Case Report: Be Alert to Parvovirus Infection in Patients with Unexplained Anemia after Cerebral Hemorrhage Surgery

Case Report: Be Alert to Parvovirus Infection in Patients with Unexplained Anemia after Cerebral Hemorrhage Surgery | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Case Report: Be Alert to Parvovirus Infection in Patients with Unexplained Anemia after Cerebral Hemorrhage Surgery Muhua Dai, Lisha Pang, Jianbiao Meng, Mahong Hu, Wei Zhang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8107211/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Human parvovirus B19 (PVB19) is a highly prevalent single-stranded DNA virus that infects a large proportion of the global population. It can involve multiple organ systems, leading to a broad spectrum of clinical manifestations. While most infections in immunocompetent individuals are mild and self-limiting, PVB19 can occasionally cause severe and diverse complications. Case Presentation: We report a rare case of an immunocompetent patient who experienced unexplained clinical deterioration following surgical evacuation of an intracerebral hemorrhage. The patient presented with refractory anemia, impaired consciousness, fever, seizures, and progressive dysfunction of the cardiac, hepatic, and renal systems. Metagenomic next-generation sequencing revealed high levels of PVB19 DNA in the cerebrospinal fluid, blood, and pleural effusion. The patient was treated with intravenous immunoglobulin (IVIG) therapy and supportive care. Following treatment, improvements were observed in consciousness, mobility, and anemia. However, renal function failed to recover and ultimately progressed to renal failure, necessitating renal replacement therapy. Conclusion： This case underscores the potential severity of PVB19 infection following cerebral hemorrhage surgery, particularly when accompanied by unexplained anemia. Accurate diagnosis requires a high index of suspicion and the use of advanced diagnostic tools. Management primarily involves IVIG therapy and supportive care. This case highlights the importance of expanding the differential diagnosis in postoperative patients presenting with unexplained anemia and multi-organ dysfunction, as early recognition of atypical infections may improve clinical outcomes. Human parvovirus B19 PVB19 refractory anemia organ failure mNGS Figures Figure 1 Figure 2 Figure 3 Introduction PVB19 is a single-stranded DNA virus first identified accidentally in 1975 by Australian virologist Yvonne Cossart [ 1 ] . The global population is generally susceptible to infection, with both sporadic cases and outbreaks reported worldwide. In some countries, the seroprevalence of PVB19 exceeds 76% [ 2 ] . The clinical manifestations of PVB19 infection vary widely in severity, depending largely on the host’s immune status and the pathogenicity of the virus. In immunocompetent individuals [ 3 ] , PVB19 infection typically causes erythema infectiosum a mild rash illness primarily affecting children and may lead to polyarthritis or arthralgia in adults. In pregnant women, infection can result in fetal hydrops, intrauterine fetal death, or miscarriage [ 4 ] . Among immunocompromised patients, PVB19 is associated with pure red cell aplasia (PRCA) and transient aplastic crisis (TAC) [ 5 , 6 ] . Recent studies have broadened the recognized clinical spectrum of PVB19, linking it to systemic sclerosis, hepatitis, myocarditis, encephalitis, meningitis, hemophagocytic lymphohistiocytosis, and renal impairment [ 7 – 9 ] . The underlying pathogenic mechanisms remain incompletely understood but are thought to be primarily immune-mediated [ 7 , 10 , 11 ] . Currently, no specific antiviral therapy exists; treatment is largely supportive, focusing on symptom control and organ function preservation. In severe cases, IVIG therapy or blood transfusion may be required. Reports of multiple organ dysfunction or failure caused by PVB19 infection in previously immunocompetent individuals are rare. To date, no cases have been documented in postoperative intracerebral hemorrhage patients developing multiple organ failure secondary to PVB19 infection. Here, we describe such a case involving an immunocompetent patient who developed sepsis and multiple organ dysfunction syndrome (MODS) following surgical evacuation of an intracerebral hemorrhage. The patient exhibited extensive multi-system involvement with an exceptionally high viral load. Through comprehensive management including mechanical ventilation, continuous renal replacement therapy (CRRT), and IVIG administration the patient’s consciousness gradually recovered, organ function improved significantly, and overall clinical status stabilized. Case presentation The patient was a 51-year-old obese male teacher admitted to the hospital with a diagnosis of cerebellar hemorrhage. His medical history was significant for hypertension and type 2 diabetes mellitus. He had not adhered to dietary recommendations or maintained regular physical activity, resulting in poor glycemic control. On emergency admission, his serum creatinine level was 140 µmol/L, although he denied any prior history of kidney disease. Surgical evacuation of the cerebellar hematoma was performed, and the patient was transferred to the intensive care unit (ICU) postoperatively. As his level of consciousness improved, he became able to follow commands and move spontaneously. One week later, after successful ventilator weaning, he was transferred to the neurosurgery ward, at which time his hemoglobin level was 95 g/L. During his stay in the neurosurgery ward, the patient developed a progressive decline in hemoglobin levels (95 g/L → 58 g/L), accompanied by persistent fever and new-onset neurological symptoms, including speech disturbance and facial twitching. Lumbar puncture revealed an opening pressure of 310 mmH₂O. Cerebrospinal fluid (CSF) analysis showed a white blood cell count of 12 × 10⁶/L, with 70% lymphocytes. Biochemical examination of the CSF indicated a glucose level of 2.81 mmol/L, chloride concentration of 120.6 mmol/L, and protein concentration of 641 mg/L. Synchronous blood tests showed a glucose level of 7.14 mmol/L and chloride of 103.2 mmol/L. Brain MRI