Sepsis is one of the leading causes of neonatal morbidity and mortality. Because of difference in local epidemiology and variation with time, regular monitoring and updates on pathogen and their antimicrobial sensitivity pattern is important for prevention and treatment.

Neonatal sepsis is a systemic inflammatory response to infection and/or isolation of bacteria from the blood stream in the first 28 days of life. When pathogenic organisms access into the blood-stream, they can cause an overwhelming infection which leads to develop septicemia. When these organisms predominantly localized to the lung or the meninges they may cause pneumonia and meningitis, respectively [1].

Systemic inflammatory response also describes a clinical syndrome in which there are two or more of the following symptoms: fever, hypothermia, tachycardia, tachypnoea and abnormal white blood cells in immature forms [1].

It is one of the most common causes of neonatal hospital admissions [2–4] and is estimated to cause 26% of all neonatal deaths worldwide [5]. It contributes to 30 to 50% of neonatal deaths in developing countries [6]. In India, the incidence of blood culture proven sepsis was reported as 8.5 per 1,000 live births for the year 2002–2003 by the National Neonatal Perinatal Database (NNPD report 2002-03) [7].

Neonatal sepsis is classified as early onset when it occurs within the first 72 hours of life and late onset when it occurs after 72 hours [8,9]. Early onset sepsis is caused by organisms prevalent in the maternal genital tract, labour room or operating theatre [10, 11] while late onset sepsis usually results from nosocomial or community-acquired infection [3, 11].Neonates are susceptible to sepsis as a result of their immature immune system, the decreased phagocytic activity of their white blood cells and their incompletely developed skin barriers [12–14]. Common risk factors for neonatal sepsis have been identified as prematurity and low birth weight, prolonged rupture of foetal membranes, maternal peri-partum pyrexia, obstructed labour and birth asphyxia [15–19].

The organisms commonly associated with late onset sepsis include coagulase-negative Staphylococci (CONS), Staphylococcus aureus, Klebsiella pneumoniae, Escherichia coli, Enterobacter spp., Pseudomonas aeruginosa and Acinetobacter species. The bacteriological profile for causative organisms of neonatal sepsis differs significantly between developed and developing countries a pneumoniae is the most common bacterial agent causing neonatal sepsis in developing countries, while group B Streptococcus and coagulase-negative staphylococci (CONS) are the common agents in developed countries [11,20].

Even among developing countries, regional variation in prevalence of the bacterial agents causing neonatal sepsis exists. The spectrum of organisms that causes neonatal sepsis changes over times and varies from region to region, due to the changing pattern of antibiotic use and changes in lifestyle [21]. Therefore, periodic evaluation of organisms responsible for neonatal sepsis and their antibiotic sensitivity pattern is essential for the appropriate management of neonates.

After 2002 no major clinical study has been undertaken in India with respect to culture positive late onset sepsis & antibiotic sensitivity. Hence, this study was undertaken to provide further evaluation of culture positive late onset septicemia with reference to antibiotic sensitivity in tertiary care center in India.

Our aim was to assess the incidence of late onset culture positive sepsis in a tertiary care, neonatal intensive care unit in Hapur, India and to study the sensitivity pattern and outcome of the same.

MATERIALS AND METHODS: -

A Prospective observational hospital-based study was carried out among all the babies admitted or referred to SIMS, Hapur NICU from January 2024 to July 2024.

All the neonates with features suggestive of late onset sepsis were included in the study after obtaining consent from their relatives.

Blood, CSF and urine culture and sensitivity analysis was done in department of microbiology, of our hospital.

The data regarding the 100 culture positivity status was plotted according to the causative organism and sensitivity to current antibiotics used in the NICU.

Blood culture and CSF culture were done on automated Bac T alert systems.

Culture reports were evaluated with regards to microorganism typing as well as antibiotic sensitivity based on disc diffusion.

Neonates with late onset culture positive sepsis were treated with appropriate antibiotics as indicated and were followed up with regards to short term outcome.

Statistical Analysis

All the collected data was entered in Microsoft Excel Sheet 2013.The data was then transferred and analyzed using SPSS ver. 21.  Qualitative data was represented in the form of frequency and percentage while quantitative data was represented using Mean +/- S.D. Appropriate statistical tests were applied on the basis of type and distribution of data. A p-value of < 0.05 was taken as level of significance.

