Figure 1: Placental villi are seen not following their normal morphological pattern
Figure 2:Terminal villi rush out disorderly with characteristics of immaturity
Globular terminal villi depressions were observed on the cell surface of the syncytium and extensive prolongations of plasma membrane can to be noted (Figure 3). Mesenchymal villi show transition into mature intermediate villi and these are seen growing with deficiency of terminal villi covered by fibrinoid (Figure 4).
Figure 3: Globular villi are noted with depressions and prolongations of the plasma membrane.
Figure 4: Mesenchymal villi are originating mature intermediate villi which not present terminal villi in their longitudinal axis.
From extensive zones of fibrinoid deposition upon immature villi are originating villi news (Figure 5). Numerous placental villi are covered with fibrinoid (Figure 6). Deep depressions of the cell surface of the trophoblast are exhibited with fissure or cracks (Figure 7). Frequently are observed figures of intermediate placental villi in curvilinear fashion or aspect of letter “s” which present proliferation of terminal villi in their extremity (Figure 8).
Figure 5: Immature villi cover by fibrinoid is seen in the central and lower region.
Figure 6:Deposition of fibrinoid is exhibited on the cell surface of many villi.
Figure 7:Detail of fig4.Cracks or deep depressions are showed in the trophoblast of placental villi.
Figure 8:Bad development of villi with curvilinear trajectory and proliferation of terminal villi in their extremity.
During preeclampsia the placenta is exposure to reduced placental perfusion or hypoperfusion, increased branching of villi, area and volume of reduced terminal villus, inflammation and oxidative stress .
Maternal anemia results in increased proliferation of trophoblast and stromal cells . Marginal insertion of umbilical cord associated with vasa praevia can to produce rupture of blood vessels during delivery in the placenta with the consequent hemorrhage .
Zika virus placental infection induces proliferation and hyperplasia of Hofbauer cells in the chorionic villi but does not elicit villous necrosis, maternal or acute inflammatory cell reaction . Although Rosenberg et al not could to observe necrosis in the placental villi we have demonstrated notable degenerative changes in the syncytium provoked by Zika virus including necrosis [5,9]. It is possible that the differences observed by us are caused by advanced age during pregnancy or by Zikav infection when it is complicated with another sickness [1,5].
Curvilinear aspect of terminal villi is provoked by degenerative changes observed in stromal region as has been noted in previous work . When placental villi maintain the organization of the stromal region entire; these are straight and they are curved when there is disorganization of placental stroma. Curved villi are own of preeclampsia.
Placental immaturity feature has been seen in villi being affected only by Zika virus infection, by Chikungunya virus and placenta infected by HIV and HPV [5,10-12]. It appears that the virus affect noticeably the immature intermediate villi provoking diminished development of the placental villi.
In preeclampsia it has been described a reduction of the microvilli of the syncytium, excessive syncytial knothing or budding sprouting, which is known as Tenney-Parker change, and alterations in their thickness which can be the origin of the depressions observed on the syncytium [1,2].
The intervillous space is obliterated in many villi that are in intimate association and lack of circulation in hypoxic condition. It leads to degenerative changes described in previous work . This condition is increased by the megaloblastic macrocytic anemia that could to produce mesenchymal villi which originate villi with deficiency of terminal villi and placental villi ramifying from immature villi in irregular aspect.
Fissure or cracks seen in the syncytium correspond with regions where the trophoblast was deportated to the intervillous space into the maternal circulation in this preeclamptic pregnancy [13,14].
In the formation of these fissures the activity of Zikav could to be contributing with lysis of the syncytial plasma membrane as has been suggested .
Figures of intermediate placental villi in curvilinear appearance were also seen in sickle cell disease associate to depressions and fibrinoid deposition .
Placental villi as observed in Figure 8 or with aspect of letter “S” are examples of bad development. Marginal insertion is related with thrombosis, fewer penetrating artery, fewer cotyledons and abnormal blood flow [16,17]. In our case, preeclampsia progress with reduction of blood flow and Zikav provoke damage to blood vessels that transport blood associate to megaloblastic macrocytic anemia .
These events combined carry to bad development of the villous tree. In this case terminal villi are small, being of 50um when compared with normal terminal villi of 60um . Zikav and high blood pressure have produced a general disorganization of the structure of the villi. High blood pressure, viral activity, and the hypoxia induced by marginal insertion and megaloblastic macrocytic anemia have originated this morphological disorder in the villous ramifications.
It has been described that Zikav infection has a low fatality rate in adults and few cases occurred of death are associate with another conditions such as lupus and sickle cell anemia . In our case associate to fetal death Zikav infection has been interacting with preeclampsia, macrocitic anemia and marginal insertion of the umbilical cord which have created a severe case of hypoxia. And this condition has been considered as very important cause of mortality .
In conclusion, the villous tree was found with small terminal villi, deficiency of terminal villi and bad development of villi which have provoked high risk for the interchange of gases or nutrients contributing with the fetal death.
We are grateful to Dr. Nora López of the service of Obstetrics and Gynecology of Clinic Medicine ”The Floresta” in Maracay by the obtention of the placental material and to our secretary Laury Rosely of Ovalles by to transcribe the manuscript.
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