revealed acute cerebral infarctions near the splenium of the corpus callosum and the posterior horns of the lateral ventricles (Fig. 1 A). However, these imaging findings did not fully explain the patient’s worsening mental status and persistent fever. His condition continued to deteriorate, presenting with high-grade fever (up to 39.5°C), lethargy, refractory anemia (hemoglobin decreased from 95 g/L to 58 g/L despite a negative stool occult blood test), hypoxemia (lowest SpO₂ = 85% on a reservoir mask), and generalized edema, necessitating urgent readmission to the ICU. Upon ICU readmission, the patient underwent endotracheal intubation and mechanical ventilation. Chest computed tomography revealed pulmonary infiltrates and bilateral pleural effusions (Fig. 1 B). Metagenomic next-generation sequencing detected high sequence counts of human PVB19 in the CSF, pleural fluid, and blood (Table and Fig. 2 ). The patient developed persistent severe anemia, with a hemoglobin nadir of 50 g/L, accompanied by prolonged reticulocytopenia (reticulocyte percentage: 0.14–0.26%; absolute count: 0.18–0.53 × 10¹²/L) lasting approximately one week. Serum ferritin levels were markedly elevated (> 1500 ng/mL; reference range: 23.9–336 ng/mL). Bone marrow aspiration demonstrated markedly suppressed erythropoiesis with a predominance of proerythroblasts and early erythroblasts, consistent with PRCA (Fig. 1 C). Persistent lymphopenia (0.5 × 10⁹/L) indicated an immunosuppressed state. Given the immunodeficiency and high viral load, IVIG therapy was administered. Renal function progressively deteriorated, as evidenced by rising serum creatinine levels and oliguria, necessitating CRRT. Following treatment, PVB19 levels in both the CSF and blood declined significantly (Table 1 ,Fig. 2 ). The patient regained consciousness,exhibiting improved responsiveness, resolution of facial twitching, and successful weaning from mechanical ventilation and renal replacement therapy. Normalization of reticulocyte counts prompted a transfer to nephrology for further management. Table 1 Test results of mNGS in body fluid samples of the patient. Item Specimen The types of pathogens detected by mNGS Viral DNA/RNA quantification(sequence count) CSF1( diagnosis) PVB19 558465 CSF2(12days after diagnosis) PVB19 95 CSF3(19days after diagnosis) PVB19 134 CSF4(26days after diagnosis) PVB19 7 CSF5(39days after diagnosis) CMV 56 Blood1(1day after diagnosis) PVB19、Circovirus 1074518、5 Blood2(20days after diagnosis) PVB19、CMV 3、39 Blood3(30days after diagnosis) CMV、Circovirus、PVB19 1511、14、8 Pleural effusion (1day after diagnosis) PVB19 29658 CSF: Cerebrospinal Fluid; CMV༚Cytomegalovirus; A: Head magnetic resonance imaging (MRI) examination B: Before being admitted to the ICU, the lung CT scan indicated bilateral pleural effusion. C: The result of the bone marrow puncture. A one-year follow-up was conducted for the patient. Intermittent blood tests performed by the attending physician showed a gradual improvement in reticulocyte counts, while metagenomic next-generation sequencing of peripheral blood revealed only trace levels of parvovirus B19 sequences. Consequently, further immunoglobulin therapy was deemed unnecessary. The patient’s hemoglobin level progressively increased from 50 g/L to 65 g/L. However, renal function failed to recover, necessitating ongoing maintenance hemodialysis. In addition, cardiac function progressively deteriorated, resulting in multiple ICU readmissions for episodes of acute left ventricular failure. The timeline of the patient’s clinical course, treatment interventions, and outcomes is summarized in Fig. 3 . Discussion PVB19 typically causes self-limited illnesses, such as erythema infectiosum in children and transient arthritis in healthy adults [ 3 ] . However, in immunocompromised patients or those with chronic anemia, PVB19 infection can lead to severe or even fatal complications, including chronic PRCA and hydrops fetalis [ 4 , 6 , 12 ] . In this case, the patient was a postoperative cerebral hemorrhage patient with no prior history of immunodeficiency. Nonetheless, surgical trauma and stress may have induced a relative immunosuppressed state, as evidenced by persistently low lymphocyte counts during the infection. The patient’s hemoglobin level remained persistently low. After excluding significant blood loss from gastrointestinal or other sources, PVB19-induced pure red cell aplasia was considered the most likely cause. According to current studies, the primary target of PVB19 is the erythroid precursor cells in the bone marrow. The VP1/VP2 capsid proteins of PVB19 exhibit a high affinity for these progenitor cells (colony-forming unit–erythroid, CFU-E), which can lead to arrested erythropoiesis and result in severe anemia and reticulocytopenia [ 13 ] . Bone marrow aspiration in this patient (Fig. 1 C ) demonstrated marked reductions in hemoglobin and reticulocyte counts, consistent with PVB19-associated bone marrow suppression.Notably, the patient had poorly controlled type 2 diabetes mellitus. Clinically, patients with type 2 diabetes often experience more severe and complicated infections, although the underlying mechanisms are not fully understood. Infection with PVB19 can manifest with a variety of clinical syndromes. Recent reports have described PVB19-associated encephalitis, meningitis, peripheral neuropathy, and even stroke-like presentations [ 14 ] . In this patient, mental status changes occurred following initial improvement after surgical evacuation of the cerebral hemorrhage. The underlying mechanism may involve post-surgical disruption of the blood-brain barrier combined with virus-induced inflammatory responses, which increase barrier permeability and potentially permit direct viral invasion of the central nervous system [ 15 , 16 ] . Notably, routine CSF biochemical tests including cell count, protein, and glucose showed no typical infection-related abnormalities after surgery. Therefore, in postoperative patients who develop neurological deterioration but exhibit negative results on conventional CSF testing, atypical pathogen infections should be considered, and molecular diagnostic tools, such as metagenomic next-generation