RESULTS

Out of the 100 babies with late onset Culture Positive Sepsis, 69% were males while 31% were females. 54% delivered in our hospital while rest 46% were referred cases. Only 28% new-borns weight above 2.5 Kg while 24% were low birth weight. Very low birth weight was observed in 30% babies while 18% had extremely low birth weight (< 1 kg).

About one third of mothers (36%) delivered at term while 64% were pre-term deliveries. Out of these 64 pre-term deliveries, 12 females delivered before 28 weeks.

Table 1:-Distribution of subjects based on type of culture positive specimen

Blood sample was positive in most of the cases (62%) while urine, pus and CSF was positive in 40%, 11% and 5% cases.

Table 2:-Distribution of subjects based on type of culture positive specimen

 Single organism was observed in 77% cases while in 23% cases more than one organism was isolated.

Isolated Blood culture alone was positive in 46% cases while isolated urine culture was positive in 30% cases. About 18% subjects showed positivity in more than 2 samples.

Table 3:-Distribution of subjects based on Type of organism isolated from culture

Most common organism isolated was K. Pneumonia (30%) followed by E. Coli (22%), Enterococcus species (12%), MRSA (11%), Acinetobacter Baumanni (10%) and staph. Aureus (10%). Other organisms isolated were CONS group (13%), Pseudomonas (5%), Enterobacter (3%), Burholderia cepaciae (2%), ESBL Klebsiella Pneumonia (2%), Aerococcus viridans (1%), Citrobacter (1%) and Proteus mirabilis (1%).

Table 4:-Distribution of subjects based on type of organism isolated from various specimens

 Most common organism isolate form blood culture was Klebsiella followed by CONS and from that of Pus was Staph. Aureus. E. coli was most common from urine while CONS group of organism was found in 2 out of 5 specimen of CSF.

Table 5:-Antibiotic sensitivity pattern of Klebsiella Pneumonia

Klebsiella Pneumonia was most sensitive towards Ciprofloxacin, Imipenem and Meropenem while it is resistant towards beta lactum and Cephalosporin group of antibiotics.

Table 6:-Antibiotic sensitivity pattern of E. coli

E.coli was most sensitive towards Piperacillin-Tazobactum and Amikacin while mostly resistant towards beta lactum and cephalosporin group of antibiotics.

Table 7:-Antibiotic sensitivity pattern of CONS

CONS group of organism were sensitive towards tetracycline, Vancomycin, linezolid, Rifampicin and Teicoplanin while they were resistant towards beta lactums, Ciprofloxacin and Clindamycin.

Table 8:-Antibiotic sensitivity pattern of Enterococcus

Enterococcus species were mostly sensitive towards Teicoplanin, Vancomycin, Linezolid and Nitrofurantoin while it is resistant towards beta lactum, Fluroquinolones and Gentamycin.

Table 9:-Antibiotic sensitivity pattern of Acinetobacter Baumanni

All the cases of Acinetobacter Baumanni were sensitive to Colistin while 80% were sensitive to Tigecycline while it is resistant towards most other groups of antibiotics.

Table 10;-Antibiotic sensitivity pattern of Staph. Aureus

All the cases of Staph. Aureus were sensitive towards Tetracycline, Teicoplanin and Vancomycin while 90% were sensitive towards Linezolid and Rifampicin. About 70% of these organisms were resistant to beta lactums.

Table 11:-Antibiotic sensitivity pattern of Methicillin resistant Staph. Aureus

Most of the cases of MRSA were sensitive towards Tetracycline, Teicoplanin, Linezolid and Vancomycin while most of these were resistant to beta lactums.

Table 12:-Antibiotic sensitivity pattern of Pseudomonas Aeruginosa

Over half of the cases of P. Aeruginosa were sensitive to Amikacin, Imipenem, Meropenem and Colistin. While maximum resistant was seen to beta lactams, Ceftriaxone, ciprofloxacin and Nalidixic acid.

Table 13:-Antibiotic sensitivity pattern of Enterobacter Species

All the cases of Enterobacter species were sensitive to Imipenem, Meropenem and Colistin while all are resistant to Cefuroxime.

