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PRESENTED BY
DR.MAYANK SHARMA
GOVT MEDICAL,KOTA
   SYSTEMIC BACTERIAL INFECTIONS IN
    NEONATES IS KNOWN AS NEONATAL
    SEPSIS(NNS).
   NNS IS THE MOST COMMON MORBIDITIES
    SEEN AT THE COMMUNITY AND FACILITY
    LEVEL.
   IT INCORPORATES
    PNEUMONIA,MENINGITIS,
    GASTROENTRITIS AND POLYNEPHRITIS.
   ESCHERICHIA COLI,STAPHYLOCOCCUS
    AUREUS AND KLEBSIELLA SP.
    ARERESPONSIBLE FOR MOST CASES OF
    NNS.
   OTHERS ARE
    ADENOVIRUS,ENTEROVIRUS,TORCH,TRIC
    HOMONIASIS,SYPHILIS,GONORRHOEA.
   CH.PNEUMONAE,H.INFLUENZAE,SPECIES
    OF BACTEROIDES AND CLOSTRIDIUM
    HAVE BEEN FOUND WITH NNS.
   NNS IS OF TWO TYPES:-

   1 EARLY NNS(LESS THAN 72 HOURS AFTER
    BIRTH).

   2 LATE NNS(GREATER THAN 72 HOURS AND
    WITHIN 90 DAYS OF BIRTH).
EARLY NSS                         LATE NNS
1 WITHIN 72 HOURS.                1 FROM 72 HOURS TO 90 DAYS.
2 CAUSED BY ORGANISM PRESENT IN   2 CAUSED BY ORGANISM PRESENT IN
MATERNAL GUT.                     THE EXTERNAL ENVIORMENT.
3 PREDISPOSING FACTORS:-
A. LBW                            A.LBW
B.PROLONG RUPTURE OF              B.LACK OF BREAT FEEDING,POOR
.MEMBRANES,PROLONGED LABOR.       CORD CARE
C. FOUL SMELLING                  C. SUPERFICIAL INFECTION.
LIQUOR,ASPIRATION OF MECONIUM.
D.MULTIPLE PERVAGINUM             D.ASPIRATION OF FEEDS,DISRUPTION
EXAMINATION.                      OF SKIN INTEGRITY WITH NEEDLE
                                  PRICKS,USE OF IV FLUIDS.
   NEONATAL IMMUNE SYSTEM IS LESS
    DEVELOPED.

   PMNs ARE DEFICIENT IN CHEMOTAXIS AND
    KILLING CAPACITY.

   THEY ARE LESS DEFORMABLE.

   CAPACITY OF NEONATAL PMNs FOR
    PHAGOCYTOSIS ARE REDUCED.
   FINALLY PMN RESERVES ARE EASILY
    DEPLETED.

   MACROPGHAGE CHEMOTAXIS IS
    IMPAIRED.

   THERE NUMBER IS ALSO DECREASED.

   CYTOKININ PRODUCTION IS DECREASED.
   POPULATION OF T-CELLS IN NEONATES
    ALSO IMMATURE.

   B-CEEL STIMULATION AND
    PROLIFERATION ALSO DECREASED.

   ALL THESE REASONS LEAD TO NNS.
Etiopathogenesis of neonatal sepsis

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Etiopathogenesis of neonatal sepsis

  • 2. SYSTEMIC BACTERIAL INFECTIONS IN NEONATES IS KNOWN AS NEONATAL SEPSIS(NNS).  NNS IS THE MOST COMMON MORBIDITIES SEEN AT THE COMMUNITY AND FACILITY LEVEL.  IT INCORPORATES PNEUMONIA,MENINGITIS, GASTROENTRITIS AND POLYNEPHRITIS.
  • 3. ESCHERICHIA COLI,STAPHYLOCOCCUS AUREUS AND KLEBSIELLA SP. ARERESPONSIBLE FOR MOST CASES OF NNS.  OTHERS ARE ADENOVIRUS,ENTEROVIRUS,TORCH,TRIC HOMONIASIS,SYPHILIS,GONORRHOEA.  CH.PNEUMONAE,H.INFLUENZAE,SPECIES OF BACTEROIDES AND CLOSTRIDIUM HAVE BEEN FOUND WITH NNS.
  • 4. NNS IS OF TWO TYPES:-  1 EARLY NNS(LESS THAN 72 HOURS AFTER BIRTH).  2 LATE NNS(GREATER THAN 72 HOURS AND WITHIN 90 DAYS OF BIRTH).
  • 5. EARLY NSS LATE NNS 1 WITHIN 72 HOURS. 1 FROM 72 HOURS TO 90 DAYS. 2 CAUSED BY ORGANISM PRESENT IN 2 CAUSED BY ORGANISM PRESENT IN MATERNAL GUT. THE EXTERNAL ENVIORMENT. 3 PREDISPOSING FACTORS:- A. LBW A.LBW B.PROLONG RUPTURE OF B.LACK OF BREAT FEEDING,POOR .MEMBRANES,PROLONGED LABOR. CORD CARE C. FOUL SMELLING C. SUPERFICIAL INFECTION. LIQUOR,ASPIRATION OF MECONIUM. D.MULTIPLE PERVAGINUM D.ASPIRATION OF FEEDS,DISRUPTION EXAMINATION. OF SKIN INTEGRITY WITH NEEDLE PRICKS,USE OF IV FLUIDS.
  • 6. NEONATAL IMMUNE SYSTEM IS LESS DEVELOPED.  PMNs ARE DEFICIENT IN CHEMOTAXIS AND KILLING CAPACITY.  THEY ARE LESS DEFORMABLE.  CAPACITY OF NEONATAL PMNs FOR PHAGOCYTOSIS ARE REDUCED.
  • 7. FINALLY PMN RESERVES ARE EASILY DEPLETED.  MACROPGHAGE CHEMOTAXIS IS IMPAIRED.  THERE NUMBER IS ALSO DECREASED.  CYTOKININ PRODUCTION IS DECREASED.
  • 8. POPULATION OF T-CELLS IN NEONATES ALSO IMMATURE.  B-CEEL STIMULATION AND PROLIFERATION ALSO DECREASED.  ALL THESE REASONS LEAD TO NNS.