sequencing, should be employed promptly [ 17 ] . The patient also developed impaired hepatic and renal function. The mechanisms underlying both acute and chronic renal impairment in this case remain unclear but are likely multifactorial. Contributing factors may include pre-existing chronic kidney disease, PVB19-induced endothelial injury triggering thrombotic microangiopathy (TMA) and impairing renal perfusion, and high-grade viremia activating a cytokine storm that exacerbates organ damage [ 18 ] . Renal pathology following PVB19 infection may also involve deposition of circulating immune complexes, local in-situ immune complex formation, or both processes occurring simultaneously [ 19 ] . The uniqueness of this case lies in the development of multiple organ dysfunction secondary to PVB19 infection. Unfortunately, the patient and family declined biopsy procedures, preventing direct histological confirmation of viral organ injury. Additionally, the route of infection could not be definitively determined. Based on differences in viral sequence counts across various specimens, we speculate that the infection likely originated in the bloodstream. These factors represent the main limitations of this report. Currently, no specific antiviral therapy exists for PVB19 infection, and management primarily relies on immune modulation and supportive care. Existing guidelines do not provide definitive recommendations regarding the dosage or duration of IVIG therapy for PVB19. In patients with severe anemia, IVIG is commonly administered at 400 mg/kg/day for five consecutive days, providing neutralizing antibodies that may accelerate viral clearance [ 12 ] . In this patient, IVIG treatment was extended to 21 days, during which serial monitoring demonstrated a marked reduction in viral load. The prolonged course was necessitated by persistent severe pure red cell aplasia and a subsequent hospital-acquired, drug-resistant bacterial infection. Although the optimal timing and duration of IVIG therapy remain controversial, a prolonged regimen may be warranted in patients with severe anemia complicated by multiple organ failure. For patients presenting with unexplained anemia following cerebral hemorrhage surgery, postoperative differential diagnosis should include atypical pathogens, such as PVB19, particularly when conventional antimicrobial therapy is ineffective and major sources of bleeding have been excluded. Metagenomic next-generation sequencing [ 20 ] is a valuable tool for identifying complex infections and can substantially reduce the time to diagnosis. Conclusion This case highlights the rare but potentially severe clinical manifestations of PVB19 infection following cerebral hemorrhage surgery, particularly in patients presenting with unexplained anemia. Accurate diagnosis requires clinician vigilance and the use of advanced molecular testing techniques, while effective management depends on a comprehensive approach, including IVIG therapy and supportive care to preserve multi-organ function. This report offers valuable insights into the diagnosis and management of severe anemia in postoperative patients, emphasizing the importance of broadening differential diagnoses in cases of unexplained anemia with concomitant multi-organ dysfunction. Early recognition of atypical infections may improve patient outcomes. Declarations Informed Consent and Approval of Ethical Standards This case report adheres to the principles of the Declaration of Helsinki. Written informed consent for publication was obtained from the patient’s legal guardian, as the patient was unable to provide consent independently. The guardian fully understood that the clinical details and accompanying images would be published while maintaining the patient’s anonymity. This study was approved by the Ethics Committee of Tongde Hospital of Zhejiang Province (Approval No. 2025-038(K)). All efforts were made to preserve patient confidentiality, and no identifiable personal information is included in this manuscript. Data Availability Statement, DAS The datasets generated and analysed during the current study are available in the Genome Sequence Archive (GSA) under assigned accession of the submission is: CRA034063.The data can be accessed at: https://ngdc.cncb.ac.cn/gsa/browse/CRA034063 Funding This research received funding from the Zhejiang Traditional Chinese Medicine Science and Technology Plan (No. 2025ZL252; 2024ZR044). Disclosure The writers affirm that the study was carried out without any monetary affiliations that might be interpreted as a possible conflict of interest. Contributions by Authors Muhua Dai, Jianbiao Meng: Data curation, Writing – original draft; Mahong Hu,Wei Zhang: Formal Analysis, Writing Tables and Figures. Lisha Pang, Mahong Hu:Conceptualization, Supervision, Validation, Visualization, Writing – review & editing. All authors contributed to the manuscript and approved the final version for submission. References Cossart YE, Field AM, Cant B, Widdows D. Parvovirus-like particles in human sera. Lancet. 1975;1(7898):72–3. Khameneh ZR, Hanifian H, Barzegari R, Sepehrvand N. Human parvovirus B19 in Iranian pregnant women: a serologic survey. Indian J Pathol Microbiol. 2014;57(3):442–4. de Vries LS. Viral Infections and the Neonatal Brain. Semin Pediatr Neurol. 2019;32:100769. Landry ML, Parvovirus B. Microbiol Spectr. 2016;4(3). Means RT Jr. Pure red cell aplasia. Blood. 2016;128(21):2504–9. Burton PR. Vomeronasal and olfactory nerves of adult and larval bullfrogs: II. Axon terminations and synaptic contacts in the accessory olfactory bulb. J Comp Neurol. 1990;292(4):624–37. Ferri C, Arcangeletti MC, Caselli E, Zakrzewska K, Maccari C, Calderaro A, et al. Insights into the knowledge of complex diseases: Environmental infectious/toxic agents as potential etiopathogenetic factors of systemic sclerosis. J Autoimmun. 2021;124:102727. Bihari C, Rastogi A, Saxena P, Rangegowda D, Chowdhury A, Gupta N, et al. Parvovirus b19 associated hepatitis. Hepat Res Treat. 