Table 14:-Antibiotic sensitivity pattern of Burholderia cepacia

Burholderia cepaciae were seen to be resistant towards most of the groups of antibiotics while 1 out of 2 cases were sensitive towards ceftriaxone, Meropenem and Trimethoprim + Sulphamethoxazole.

Table 15:-Antibiotic sensitivity pattern of Extended-spectrum beta-lactamases producing (ESBL) Klebsiella Pneumonia

Two cases of extended-spectrum beta-lactamases producing (ESBL) Klebsiella Pneumonia were sensitive towards Piperacillin-Tazobactum, Amikacin, Ciprofloxacin, Imipenem, Meropenem, Colistin and Tigecycline while both were resistant to beta lactum and Cephalosporin’s.

Table 16:-Antibiotic sensitivity pattern of Aerococcus viridans

One case of Aerococcus viridans was resistant to Penicillin and Trimethoprim+ Sulphamethoxazole while it was resistant to all other tested drugs.

Table 17:-Antibiotic sensitivity pattern of Citrobacter Species

One case of Citrobacter species was sensitive to Piperacillin-Tazobactum, Chloramphenicol, Cefotaxime, Cefipime, Ciprofloxacin, Imipenem and Meropenem and Trimethoprim-Sulphamethoxazole. 

Table 18:-Antibiotic sensitivity pattern of Proteus Mirabilis

One case of Proteus Mirabilis was sensitive to Piperacillin-Tazobactum, Amoxicillin-clavulunate, Amikacin, Imipenem and Meropenem.

DISCUSSION

Sepsis is one of the most common causes of neonatal hospital admissions [2-4] and is estimated to cause 26% of all neonatal deaths worldwide [5]. Late onset sepsis usually presents after 72 hours of age. The source of infection is either nosocomial or community-acquired and neonates usually present with septicemia, pneumonia or meningitis [1]. Nosocomial sepsis frequency and microorganism profiles vary widely from center to center and from country to country [32].

In present study, out of the total 1473 admitted in NICU during study period, 100 cases were observed to be culture positive. So, the overall incidence of sepsis in neonates admitted in the NICU was reported as 6.7%. In a similar study by Resende et al. in Brazil, out of 551 neonates admitted in the NICU during the study period, 112 neonates developed sepsis (20.3%) [33]. Our results were also similar to the rates reported in developing countries [34,35].

Demography

Out of the 100 babies with late onset Culture Positive Sepsis, 69% were males while 31% were females.

Male predominance was also noted in a similar study by Nayak et al., where out of 195 suspected cases of neonatal sepsis, 121 (62.05%) male and 74 (37.95%) were female neonates, with the male to female ratio of 1.63:1 [96]. Jyothi P et al. noted were 65.5% males and 34.5% females in their study with male to female ration of 1.9:1 [89]. Male to female ratio was noted as 2.5:1 by Shah et al. [30]. In a similar study by Vaniya et al., out of the 713 patients with neonatal sepsis, 449 (62.97%) were male and 264 (37.03%) were female subjects [27]. Sawhney et al. observed the prevalence of Male to female prevalence as 59.5% and 40.5% [25].

Thus our results are similar to the previous studies carried out by various authors who hypothesized that incidence of septicemia was higher in males ranging from 59%-82% due to the presence of factors regulating the synthesis of gamma globulin on X chromosome [36]. This may also be due to a gender bias in presentation to hospital prevalent in our community.

Organism Isolated

In present study most common organisms isolated were K. Pneumonia (30%) followed by E. Coli (22%), Staph. Aureus (21% including MRSA 11%), Enterococcus species (12%) and Acinetobacter Baumanni (10%). Other organisms isolated were CONS group (13%), Pseudomonas (5%), Enterobacter (3%), Burholderia cepaciae (2%), ESBL Klebsiella Pneumonia (2%), Aerococcus viridans (1%), Citrobacter (1%) and Proteus mirabilis (1%).

Thus in present study, gram-negative bacteria were the principle pathogens, which caused septicemia. Similar results were reported by Roy et al. and Jain A et al. [37,38]. Similar preponderance of the gram-negative rods has been reported in other studies conducted in India [25,27-30].

