Modern Pathology https://doi.org/10.1038/s41379-021-00827-5 ARTICLE Diffuse trophoblast damage is the hallmark of SARS-CoV-2- associated fetal demise Marta Garrido-Pontnou1 Alexandra Navarro2 Jessica Camacho2 Fàtima Crispi3 Marina Alguacil-Guillén 4 ● ● ● ● ● Anna Moreno-Baró2,5 Javier Hernandez-Losa 2,6 Marta Sesé2,6 Santiago Ramón y Cajal 1 Itziar Garcia Ruíz7 ● ● ● ● ● Berta Serrano7 Paula Garcia-Aguilar7 Anna Suy7 Joan Carles Ferreres8 Alfons Nadal 9,10,11 ● ● ● ● Received: 25 March 2021 / Revised: 26 April 2021 / Accepted: 27 April 2021 © The Author(s), under exclusive licence to United States & Canadian Academy of Pathology 2021 Abstract Placental pathology in SARS-CoV-2-infected pregnancies seems rather unspecific. However, the identification of the placental lesions due to SARS-CoV-2 infection would be a significant advance in order to improve the management of these pregnancies and to identify the mechanisms involved in a possible vertical transmission. The pathological findings in placentas delivered from 198 SARS-CoV-2-positive pregnant women were investigated for the presence of lesions 1234567890();,: 1234567890();,: associated with placental SARS-CoV-2 infection. SARS-CoV-2 infection was investigated in placental tissues through immunohistochemistry, and positive cases were further confirmed by in situ hybridization. SARS-CoV-2 infection was also investigated by RT-PCR in 33 cases, including all the immunohistochemically positive cases. Nine cases were SARS-CoV- 2-positive by immunohistochemistry, in situ hybridization, and RT-PCR. These placentas showed lesions characterized by villous trophoblast necrosis with intervillous space collapse and variable amounts of mixed intervillous inflammatory infiltrate and perivillous fibrinoid deposition. Such lesions ranged from focal to massively widespread in five cases, resulting in intrauterine fetal death. Two of the stillborn fetuses showed some evidence of SARS-CoV-2 positivity. The remaining 189 placentas did not show similar lesions. The strong association between trophoblastic damage and placenta SARS-CoV-2 infection suggests that this lesion is a specific marker of SARS-CoV-2 infection in placenta. Diffuse trophoblastic damage, massively affecting chorionic villous tissue, can result in fetal death associated with COVID-19 disease. Introduction Several reports based largely in placentas delivered by SARS-CoV-2 positive mothers describe different placental COVID-19 dramatically changed the management of many pathologic findings in SARS-CoV-2 affected pregnancies. clinical conditions and scenarios. Pregnancy raised particular These findings included maternal and fetal vascular mal- concern because SARS-CoV-2 infection complications can perfusion, perivillous fibrin deposition, and inflammatory affect two different individuals such as the mother and the lesions such as villitis, intervillitis, and chorioamnionitis. A baby. According to the published literature, placental infec- few fetal deaths were reported associated with inflammatory tion occurs at a low rate estimated in 21% of pregnancies, but and ischemic placental findings [2]. However, most of pla- only 2% of neonates show SARS-CoV-2 positivity [1]. cental findings are not severe and corresponding babies were discharged in good health [3–6]. Recently, a previously unreported placental lesion char- acterized by trophoblast necrosis was identified in cases with evidence of SARS-CoV-2 placental infection [7–9]. These authors contributed equally: Marta Garrido-Pontnou, Alexandra Navarro, Jessica Camacho We report here the findings associated with placental SARS-CoV-2 infection that may result in fetal loss depend- These authors jointly supervised this work: Anna Suy, Joan Carles ing on the extent of the lesion. We suggest the name of Ferreres, Alfons Nadal “trophoblastic damage associated with placental SARS-CoV- * Alfons Nadal 2 infection” for this condition that can display either a focal anadal@clinic.cat or a diffuse pattern. This “diffuse trophoblastic damage” is Extended author information available on the last page of the article linked with a very poor fetal outcome. M. Garrido-Pontnou et al. Material and methods Table 1 Association between trophoblastic damage and SARS-CoV-2 infection. A total of 198 placentas delivered from SARS-CoV-2-positive Trophoblastic damage pregnant women were submitted for conventional pathological Yes No p value analysis. Sampling was performed according to recommenda- tions of the Amsterdam Consensus for placental sampling Maternal SARS-CoV-2 positive at <0.006 admission for delivery and report statements [10]. All placentas were immunohisto- Yes 7 68 chemically investigated for the presence of SARS-CoV-2 with No 2 121 the anti-SARS-CoV-2 nucleoprotein (Sino Biological, Wayne, PA) according to