2013;2013:472027. Williams JL, Jacobs HM, Lee S. Pediatric Myocarditis. Cardiol Ther. 2023;12(2):243–60. Rigante D, Mazzoni MB, Esposito S. The cryptic interplay between systemic lupus erythematosus and infections. Autoimmun Rev. 2014;13(2):96–102. Elbadry MI, Khaled S, Ahmed NM, Abudeif A, Abdelkareem RM, Ezeldin M, et al. Acute human parvovirus B19 infection triggers immune-mediated transient bone marrow failure syndrome, extreme direct hyperbilirubinaemia and acute hepatitis in patients with hereditary haemolytic anaemias: multicentre prospective pathophysiological study. Br J Haematol. 2021;193(4):827–40. Crabol Y, Terrier B, Rozenberg F, Pestre V, Legendre C, Hermine O, et al. 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Virology. 2009;385(2):425–33. Herberts P, Ahnfelt L, Malchau H, Strömberg C, Andersson GB. Multicenter clinical trials and their value in assessing total joint arthroplasty. Clin Orthop Relat Res. 1989;(249):48–55. Huang L, Zhang X, Fang X. Case Report: Epstein-Barr Virus Encephalitis Complicated With Brain Stem Hemorrhage in an Immune-Competent Adult. Front Immunol. 2021;12:618830. Waldman M, Kopp JB. Parvovirus B19 and the kidney. Clin J Am Soc Nephrol. 2007;2(Suppl 1):S47–56. Takeda S, Takaeda C, Takazakura E, Haratake J. Renal involvement induced by human parvovirus B19 infection. Nephron. 2001;89(3):280–5. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8107211","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":556554894,"identity":"020cbb39-4b6b-4794-a53b-0adca69a5181","order_by":0,"name":"Muhua Dai","email":"","orcid":"","institution":"Medicine，Tongde Hospital of Zhejiang Province Afflicted to Zhejiang Chinese Medical University (Tongde hospital of Zhejiang Province)","correspondingAuthor":false,"prefix":"","firstName":"Muhua","middleName":"","lastName":"Dai","suffix":""},{"id":556554895,"identity":"41f70188-4ef7-4433-885e-ce8e1c6fbe22","order_by":1,"name":"Lisha 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1","display":"","copyAsset":false,"role":"figure","size":350256,"visible":true,"origin":"","legend":"\u003cp\u003eResults of Head MRI, lung CT and bone marrow puncture\u003c/p\u003e\n\u003cp\u003eA：Head magnetic resonance imaging (MRI) examination\u003c/p\u003e\n\u003cp\u003eB: Before being admitted to the ICU, the lung CT scan indicated bilateral pleural effusion.\u003c/p\u003e\n\u003cp\u003eC: The result of the bone marrow puncture.\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-8107211/v1/2144ab3927ce038ca4244b55.png"},{"id":97896247,"identity":"865f5d88-6f4b-494c-acab-ddd575f9824f","added_by":"auto","created_at":"2025-12-10 15:36:14","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":706443,"visible":true,"origin":"","legend":"\u003cp\u003eResults of next-generation sequencing in the peripheral blood. Mapping results of nucleotide sequences distributed along the genome of parvovirus B19 in the peripheral blood to parvovirus B19 reference genome NC_000883.\u003c/p\u003e","description":"","filename":"floatimage2.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8107211/v1/e6353d52ae61138881fb6f2c.jpeg"},{"id":97766416,"identity":"8cef77a3-6495-41ed-947f-3ed2264ea7dd","added_by":"auto","created_at":"2025-12-09 07:15:55","extension":"jpeg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":43983,"visible":true,"origin":"","legend":"\u003cp\u003eTimeline depicting the disease course of the patient.\u003c/p\u003e\n\u003cp\u003eThe timeline illustrates the different events in this patient’s treatment and disease progression and prognosis.\u003c/p\u003e","description":"","filename":"floatimage3.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8107211/v1/3ef178e49ca4cda0d19e077f.jpeg"},{"id":99272977,"identity":"9230bd58-3074-4c24-bc96-e4c355496106","added_by":"auto","created_at":"2025-12-31 06:24:25","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1701409,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8107211/v1/1cb4bad8-7693-49f2-a885-67ba9526b51b.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Case Report: Be Alert to Parvovirus Infection in Patients with Unexplained Anemia after Cerebral Hemorrhage Surgery","fulltext":[{"header":"Introduction","content":"\u003cp\u003ePVB19 is a single-stranded DNA virus first identified accidentally in 1975 by Australian virologist Yvonne Cossart \u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/sup\u003e. The global population is generally susceptible to infection, with both sporadic cases and outbreaks reported worldwide. In some countries, the seroprevalence of PVB19 exceeds 76% \u003csup\u003e[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]\u003c/sup\u003e. The clinical manifestations of PVB19 infection vary widely in severity, depending largely on the host\u0026rsquo;s immune status and the pathogenicity of the virus. In immunocompetent individuals\u003csup\u003e[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/sup\u003e, PVB19 infection typically causes erythema infectiosum a mild rash illness primarily affecting children and may lead to polyarthritis or arthralgia in adults. In pregnant women, infection can result in fetal hydrops, intrauterine fetal death, or miscarriage\u003csup\u003e[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]\u003c/sup\u003e. Among immunocompromised patients, PVB19 is associated with pure red cell aplasia (PRCA) and transient aplastic crisis (TAC) \u003csup\u003e[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]\u003c/sup\u003e. Recent studies have broadened the recognized clinical spectrum of PVB19, linking it to systemic sclerosis, hepatitis, myocarditis, encephalitis, meningitis, hemophagocytic lymphohistiocytosis, and renal impairment \u003csup\u003e[\u003cspan additionalcitationids=\"CR8\" citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]\u003c/sup\u003e. The underlying pathogenic mechanisms remain incompletely understood but are thought to be primarily immune-mediated\u003csup\u003e[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]\u003c/sup\u003e. Currently, no specific antiviral therapy exists; treatment is largely supportive, focusing on symptom control and organ function preservation. In severe cases, IVIG therapy or blood transfusion may be required.\u003c/p\u003e\u003cp\u003eReports of multiple organ dysfunction or failure caused by PVB19 infection in previously immunocompetent individuals are rare. To date, no cases have been documented in postoperative intracerebral hemorrhage patients developing multiple organ failure secondary to PVB19 infection. Here, we describe such a case involving an immunocompetent patient who developed sepsis and multiple organ dysfunction syndrome (MODS) following surgical evacuation of an intracerebral hemorrhage. The patient exhibited extensive multi-system involvement with an exceptionally high viral load. Through comprehensive management including mechanical ventilation, continuous renal replacement therapy (CRRT), and IVIG administration the patient\u0026rsquo;s consciousness gradually recovered, organ function improved significantly, and overall clinical status stabilized.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eThe patient was a 51-year-old obese male teacher admitted to the hospital with a diagnosis of cerebellar hemorrhage. His medical history was significant for hypertension and type 2 diabetes mellitus. He had not adhered to dietary recommendations or maintained regular physical activity, resulting in poor glycemic control. On emergency admission, his serum creatinine level was 140 \u0026micro;mol/L, although he denied any prior history of kidney disease. Surgical evacuation of the cerebellar hematoma was performed, and the patient was transferred to the intensive care unit (ICU) postoperatively. As his level of consciousness improved, he became able to follow commands and move spontaneously. One week later, after successful ventilator weaning, he was transferred to the neurosurgery ward, at which time his hemoglobin level was 95 g/L.\u003c/p\u003e\u003cp\u003eDuring his stay in the neurosurgery ward, the patient developed a progressive decline in hemoglobin levels (95 g/L \u0026rarr; 58 g/L), accompanied by persistent fever and new-onset neurological symptoms, including speech disturbance and facial twitching. Lumbar puncture revealed an opening pressure of 310 mmH₂O. Cerebrospinal fluid (CSF) analysis showed a white blood cell count of 12 \u0026times; 10⁶/L, with 70% lymphocytes. Biochemical examination of the CSF indicated a glucose level of 2.81 mmol/L, chloride concentration of 120.6 mmol/L, and protein concentration of 641 mg/L. Synchronous blood tests showed a glucose level of 7.14 mmol/L and chloride of 103.2 mmol/L. Brain MRI revealed acute cerebral infarctions near the splenium of the corpus callosum and the posterior horns of the lateral ventricles (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eA). However, these imaging findings did not fully explain the patient\u0026rsquo;s worsening mental status and persistent fever. His condition continued to deteriorate, presenting with high-grade fever (up to 39.5\u0026deg;C), lethargy, refractory anemia (hemoglobin decreased from 95 g/L to 58 g/L despite a negative stool occult blood test), hypoxemia (lowest SpO₂ = 85% on a reservoir mask), and generalized edema, necessitating urgent readmission to the ICU.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eUpon ICU readmission, the patient underwent endotracheal intubation and mechanical ventilation. Chest computed tomography revealed pulmonary infiltrates and bilateral pleural effusions (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eB). Metagenomic next-generation sequencing detected high sequence counts of human PVB19 in the CSF, pleural fluid, and blood (Table and Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e ). The patient developed persistent severe anemia, with a hemoglobin nadir of 50 g/L, accompanied by prolonged reticulocytopenia (reticulocyte percentage: 0.14\u0026ndash;0.26%; absolute count: 0.18\u0026ndash;0.53 \u0026times; 10\u0026sup1;\u0026sup2;/L) lasting approximately one week. Serum ferritin levels were markedly elevated (\u0026gt;\u0026thinsp;1500 ng/mL; reference range: 23.9\u0026ndash;336 ng/mL). Bone marrow aspiration demonstrated markedly suppressed erythropoiesis with a predominance of proerythroblasts and early erythroblasts, consistent with PRCA (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eC). Persistent lymphopenia (0.5 \u0026times; 10⁹/L) indicated an immunosuppressed state. Given the immunodeficiency and high viral load, IVIG therapy was administered. Renal function progressively deteriorated, as evidenced by rising serum creatinine levels and oliguria, necessitating CRRT. Following treatment, PVB19 levels in both the CSF and blood declined significantly (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e,Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The patient regained consciousness,exhibiting improved responsiveness, resolution of facial twitching, and successful weaning from mechanical ventilation and renal replacement therapy. Normalization of reticulocyte counts prompted a transfer to nephrology for further management.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eTest results of mNGS in body fluid samples of the patient.\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;Item\u003c/p\u003e\u003cp\u003eSpecimen\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eThe types of pathogens detected by mNGS\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003eViral DNA/RNA quantification(sequence count)\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eCSF1( diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePVB19\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e558465\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eCSF2(12days after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePVB19\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e95\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eCSF3(19days after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePVB19\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e134\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eCSF4(26days after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePVB19\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e7\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eCSF5(39days after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eCMV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e56\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eBlood1(1day