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Neonatal sepsis

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

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

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 72 hours of birth) or late-onset (infection arising more than 72 hours 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 8 of every 1000 live births and 71 of every 1000 neonatal admissions.  Of these infections, 82% occur in premature babies (less than 37 weeks) and 81% in low birthweight babies (below 2500 grams) 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 Group B Streptococcus Escherichia coli Late onset neonatal sepsis Coagulase-negative staphylococci Staphylococcus aureus Escherichia coli Listeria monocytogenes Coagulase-negative Staphylococcus Haemophilus influenzae Klebsiella Pseudomonas Enterobacter Candida Group B Streptococcus Serratia Acinetobacter Anaerobes 14 Streptococcus pneumoniae

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

18. 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

19. BACTERIAL INFECTIONS 20

20. 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

21. 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

22. 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 23  Presence of microorganism in CSF sample

23. 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

24. 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

25. 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

26. 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

27. VIRAL INFECTIONS 28

28. 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

29. 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 30  Prevention – MMR vaccination

30. 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

31. HIV INFECTION  Acquired via transplacental 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

32. 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

33. 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

34. 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

35. 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

36. 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 5 kg with uncomplicated P. falciparum, WHO recommends treatment with an ACT at the same mg/kg body weight dose as for children weighing 5 kg 7  Quinine or artesunate for severe malaria  Prevention – use of LLIN in pregnant women, IPT, adequate treatment of pregnant women with malaria 37

37. 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

38. CONCLUION  Neonatal infections are a major cause of morbidity and mortality in the newborn.  Although GBS and E. coli are the most common pathogens associated, other organisms as well as multidrug resistant pathogens need to be considered.  Development of accurate and early diagnostic markers will allow clinicians to better assess the risk of infection and institute appropriate therapy.  Adherence to infection control policies including attention to strict hand hygiene, antibiotic stewardship and catheter management are required to decrease the number of infections in hospitalized neonates. 39

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

40. THANK YOU 41