manufacturer’s instructions. Immunohisto- Placenta SARS-CoV-2 infection chemically positive cases were further analyzed by in situ IHC <0.001 hybridization (ISH) with the RNAscope-ProbeV-nCoV2019-S Positive 9 0 (Advanced Cell Diagnostics, Hayward, CA). Thirty-three pla- Negative 0 189 centas were investigated for SARS-CoV-2 infection through RT-PCR <0.001 retrotranscriptase PCR (RT-PCR). Fresh tissue samples and/or Positive 9 0 swabs were investigated by RT-PCR for SARS-CoV-2 with Negative 0 24 either the Allplex 2019-nCoV Assay (Seegene, Seoul, South Total 9 189 Korea) or the Taqman 2019-nCoV Assay kit v.2 (Thermo- Fisher Scientific, Waltham, MA, US). For formaldehyde-fixed, paraffin embedded samples, RNA was obtained by High Pure with a tigroid appearance with white irregular deposits FFPET extraction kit (Roche Diagnostics Gmbh) and further (Fig. 1). These five cases showing a diffuse trophoblastic analyzed with CLART®COVID-19 (Genomica SAU) follow- damage were the only that resulted in fetal loss among the ing the manufacturer’s instructions. Clinical data were retrieved nine cases with SARS-CoV-2-infected placentas (p = from the institutional records. Significance of association 0.0079). Four of the stillborns were submitted for fetal between qualitative variables was tested by Fisher’s exact test autopsy, showing no significant results. Two of the fetuses with an α-risk of 0.05. had at least one SARS-CoV-2 RT-PCR positive test (lung and nasopharyngeal swab each) (Table 2). The small foci identified in the four placentas from surviving fetuses were Results positive both for IHC and ISH (Fig. 2). Two of the focally affected placentas were the only that occurred in pregnan- Immunohistochemistry (IHC) for SARS-CoV-2 showed cies negative for SARS-CoV-2 at admission for delivery. cytoplasmic positivity in trophoblastic lining in nine cases Last positive test was obtained 19 days and 17 weeks before with histological evidence of trophoblast necrosis. Pattern delivery, respectively. None of the 189 remaining placentas of staining was patchy both in necrotic and viable tropho- showed similar trophoblastic lesions. IHC for SARS-CoV-2 blast. SARS-CoV-2 ISH was positive with a similar pattern was negative in all of them. Twenty-four of these placentas in the nine immunohistochemically positive cases tested. were tested by RT-PCR giving negative results (Table 1). The nine SARS-CoV-2 positive cases for IHC and ISH Only an additional fetal loss was identified among the were also positive by RT-PCR (Table 1). 189 negative placentas. It occurred in a second trimester The nine immunohistochemically positive placentas SARS-CoV-2 actively infected pregnant woman. Placenta showed similar pathologic findings consisting in villous was small for gestational age and showed acute chor- trophoblast necrosis with collapse of the intervillous space. ioamnionitis with severe stage 3 maternal response and non- Trophoblast necrosis was continuous, outlining the villi. In severe stage 1 fetal response. No signs of trophoblast contrast, villous stroma was rather spared. Some of the foci necrosis were identified. RT-PCR and IHC of placenta were showed a moderate amount of intervillous fibrinoid negative for SARS-CoV-2. deposition and very variable polymorphous inflammatory infiltrates composed mainly by histiocytes with lower numbers of neutrophils and scattered CD-3 positive T-cell Discussion lymphocytes. Small groups of preserved villi were found merged among the areas of trophoblast necrosis. In five Few diseases along human history generated an impact that cases, this pattern of trophoblast necrosis was diffuse, could be compared to the COVID-19 pandemic. Serious involving 80–90% of chorionic tissue. Macroscopically concerns raised on COVID-19 consequences in pregnancy. these five placentas had striking gross findings. The pla- Some early fetal losses were reported [2, 11, 12]. Series on cental disks were stiffed and showed increased consistency placental pathology showed inconsistent results with little Diffuse trophoblast damage is the hallmark of SARS-CoV-2-associated fetal demise Fig. 1 Pathology of diffuse trophoblastic damage. A Grossly the placenta is pale and stiffed. B Histologically, there is diffuse collapse of intervillous space resulting in close contact among chorionic villi with necrosis of trophoblast that stains homogeneously with eosin (H&E, original magnification 20x). C At higher power nuclear signs of cell necrosis can be readily seen in the involved trophoblast whereas villous stroma is spared (H&E, original magnification 60x). D Occasional groups of preserved chorionic villi are totally surrounded of villi involved by diffuse trophoblastic damage (H&E, original magnification 10x). E immunohistochemistry for SARS-CoV-2 shows patchy trophoblast