The events during the pathogenesis of chicken anemia virus (CAV) infection following intramuscular (IM) and oral inoculation were further elucidated and compared by sequential clinical, pathologic, and morphometric histopathologic evaluations, and by sequential determination of CAV genome concentrations in different organs. Specific-pathogen-free chickens were inoculated by IM or oral routes with the same dose (2 x 10(6) mean tissue culture infective dose [TCID50]) of CAV isolate 03-4876 at 1 day of age. Weights and hematocrits were obtained at 7, 10, 14, 18, 21, 25, and 28 days postinoculation (DPI). Seven birds from each group were necropsied at 7, 10, 14, and 28 DPI, and samples of thymus, Harderian gland, and cecal tonsils (CT) were obtained for histopathologic examination and CAV genome quantification by real-time polymerase chain reaction. Peak CAV genome concentrations were detected in the thymus at 10 and 14 DPI in the IM and orally infected chickens, respectively. High CAV DNA concentrations were maintained throughout the experimental period until 28 DPI, despite specific seroconversion occurring by 14 DPI in the IM-inoculated chickens. CAV was isolated from both orally and IM-infected chickens 28 DPI. Peak CAV genomes in the thymuses of IM and orally infected chickens coincided with peak lymphocyte depletion in these organs. Lymphocyte repopulation of the thymus occurred by 28 DPI in spite of the presence of the virus in the organs of both infected chicken groups. CAV genomes were detected in the CT, but histopathologic changes were not observed. Compared with the IM route of infection, orally infected chickens did not show apparent signs of illness. Clinical parameters, including reduction of weight gains and hematocrits, and gross and histopathologic changes were delayed and less severe in the orally inoculated chickens. This was concurrent with a delay in accumulation of CAV genomes in the thymus of these chickens.

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Premature birth (PB) is a polyetiological problem that depends on many factors, accompanied by violations of the placenta functional competence, changes in its metabolic, hormone-producing and protective functions. The objective: to establish the importance of placental factors in the development of PB in pregnant women with comorbid pathology. Materials and methods. The levels of fetal and placental proteins (placental alfa microglobulin-1, α2-microglobulin of fertility, trophoblastic β1-glycoprotein) and hormones (estriol, placental lactogen, progesterone) were determined in 33 pregnant women with threat of PB at 26–34 weeks of gestation (main group), who had concomitant comorbid pathology in the stage of unstable remission. The control group included 26 healthy pregnant women who were representative for gestational age. Results. In pregnant women with comorbid pathology a decrease of the placenta protein-synthesizing function and the hormone-producing function of the trophoblast was found, which makes it difficult to launch the syntoxic adaptation programs of the mother’s organism, which are responsible for maintaining the pregnancy with the subsequent development of placental dysfunction, the result of which is PB.The markers of these disorders are a 3-fold decrease in the level of trophoblastic β1-glycoprotein (p<0.0001) and a 1.7-fold decrease in the concentration of α2-microglobulin of fertility (p<0.0001) with a simultaneous 4-fold increase of placental alfa microglobulin-1 concentration (p<0.0001) and a decrease in the levels of placental lactogen by 1.6 times (p<0.0001), estradiol by 40 % (p<0.0001) and progesterone by more than 2 times (p<0.0001) compared to healthy pregnant women.Conclusions. In patients with comorbid pathology there are disorders in the secretion of pregnancy proteins due to a decrease in the levels of trophoblastic β1-glycoprotein and α2-microglobulin of fertility and an increase in the level of placental alfa microglobulin-1 and disorders of the hormone-producing function of the trophoblast due to a decrease in the secretion of placental lactogen, progesterone, and estradiol. The disturbance of the secretion of the pregnancy zone proteins and hormones are the early markers for the initiation of premature birth caused by placental dysfunction in pregnant women with comorbid pathology.

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Встановлено, що у жінок, у яких мають місце соціальні і/або медичні фактори ризику під час вагітності, частіше розвиваються такі акушерські чи перинатальні ускладнення, як дисфункція плаценти, невиношування, затримка росту плода, прееклампсія, патологічний перебіг пологів тощо. Однією з причин розвитку цих ускладнень може бути недостатнє забезпечення вітамінами та мікроелементами жінки під час гестації. Впровадження комплексу лікувально-профілактичних заходів з використанням вітамінномінерального препарату емфетал сприяє достовірному зниженню розвитку найчастіших акушерських ускладнень.