Neonatal infections

Common neonatal infections

1. 1
NEONATAL
INFECTIONS
BY
DR. AYODELE, NOSRULLAH S
FMC, BIRNIN KEBBI

2. OUTLINE
INTRODUCTION
EPIDEMIOLOGY
PREDISPOSING FACTORS
AETIOLOGY
PATHOGENESIS
CLINICAL PRESENTATION
INVESTIGATIONS
MANAGEMENT
PREVENTION
SUMMARY
CONCLUSION
REFERENCES
2

3. INTRODUCTION
Infection is a major cause of morbidity and mortality in
the newborn
1
It can lead to life-threatening sepsis and accounts for
10%of all neonatal mortality.
It may be early-onset (infection arising within 72hours of
birth) or late-onset (infection arising more than 72hours
after birth)
2
Early-onset neonatal infection is less common than late-
onset neonatal infection but often more severe
2
3

4. INTRODUCTION
Of newborns with early-onset sepsis, 85% present within
24 hours, 5% present at 24-48 hours, and a smaller
percentage present within 48-72 hours
3
Early-onset infection is associated with acquisition of
microorganisms from the mother e.g. via the placenta or
while passing through the birth canal.
Most late onset infections are acquired from the
environment
Pathogens causing infection may be bacteria, viruses,
fungi or protozoa
4

5. INTRODUCTION
Premature and ill infants are more susceptible to sepsis
and may present with subtle nonspecific symptoms.
Considerable vigilance is therefore required in these
patients so that sepsis can be effectively identified and
treated.
When infection is suspected, treatment should be
initiated immediately
5

6. EPIDEMIOLOGY
Over one-third of the estimated four million neonatal
deaths around the world each year are caused by severe
infections and around one million deaths are due to
neonatal sepsis/pneumonia alone.
4
Neonatal infection is present in 8of every 1000live
births and 71of every 1000neonatal admissions.
Of these infections, 82% occur in premature babies (less
than 37weeks) and 81% in low birthweight babies
(below 2500grams)
2
6

7. EPIDEMIOLOGY
In Nigeria, sepsis-related case fatality rates over the last
2 decades ranged over the last 2 decades from
6
26.7% in Abakaliki,
27.3% in Jos,
33.3% in Ile-Ife
7

8. PREDIPOSING FACTORS
Newborn babies are more susceptible to infections due
to the following reasons:
Reduced phagocytic activity of polymorphs
Reduced response to chemotactic factors
Low serum properdin level and defective opsonization
Deficiency of serum complements C1q, C3, and C5
Low levels of IgA and IgM
8

9. PREDIPOSING FACTORS
Deficiency in mechanical barrier-thin skin, low secretion
(mucus, lachrymal), poor ciliary activity
Deficiency in non-specific immune factors -reduced
phagocytosis by polymorphs, opsonization,
complements, cytokines, TNF, IFN
Deficiency in specific immunity -low levels of IgA, IgM
and IgE
9

10. PREDIPOSING FACTORS
Early Onset (EONS) Late onset (LONS)
Maternal GBS Colonization Breakage of the natural barriers (skin and
mucosa)
Chorioamnionitis Prolonged indwelling catheter use
Premature rupture of membranes Invasive Procedures (e.g. Endotracheal
intubation)
Prolonged rupture of membranes (>18
hours)
Necrotizing Enterocolitis
Maternal urinary tract infection Prolonged use of Antibiotics
Multiple pregnancies H
2-receptor blocker or proton pump inhibitor
use
Preterm Delivery (<37 weeks)
Birth trauma
10

11. MODES OF INFECTION
TRANSFER
Early prenatal transplacental transmission –syphilis,
CMS, toxoplasmosis, rubella malaria and HIV
Vertical transmission through infected amniotic fluid
(PROM, aspiration of infected amniotic fluid) –hepatitis,
HIV
Direct infection acquisition during passage through birth
canal –GBS, gonococcus, herpes simplex virus,
Hepatitis, HIV
Postnatal acquisition –community or hospital acquired
(direct contacts with people or contaminants, breast
milk)-Hepatitis, HIV, TB
11

12. MODES OF INFECTION
TRANSFER
Factors influencing which colonized infant will
experience disease include
5
prematurity,
underlying illness,
invasive procedures,
inoculum size,
virulence of the infecting organism,
genetic predisposition,
the innate immune system,
host response, and
transplacental maternal antibodies
12

13. AETIOLOGY
Bacteria
Viruses
Fungi
Protozoa
Mycoplasma
13

14. AETIOLOGY (BACTERIAL)
Early Onset neonatal sepsis Late onset neonatal sepsis
Group B Streptococcus Coagulase-negative staphylococci
Escherichia coli Staphylococcus aureus
Listeria monocytogenes Escherichia coli
Coagulase-negative Staphylococcus Klebsiella
Haemophilus influenzae Pseudomonas
Enterobacter
Candida
Group B Streptococcus
Serratia
Acinetobacter
Anaerobes
Streptococcus pneumoniae
14

