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      The Bacteriology and Its Virulence Factors in Neonatal Infections: Threats to Child Survival Strategies

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          Abstract

          Background

          Neonatal infection refers to the infection of the newborn during the first twenty-eight days of life. It is one of the causes of infant morbidity and mortality worldwide. The aim of the study is to determine the relative contribution of the different pathogens to the overall disease burden. It will also determine the mechanisms of virulence of these pathogens that cause neonatal infections at Chukwuemeka Odumegwu Ojukwu University Teaching Hospital (COOUTH), Awka.

          Methods

          Biological samples were collected from 30 neonates admitted at the special care baby unit (SCBU) of COOUTH and cultured using selective media and nutrient agar. The isolates were identified using microbiological and biochemical tests. The antibiogram study was determined using Kirby-Bauer disc diffusion method on Mueller Hinton Agar. Several methods previously reported in literature were used for the characterization of the virulence factors.

          Results

          From the 30 blood samples collected, Pseudomonas spp. (19.7%), Escherichia coli (23%), Salmonella spp. (24.6%), and Staphylococcus aureus (32.8%) were isolated. Male to female ratio of study population was 1.5: 1. The isolates were 100 % resistant to ticarcillin, cephalothin, ceftazidime, and cefuroxime but appreciably susceptible to only levofloxacin (88.85%). They were moderately susceptible to ceftriaxone/sulbactam (39.05%) and azithromycin (26.46%). Common virulence factors identified among the isolates (up to 90 %) were hemolysin, biofilm formation, and acid resistance. Less common virulence factors were proteases (50 %), deoxyribonucleases (50 %), enterotoxins (63%), and lipopolysaccharide (70%). The virulence factors were found mostly among the S. aureus isolates.

          Conclusions

          Pseudomonas spp., Escherichia coli, Salmonella spp., and Staphylococcus aureus were implicated in neonatal infections in the center and most of them were resistant to conventional antibiotics. The organisms showed marked virulence and multidrug resistance properties. Levofloxacin, a fluoroquinolone, had superior activity on the isolates compared to other antibiotics used in the study.

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          Most cited references41

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          Oxidative stress responses in Escherichia coli and Salmonella typhimurium.

          Oxidative stress is strongly implicated in a number of diseases, such as rheumatoid arthritis, inflammatory bowel disorders, and atherosclerosis, and its emerging as one of the most important causative agents of mutagenesis, tumorigenesis, and aging. Recent progress on the genetics and molecular biology of the cellular responses to oxidative stress, primarily in Escherichia coli and Salmonella typhimurium, is summarized. Bacteria respond to oxidative stress by invoking two distinct stress responses, the peroxide stimulon and the superoxide stimulon, depending on whether the stress is mediated by peroxides or the superoxide anion. The two stimulons each contain a set of more than 30 genes. The expression of a subset of genes in each stimulon is under the control of a positive regulatory element; these genes constitute the OxyR and SoxRS regulons. The schemes of regulation of the two regulons by their respective regulators are reviewed in detail, and the overlaps of these regulons with other stress responses such as the heat shock and SOS responses are discussed. The products of Oxy-R- and SoxRS-regulated genes, such as catalases and superoxide dismutases, are involved in the prevention of oxidative damage, whereas others, such as endonuclease IV, play a role in the repair of oxidative damage. The potential roles of these and other gene products in the defense against oxidative damage in DNA, proteins, and membranes are discussed in detail. A brief discussion of the similarities and differences between oxidative stress responses in bacteria and eukaryotic organisms concludes this review.
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            Respiratory distress in the newborn.