after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePVB19、Circovirus\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e1074518、5\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eBlood2(20days after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePVB19、CMV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e3、39\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eBlood3(30days after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eCMV、Circovirus、PVB19\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e1511、14、8\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePleural effusion\u003c/p\u003e\u003cp\u003e(1day after diagnosis)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePVB19\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e29658\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003ctfoot\u003e\u003ctr\u003e\u003ctd colspan=\"3\"\u003eCSF: Cerebrospinal Fluid; CMV༚Cytomegalovirus;\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd colspan=\"3\"\u003eA: Head magnetic resonance imaging (MRI) examination\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd colspan=\"3\"\u003eB: Before being admitted to the ICU, the lung CT scan indicated bilateral pleural effusion.\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd colspan=\"3\"\u003eC: The result of the bone marrow puncture.\u003c/td\u003e\u003c/tr\u003e\u003c/tfoot\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eA one-year follow-up was conducted for the patient. Intermittent blood tests performed by the attending physician showed a gradual improvement in reticulocyte counts, while metagenomic next-generation sequencing of peripheral blood revealed only trace levels of parvovirus B19 sequences. Consequently, further immunoglobulin therapy was deemed unnecessary. The patient\u0026rsquo;s hemoglobin level progressively increased from 50 g/L to 65 g/L. However, renal function failed to recover, necessitating ongoing maintenance hemodialysis. In addition, cardiac function progressively deteriorated, resulting in multiple ICU readmissions for episodes of acute left ventricular failure. The timeline of the patient\u0026rsquo;s clinical course, treatment interventions, and outcomes is summarized in Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003ePVB19 typically causes self-limited illnesses, such as erythema infectiosum in children and transient arthritis in healthy adults \u003csup\u003e[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/sup\u003e. However, in immunocompromised patients or those with chronic anemia, PVB19 infection can lead to severe or even fatal complications, including chronic PRCA and hydrops fetalis \u003csup\u003e[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eIn this case, the patient was a postoperative cerebral hemorrhage patient with no prior history of immunodeficiency. Nonetheless, surgical trauma and stress may have induced a relative immunosuppressed state, as evidenced by persistently low lymphocyte counts during the infection. The patient\u0026rsquo;s hemoglobin level remained persistently low. After excluding significant blood loss from gastrointestinal or other sources, PVB19-induced pure red cell aplasia was considered the most likely cause. According to current studies, the primary target of PVB19 is the erythroid precursor cells in the bone marrow. The VP1/VP2 capsid proteins of PVB19 exhibit a high affinity for these progenitor cells (colony-forming unit\u0026ndash;erythroid, CFU-E), which can lead to arrested erythropoiesis and result in severe anemia and reticulocytopenia \u003csup\u003e[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/sup\u003e. Bone marrow aspiration in this patient (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eC\u003cb\u003e)\u003c/b\u003e demonstrated marked reductions in hemoglobin and reticulocyte counts, consistent with PVB19-associated bone marrow suppression.Notably, the patient had poorly controlled type 2 diabetes mellitus. Clinically, patients with type 2 diabetes often experience more severe and complicated infections, although the underlying mechanisms are not fully understood.\u003c/p\u003e\u003cp\u003eInfection with PVB19 can manifest with a variety of clinical syndromes. Recent reports have described PVB19-associated encephalitis, meningitis, peripheral neuropathy, and even stroke-like presentations\u003csup\u003e[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]\u003c/sup\u003e. In this patient, mental status changes occurred following initial improvement after surgical evacuation of the cerebral hemorrhage. The underlying mechanism may involve post-surgical disruption of the blood-brain barrier combined with virus-induced inflammatory responses, which increase barrier permeability and potentially permit direct viral invasion of the central nervous system \u003csup\u003e[\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]\u003c/sup\u003e. Notably, routine CSF biochemical tests including cell count, protein, and glucose showed no typical infection-related abnormalities after surgery. Therefore, in postoperative patients who develop neurological deterioration but exhibit negative results on conventional CSF testing, atypical pathogen infections should be considered, and molecular diagnostic tools, such as metagenomic next-generation sequencing, should be employed promptly\u003csup\u003e[\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]\u003c/sup\u003e. The patient also developed impaired hepatic and renal function. The mechanisms underlying both acute and chronic renal impairment in this case remain unclear but are likely multifactorial. Contributing factors may include pre-existing chronic kidney disease, PVB19-induced endothelial injury triggering thrombotic microangiopathy (TMA) and impairing renal perfusion, and high-grade viremia activating a cytokine storm that exacerbates organ damage\u003csup\u003e[\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]\u003c/sup\u003e. Renal pathology following PVB19 infection may also involve deposition of circulating immune complexes, local in-situ immune complex formation, or both processes occurring simultaneously\u003csup\u003e[\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]\u003c/sup\u003e. The uniqueness of this case lies in the development of multiple organ dysfunction secondary to PVB19 infection. Unfortunately, the patient and family declined biopsy procedures, preventing direct histological confirmation of viral organ injury. Additionally, the route of infection could not be definitively determined. Based on differences in viral sequence counts across various specimens, we speculate that the infection likely originated in the bloodstream. These factors represent the main limitations of this report.\u003c/p\u003e\u003cp\u003eCurrently, no specific antiviral therapy exists for PVB19 infection, and management primarily relies on immune modulation and supportive care. Existing guidelines do not provide definitive recommendations regarding the dosage or duration of IVIG therapy for PVB19. In patients with severe anemia, IVIG is commonly administered at 400 mg/kg/day for five consecutive days, providing neutralizing antibodies that may accelerate viral clearance\u003csup\u003e[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]\u003c/sup\u003e. In this patient, IVIG treatment was extended to 21 days, during which serial monitoring demonstrated a marked reduction in viral load. The prolonged course was necessitated by persistent severe pure red cell aplasia and a subsequent hospital-acquired, drug-resistant bacterial infection. Although the optimal timing and duration of IVIG therapy remain controversial, a prolonged regimen may be warranted in patients with severe anemia complicated by multiple organ failure. For patients presenting with unexplained anemia following cerebral hemorrhage surgery, postoperative differential diagnosis should include atypical pathogens, such as PVB19, particularly when conventional antimicrobial therapy is ineffective and major sources of bleeding have been excluded. Metagenomic next-generation sequencing\u003csup\u003e[\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]\u003c/sup\u003e is a valuable tool for identifying complex infections and can substantially reduce the time to diagnosis.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case highlights the rare but potentially severe clinical manifestations of PVB19 infection following cerebral hemorrhage surgery, particularly in patients presenting with unexplained anemia. Accurate diagnosis requires clinician vigilance and the use of advanced molecular testing techniques, while effective management depends on a comprehensive approach, including IVIG therapy and supportive care to preserve multi-organ function. This report offers valuable insights into the diagnosis and management of severe anemia in postoperative patients, emphasizing the importance of broadening differential diagnoses in cases of unexplained anemia with concomitant multi-organ dysfunction. Early recognition of atypical infections may improve patient outcomes.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eInformed Consent and Approval of Ethical Standards\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis case report adheres to the principles of the Declaration of Helsinki. Written informed consent for publication was obtained from the patient’s legal guardian, as the patient was unable to provide consent independently. The guardian fully understood that the clinical details and accompanying images would be published while maintaining the patient’s anonymity. This study was approved by the Ethics Committee of Tongde Hospital of Zhejiang Province (Approval No. 2025-038(K)). All efforts were made to preserve patient confidentiality, and no identifiable personal information is included in this manuscript.\u003c/p\u003e\n\u003cp\u003eData Availability Statement, DAS\u003c/p\u003e\n\u003cp\u003eThe datasets generated and analysed during the current study are available in the Genome Sequence Archive (GSA) under assigned accession of the submission is:\u0026nbsp;CRA034063.The data can be accessed at:\u0026nbsp;https://ngdc.cncb.ac.cn/gsa/browse/CRA034063\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research received funding from the Zhejiang Traditional Chinese Medicine Science and Technology Plan (No. 2025ZL252; 2024ZR044).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDisclosure\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe writers affirm that the study was carried out without any\u0026nbsp;monetary affiliations that might be interpreted as a possible conflict of interest.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eContributions by Authors\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eMuhua Dai, Jianbiao Meng: Data curation, \u0026nbsp; Writing – original draft; Mahong Hu,Wei Zhang: Formal Analysis, Writing Tables and Figures. Lisha Pang, Mahong Hu:Conceptualization, Supervision, Validation, Visualization, Writing – review \u0026amp; editing. All authors contributed to the manuscript and approved the final version for submission.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eCossart YE, Field AM, Cant B, Widdows D. Parvovirus-like particles in human sera. Lancet. 1975;1(7898):72\u0026ndash;3.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eKhameneh ZR, Hanifian H, Barzegari R, Sepehrvand N. Human parvovirus B19 in Iranian pregnant women: a serologic survey. Indian J Pathol Microbiol. 2014;57(3):442\u0026ndash;4.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ede Vries LS. Viral Infections and the Neonatal Brain. Semin Pediatr Neurol. 2019;32:100769.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLandry ML, Parvovirus B. Microbiol Spectr. 2016;4(3).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMeans RT Jr. Pure red cell aplasia. Blood. 2016;128(21):2504\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBurton PR. Vomeronasal and olfactory nerves of adult and larval bullfrogs: II. Axon terminations and synaptic contacts in the accessory olfactory bulb. J Comp Neurol. 1990;292(4):624\u0026ndash;37.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eFerri C, Arcangeletti MC, Caselli E, Zakrzewska K, Maccari C, Calderaro A, et al. Insights into the knowledge of complex diseases: Environmental infectious/toxic agents as potential etiopathogenetic factors of systemic sclerosis. J Autoimmun. 2021;124:102727.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBihari C, Rastogi A, Saxena P, Rangegowda D, Chowdhury A, Gupta N, et al. Parvovirus b19 associated hepatitis. Hepat Res Treat. 2013;2013:472027.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eWilliams JL, Jacobs HM, Lee S. Pediatric Myocarditis. Cardiol Ther. 2023;12(2):243\u0026ndash;60.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRigante D, Mazzoni MB, Esposito S. The cryptic interplay between systemic lupus erythematosus and infections. Autoimmun Rev. 2014;13(2):96\u0026ndash;102.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eElbadry MI, Khaled S, Ahmed NM, Abudeif A, Abdelkareem RM, Ezeldin M, et al. Acute human parvovirus B19 infection triggers immune-mediated transient bone marrow failure syndrome, extreme direct hyperbilirubinaemia and acute hepatitis in patients with hereditary haemolytic anaemias: multicentre prospective pathophysiological study. Br J Haematol. 2021;193(4):827\u0026ndash;40.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eCrabol Y, Terrier B, Rozenberg F, Pestre V, Legendre C, Hermine O, et al. Intravenous immunoglobulin therapy for pure red cell aplasia related to human parvovirus b19 infection: a retrospective study of 10 patients and review of the literature. Clin Infect Dis. 2013;56(7):968\u0026ndash;77.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eIsa A, Lundqvist A, Lindblom A, Tolfvenstam T, Broliden K. Cytokine responses in acute and persistent human parvovirus B19 infection. Clin Exp Immunol. 2007;147(3):419\u0026ndash;25.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGray V, Chen W, Tan R, Teo J, Huang Z, Fong CH, et al. Hyperglycemia-triggered lipid peroxidation destabilizes STAT4 and impairs anti-viral Th1 responses in type 2 diabetes. Cell Metab. 2024;36(12):2511\u0026ndash;e277.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eDouvoyiannis M, Litman N, Goldman DL. Neurologic manifestations associated with parvovirus B19 infection. Clin Infect Dis. 2009;48(12):1713\u0026ndash;23.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eVerma S, Lo Y, Chapagain M, Lum S, Kumar M, Gurjav U, et al. West Nile virus infection modulates human brain microvascular endothelial cells tight junction proteins and cell adhesion molecules: Transmigration across the in vitro blood-brain barrier. Virology. 2009;385(2):425\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHerberts P, Ahnfelt L, Malchau H, Str\u0026ouml;mberg C, Andersson GB. Multicenter clinical trials and their value in assessing total joint arthroplasty. Clin Orthop Relat Res. 1989;(249):48\u0026ndash;55.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHuang L, Zhang X, Fang X. Case Report: Epstein-Barr Virus Encephalitis Complicated With Brain Stem Hemorrhage in an Immune-Competent Adult. Front Immunol. 2021;12:618830.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eWaldman M, Kopp JB. Parvovirus B19 and the kidney. Clin J Am Soc Nephrol. 2007;2(Suppl 1):S47\u0026ndash;56.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eTakeda S, Takaeda C, Takazakura E, Haratake J. Renal involvement induced by human parvovirus B19 infection. Nephron. 2001;89(3):280\u0026ndash;5.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Human parvovirus B19, PVB19, refractory anemia, organ failure, mNGS","lastPublishedDoi":"10.21203/rs.3.rs-8107211/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8107211/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground: \u003c/strong\u003eHuman parvovirus B19 (PVB19) is a highly prevalent single-stranded DNA virus that infects a large proportion of the global population. It can involve multiple organ systems, leading to a broad spectrum of clinical manifestations. While most infections in immunocompetent individuals are mild and self-limiting, PVB19 can occasionally cause severe and diverse complications.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase Presentation:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe report a rare case of an immunocompetent patient who experienced unexplained clinical deterioration following surgical evacuation of an intracerebral hemorrhage. The patient presented with refractory anemia, impaired consciousness, fever, seizures, and progressive dysfunction of the cardiac, hepatic, and renal systems. Metagenomic next-generation sequencing revealed high levels of PVB19 DNA in the cerebrospinal fluid, blood, and pleural effusion. The patient was treated with intravenous immunoglobulin (IVIG) therapy and supportive care. Following treatment, improvements were observed in consciousness, mobility, and anemia. However, renal function failed to recover and ultimately progressed to renal failure, necessitating renal replacement therapy.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion：\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis case underscores the potential severity of PVB19 infection following cerebral hemorrhage surgery, particularly when accompanied by unexplained anemia. Accurate diagnosis requires a high index of suspicion and the use of advanced diagnostic tools. Management primarily involves IVIG therapy and supportive care. This case highlights the importance of expanding the differential diagnosis in postoperative patients presenting with unexplained anemia and multi-organ dysfunction, as early recognition of atypical infections may improve clinical outcomes.\u003c/p\u003e","manuscriptTitle":"Case Report: Be Alert to Parvovirus Infection in Patients with Unexplained Anemia after Cerebral Hemorrhage Surgery","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-09 07:15:51","doi":"10.21203/rs.3.rs-8107211/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"9a3a73d6-7f58-49bf-b014-d774ea2b179d","owner":[],"postedDate":"December 9th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-12-31T06:23:16+00:00","versionOfRecord":[],"versionCreatedAt":"2025-12-09 07:15:51","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8107211","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8107211","identity":"rs-8107211","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}