In a study by Gupta et al. Klebsiella pneumonia and Escherichia coli were the commonest isolates in 42.30% and 38.46% of cases, respectively [26]. In a study by Sawhney et al., Klebsiella spp has been found to be the predominant pathogen (45.75%) of the culture positive cases followed by staphylococcus aureus (25.7%). Vaniya et al. found that common isolates in neonatal sepsis were Klebsiella, Staphylococcus aureus, and coagulase-negative Staphylococci [27]. Pooja R also observed that Klebsiella spp. were the most common pathogens followed by S.aureus [28]. Klebsiella pneumoniae (30.66%) was the most common organism isolated in another similar study by Nayak et al [29]. Klebsiella pneumoniae (41%) and Coagulase Negative Staphylococcus (31.32%) were the common organisms isolated in a study by Bhurle teet al. [31].

Klebsiella and Staphylococcus aureus can survive in the environment for a relatively long time and fairly widely distributed in the hospital environment, and, therefore, have the potential for being transmitted from the environment to the patients through practices that breach infection control measures. This emphasizes the need for the establishment of effective and functional infection control programs in hospitals [30].

Antibiotic Sensitivity Pattern

Klebsiella Pneumonia was most sensitive towards Ciprofloxacin, Imipenem and Meropenem while it is resistant towards beta lactum and cephalosporin group of antibiotics. In a similar study by Nayak et al. almost 80% of the Klebsiella isolates were resistant to commonly used antibiotics, especially gentamicin and the second and third generation cephalosporin’s. Antibiotic sensitivity testing showed high resistance to multiple drugs while imipenem is still the best for infections with multidrug-resistant organism [29]. Similarly in a study by Jyothi et al., highest sensitivity by K. pneumonia was shown towards Imipenem [22]. In another study by Vaniya et al. Klebsiella Pneumonia was most sensitive towards ciprofloxacin and Gatifloxacin while it is resistant towards beta lactum and cephalosporin group of antibiotics [27]. Sawhney et al. observed Klebsiella Pneumonia to be most sensitive towards Cotrimoxazole, Gentamycin and ciprofloxacin while almost all organisms were resistant towards beta lactum and cephalosporin group of antibiotics [25]. 

In present study, E.coli was most sensitive towards Amikacin and Piperacillin-Tazobactum while mostly resistant towards Ampicillin / Amoxicillin and cephalosporin group of antibiotics. In a study by Nayak et al. two third of the E.coli isolates were resistant to Ampicillin [29]. Shah et al. observed E.Coli to be maximally sensitive towards Amikacin and maximum resistance was towards Cephalosporin [30]. Vaniya et al. observed E.coli isolates to be Fluroquinolones and chloramphenicol and resistant towards Cephalosporin [27].  

In present study, all the cases of Staph. Aureus were sensitive towards Tetracycline, Teicoplanin and Vancomycin while 90% were sensitive towards Linezolid and Rifampicin. About 70% of these organisms were resistant to beta lactums. Most of the cases of MRSA were sensitive towards Tetracycline, Teicoplanin, Linezolid and Vancomycin while most of these were resistant to beta lactums. Similar results were also observed in the studies done by Shrestha et al.[20] and Rahman et al.[39] Our results also matched the reports of Narang A et al., where most of the S. aureus isolates responded very well to Vancomycin [38]. Shah et al. observed maximum resistant towards Cephalosporin and Nalidixic acid [30]. Vaniya et al. observed over 90% sensitivity towards Linezolid while more than 80% resistance was observed for beta lactums [27].  Sawhney et al. observed 84% resistance towards Amoxicillin and 100% sensitivity towards Vancomycin [25].

The clinical significance of relatively low virulence isolates, such as CONS is difficult to ascertain. These organisms can cause true bacteremia or their isolation may represent simple contamination. It would be unfair to ignore such isolates as contaminants. In present study, CONS group of organism were sensitive towards Tetracycline, Vancomycin, Linezolid, Rifampicin and Teicoplanin while they were resistant towards beta lactums, Ciprofloxacin and clindamycin. Sawhney et al. observed 100% resistant towards Amoxicillin among CONS isolates [25]. Vaniya et al. observed maximum sensitivity of CONS towards Levofloxacin, Linezolid and gentamycin. Shah et al. in a similar study, observed maximum resistant among CONS for Clindamycin, ciprofloxacin and Nalidixic acid [30].