15. AETIOLOGY (NON-BACTERIAL)
15
*
*
*
*
*More common

16. PATHOGENESIS
16

17. CLINICAL PRESENTATION
5
Are usually subtle and non-specific
High index of suspicion is needed
17

19. INVESTIGATIONS
FBC –anaemia, leukopenia/leukocytosis, increased
band forms, thrombocytopenia
Erythrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
Sepsis work up –urine, blood, discharge, CSF
PCR –CMV, HSV, Toxoplasmosis
Serology –Syphilis, Rubella, Toxoplasmosis
19

20. 20
BACTERIAL INFECTIONS

21. NEONATAL SEPTICAEMIA
Can be early onset or late onset
Different organisms implicated
Presentation may be non-specific
Investigations –FBC, culture
Treatment
Broad spectrum antibiotics to cover for both gram negative
and gram positive (based on common pathogens in the
area) commenced as early as sample are taken for
investigations
Common combinations include penicillins (e.g. ampicillin)
and aminoglycoside (e.g. gentamicin) or cefotaxime
21

22. NEONATAL SEPTICAEMIA
Supportive therapy
Fluid, electrolyte and acid-base balance
Correction of hypoglycaemia if present
Ensuring adequate caloric intake
Maintenance of thermo-neutral environment
Correction of anaemia with blood transfusion
Anticonvulsant for seizures
Ventilatory support for respiratory failure
Exchange blood transfusion in severe sepsis or DIC
22

23. NEONATAL MENINGITIS
Commonly by GBS, E.coli, L. monocytogens
Less commonly by Streptococcus pneumoniae and
Staph aureus
Presentation as for septicaemia, others may include
bulging anterior fontanelle, focal or generalized seizure,
nuchal rigidity
Lumbar puncture must always be done for chemistry,
microscopy, culture and sensitivity
WBC >32/mm
3
predominantly polymorphs (>60%)
CSF sugar <50% of simultaneously obtained blood sugar
CSF protein >150mg/dl
Presence of microorganism in CSF sample
23

24. NEONATAL MENINGITIS
Blood culture and urine culture be obtained
Treatment
same principles guiding antimicrobial treatment of neonatal
septicaemia
Cefotaxime+ampicillin
To be treated for at least 14 days
24

25. OPHTHALMIA NEONATORUM
Inflammation of the conjunctiva in neonatal period
May be caused by gonococcus or chlamydia.
Others include: Staph. Strept., gram negative bacilli
It is a major cause of blindness in the developing world
It is acquired during delivery as the baby passes through
an infected birth canal.
May present with profuse purulent eye discharge with
varied oedema of the eyelids and conjunctiva 2-3 days
after birth.
Diagnosis is by gram staining and culture of the
discharge (ELISA or DNA probe testing for chlamydia)25

26. OPHTHALMIA NEONATORUM
Treatment -antibiotics.
Mild infection –
erythromycin/gentamicin/ciprofloxacin/chloramphenicol eye
drops/ointment may be used
Non-penicillinase producing gonococci will respond readily
to penicillin {benzyl penicillin 30mglkg/ day. for 7 days)
Penicillinase-producing gonococcus respond to third
generation cephalosporin
Chlamydia –erythromycin 50mg/kg/day in 4 divided doses
for 14 days
Prevention –instill into the eye freshly prepared 1%
silver nitrate or 1% tetracycline (Crede's prophylaxis).26

27. CORD OMPHALITIS
An acute bacterial infection of the umbilical cord, stump
and peri-umbilical tissue
Usually caused by Staph. aureus and gram negative
organisms
Characterized by purulent discharge with or without
offensive odour
Treatment –Cefuroxime 50-75mg/kg/day in 2 divided
doses for 5 days
Prevention –cord care with spirit or chlorhexidine
27

28. VIRAL INFECTIONS
28

29. CYTOMEGALOVIRUS
INFECTION
Acquired by transplacentally, through birth canal or
breast feeding
Perinatal infection less severe than congenital
Presentation-the severe form of the disease may
manifest with low birth weight, hepatosplenomegaly,
jaundice, petechiae, microcephaly, chorioretinitis and
intracranial calcification
Diagnosis -demonstration of the virus in the urine or
throat washing, raised complement fixing antibody and
lgM specific antibodies at birth
Treatment -ganciclovir for 6 weeks may help, supportive
5
Prevention –?vaccine (under various reviews)
29

30. RUBELLA INFECTION
Single stranded RNA virus
Infection occurs almost exclusively by vertical
transmission through the placenta
Risk of infection is very high in early pregnancy and
affects embryogenesis with severe consequences
Presentation –classical triad of cataract, congenital
heart disease (PDA, VSD, TOF) and deafness. Others –
microphthalmia, microcephaly, LBW, meningoencehalitis
Diagnosis –history of skin rash in the mother, isolation of
virus in urine, blood, CSF or nasopharyngeal washings
Treatment –no specific, supportive and rehabilitative
Prevention –MMR vaccination
30

31. HEPATITIS
Hepatitis B –double stranded DNA, Hepatitis C single
stranded RNA
Risk of infection is low in early pregnancy and high in
late pregnancy
Presentation –asymptomatic, chronic carriers. May
develop liver problems later in live (carcinoma, cirrhosis)
Prevention –universal preventive measures at birth,
vaccination (passive –immunoglobulin, active –hepatitis
vaccine)
31