staining (original magnification 30x). F in situ hybridization shows a granular pattern of staining in trophoblast lining of chorionic villi (original magnification 30x). Table 2 Clinicopathologic Case 1 2 3 4 5 6 7 8 9 features of feto-maternal dyads with SARS-CoV-2 infected Maternal age (yr) 38 24 32 38 34 35 37 34 39 placentas. Gestational age 37.4 27.0 28.1 35.3 31.4 40.4 20.2 38.3 41.3 Fetal death Yes Yes Yes No Yes No Yes No No Autopsy Yes Yes No No Yes No Yes No No Fetal weight (g) 2935 781.5 950 2200 1580 3950 313 2580 3740 Fetal gender F M M F F F M M M Placental disk weight (g) 590 126 212 314 234 636 105 300 586 SARS-CoV-2 RT-PCR Fetal tissues Neg. Neg. Pos. Fetal secretions Pos. Neg. Placenta Pos. Pos. Pos. Pos. Pos. Pos. Pos. Pos. Pos. SARS-CoV-2 IHC Fetal tissues Neg. Neg. Neg. Placenta Pos. Pos. Pos. Pos. Pos. Pos. Pos. Pos. Pos. Extent of placental lesions 80% 80% 90% 20% 80% Focal 90% 7% 3% reproducibility among them. However, those series were looked like placental lesions among COVID-19 affected mainly based in maternal SARS-Cov-2 positivity instead of pregnancies were not particularly different from non- placental infection [3, 4, 6]. Taken their results together it affected ones [6]. Besides, placental lesions had little, if M. Garrido-Pontnou et al. Fig. 2 Focal trophoblastic damage. A In this grossly normal-looking placenta few small foci of intervillous space collapse were found as the two here depicted. Inset is shown at a higher magnification in (B) (H&E, original magnification 10x). B Intervillous space collapse and trophoblastic necrosis looks quite similar to more extensive lesions depicted in Fig. 1 (original magnification, 20X). C Immunohistochemical staining for SARS-CoV-2 nucleoprotein shows staining in the injured villi but also in the surrounding normal-looking villi (original magnification 10X). D In situ hybridization with the RNAscope probe replicates the image of immunohistochemistry (original magnification 10x). any impact at all in newborn outcome in those series. Fetal case, pointing to the trophoblast necrosis as the primary losses in COVID-19 pregnancies were clinically attributed lesion in these placentas. to SARS-CoV-2 infection, with two out of three tested cases The combination of trophoblast necrosis and intervillous having evidence of placental or amniotic fluid infection [2]. space collapse can be seen in ischemic lesions such as Vertical transmission or placental infection is supposed to recent villous infarcts or villous agglutination (micro- occur at a low rate [1]. In fact, the existence of a “placental infarcts). Massive infarctions can be seen in abruptio pla- barrier” that prevents fetal infection was suggested [13]. centae, but there were neither clinical nor pathological SARS-CoV-2 infection in placenta was confidently findings supporting this condition in the more severe cases, proved in several cases with consistent results indicating that and the finding of spared small groups of villi surrounded SARS-CoV-2 infects mainly trophoblastic cells outlining by extensive necrotic areas and the relative sparing of the placental villi. Babies affected had an uneventful course and villous stroma in contrast with the extensive trophoblastic were discharged home in good health [7–9, 14]. Placental involvement go against an ischemic origin of necrosis. pathology was interpreted as inflammatory by most of the The inflammatory infiltrate is reported as the main lesion authors except for Debelenko et al., who focused their in most of reports, but our findings do not support its attention in the necrosis of the trophoblast and the acute and leading role. First, although this infiltrate is present in all chronic component of the inflammatory infiltrate [7]. Our cases, it represents just a fraction of the injured tissue, being findings agree with this description. SARS-CoV-2-positive greatly surpassed by the extent of necrosis itself, even in the placentas show a particular lesion characterized by tropho- less severe cases. Moreover, the nature of the infiltrate, with blast necrosis and intervillous space collapse. It can be seen and admixture of histiocytes and greater number of neu- as tiny foci in the less affected cases or as massively exten- trophils than lymphocytes, resembles a reaction to necrosis, sive lesions in the more severe ones. When subtle, ancillary rather than its cause. Massive diffuse trophoblast necrosis is techniques for SARS-CoV-2 detection in placental tissues not a common finding in chronic intervillositis, whereas (IHC, ISH, RT-PCR) are required. Otherwise, they can be mixed inflammatory reaction is common in villous or tro- missed as ischemic lesions. Trophoblast necrosis can be phoblastic necrosis. Although an increase in perivillous found alone or in combination with