Enterococcus species were mostly sensitive towards Teicoplanin, Vancomycin, Linezolid and Nitrofurantoin while it is resistant towards beta lactum, Fluroquinolones and gentamycin. Similar pattern of resistance was noted in the study by Vaniya et al. and Jyothi et al [22].

All the cases of Acinetobacter Baumanni were sensitive to Colistin while 80% were sensitive to Tigecycline while it is resistant towards most other groups of antibiotics. Similar pattern of high resistant to most antibiotics in Acinetobacter species was observed by Nayak et al [29]. A similar observation was also made by Vaniya et al. where Acinetobacter species showed good sensitivity only to Gatifloxacin while they were resistant to all other antibiotics [27].

In present study, over half of the cases of P. Aeruginosa were sensitive to Amikacin, Imipenem, Meropenem and Colistin. While maximum resistant was seen to beta lactums, Ceftriaxone, Ciprofloxacin and Nalidixic acid. Shah et al. observed maximum resistance of pseudomonas isolates towards Cephalosporins, Nalidixic acid and chloramphenicol while maximum sensitivity was observed towards Amikacin [30]. Vaniya et al. also observed poor sensitivity towards cephalosporins and beta lactums with maximum sensitivity towards Gatifloxacin [27]. In the studies done by Bhat et al. [40] and Aletayeb et al. [41] Pseudomonas sp. were the most sensitive to aminoglycoside antibiotics such as amikacin and gentamicin.

Thus present study observed a decreased sensitivity of microorganisms to the commonly used drugs such as ampicillin, amoxicillin and aminoglycosides. Sensitivity of gram-negative and gram positive organisms to the third generation cephalosporins was quite high, which is of great concern. Sensitivity to higher antibiotics like linezolid and Carbapenems was much higher than that to other antibiotics, but it should not be used indiscriminately and be kept as a reserve drug; otherwise, resistance to even these drugs may develop soon, thereby limiting our treatment options. Sensitivity pattern of ciprofloxacin and other fluoroquinolones was also promising. In neonatology, the use of ciprofloxacin in life-threatening infections, although rare, is justified by the fact that clinical benefits largely overweight the potential risks. The various studies indicate a gradual increase in the emergence of antibiotics-resistant organisms. However, many factors play a role in the development of resistance such as no uniformity in the usage of antibiotics, indiscriminate use, and availability of antibiotics. Antibiogram may vary depending on the study group and the hospital setup. So, it is highly recommended that antibiotics should be used depending on the antibiotic sensitivity pattern of the isolates.

CONCLUSIONS

This study indicated that Klebsiella, E.coli and Staphylococcus aureus species remain the principal organisms causing neonatal sepsis. Many multi-drug-resistant organisms were isolated from neonatal septicemia. Therefore, great caution is required in selection of antibiotics. We thus recommend that resistance pattern of the organisms should be considered essential for deciding the empirical treatment. Prompt treatment of neonatal sepsis with judicious use of appropriate antibiotics can minimize the morbidity and mortality, besides reducing the emergence of multidrug resistant organisms in NICU.

