Early-onset neonatal sepsis due to Streptococcus Pneumoniae: A rare causative organism in neonates



   Table of Contents   CASE REPORT Year : 2021  |  Volume : 10  |  Issue : 1  |  Page : 48-51

Early-onset neonatal sepsis due to Streptococcus Pneumoniae: A rare causative organism in neonates

Sana Niaz, Azeem Khan, Vikram Kumar, Syed Rehan Ali
Department of Neonatal Paediatrics, The Indus Hospital, Karachi, Pakistan

Date of Submission04-Jun-2020Date of Decision10-Sep-2020Date of Acceptance17-Sep-2020Date of Web Publication08-Feb-2021

Correspondence Address:
Dr. Syed Rehan Ali
Department of Neonatal Pediatrics, The Indus Hospital, Plot C-76, Sector 39, Korangi, Karachi
Pakistan
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Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/jcn.JCN_73_20

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Streptococcus pneumoniae (pneumococcus) is a common respiratory tract pathogen in children causing otitis media, sinusitis, bacteremia, and meningitis. Although comparatively rare, this pathogen can also cause early-onset neonatal sepsis (EONS) as well as late-onset neonatal sepsis and can mimic Group B streptococcal sepsis-like illness in neonates. S. pneumoniae can be transmitted vertically from maternal vaginal tract colonization or from the placenta through hematogenous spread. Two consecutive case reports of EONS are reported. Vaccination of the mother with pneumococcal polysaccharide vaccine during the third trimester may provide protection to infants by enhancing the transplacental transfer of active immunoglobulin (IgG) to the fetus, as well as improving the availability of secretory antibodies for the fetus through mother's milk. Immunization of the mother may also prevent genital colonization through resulting high levels of IgG plus mucosal CD17 lymphocytes.

Keywords: Neonatal, Pneumococcus, Sepsis, Streptococcus pneumoniae


How to cite this article:
Niaz S, Khan A, Kumar V, Ali SR. Early-onset neonatal sepsis due to Streptococcus Pneumoniae: A rare causative organism in neonates. J Clin Neonatol 2021;10:48-51
How to cite this URL:
Niaz S, Khan A, Kumar V, Ali SR. Early-onset neonatal sepsis due to Streptococcus Pneumoniae: A rare causative organism in neonates. J Clin Neonatol [serial online] 2021 [cited 2021 Dec 5];10:48-51. Available from: https://www.jcnonweb.com/text.asp?2021/10/1/48/308846   Introduction Top

Early-onset neonatal sepsis (EONS) is the reason behind 30%–50% of neonatal deaths in developing countries each year, remains the main cause of neonatal mortality worldwide.[1] EONS is known as a condition triggered by bacterial pathogens which spread vertically from mother to infant either before or during delivery within the first 3 days of life. There is limited data available on the incidence of neonatal sepsis in Pakistan; however, it is said to vary from 1.13 to 3.8/1000 live births.[2]

There are different organisms responsible for EONS. Streptococcal pneumonia, although mainly described as a respiratory pathogen, is associated with vaginal colonization in 0.03%–0.75% of pregnant women. Other associations are with prolonged rupture of membrane (PROM), chorioamnionitis, pneumonia, and meningitis in mothers.[3] Immunization of a pregnant mother with 23-valent pneumococcal vaccine resulted in a considerably higher concentration (80%–90%) of IgG antibodies against pneumococcus at birth and at 1-month postnatal age.[4]Streptococcus pneumoniae is one of the rare causative organisms responsible for 1%–11% of EONS.[3],[4] It is, however, linked to high morbidity and mortality of approximately 14.3%–60%, causing neonatal sepsis, congenital pneumonia (<72 h), and meningitis.[5] Since pneumococcal vaccination is not currently recommended to be given at neonatal age, the pneumococcal vaccine for mother in the third trimester and appropriate treatment of suspected neonates is the best option as of now. We have reported consecutive case reports of two cases that presented with early-onset pneumococcal sepsis at birth.