            Respiratory distress presents as tachypnea, nasal flaring, retractions, and grunting and may progress to respiratory failure if not readily recognized and managed. Causes of respiratory distress vary and may not lie within the lung. A thorough history, physical examination, and radiographic and laboratory findings will aid in the differential diagnosis. Common causes include transient tachypnea of the newborn, neonatal pneumonia, respiratory distress syndrome (RDS), and meconium aspiration syndrome (MAS). Strong evidence reveals an inverse relationship between gestational age and respiratory morbidity. (1)(2)(9)(25)(26) Expert opinion recommends careful consideration about elective delivery without labor at less than 39 weeks’ gestation. Extensive evidence, including randomized control trials, cohort studies, and expert opinion, supports maternal group B streptococcus screening, intrapartum antibiotic prophylaxis, and appropriate followup of high-risk newborns according to guidelines established by the Centers for Disease Control and Prevention. (4)(29)(31)(32)(34) Following these best-practice strategies is effective in preventing neonatal pneumonia and its complications. (31)(32)(34). On the basis of strong evidence, including randomized control trials and Cochrane Reviews, administration of antenatal corticosteroids (5) and postnatal surfactant (6) decrease respiratory morbidity associated with RDS. Trends in perinatal management strategies to prevent MAS have changed. There is strong evidence that amnioinfusion, (49) oropharyngeal and nasopharyngeal suctioning at the perineum, (45) or intubation and endotracheal suctioning of vigorous infants (46)(47) do not decrease MAS or its complications. Some research and expert opinion supports endotracheal suctioning of nonvigorous meconium-stained infants (8) and induction of labor at 41 weeks’ gestation (7) to prevent MAS.
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              Stillbirth in developing countries: a review of causes, risk factors and prevention strategies.

              To understand the rates, causes and risk factors for stillbirth in developing countries as well as the strategies that have been evaluated to reduce stillbirth. We searched the English literature for 2003-2008 for all articles related to stillbirth and perinatal mortality in developing countries and reviewed all related publications. Despite the large number of stillbirths worldwide, the topic of stillbirths in developing countries has received very little research, programmatic or policy attention. In many developing countries, almost half of the deliveries occur at home, and under-reporting of stillbirths is a significant problem. Reliable data about rates and causes are unavailable in many areas of the world. Nevertheless, of the estimated 3.2 million stillbirths that occur yearly world-wide, the vast majority occur in developing countries. Rates in many developing countries are 10-fold greater or more than in developed countries. There is not a standard international classification system that defines cause of death, nor is there agreement about the lower limits of birthweight or gestational age that define stillbirth, making comparisons of causes of stillbirth or rates over time or between sites problematic. From available data, prolonged and obstructed labour, pre-eclampsia and various infections, all without adequate treatment, appear to account for the majority of stillbirths in developing countries. Identification and treatment of maternal syphilis has been effective in reducing stillbirth risk, as has improvements in access to emergency obstetrical services and particularly caesarean section. Further research is needed to understand the causes and the best preventive strategies for stillbirth specific to geographic areas. However, based on current data, better access to appropriate obstetric care, particularly during labour and delivery and better screening and treatment of syphilis should reduce developing country stillbirth rates dramatically.
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                Author and article information

                Contributors
                Journal
                J Pathog
                J Pathog
                JPATH
                Journal of Pathogens
                Hindawi
                2090-3057
                2090-3065
                2018
                2 July 2018
                : 2018
                : 4801247
                Affiliations
                1Department of Pediatrics, Chukwuemeka Odumegwu Ojukwu University, Awka, Anambra State, Nigeria
                2Department of Pharmaceutical Microbiology and Biotechnology, Faculty of Pharmaceutical Sciences, Agulu, Nnamdi Azikiwe University, Anambra State, Nigeria
                3Department of Pediatrics, College of Health Sciences, Faculty of Medicine, Nnamdi Azikiwe University, Nnewi Campus, Anambra State, Nigeria
                4Department of Medical Laboratory Science, Faculty of Health Science and Technology, Nnamdi Azikiwe University, Nnewi Campus, Anambra State, Nigeria
                5Department of Clinical Laboratory Science, School of Health Sciences, Winston-Salem State University, Winston-Salem, NC, USA
                6Department of Nursing Sciences, Faculty of Health Science and Technology, Nnamdi Azikiwe University, Nnewi Campus, Nigeria
                Author notes

                Academic Editor: Hin-Chung Wong

                Author information
                http://orcid.org/0000-0001-8519-2555
                Article
                10.1155/2018/4801247
                6077539
                30112215
                e7ab5f1a-faff-43d7-952a-ca522118fe87
                Copyright © 2018 Obiora Shedrach Ejiofor et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 24 January 2018
                : 23 April 2018
                : 19 May 2018
                Categories
                Research Article

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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