32. HIV INFECTION
Acquired viatransplacental transfer in utero, in the birth
canal as the baby is delivered and through ingestion of
breast milk
Presentation -asymptomatic during the neonatal period,
intrauterine growth restriction, features of LBW and
failure to thrive
Diagnosis –history of HIV in the mother, early diagnosis
can be made by use of DNA PCR assay (done at birth,
repeated at 1-2 months, 4 months and at 12 months or
older.
Negative test at 4 months or older gives near 100%
assurance that the infant is not infected.
32

33. HIV INFECTION
Treatment –not specific, supportive
Prevention (PMTCT)
Voluntary counselling and testing of all pregnant women
HIV infected pregnant women to be started on HAART for
life (Option B)
Precautions to limit transmission at delivery
Prophylactic treatment on nevirapine ±zidovudine
(depending on the risk)
Feeding –exclusive or formula feeding
33

34. VARICELLA INFECTION
Infants whose mothers demonstrate varicella in the
period from 5 days prior to delivery to 2 days afterward
are at high risk for severe varicella
Usually acquired transplacentally from maternal viremia
Presentation –rash, LBW, congenital varicella syndrome
Treatment -acyclovir 10 mg/kg every 8 hr IV
Prevention –VZIG or IVIG
34

35. NEONATAL CANDIDIASIS
Caused by Candida albicans giving either oral thrush or
diaper dermatitis
Acquired while passing through birth canal
Presentation –whitish adherent patches on the tongue
and buccal mucosa, erythematous, scaly and popular
eruptions on the perineal skin
Treatment
oral thrush –nystatin oral suspension 100,000IU qds for
10-14days
Dermatitis –keep area dry,2% nystatin, 2% miconazole or
1% clotrimazole cream applied topically are effective
35

36. NEONATAL MALARIA
Acquired congenitally by transplacental transmission or
postnatally, usually iatrogenically through blood
transfusion
Infection through mosquito bite may occur in late
neonatal life
Congenital malaria is associated with low birth weight.
Presentation –similar to neonatal septicaemia. In less
severe cases -jaundice, anaemia, hepatosplenomegaly,
persistent low grade pyrexia and poor weight gain
Diagnosis -demonstration of parasites in blood films
(thick and thin)
36

37. NEONATAL MALARIA
Treatment
Chloroquine, 5mglkg /day in once daily doses for three
days
Sulphadoxine/ pyrimethamine
Artemesinin combination therapy are currently
recommended for neonates. For infants weighing less than
5kg with uncomplicated P.falciparum, WHO recommends
treatment with an ACT at the same mg/kg body weight
dose as for children weighing 5kg
7
Quinine or artesunate for severe malaria
Prevention –use of LLIN in pregnant women, IPT,
adequate treatment of pregnant women with malaria37

38. SUMMARY
Neonatal infection is a major cause of morbidity and
mortality in the newborn
Organisms implicated may be bacteria, virus, fungi or
protozoa
Some of the infections may be highly fatal or cause long
term disability in the baby
Presentation of infection may be simply by unspecific
symptoms, hence, high index of suspicion is needed for
diagnosis
Investigations e.g. septic work-up enhance accurate
diagnosis
38

39. CONCLUION
Neonatalinfectionsareamajorcauseofmorbidityand
mortalityinthenewborn.
AlthoughGBSandE.coliarethemostcommon
pathogensassociated,otherorganismsaswellas
multidrugresistantpathogensneedtobeconsidered.
Developmentofaccurateandearlydiagnosticmarkers
willallowclinicianstobetterassesstheriskofinfection
andinstituteappropriatetherapy.
Adherencetoinfectioncontrolpoliciesincludingattention
tostricthandhygiene,antibioticstewardshipand
cathetermanagementarerequiredtodecreasethe
numberofinfectionsinhospitalizedneonates.
39

40. REFERENCES
1.Azubuike JC, Nkanginieme KE. Paediatrics and child health in a tropical
region. 2
nd
edition. African Educational Services;. Pp 197-215
2.NICE guidelines:
https://www.nice.org.uk/guidance/qs75/chapter/Introduction
3.Medscape https://emedicine.medscape.com/article/978352-
overview?pa=PHQtUZy%2FyJ4c0w8HZi2Fmtk4YIRaC2txDHetkMNZPIV1
Y8pD%2B%2BORoV7GqCLEie1TVrJxKJt4DRD8mxYr6kYfOw%3D%3D#
a5
4.http://www.who.int/maternal_child_adolescent/news_events/news/2009/19
_01/en/
5.Kliegman, Robert, Richard E. Behrman, and Waldo E. Nelson. Nelson
textbook of pediatrics. 20
th
edition (2016).
6.Ogunlesi TA, Ogunfowora OB. Predictors of mortality in neonatal
septicemia in an underresourced setting. Journal of the National Medical
Association. 2010 Oct 1;102(10):915.
7.http://www.who.int/malaria/areas/high_risk_groups/infants/en/
40

41. THANK YOU
41