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Aim. To determine the structure and detection rate of some opportunistic infections in premature birth.Materials and methods. The study was carried out at the premises of the Research Institute of Maternity and Childhood Protection and the Pathology Department of the Khabarovsk Perinatal Center. We studied 62 placentas from women whose pregnancy ended prematurely and placentas and organ samples (heart, lungs, liver, and kidneys) from 14 premature infants who died in the early neonatal period. Thirty placentas of women who delivered full-term live babies were classified as a control group. Genomes of Chlamydia trachomatis, Mycoplasma hominis, Mycoplasma genitalium, Ureaplasma species (Ureaplasma urealyticum + Ureaplasma parvum), Cytomegalovirus, Herpes simplex virus, Human herpesvirus 4 type, Human herpesvirus 6 type, Parvovirus B19, Listeria monocytogenes, Streptococcus agalactiae, Streptococcus species, Streptococcus pyogenes, Haemophilus influenza, Klebsiella pneumoniae, Candida albicans were detected by polymerase chain reaction (PCR) in samples of placental tissue and samples of internal organs of deceased newborns. Results. The rate of opportunistic agent detection in the placentas from women with preterm birth made 59.6% and in the sectional material from premature newborns who died in the early neonatal period (78.6%), which figures exceeded the same indicator in the control group (30.0%) respectively, by 2.0 (p=0.007) and 2.6 (p=0.002), respectively. In 47.9±7.2% of cases of all positive results, the material from women with preterm birth presented with various combinations of two, three, and four infectious agents, having common pathogenic links, which contributes to the aggravation of pathogenic processes, comorbidity or multimorbidity. According to the detection rates, in terms of total monoinfections and mixed infection components, pathogens detected during preterm birth were distributed as follows: U. urealyticum ‒ 34,2±5,4%; S. agalactiae ‒ 17,1±4,3%; M. hominis ‒ 15,8±4,1%; S. species (S. sanguis, S. salivarius, S. mitis, S. mutans) ‒ 13,1±3,8%; Cytomegalovirus ‒ 11,8±3,7%; Human herpesvirus 4 type – 9,2±3,3%; M. genitalium ‒ 2,6±1,8%. Conclusion. PCR testing showed that placentas from women whose pregnancy ended prematurely and samples of placenta and organs of premature infants who died in the early neonatal period presented with opportunistic agents colonizing female genital tract (streptococci, mycoplasmas) or ubiquitous herpesviruses persistent and reproduced in human lymphocytes (Cytomegalovirus, Human herpesvirus 4 type). Associations of microorganisms that cause comorbidity or multimorbidity account for a significant portion of the infectious agents detected. The context for a microbiota-integrated opportunistic agent to transform into a pathogenic strain, identification of transformation predictors, and possible tools to correct the disorders – all these require further research.
Aim. To determine the structure and detection rate of some opportunistic infections in premature birth.Materials and methods. The study was carried out at the premises of the Research Institute of Maternity and Childhood Protection and the Pathology Department of the Khabarovsk Perinatal Center. We studied 62 placentas from women whose pregnancy ended prematurely and placentas and organ samples (heart, lungs, liver, and kidneys) from 14 premature infants who died in the early neonatal period. Thirty placentas of women who delivered full-term live babies were classified as a control group. Genomes of Chlamydia trachomatis, Mycoplasma hominis, Mycoplasma genitalium, Ureaplasma species (Ureaplasma urealyticum + Ureaplasma parvum), Cytomegalovirus, Herpes simplex virus, Human herpesvirus 4 type, Human herpesvirus 6 type, Parvovirus B19, Listeria monocytogenes, Streptococcus agalactiae, Streptococcus species, Streptococcus pyogenes, Haemophilus influenza, Klebsiella pneumoniae, Candida albicans were detected by polymerase chain reaction (PCR) in samples of placental tissue and samples of internal organs of deceased newborns. Results. The rate of opportunistic agent detection in the placentas from women with preterm birth made 59.6% and in the sectional material from premature newborns who died in the early neonatal period (78.6%), which figures exceeded the same indicator in the control group (30.0%) respectively, by 2.0 (p=0.007) and 2.6 (p=0.002), respectively. In 47.9±7.2% of cases of all positive results, the material from women with preterm birth presented with various combinations of two, three, and four infectious agents, having common pathogenic links, which contributes to the aggravation of pathogenic processes, comorbidity or multimorbidity. According to the detection rates, in terms of total monoinfections and mixed infection components, pathogens detected during preterm birth were distributed as follows: U. urealyticum ‒ 34,2±5,4%; S. agalactiae ‒ 17,1±4,3%; M. hominis ‒ 15,8±4,1%; S. species (S. sanguis, S. salivarius, S. mitis, S. mutans) ‒ 13,1±3,8%; Cytomegalovirus ‒ 11,8±3,7%; Human herpesvirus 4 type – 9,2±3,3%; M. genitalium ‒ 2,6±1,8%. Conclusion. PCR testing showed that placentas from women whose pregnancy ended prematurely and samples of placenta and organs of premature infants who died in the early neonatal period presented with opportunistic agents colonizing female genital tract (streptococci, mycoplasmas) or ubiquitous herpesviruses persistent and reproduced in human lymphocytes (Cytomegalovirus, Human herpesvirus 4 type). Associations of microorganisms that cause comorbidity or multimorbidity account for a significant portion of the infectious agents detected. The context for a microbiota-integrated opportunistic agent to transform into a pathogenic strain, identification of transformation predictors, and possible tools to correct the disorders – all these require further research.
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