intervillous inflammation fibrin deposition was present in all cases, it was not a and/or and intervillous fibrinoid deposition. The opposite— prominent feature in any of them. The macroscopic features intervillous inflammation or intervillous fibrinoid deposition resembling massive perivillous fibrinoid deposition could in the absence of trophoblast necrosis—was not found in any be explained by the intervillous space collapse that would Diffuse trophoblast damage is the hallmark of SARS-CoV-2-associated fetal demise produce both the tissue stiffness and the white stripes Data availability crossing the placental tissue, due to the absence of blood normally present in the intervillous space. Data available from the authors upon reasonable request. SARS-CoV-2 infection of trophoblastic cells could be the lesional mechanism in these cases. Sincytiotrophoblast Author contributions MG-P, AN, JC, JCF, and AN performed study express high levels (even higher than pneumocytes) of ACE- concept and design, data acquisition, interpretation of data, writing, review, and revision of the paper. AN performed statistical analysis. 2, the receptor for SARS-CoV-2 cell entry in human cells FC, MA-G, AM-B, IG-R, BS, PG-A, AS participated in data acqui- [13, 15]. Diffuse trophoblastic damage, with trophoblastic sition. JH-L and MS provided technical support and S. RyC, provided necrosis and intervillous space collapse with variable inter- material support. All authors read and approved the final paper. villous inflammatory infiltrates and perivillous fibrinoid deposition could be the placental counterpart of diffuse Funding The authors received no specific funding for this work. alveolar damage of the lung, which is the main histopatho- logic finding in COVID-19 pneumonia. A transcriptional Compliance with ethical standards pattern similar to that of SARS-CoV-2-infected lungs was found in samples of a SARS-CoV-2-infected placenta with a Conflict of interest The authors declare no competing interests. high viral load [16]. In lungs the virus is detected in the Ethics statement The article does not contain any studies with human acute but not in the organizing phase of DAD, suggesting a participants or animals performed by any of the authors. major role for SARS-CoV-2 in initiating the acute lung injury [15]. The presence of the virus in trophoblast even in Publisher’s note Springer Nature remains neutral with regard to the earliest placental lesions would support this view. jurisdictional claims in published maps and institutional affiliations. This peculiar pattern of injury of diffuse trophoblastic damage with trophoblast necrosis plus intervillous space collapse with variable amounts of intervillous inflammation References and perivillous fibrin deposition is either reported [7– 9, 14, 16, 17] or identifiable in the pictures [2, 6, 18, 19] 1. Sharps MC, Hayes DJL, Lee S, Zou Z, Brady CA, Almoghrabi Y, et al. 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Affiliations Marta Garrido-Pontnou1 Alexandra Navarro2 Jessica Camacho2 Fàtima Crispi3 Marina Alguacil-Guillén 4 ● ● ● ● ● Anna Moreno-Baró2,5 Javier Hernandez-Losa 2,6 Marta Sesé2,6 Santiago Ramón y Cajal 1 Itziar Garcia Ruíz7 ● ● ● ● ● Berta Serrano7 Paula Garcia-Aguilar7 Anna Suy7 Joan Carles Ferreres8 Alfons Nadal 9,10,11 ● ● ● ● 1 6 Pathology Department, Hospital Universitari Vall d’Hebron, Pathology Department, Hospital Universitari Vall d’Hebron. Department of Morphological Sciences, School of Medicine, Translational Molecular Pathology, Vall d’Hebron Institute of Universitat Autònoma de Barcelona, Barcelona, Spain Research (VHIR)., Universitat Autònoma de Barcelona, 2 Barcelona, Spain Pathology Department, Hospital Universitari Vall d’Hebron, 7 Barcelona, Spain Obstetrics Department, Hospital Universitari Vall d’Hebron, 3 Barcelona, Spain Department of Maternal-Fetal Medicine, BCNatal, Barcelona 8 Center for Maternal-Fetal and Neonatal Medicine, Hospital Clínic Pathology Department. Parc Taulí Hospital Universitari. Institut and Hospital Sant Joan de Déu, IDIBAPS, Universitat de d’Investigació i Innovació Parc Taulí I3PT. Department of Barcelona, Barcelona, Spain Morphological Sciences, School of Medicine, Universitat 4 Autònoma de Barcelona, Sabadell, Spain Microbiology Department, Parc Taulí Hospital Universitari. Institut 9 d’Investigació i Innovació Parc Taulí I3PT, Universitat Autònoma Pathology Department, Hospital Clínic, Barcelona, Spain de Barcelona, Sabadell, Spain 10 Department of Basic Clinical Practice, School of Medicine, 5 Obstetrics Department, Parc Taulí Hospital Universitari. Institut Universitat de Barcelona, Barcelona, Spain d’Investigació i Innovació Parc Taulí I3PT, Universitat Autònoma 11 de Barcelona, Sabadell, Spain August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain