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Brief Report

Detection of SARS-CoV-2 in Ascitic Fluid of Cirrhotic COVID-19 Patients: Case Series and Literature Review

by
Grazia Caci
1,2,†,
Andrea Marino
3,*,†,
Edoardo Campanella
3,4,
Ylenia Russotto
4,
Cristina Micali
4,
Natascia Laganà
4,
Aldo Sitibondo
4,
Roberto Filomia
5,
Antonino Botindari
4,
Serena Spampinato
3,4,
Giuseppe Mancuso
6,
Angelina Midiri
6,
Giovanni Francesco Pellicanò
4,
Giuseppe Nunnari
3 and
Emmanuele Venanzi Rullo
4
1
Infectious Disease Department, University Hospital Policlinico “G. Rodolico- San Marco” of Catania, 95121 Catania, Italy
2
Department of General Surgery and Medical-Surgical Specialities, University of Catania, 95122 Catania, Italy
3
Unit of Infectious Diseases, Department of Clinical and Experimental Medicine, University of Catania, 95122 Catania, Italy
4
Unit of Infectious Diseases, Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
5
Division of Medicine and Hepatology, Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
6
Unit of Microbiology, Department of Adult and Childhood Human Pathology “G. Barresi”, University of Messina, 98125 Messina, Italy
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
COVID 2025, 5(4), 58; https://doi.org/10.3390/covid5040058
Submission received: 8 February 2025 / Revised: 28 March 2025 / Accepted: 4 April 2025 / Published: 18 April 2025
(This article belongs to the Section COVID Clinical Manifestations and Management)
Review Reports Versions Notes

Abstract

:
SARS-CoV-2 has been identified in multiple organs and fluids, including the liver and peritoneal fluid. Gastrointestinal symptoms, such as abdominal pain, diarrhea, nausea, and vomiting, can exacerbate COVID-19 outcomes by contributing to complications, like acid–base imbalances and cardiovascular dysfunction, particularly in patients with pre-existing conditions. We report three cases of COVID-19 cirrhotic patients with SARS-CoV-2 detected in their ascitic fluid and review the relevant literature on the virus’s presence and clinical significance in peritoneal fluid. These findings underscore diagnostic and prognostic challenges in managing COVID-19 in patients with chronic liver disease and highlight the need for further research to clarify viral dissemination mechanisms and optimize protective measures for healthcare workers during surgical procedures.

1. Introduction

The first case of Coronavirus Disease 2019 (COVID-19) was reported in Wuhan, Hubei Province, China, in December 2019, and the pathogen was named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) [1]. SARS-CoV-2 primarily spreads through the respiratory tract via droplets, respiratory secretions, and direct contact. Additionally, the virus has been isolated from fecal swabs and blood, indicating multiple routes of transmission [2,3].
The detection of SARS-CoV-2 in various clinical samples has provided critical insights into its pathogenesis. A dysregulated inflammatory response has been demonstrated and its understanding used for early strategies for treatment [4]. Notably, the virus utilizes angiotensin-converting enzyme 2 (ACE2) receptors, which are expressed in a wide range of human cells, including pneumocytes, ileal and colonic enterocytes, hepatocytes, and cholangiocytes [5]. An enhanced ACE2 expression in the liver, particularly in patients with hepatitis C, steatosis, and non-alcoholic steatohepatitis, suggests a potential mechanism for liver involvement [6,7].
Liver injury in COVID-19 patients can range from the asymptomatic elevations of liver enzymes to severe hepatic decompensation. The injury is primarily hepatocellular rather than cholestatic, likely due to the overactivation of Kupffer cells, virus-induced cytotoxic T cell response, and innate immune response [8]. The American Gastroenterological Association notes that liver injury in COVID-19 may be related to systemic inflammation, hypoxia, hepatic congestion, and drug-induced liver injury [9].
Patients with chronic liver diseases, such as cirrhosis, are at higher risk of severe COVID-19 outcomes. Studies have shown that mortality rates in patients with cirrhosis and COVID-19 can be significantly higher, with increased rates of hepatic decompensation and acute-on-chronic liver failure [10,11]. Understanding the mechanisms of liver injury and the impact of SARS-CoV-2 on patients with pre-existing liver conditions is crucial for developing effective management strategies. Furthermore, positive test results of SARS-CoV-2 in peritoneal fluid are reported in the recent medical literature, although the significance of this finding remains uncertain [12,13].
We report three cases of cirrhotic COVID-19 patients in which SARS-CoV-2 has been detected in the ascitic fluid, independently of its presence in nasopharyngeal swabs.

2. Materials and Methods

Nasal and oropharyngeal swabs were collected and stored in the universal transport medium (UTM) with 3 mL of Hank’s Balanced Salt solution (HBSS) (Merck KGaA, Darmstadt, Germany). Ribonucleic acid (RNA) extraction was performed in all specimens with Promega Maxwell RSC 48 RNA extraction system (Promega, Madison, WI, USA).
Ascitic fluid was collected with a sterile syringe following abdominal punction with aseptic technique. After that, real time-PCR (RT-PCR) assay testing for three SARS-CoV-2 target genes (Envelope, Nucleocapsid, and RNA-dependent-RNA-polymerase) was performed (Arrow diagnostics, Seegene Allplex SARS-CoV-2 Assay, Seoul, Republic of Korea). SARS-CoV-2 RNA detection was performed using RT-PCR with a limit of detection of 50 copies per 20 µL. Samples were considered positive if amplification occurred within 40 cycles (Cycle Threshold ≤ 40). Ct values below 30 were interpreted as indicative of high viral load, while values between 30 and 40 suggested low viral load or residual RNA. The assay was not optimized for this type of sample.
We conducted a literature search for articles about presence and/or testing of SARS-CoV-2 in abdominal fluids. We searched the National Library of Medicine (PubMed) database, using the terms: “COVID-19” or “SARS-CoV-2” and “ascites”, “peritoneal dialysis”, “gastrointestinal tract”, and “peritoneal fluid” in various combinations. We also searched for the Google Scholar database using the same queries. The search was not limited by language or geographic region. Case reports, systematic reviews, and meta-analyses were included.

3. Results

  • Case 1
A 78-year-old white male patient showing severe oxygen desaturation (SpO2 80%) in room air and a positive RT-PCR for SARS-CoV-2 on a nasopharyngeal swab was admitted to our COVID-hospital. His past clinical history showed arterial hypertension, dyslipidemia, and a previous episode of acute myocardial infarction. He was in follow-up at the Hepatology Unit of our hospital due to decompensated cryptogenic hepatic cirrhosis and esophageal varices, which were treated endoscopically. During the last 8 months, he underwent several diagnostic and therapeutic paracentesis procedures; the last one was scheduled for the day of admission.
At admission, he was in poor general condition, with an increased respiratory rate (36 breaths per minute) and peripheral vasoconstriction with arterial hypotension (100/70 mmHg). A chest X-ray showed parenchymal thickening spread to both lungs, which was more evident in the mid-lower lung area on the right.
Oxygen therapy with a Venturi Mask FiO2 60% 12 lt/min and corticosteroid therapy with dexamethasone were started.
Moreover, his blood tests (Table 1) highlighted a worsening liver function compared with his last check-up. Amylases and lipases were also increased. Cholestasis indices were in range at admission. A paracentesis was performed to improve respiratory function. A SARS-CoV-2 test of his peritoneal fluid was positive. During the hospitalization the patient was mostly unresponsive and showed a general slowness and worsening dyspnea. He died three days later due to severe pulmonary edema.
  • Case 2
A 74-year-old white male patient was admitted to the Hepatology Unit due to decompensated ascites. The patient was admitted to our COVID-hospital with a positive RT-PCR for SARS-CoV-2 on a nasopharyngeal swab.
He had a history of ischemic heart disease, arterial hypertension, dyslipidemia, type 2 diabetes mellitus, gallbladder stones, portal hypertension, alcoholic liver cirrhosis Child-Pugh B, F1 esophageal varices, chronic kidney disease, and polyposis of the rectum and sigma. He reported alcohol abuse.
Soon after his admission, an RT-PCR for SARS-CoV-2 on his nasopharyngeal swab resulted in a positive result and he was transferred to the Infectious Diseases Unit. At admission, a physical examination revealed a fever (37.8 °C), blood pressure of 100/60 mmHg, heart rate of 70 bpm, respiratory rate of 20 breaths per minute, and oxygen saturation in room air of 98%.
Serological studies were negative for HBV, HCV, and HIV. He had an IgG serology positive for HAV, with a negative IgM.
A chest CT scan showed bilateral parenchymal thickening with mixed characters, partly ground glass and partly consolidative, which was predominantly peripheral with the involvement of the lower lobes. At admission, his blood exams showed an alteration in the liver function and cholestasis indices (Table 1).
After 20 days of hospitalization, the patient’s nasopharyngeal swab tested negative for SARS-CoV-2.
Due to his fever, abdomen pain, and the patient’s worsening clinical conditions we proceeded with paracentesis. The microbiological markers, both in cultures and Filmarray, in the ascitic fluid tested negative. However, SARS-CoV-2 was detected in the peritoneal fluid. Empiric antibiotic therapy was started with ceftriaxone. The patient died due to cardiac arrest after 36 days of hospitalization.
  • Case 3
A 73-year-old white male patient was admitted to the Hepatology Unit. He had a history of arterial hypertension, dyslipidemia, type 2 diabetes mellitus, hepatic trans-arterial chemo embolization (TACE) S5 and S8 in 2017 and 2018, subsequent degeneration into hepatocellular carcinoma (HCC), dysmetabolic liver cirrhosis, history of ruptured esophageal varices F3 in 2016, and hypoacusis bilateral due to professional reasons since 2008. He also had a history of bladder stones with recurrent urinary tracts infections (UTIs) and sigma polyposis and an endoscopic resection in 2018.
Six days after admission, a nasopharyngeal swab for SARS-CoV-2 detection tested positive; he was therefore transferred to the Infectious Diseases Unit. At admission, the patient presented in a poor clinical condition. A physical examination revealed a blood pressure of 125/70 mmHg, heart rate of 73 bpm, respiratory rate of 18 breaths per minute, and peripheral oxygen saturation in room air of 97%. Diuresis was valid from the catheter, hyperchromic urine. The abdomen was tense but not painful on palpation. A thorax CT scan showed bilateral and diffuse parenchymal thickening. The blood examination showed thrombocytopenia, increased transaminases, and cholestasis indices (Table 1).
Due to the development of abdomen pain along with sensory loss, we proceeded to a diagnostic paracentesis to rule out spontaneous bacterial peritonitis (SBP). The peritoneal fluid tested positive for SARS-CoV-2. Twenty days after admission the patient died due to liver failure.
The presence of SARS-CoV-2 in peritoneal fluid has been documented in several studies, although the findings are inconsistent (Table 2).

4. Discussion

As is known, SARS-CoV-2 is considered a hepatotropic virus causing acute hepatitis up to hepatic failure, especially in patients suffering from chronic liver diseases [21]. It has also been shown that increased liver enzymes correlate with the severity of COVID-19 [21,22,23]. SARS-CoV-2 also reportedly worsens the clinical course of patients affected by different diseases [24], such as viral hepatitis and especially hepatitis B infection [25]. Therefore, as shown in our case series, it seems that people already suffering from hepatic disorders are at a higher risk of developing severe disease [23,24,25,26,27,28].
SARS-CoV-2 can reach the peritoneal cavity through several potential mechanisms:
1. Hematogenous Spread: SARS-CoV-2 RNA has been detected in blood samples, suggesting that the virus can disseminate via the bloodstream to various organs, including the peritoneal cavity. This hematogenous spread is facilitated by the presence of ACE2 receptors in multiple tissues, including the liver and gastrointestinal tract [13,29].
2. Lymphatic Drainage: The virus may also spread through the lymphatic system. The lymphatic drainage from the gastrointestinal tract and other abdominal organs can carry the virus to the peritoneal cavity, contributing to its presence in peritoneal fluid [29].
3. Direct Viral Shedding from the Gastrointestinal Tract: SARS-CoV-2 can infect the gastrointestinal tract, where ACE2 receptors are highly expressed. The virus can cause damage to the intestinal epithelial barrier, leading to the translocation of the virus from the gut lumen into the peritoneal cavity. This mechanism is supported by the detection of viral RNA in fecal samples and the presence of gastrointestinal symptoms in COVID-19 patients [2,5].
SARS-CoV-2 utilizes the angiotensin-converting enzyme 2 (ACE2) receptors to infiltrate human cells, which is expressed not only in pneumocytes (type II alveolar cells) but also in a wide range of human cells, such ileal and colonic enterocytes, hepatocytes, and cholangiocytes [30].
Studies have revealed an enhanced ACE2 expression in the livers of patients with hepatitis C, steatosis, and non-alcoholic steatohepatitis [31,32]. However, despite the fact that cholangiocytes express higher levels of ACE2 receptors compared to hepatocytes, liver injury is primarily due to hepatocyte injury rather than cholestasis. This injury may be related to the overactivation of Kupffer cells, virus-induced cytotoxic T cell response, and innate immune responses. In addition, SARS-CoV-2 can also trigger the massive release of pro-inflammatory cytokines, which can exacerbate underlying liver injuries [33,34,35]. Furthermore, ACE2 receptors have been detected in macrophages, which could be in patients’ peritoneal fluid and may facilitate viral shedding through different tissues and cause peritoneal effusion [36,37].

Gut–Liver Axis and SARS-CoV-2

The gut–liver axis plays a significant role in the pathogenesis of the SARS-CoV-2 infection and its dissemination to the peritoneal cavity. The gut–liver axis involves bidirectional communication between the gut and the liver, mediated by the portal vein, bile acids, and immune signaling pathways. SARS-CoV-2 can infect the gastrointestinal tract, where ACE2 receptors are highly expressed, leading to intestinal barrier dysfunction and increased intestinal permeability. This disruption allows the translocation of microbial products and the virus itself into the portal circulation, potentially reaching the liver and peritoneal cavity [29,38,39].
The presence of SARS-CoV-2 in peritoneal fluid may be indicative of a severe systemic involvement. Studies have shown that patients with higher viral loads in respiratory samples are more likely to have viral dissemination to extrapulmonary organs, including the peritoneal cavity. This suggests that the detection of SARS-CoV-2 in peritoneal fluid could be a marker of disease severity and a predictor of poor outcomes, particularly in patients with pre-existing liver conditions [2,13,40,41].
Conflicting findings in the literature regarding the presence of SARS-CoV-2 in peritoneal fluid, especially in cirrhotic patients, can be attributed to several factors. Variations in the timing of sample collection, the severity of the disease, methodological differences in RT-PCR assays, and differences in patient populations may all contribute to inconsistent results. For instance, studies reporting negative results may have sampled patients at different stages of infection or used less sensitive detection methods [13,42,43].
In conclusion, the gut–liver axis is a critical pathway for the dissemination of SARS-CoV-2 to the peritoneal cavity. The presence of the virus in peritoneal fluid may serve as a marker of severe disease and a poor prognosis, highlighting the need for further research to understand the factors influencing viral dissemination and to improve patient management strategies.
Conflicting Findings in the Literature:
Studies have reported both positive and negative results for SARS-CoV-2 in peritoneal fluid. Tartaglia et al. found that 15% of patients undergoing emergency abdominal surgery had SARS-CoV-2 in their peritoneal fluid. In contrast, other studies have reported negative results, such as those by Jakimiuk et al. and Vimalachandran et al., who did not detect the virus in peritoneal fluid samples from patients undergoing cesarean sections or abdominal surgeries [13].
Explanations for Discrepancies:
1. Timing of Sample Collection: The viral load in different body compartments may vary over the course of the infection. Samples collected at different stages of the disease may yield different results.
2. Severity of Disease: patients with severe COVID-19 and higher viral loads in respiratory samples are more likely to have a viral dissemination to extrapulmonary organs, including the peritoneal cavity [13].
3. Methodological Differences: variations in the sensitivity and specificity of the RT-PCR assays used to detect viral RNA can contribute to inconsistent findings.
4. Patient Population: Differences in the underlying health conditions of the patient populations studied, such as the presence of chronic liver disease, may influence the likelihood of detecting the virus in peritoneal fluid.
In conclusion, while the presence of SARS-CoV-2 in peritoneal fluid has been documented, the variability in detection rates highlights the need for further research to understand the factors influencing the viral dissemination to the peritoneal cavity.
Finally, Shankar et al. found out that in a total of 246 samples from different organs of 21 patients who died due to severe COVID-19, SARS-CoV-2 was detected in 181 samples with a positivity of SARS-CoV-2 in the peritoneal fluid around 80%. Furthermore, in this study it seems that patients with higher viral loads in respiratory samples (low Ct value) are more likely to have dissemination to extrapulmonary organs. For this reason, the authors recommend monitoring patients more closely for any warning signs during the acute phase of the illness to address the involvement of other organs [44].
Furthermore, theoretically the presence of SARS-CoV-2 in peritoneal fluid could represent a risk of contagion for operating teams, especially during laparoscopy because of the aerosolized particles originating during this procedure [12]. However, despite the need for larger studies, some evidence seems to show that patients with a positive peritoneal swab are unlikely to contaminate an operating room and that the adopted precautions are effective in protecting the exposed health workers from infection, and abdominal or gynecological surgeries must be considered low-risk procedures [15].
The cases we reported describe patients in severe clinical conditions suffering from chronic hepatic diseases. All of them tested positive for SARS-CoV-2 in their peritoneal fluid. This is a very small case series, and more evidence is needed to determine if there is a correlation between the presence of SARS-CoV-2 in the peritoneal/ascitic fluid and the severity of COVID-19. However, it is possible to hypothesize a correlation between liver failure and the presence of SARS-CoV-2 in peritoneal fluid. It is not known whether the presence of SARS-CoV-2 in the same fluid is correlated with other disorders concerning abdominal organs. All the patients that test positive for SARS-CoV-2 with increased liver enzymes should undergo a careful examination of their clinical history, to find any possible risk factors for liver disorders. Moreover, they should undergo a careful clinical examination, periodic blood tests, screenings for viral hepatitis, and possibly an abdominal ultrasound or computer tomography to promptly identify and treat the causes of liver failure.

5. Conclusions

The detection of SARS-CoV-2 in ascitic fluid in our case series, even after the negativization of nasopharyngeal swabs, highlights the persistence of peripheral viral replication and its potential association with severe clinical outcomes.
While our findings do not establish a direct causal link, they emphasize the need to investigate the mechanisms of viral dissemination to the abdominal cavity and their clinical significance in patients with chronic liver disease. Previous studies on viruses such as hepatitis B virus (HBV) [45], human papillomavirus virus (HPV) [46], and human immunodeficiency virus 1 (HIV-1) [47] confirmed that it could be possible detected the virus in vapors created by power surgical instruments [12].
Future research should focus on larger cohort studies to confirm these findings and provide robust epidemiological data. Additionally, mechanistic studies are necessary to elucidate how SARS-CoV-2 infiltrates the peritoneal cavity and whether this contributes to disease progression or complications. Moreover, it is essential to determine the clinical–prognostic significance and, in the event of abdominal surgery, if there is a need to take more precautions to protect healthcare workers from the droplet effect that could result from it. Addressing these areas will enhance our understanding of the SARS-CoV-2 pathogenesis and improve clinical management strategies for at-risk patients.

Author Contributions

G.C. and A.M. (Andrea Marino) wrote the final version of the manuscript. G.M. and A.M. (Angelina Midiri) coordinated the sample analysis and ran the RT-PCR. G.C., A.B., N.L., A.S., R.F. and E.C. collected samples and clinical data, G.C., Y.R., C.M., S.S., G.F.P. and G.N. revised the manuscript, E.V.R. coordinated the experiment and revised the final manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of Azienda Ospedaliera Universitaria “Gaetano Martino” (Prot. 63-20 BIS, 22 May 2022).

Informed Consent Statement

Informed consent was obtained from all subjects involved in this study.

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author(s).

Conflicts of Interest

The authors declare no conflicts of interest.

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Table 1. Blood chemistry. Table shows laboratory findings of 3 patients described above.
Table 1. Blood chemistry. Table shows laboratory findings of 3 patients described above.
Case #WBC/mm3N%Lf%PLT/mm3AST U/LALT U/LγGT U/LBilirubin Total mg/dLDirect Bilirubin mg/dLLDH U/LAmmoniemia μg/dL
Case 1 38008211301,000495280.760.56930N/A
Case 27200573592,000124452323.702.43523125
Case 33800771833,0003257346.024.98217109
Abbreviations: WBC: white blood cells, N: neutrophils, Lf: lymphocyte, PLT: platelets, AST: Aspartate Aminotransferase, ALT: alanine aminotransferase, γGT: gamma-glutamil transpeptidase, and LDH: Lactate Dehydrogenase.
Table 2. Overview of studies assessing SARS-CoV-2 detection in peritoneal and abdominal samples.
Table 2. Overview of studies assessing SARS-CoV-2 detection in peritoneal and abdominal samples.
StudySample SizePatient CharacteristicsMethodsResultsReferences
Coccolini et al. (2020)1COVID-19-positive patient undergoing emergency surgeryRT-PCR on peritoneal fluid1/1 positive for SARS-CoV-2[13]
Tartaglia et al. (2022)13Patients with positive nasopharyngeal swabs undergoing emergency surgeryRT-PCR on peritoneal swabs2/13 (15%) positive for SARS-CoV-2[14]
Jones et al. (2021)113Patients undergoing abdominal surgery, presumed COVID-19-negativeRT-PCR on peritoneal and vaginal swabs0/102 peritoneal samples positive[15]
Romero-Velez et al. (2020)1Asymptomatic COVID-19-positive patientRT-PCR on peritoneal fluid0/1 peritoneal sample positive[16]
Romero-Velez et al. (2023)295Mixed, including severe COVID-19 casesSystematic review of RT-PCR on abdominal samples21/357 (5.9%) positive for SARS-CoV-2[17]
Candellier et al. (2020)3Peritoneal dialysis patients with COVID-19RT-PCR on peritoneal effluent0/3 peritoneal effluent samples positive[18]
Safari et al. (2020)4Patients undergoing emergent abdominal surgeryRT-PCR on abdominal fluid and tissues0/4 peritoneal samples positive[19]
Romero-Velez et al. (2021)6COVID-19 positive patients undergoing abdominal surgeryRT-PCR on abdominal fluid samples0/6 peritoneal samples positive[20]
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Caci, G.; Marino, A.; Campanella, E.; Russotto, Y.; Micali, C.; Laganà, N.; Sitibondo, A.; Filomia, R.; Botindari, A.; Spampinato, S.; et al. Detection of SARS-CoV-2 in Ascitic Fluid of Cirrhotic COVID-19 Patients: Case Series and Literature Review. COVID 2025, 5, 58. https://doi.org/10.3390/covid5040058

AMA Style

Caci G, Marino A, Campanella E, Russotto Y, Micali C, Laganà N, Sitibondo A, Filomia R, Botindari A, Spampinato S, et al. Detection of SARS-CoV-2 in Ascitic Fluid of Cirrhotic COVID-19 Patients: Case Series and Literature Review. COVID. 2025; 5(4):58. https://doi.org/10.3390/covid5040058

Chicago/Turabian Style

Caci, Grazia, Andrea Marino, Edoardo Campanella, Ylenia Russotto, Cristina Micali, Natascia Laganà, Aldo Sitibondo, Roberto Filomia, Antonino Botindari, Serena Spampinato, and et al. 2025. "Detection of SARS-CoV-2 in Ascitic Fluid of Cirrhotic COVID-19 Patients: Case Series and Literature Review" COVID 5, no. 4: 58. https://doi.org/10.3390/covid5040058

APA Style

Caci, G., Marino, A., Campanella, E., Russotto, Y., Micali, C., Laganà, N., Sitibondo, A., Filomia, R., Botindari, A., Spampinato, S., Mancuso, G., Midiri, A., Pellicanò, G. F., Nunnari, G., & Venanzi Rullo, E. (2025). Detection of SARS-CoV-2 in Ascitic Fluid of Cirrhotic COVID-19 Patients: Case Series and Literature Review. COVID, 5(4), 58. https://doi.org/10.3390/covid5040058

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