BIBLIOGRAPHY

1. Chiesa C, Panero A, Osborn JF, et al. Neonatal sepsis: a clinical and laboratory challenge. Clin Chem 2004; 50(2): 279–287. 
2. Darmstadt GL, Batra M, Zaida AKM. Parenteral antibiotics for the treatment of serious neonatal bacterial infections in developing country settings. Pediatr Infect Dis J 2009; 28(1): S37–S42. 
3. Sankar MJ, Agarwal R, Deorari AK, et al. Sepsis in the newborn. Indian J Pediatr 2008; 75(3): 261–272. 
4. Sundaram V, Kumar P, Dutta S, et al. Blood culture confirmed bacterial sepsis in neonates in North Indian tertiary care centre: changes over the last decade. Jpn J Infect Dis 2009; 62(1): 46–50. 
5. Lawn JE, Cousens S, Zupan J, et al. 4 million neonatal deaths: When? Where? Why? Lancet 2005; 365(9462): 891–900. 
6. Antia-Obong CE, Utsalo SJ, Udo JJ, et al. Neonatal Septicaemia in Calabar, Nigeria. Central Afr J Med 1992; 36: 161–165
7. National Neonatal Perinatal Database. [Internet]. NNPD report 2002-03 [cited 2010 Sep 22]. Available from: http:// www.newbornwhoccorg/pdf/nnpd_r eport_2002-03 PDF; 2005
8. Bukhari EE, Alrabiaah AA. A review of clinically suspected sepsis and meningitis in infants under 90 days old in a tertiary care centre in Saudi Arabia. J Microbiol Infect Dis 2011; 1(2): 47–52.
9. Chacko B, Sohi I. Early onset sepsis. Indian J Pediatr 2005; 72(1): 23–26.
10. Bellig LL, Ohning BL. Neonatal Sepsis. [Retrieved 6th June 2013]; Available: http://www.emedicine.com/ped/topic2630.html.
11. Zaidi AK, Thaver D, Ali SA, et al. Pathogens associated with sepsis in newborns and young infants in developing countries. Pediatr Infect Dis J 2008; 28(1 Suppl): S10–S18.
12. Levy O. Innate immunity of the newborn: basic mechanisms and clinical correlates. Nat Rev Immunol 2007; 7(5): 379–390.
13. Shah GS, Budhathoki S, Das BK, et al. Risk factors in early neonatal sepsis. Kathmandu Univ Med J 2006; 4(2): 187–191.
14. Trotman H, Bell Y, Thame M, et al. Predictor of poor outcome in neonates with bacterial sepsis admitted to the University Hospital of the West Indies. West Indian Med J 2006; 55(2): 80–83.
15. Ben Hamida Nouaili E, Harouni M, Chaouachi S, et al. Early onset neonatal bacterial infections: a retrospective series of 144 cases. Tunis Med 2008; 86(2): 136–139.
16. Bomela HN, Ballot DE, Cooper PA. Is prophylaxis of early onset group B Streptococcal disease appropriate for South Africa? South Afr Med J 2001; 91(10): 858–860.
17. Laving AM, Musoke RN, Wasunna AO, et al. Neonatal bacterial meningitis at the newborn unit of Kenyatta National Hospital. East Afr Med J 2003; 80(9): 456–462.
18. Madhi SA, Radebe K, Crewe-Brown H, et al. High burden of invasive Streptococcus agalactiae in South African Infants. Ann Trop Paediatr 2003; 23(1): 15–23.
19. Viswanathan R, Singh AK, Ghosh C, Dasgupta S, Mukherjee S, Basu S. Profile of neonatal septicaemia at a district-level sick newborn care unit. Journal of health, population and nutrition. 2012 Mar 1:41-8.
20. Shrestha P, Das BK, Bhatta NK, Jha DK, Das B, Setia A, et al. Clinical and bacteriological profiles of blood culture positive sepsis in newborns. J Nepal Paediatr Soc. 2008;27:64–7.
21. Edwards MS, Baker CJ. Sepsis in the Newborn. In: Krugman's Infectious Diseases of Children, 11th ed, Gershon AA, Hotez PJ, Katz SL (Eds), Mosby, Philadelphia 2004. p.545.
22. Jyothi P, Basavaraj MC, Basavaraj PV. Bacteriological profile of neonatal septicemia and antibiotic susceptibility pattern of the isolates. Journal of Natural Science, Biology and Medicine. 2013 Jul 1;4(2):306.
23. Shah AJ et al. Neonatal Sepsis: High Antibiotic Resistance of the Bacterial Pathogens in a Neonatal Intensive Care Unit of a Tertiary Care Hospital. J Clin Neonatol. 2012 Apr-Jun; 1(2): 72–75.