  Case Reports Top

Case report 1

A baby boy born to an 18-year-old G2P1 + 1 mother by normal vaginal delivery at 38 weeks of gestation, with a weight of 2600 g. There is a history of one neonatal death on the 2nd DOL due to respiratory distress and grunting. There is no history of pyrexia, PROM, vaginal discharge, or urinary tract infection (UTI) in the mother. The baby developed respiratory distress at 2½ of life and was shifted to the neonatal intensive care unit (NICU) from the postnatal ward. His vitals revealed respiratory rate 76 breaths/min, heart rate 152 beats/min, oxygen saturation 94%, and blood pressure (BP) 78/35 mmHg. Oxygen support and antibiotics (cefotaxime/amikacin) were started after sending septic workup. The baby developed frequent apnea's with desaturations and an increase in oxygen requirements for which he required ventilatory support with synchronized intermittent mandatory ventilation. Chest X-ray showed a dense bilateral air space-filling process with bronchograms bilaterally [Figure 1]. Blood gas revealed respiratory acidosis (PH 7.08, PCO2 70 mmHg, HCO3 20 mEq/L). His initial blood counts revealed white blood cell (WBC) 12 × 109 with 60% neutrophils. C-reactive protein (CRP) of 38 mg/L. Cerebrospinal fluid DR and culture were unremarkable. He was subsequently weaned and extubated on the 3rd day of life. Feeding was established, and he was discharged home on day 7 of life. Gram stain showed Gram-positive cocci, which later identified as S. pneumoniae sensitive to penicillin and other first-line antibiotics. Mother high vaginal swab and throat swab sent, which came to be negative.

Figure 1: Dense bilateral air space-filling process with bronchograms bilaterally

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Case report 2

A 2200 g baby boy was born to 17-year-old primigravida mother at 37 + 6 weeks of gestation by SVD. She was booked pregnancy. There was no history of fever, PROM, or UTI in the mother before delivery. The baby was born with APGAR score of 9 at 1 and 5 min, respectively. The baby was shifted with the mother to the postnatal ward. At 4 h of life, the baby had issues of grunting and peripheral cyanosis. His saturation in room air was 83% and noted to be significantly lethargic with poor perfusion. The baby was shifted to NICU. Vitals revealed temperature of 36.5o C, respiratory rate 70 breaths/min, HR 160/min, BP was 61/28 (mean 37 mmHg). First-line antibiotics (ampicillin and gentamycin) were started after sending workup. Chest X-ray showed homogenous opacity involving the right upper middle zone [Figure 2]. His blood count shows WBC 3.3 × 109 with 68% neutrophils and CRP was 78 mg/L. His blood culture grew S. pneumoniae susceptible to penicillin, cefotaxime, and co-trimoxazole. Cerebrospinal fluid DR and culture were unremarkable. The baby was put on high flow nasal cannula with 40% oxygen, which was tapered gradually over the next 3 days. Direct breastfeed trial was given and established. The baby was discharged home on injectable antibiotics for total 7 days with a follow-up in the clinic.

The mother developed a fever spike (38°C) on the 2nd postnatal day. Her CBC showed neutrophilic leukocytosis with a WBC 23500 × 109 (Neutrophils 88%). Her urine DR showed pus cells of 10–15, leucocyte esterase and nitrites were negative along with urine culture. Her blood film for malarial parasite and Dengue NS1 antigen was negative. Mother's throat and high vaginal swab sent, which came out to be negative.

  Discussion Top

Neonatal sepsis is defined as systemic infections of newborn up to 28 days of life.[5] It is separated into early-onset sepsis occurs within 72 h of life, and late-onset sepsis, which occurs from the 4th day to 28th days of life. The mortality rate of EONS is from 15% to 40%, while it is around 5% for late neonatal sepsis.[6] Studies carried out in Pakistan have shown that the majority of early-onset sepsis is caused by Gram-negative organisms, whereas Gram-positive organisms are predominantly responsible for late-onset sepsis: the latter due to interventions associated with neonatal care like intravenous lines and percutaneous central catheters. However, these reports are focused on large, academic NICUs and may not provide accurate findings in regard to other units.

S. pneumonia e was first discovered by Louis Pasteur in 1881. The polysaccharide capsule of pneumococcus helps it from host defense and contributes to major virulence factors.[7] Early-onset sepsis with Group B streptococcus (GBS) and that with S. pneumoniae can have symptoms that are similar, such as respiratory distress, pneumonia, fever, cyanosis, irritability, leukopenia, shock, and rapid clinical deterioration. This consequently makes it difficult to distinguish between the two organisms based on clinical grounds.[8] These two organisms, however, differ significantly in the way they carry out maternal colonization as well as the rate of infection in the neonatal population. GBS is commonly found in the female genital tract, and the frequency of invasive disease by this organism is low, but S. pneumoniae is seldom isolated from the female genital tract (0.03%) but can lead to more invasive disease and causing 1%–11% of cases of neonatal sepsis.

