Placental infectious villitis versus villitis of unknown etiology

Stanek, Jerzy

doi:10.5114/pjp.2017.67616

Cited by 15 publications

(9 citation statements)

References 34 publications

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“…52 The frequency of chronic VUE was mildly but statistically significantly increased (16%) in LOPE, but in the EOPE and the comparative group, the frequency was below the 9% incidence of our total database. 34 VUE is likely a result of an immune ''rejection-like'' reaction observed in association with FGR [53][54][55] but not really with PE. 55 In our previous study, VUE statistically significantly clustered with several conditions (maternal diabetes mellitus among others), 31 but its more common occurrence in term pregnancies corresponds to its correlation with LOPE ( Table 2).…”

Section: Discussionmentioning

confidence: 99%

Histological Features of Shallow Placental Implantation Unify Early-Onset and Late-Onset Preeclampsia

Stanek

2018

Pediatr Dev Pathol

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Preeclampsia is distinguishable from other hypertensive conditions of pregnancy by its high rates of decidual arteriopathy, the uterine type of chronic hypoxic placental injury, the occurrence of villous infarctions, and clusters of multinucleate trophoblasts in the maternal floor. To retrospectively study the clinical and placental phenotypes of 230 women with early-onset preeclampsia, 261 women with late-onset preeclampsia, and 5059 women without hypertension in pregnancy (comparative group), 24 clinical and 46 placental phenotypes were statistically compared (analysis of variance, 2 with Bonferroni correction). The frequency of decidual arteriopathy (both hypertrophic and atherosis), patterns of chronic hypoxic placental injury, villous infarction, membrane laminar necrosis, membrane microscopic chorionic pseudocysts, clusters of maternal floor multinucleated trophoblasts, excessive number of extravillous trophoblasts, and intervillous thrombi was strikingly higher in both late-onset preeclampsia and early-onset preeclampsia than in the comparative group without hypertension in pregnancy. All 3 patterns of chronic hypoxic placental injury were 2-to 3-fold more common in preeclampsia. Although the preuterine pattern was as common in early-onset preeclampsia as it was in late-onset preeclampsia, the postuterine pattern was 2-fold more common in early-onset preeclampsia, and chronic villitis of unknown etiology was more common in lateonset preeclampsia than in the other 2 groups. Features of shallow placental implantation occurred at the same frequency in early-onset preeclampsia as in late-onset preeclampsia, which reflects an underlying common pathological mechanism in both subgroups of preeclampsia, while hypoxic lesions and patterns of placental injury were more common in early-onset preeclampsia than in late-onset preeclampsia, which correlates with more severe clinical outcomes of the former.

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Section: Discussionmentioning

confidence: 99%

Histological Features of Shallow Placental Implantation Unify Early-Onset and Late-Onset Preeclampsia

Stanek

2018

Pediatr Dev Pathol

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“…Villitis of unknown etiology (VUE) is a diagnosis of exclusion, requiring first that infectious causes be ruled out adequately . VUE is far more common than its infectious counterpart and the two present differently: in cases of the latter, usually there are signs and symptoms of infection in the mother or fetus/neonate . Infectious causes of villitis also are suspected at earlier gestational ages .…”

Section: Villitis Of Unknown Etiologymentioning

confidence: 99%

“…D) . The proximal form is commonly seen with fetal vascular malperfusion, such as vascular thrombosis with or without downstream villous stromal‐vascular karyorrhexis and avascular villi . Plasma cell deciduitis is commonly encountered in cases of basal VUE .…”

Section: Villitis Of Unknown Etiologymentioning

confidence: 99%

“…Villous plasma cells raise suspicion for an infectious villitis, and the pathologist must be alert to other infection‐associated pathologies such as villous stromal hemosiderin deposition and (certainly) viral inclusions as in CMV or HSV placentitis (Fig. E) . Giant cells in a specific clinical context may raise suspicion for Toxoplasma gondii or Trypanosoma cruzi infection .…”

Section: Villitis Of Unknown Etiologymentioning

confidence: 99%

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Placental pathologic lesions with a significant recurrence risk – what not to miss!

Chen

Roberts

2017

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Here, we review three important placental pathologies with significant clinical implications and recurrence risks. They are, in order of most to least frequently seen, villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition (also known as maternal floor infarction). These entities occur in both preterm and term gestations and are observed more frequently with maternal and obstetric disorders including prior pregnancy loss, hypertension/preeclampsia, and autoimmune disease. They are associated with, and probably the cause of, significant perinatal morbidity and mortality including intrauterine growth restriction, fetal and neonatal demise, and fetal/neonatal neurocompromise (seizures and cerebral palsy). All three entities have high recurrence risks, with recurrence rates ranging from 34 to 100%. The histologic features of villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition are described herein. We discuss the clinical associations and suggest the subsequent clinical and pathological evaluation. Hypotheses as to the biology of these lesions are reviewed.

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“…The placenta has typically been viewed as a sterile organ (5). Yet, it has long been known that bacterial infection of the placental amnion and chorion (15)(16)(17)(18)(19)(20)(21)(22)(23)(24) and/or villous tree (15,18,(25)(26)(27) is associated with preterm labor (16,18,(28)(29)(30)(31)(32)(33)(34), preterm prelabor rupture of the membranes (PPROM) (18,29,30,35,36), histological chorioamnionitis (15-17, 22, 23, 37, 38), clinical chorioamnionitis (15,(36)(37)(38)(39)(40)(41)(42), and congenital infection (26,(43)(44)(45)(46)(47). What is unique about many recent investigations is that they further report detection of a microbiota in placentas from uncomplicated pregnancies at term (1,…”

Section: Introductionmentioning

confidence: 99%

Bacterial profiles of the human placenta from term and preterm deliveries

Theis

Winters

Romero

et al. 2022

Preprint

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Whether the human placenta is a sterile organ is under debate. Yet, infection of the amniotic cavity, including the placenta, is causally linked to preterm birth. This study compares the bacterial profiles of term and preterm placentas through culture and 16S rRNA gene sequencing of the amnion, amnion-chorion interface, subchorion, villous tree, and basal plate, while accounting for patient identity, mode of delivery, presence/absence of labor, and potential background DNA contamination. As no evidence of a placental microbiota in term pregnancy was found, these placentas were considered as controls. Placentas from preterm birth cases were more likely to yield bacterial cultures, and their bacterial DNA profiles were less rich than those of term controls, suggesting the predominance of only a few bacteria. Nevertheless, the bacterial DNA profiles of placentas from preterm cases and term controls were not consistently different. The placentas from preterm cases may often have a microbiota but the bacteria constituting these communities varied among the women. Mode of delivery had a pronounced effect on the bacterial profiles of all sampled levels of the placenta. Specifically, the bacterial DNA profiles of vaginally delivered placentas had higher relative abundances of Finegoldia, Gardnerella, Peptoniphilus, and Prevotella (each a common resident of the vaginal microbiota) than the profiles of cesarean-delivered placentas. Collectively, these data indicate that there is a not a placental microbiota in normal term pregnancy, and that although the placentas of some preterm cases were populated by bacteria, the identities of these bacteria varied among women delivering preterm.

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Placental infectious villitis versus villitis of unknown etiology

Cited by 15 publications

References 34 publications

Histological Features of Shallow Placental Implantation Unify Early-Onset and Late-Onset Preeclampsia

Histological Features of Shallow Placental Implantation Unify Early-Onset and Late-Onset Preeclampsia

Placental pathologic lesions with a significant recurrence risk – what not to miss!

Bacterial profiles of the human placenta from term and preterm deliveries

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