24. Thakur S, Thakur K, Sood A, Chaudhary S. Bacteriological profile and antibiotic sensitivity pattern of neonatal septicaemia in a rural tertiary care hospital in North India. Indian journal of medical microbiology. 2016 Jan 1;34(1):67.
25. Sawhney N, Shinu P, Singh VA. Bacteriological Profile and Antibiotic Susceptibility Pattern of Neonatal Septicaemia in a Tertiary Care Hospital. Int. J. Curr. Microbiol. App. Sci. 2015;4(10):977-84.
26. Indrajit Gupta, Prosenjit Naskar, Gadadhar Mitra. Spectrum of bacterial infection and antimicrobial sensitivity pattern in neonatal septicemia in a peripheral tertiary care hospital in West Bengal. International Journal of Contemporary Medical Research 2016;3(9):2669-2671.
27. Vaniya HV, Patel NM, Agrawal JM, Trivedi HR, Dhanani JV, Balat JD. Antimicrobial culture sensitivity pattern in neonatal sepsis in a tertiary-care hospital. Int J Med Sci Public Health. 2016; 5(4): 661-665.
28. Rao P, Baliga S, Radhakrishna M, Bele K. A Spectrum of Bacterial Pathogens and its Antibiotic Susceptibility Pattern Isolated from Neonatal Sepsis in an NICU in a Government Pediatric Hospital. International Research Journal of Biological Sciences. 2015;4(5):50-4.
29. Nayak S, Rai R, Kumar VK, Sanjeev H, Pai A, Ganesh H R. Distribution of microorganisms in neonatal sepsis and antimicrobial susceptibility patterns in a tertiary care hospital . Arch Med Health Sci 2014;2:136-9.
30. Shah MN, Desai PB. Clinical and bacteriological profiles of blood culture positive sepsis in newborns Int. J. of Pharm. & Life Sci. (IJPLS). 2011; 2(9): 1041-1045.
31. Bhurle A, Solabannavar S. Neonatal Septicemia Isolates and Antibiotic Susceptibility Pattern in a Tertiary Care Hospital in North Karnataka. International Journal of Health Information and Medical Research. 2014 Jul 31;1(3):25-9.
32. Korpela JK, Campbell J, Singh N. Health care associated infections. In: Mhairi MG, Mullett MD, Seshia MM, editors. Avery's Neonatology: Pathophysiology and Management of the Newborn. Philadelphia: Lippincott Williams Wilkins; 2005. p. 1356-83.
33. Resende DS, Peppe AL, Reis HD, Abdallah VO, Ribas RM, Gontijo Filho PP. Late onset sepsis in newborn babies: epidemiology and effect of a bundle to prevent central line associated bloodstream infections in the neonatal intensive care unit. Brazilian Journal of Infectious Diseases. 2015 Feb;19(1):52-7.
34. L. Pessoa-Silva, S. Hugonnet, R. Pfister, et al. Reduction of health care associated infection risk in neonates by successful hand hygiene promotion Pediatrics, 120 (2007):382–90
35. C. Couto, E.A. Carvalho, T.M. Pedrosa, E.R. Pedroso, M.C. Neto, F.M. Biscione. A 10-year prospective surveillance of nosocomial infections in neonatal intensive care units. Am J Infect Control, 35 (2007):183–189.
36. Schreiber JR, Berger M. Intravenous immune globulin therapy for sepsis in premature neonates. J Pediatr 1992;121:401-4.
37. Roy A, Jain M, Kumar M, Agarwal SK. Bacteriology of neonatal septicemia in a tertiary care hospital of northern India. Indian J Med Microbiol 2002;20:156-9.
38. Narang A, Rao R, Bhakoo ON. Neonatal necrotizing enterocolitis: A clinical study. Indian Pediatr 1993;30:1417-22.
39. Rahman S, Hameed A, Roghani MT, Ullah Z. Multidrug resistant neonatal sepsis in Peshawar, Pakistan. Arch Dis Child Fetal Neonatal Ed 2002;87(1):F52–4.
40. Bhat R, Lewis LE, Vandana KE. Bacterial isolates of early-onset neonatal sepsis and their antibiotic susceptibility pattern between 1998 and 2004: An audit from a center in India. Ital J Pediatr 2011;37(32):512–7
41. Aletayeb SM, Khosravi AD, Dehdashtian M, Kompani F, Mortazavi S, Aramesh M. Identification of bacterial agents and antimicrobial susceptibility of neonatal sepsis: a 54-month study in a tertiary hospital. Afr J Microbiol Res 2011;5(5):528–31.