. Herpes simplex virus (HSV)
Three quarters of HSV neonatal infection is due to HSV type 2 and
the rest is due to type 1.
Modes of infection include
• Mostly from maternal genital tract infection
• Intrauterine infection (5%)
• Postpartum (10%)
• Transmission from a primary lesion is about 50%
• Transmission from recurrent lesions is only 1-3%.

34. • Clinical manifestations There are three major categories
1. Disseminated form commences at about 1 week of age with
constitutional signs and symptoms of sepsis and the characteristic
erythematous based vesicles
2. Skin, eye or mouth disease
3. Encephalitic form - Usually of later onset (3 wks) - Has a lower
incidence of viremia and vesicles

35. Diagnosis:
• cytologic examination,
• direct viral culture of skin, mouth or eye lesions
• analysis of IgM specific antibody response
Treatment
• IV acyclovir for 14 -21 days.
Prevention Delivery by cesarean section may reduce the risk of
neonatal infection.

36. Congenital syphilis
• Caused by treponema pallidum
• Tranmission occure in 100% result in perinatal death in 40%
Clinical manifestation:
• hepatosplenomegaly, lymphadenopathy, hemolytic anemia,
thrombocytopenia and mucocutaneous rash.
• Rhinitis (snuffles) and condylomatous lesions
• CNS abnormalities, failure to thrive, chorioretinitis, nephritis and
nephrotic syndrome

37. Diagnosis Serology:
• VDRL (Venereal Disease Research Laboratory)
• RPR (Rapid Plasma Reagin)
Treatment:
• Crystalline penicillin (100,000-150,000 IU/kg/d iv)
• Procaine penicillin (50,000 IU/kg/d im) for 10-14 days.

38. THANK YOU
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