Placental SARS-CoV-2 in a pregnant woman with mild COVID-19 disease

Abstract

The full impact of coronavirus disease 2019 (COVID-19) on pregnancy remains uncharacterized. Current literature suggests minimal maternal, fetal, and neonatal morbidity and mortality. COVID-19 manifestations appear similar between pregnant and nonpregnant women. We present a case of placental severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus in a woman with mild COVID-19 disease, then review the literature. Reverse transcriptase polymerase chain reaction was performed to detect SARS-CoV-2. Immunohistochemistry staining was performed with specific monoclonal antibodies to detect SARS-CoV-2 antigen or to identify trophoblasts. A 29-year-old multigravida presented at 40-4/7 weeks for labor induction. With myalgias 2 days prior, she tested positive for SARS-CoV-2. We demonstrate maternal vascular malperfusion, with no fetal vascular malperfusion, as well as SARS-CoV-2 virus in chorionic villi endothelial cells, and also rarely in trophoblasts. To our knowledge, this is the first report of placental SARS-CoV-2 despite mild COVID-19 disease (no symptoms of COVID-19 aside from myalgias); patient had no fever, cough, or shortness of breath, but only myalgias and sick contacts. Despite her mild COVID-19 disease in pregnancy, we demonstrate placental vasculopathy and presence of SARS-CoV-2 virus across the placenta. Evidence of placental COVID-19 raises concern for placental vasculopathy (potentially leading to fetal growth restriction and other pregnancy complications) and possible vertical transmission-especially for pregnant women who may be exposed to COVID-19 in early pregnancy. This raises important questions of whether future pregnancy guidance should include stricter pandemic precautions, such as screening for a wider array of COVID-19 symptoms, increased antenatal surveillance, and possibly routine COVID-19 testing throughout pregnancy.

Keywords: Coronavirus; SARS coronavirus; public policy.

Figure 1

Placental vasculopathy in a pregnant woman with mild COVID‐19 disease. Placental membranes showed decidua with scattered arterioles with thickened smooth muscle, consistent with hypertrophic arteriolopathy (vasculopathy) (A, umbilical cord and placental membranes) and subchorionic laminar necrosis (B, placental parenchyma under the umbilical cord). Placental disc showed focal areas of lympho‐histiocytic inflammation consistent with chronic villitis (C, central placental parenchyma) and scattered islands of extravillous trophoblasts (D, peripheral placental parenchyma)

Figure 2

Presence of SARS‐CoV‐2 virus across the placenta in a patient with mild COVID‐19 disease. IHC staining of SARS‐CoV‐2 virus in a COVID‐19 negative patient, delivery before the COVID‐19 outbreak (A). IHC of SARS‐CoV‐2 from three placental sections ((B) under umbilical cord, (C) central placental disc, (D, E) peripheral placental disc at ×20 and ×40). IHC of CK‐7 marker in control ferret nasal turbinate tissue (F). IHC of CK‐7 from three placental sections ((G) under umbilical cord, (H) central placental disc, (I, J) peripheral placental disc at ×10 and ×20). Arrows or brown staining indicate immunoreactive antigens. Bars = 20/50/100 µm shown at the right bottom corner of each panel. IHC was performed with SARS‐CoV‐2 nucleocapsid‐specific rabbit monoclonal antibody (Sino Biological) and goat anti‐rabbit IgG (Vector lab). To identify trophoblasts, IHC was performed using rabbit recombinant anti‐CK7 monoclonal antibody (Abcam) and goat anti‐rabbit IgG (Vector lab). CK‐7, cytokeratin‐7; IHC, immunohistochemistry; SARS‐CoV‐2, severe acute respiratory syndrome coronavirus 2