Invasive pneumococcal disease (IPD) is well-defined as an infection identified by the isolation of S. pneumoniae from a generally sterile site, for example, blood, pleural fluid, pericardial fluid, peritoneal fluid, biopsy tissue, joint aspiration, or cerebrospinal fluid.[9] It is possible for trans-placental passage of pneumococcus to occur secondary to maternal bacteremia, either by a colonized maternal genital tract leading to ascending infection or postnatally through horizontal transmission.[9],[10],[11] Despite the vaginal colonization rate of 0.03%–0.75% in pregnant women, newborns show high morbidity and mortality rates when compared with GBS. Oral-genital interaction in a nasopharynx carrier or upper respiratory infection by pneumococcus can cause lower genital tract colonization. Although the implementation of giving the pediatric population conjugate pneumococcal vaccine has significantly decreased the incidence of IPD, nearly 40% of identified cases in infants usually occur within the 1st week of life.[8]

Immunization of pregnant women through administering pneumococcal polysaccharide vaccine may enhance maternal protection against S. pneumoniae, and in turn, provide protection for infants during the initial few months of life against pneumococcal disease. Improvement in trans-placental antibody transfer, in addition to increased delivery of secretory antibody in the mother's milk, is accountable for this protection. Vaccination during the third trimester could lessen incidence of neonatal infections by helping to actively transfer IgG to the fetus, ultimately enhancing the availability of secretory antibodies in mother's milk as well as prevent genital tract colonization through the vaccine resulting in high levels of IgG and mucosal CD17 lymphocytes.[12]

  Conclusion Top

Many strategies are evolving to prevent streptococcal pneumoniae infection in the newborn. It can mimic a GBS like illness which can be rapidly progressive in the early neonatal period. Therefore, it is important to acquire more knowledge about this disease so that effective strategies can be adopted to prevent neonatal morbidity and mortality associated with this disease. Currently, pneumococcal vaccination is not recommended to administer at neonatal age. For this reason, maternal immunization using the pneumococcal vaccine during the third trimester of pregnancy, as well as early and appropriate treatment of suspected neonates, is deemed the best therapeutic option.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 

  References Top
1.Jarovsky D, Marchetti IC, da Silva Mori MA, de Souza RM, Almeida FJ, Palazzi Sáfadi MA, et al. Early-onset neonatal pneumococcal sepsis: A fatal case report and brief literature review. Pediatr Infect Dis J 2018;37:e111-2.  Back to cited text no. 1
    2.Sheikh A, Sajjad A, Hanif S. Neonatal sepsis: An evaluation of bacteriological spectrum, antibiotic susceptibilities and prognostic predictors at Civil Hospital, Karachi. Pak Pediatr J 2014;38:143-55.  Back to cited text no. 2
    3.Kochhar S, Edwards KM, Ropero Alvarez AM, Moro PL, Ortiz JR. Introduction of new vaccines for immunization in pregnancy - Programmatic, regulatory, safety and ethical considerations. Vaccine 2019;37:3267-77.  Back to cited text no. 3
    4.Hoffman JA, Mason EO, Schutze GE, Tan TQ, Barson WJ, Givner LB, et al. Streptococcus pneumoniae infections in the neonate. Pediatrics 2003;112:1095-102.  Back to cited text no. 4
    5.Russell FM, Carapetis JR, Tikoduadua L, Paeds D, Chandra R, Seduadua A, et al. Invasive pneumococcal disease in Fiji: Clinical syndromes, epidemiology, and the potential impact of pneumococcal conjugate vaccine. Pediatr Infect Dis J 2010;29:870-2.  Back to cited text no. 5
    6.Najeeb S, Gillani S, Rizvi SK, Ullah R, ur Rehman A. Causative bacteria and antibiotic resistance in neonatal sepsis. J Ayub Med Coll Abbottabad 2012;24:131-4.  Back to cited text no. 6
    7.Rodrigo C, Lim WS. The relevance of pneumococcal serotypes. Curr Infect Dis Rep 2014;16:403.  Back to cited text no. 7
    8.Ladhani SN, Andrews NJ, Waight P, Borrow R, Slack MP, Miller E. Impact of the 7-valent pneumococcal conjugate vaccine on invasive pneumococcal disease in infants younger than 90 days in England and wales. Clin Infect Dis 2013;56:633-40.  Back to cited text no. 8
    9.Simonsen KA, Anderson-Berry AL, Delair SF, Davies HD. Early-onset neonatal sepsis. Clin Microbiol Rev 2014;27:21-47.  Back to cited text no. 9
    10.Singh J, Dick J, Santosham M. Colonization of the female urogenital tract with Streptococcus pneumoniae and implications for neonatal disease. Pediatr Infect Dis J 2000;19:260-2.  Back to cited text no. 10
    11.Primhak RA, Tanner MS, Spencer RC. Pneumococcal infection in the newborn. Arch Dis Child 1993;69:317-8.  Back to cited text no. 11
    12.Chaithongwongwatthana S, Yamasmit W, Limpongsanurak S, Lumbiganon P, Tolosa JE. Pneumococcal vaccination during pregnancy for preventing infant infection. Cochrane Database Syst Rev 2015;1:CD004903.  Back to cited text no. 12
    
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