Mycoplasma Pneumonia Infection Complicated with Hemolytic Anemia and Persistent Leukocytosis in a Middle-Aged Woman: A Case- Report.

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Vigneshwaran V, Nanda Kumar R, Sarumathy S, Pravin Selvi Saravanan This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8131850/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 9 You are reading this latest preprint version Abstract Background: Mycoplasma pneumonia is one of the causes of community-acquired pneumonia (CAD) with rare extrapulmonary complications, including hemolytic anemia, persistent leukocytosis, Stevens-Johnson syndrome, meningoencephalitis. While these conditions are most common in children and young adults, typically those aged 5 to 20 years, this case report covers Mycoplasma pneumonia with the very rare complication of hemolytic anemia and persistent leukocytosis in a middle-aged woman. Case Presentation: A 44-year-old woman with a history of high-grade fever for 10 days, fatigue, and headache came to the emergency medicine. Laboratory evaluation revealed severe normocytic anemia (Hb 5.3 g/dL), leukocytosis (42,000/μL), and thrombocytosis (564,000/μL). Cold agglutinin testing confirmed anti-I IgM–mediated disease with high titers (1:256), and serology was positive for M. pneumoniae IgM and IgG antibodies. She was treated with warmed red cell transfusions, intravenous methylprednisolone, and clarithromycin, followed by oral levofloxacin. Her condition improved significantly. Rationale: This case highlights the diagnostic complexity in a woman patient with rare hemolytic anemias in the context of atypical infections and the approach for their diagnosis and appropriate treatment. The coexistence of IgM-mediated autoimmune hemolytic anemia and leukocytosis poses diagnostic and therapeutic challenges that are relevant to clinical practice. This case underscores the diagnostic and therapeutic challenges of cold agglutinin hemolysis secondary to M. pneumoniae infection. Mycoplasma pneumonia cold agglutinin hemolysis lymphoproliferative disorders IgM anti-I mediated cold agglutinin disease Figures Figure 1 Introduction This case report adds to Mycoplasma pneumonia , a form of CAD, caused by Mycoplasma pneumoniae , which is one of the major causative organisms of CAD and infection indeed manifests in two main ways namely respiratory tract infections and extrapulmonary diseases ranging from mild upper respiratory symptoms to severe pneumonia. The reported detection rates of atypical pneumonia range from 20–28% [ 1 ]. Cold agglutinin hemolysis which is linked to an IgM mediated complementary cascade mechanism causes extravascular hemolysis and intravascular hemolysis (less common) in patients after one to two weeks after infection[ 2 ]. Severe anemia is typically described in pediatric patients or in patients with sickle cell disease This case describes an unusual triad of severe hemolysis, persistent leukocytosis, and thrombocytosis in a middle-aged woman. Case Report A 44-year-old woman presented to the emergency department with a 10-day history of persistent high fever (up to 102°F/38.9°C), progressive generalized fatigue, and persistent headache with no significant medical history. Five days prior to admission, she sought care at an outside facility where she was empirically treated with intravenous ceftriaxone (dose not specified) and oral chloroquine (dose not specified) without any clinical improvement. Upon presentation to our institution, the patient appeared acutely ill with marked respiratory distress. Vital signs revealed tachycardia (heart rate of 110 beats per minute), tachypnea (respiratory rate of 28 breaths per minute), borderline hypertension (blood pressure of 140/90 mmHg), and significant hypoxemia (oxygen saturation of 88% on room air). The physical examination revealed bilateral inspiratory crackles on lung auscultation, but neurological examination was completely normal with a GCS score of 15 and no focal neurological deficits. Table 1 Blood parameters on the first and second days of admission followed by the last day Parameter Day − 1 Day – 2 Day − 6 Normal Range Hemoglobin (Hb) 5.3 g/dL 4.6 g/dL 8.6 g/dL 12–15 g/dL White Blood Cell (WBC) Count 42,000 cells/µL 36,390 cells/µL 9,350 cells/µL 4,000–11,000 cells/µL Platelet Count 564,000 cells/µL 488,400 cells/µL 560,100 cells/µL 150,000–450,000 cells/µL Investigations Initial laboratory investigations revealed profound hematological abnormalities including severe normocytic anemia, marked leukocytosis, and thrombocytosis as represented in Table 1 . The peripheral blood smear rrevealed a strikingly reduced red blood cell count (1.60 million/µL, reference range 3.9–5.1 million/µL) with evidence of hemolysis including polychromasia and occasional schistocytes. Biochemical markers revealed elevated serum iron (325 µg/dL, reference range 50–170 µg/dL), extremely elevated erythrocyte sedimentation rates (140 mm/hr, reference range 0–20 mm/hr), and significantly increased C-reactive protein levels (34.2 mg/L, reference range < 5 mg/L). Renal function remained normal (serum creatinine 0.6 mg/dL, reference range 0.5–1.2 mg/dL). Initial chest radiography revealed a right-sided mild pleural effusion without obvious parenchymal infiltrates. The patient was promptly administered broad-spectrum intravenous antibiotics (piperacillin-tazobactam 4.5g every 8 hours) and aggressive fluid resuscitation. However, computed tomography of the chest performed within 24 hours of admission revealed bilateral multifocal pneumonic infiltrates as presented in Fig. 1 that were not apparent on the initial chest X-ray. By the second visit at the hospital, the patient's condition had deteriorated hematologically with further decrease in hemoglobin, persistent leukocytosis, and thrombocytosis as represented in Table 1 . Additional laboratory tests confirmed ongoing hemolysis with markedly elevated lactate dehydrogenase (1329 U/L, reference range 140–280 U/L) and undetectable serum haptoglobin levels (< 0.072 g/L, reference range 0.3-2.0 g/L). Immunohematological workup revealed a blood group discrepancy due to autoagglutination that resolved when testing was performed at 37°C, ultimately confirming that the patient's blood group was O-positive. Direct antiglobulin testing was strongly positive (4+) for IgM, with a weakly positive indirect antiglobulin test (2+). Cold agglutinin testing revealed no reactivity with neonatal O-positive red blood cells (excluding anti-i specificity) but strong agglutination with adult O-positive red blood cells at 4°C with a titer of 1:256, which is consistent with anti-I IgM-mediated cold agglutinin disease. Serological testing confirmed acute Mycoplasma pneumoniae infection with elevated IgM antibodies (727 AU/mL) and IgG antibodies (197 AU/mL). The procalcitonin level was mildly elevated at 0.33 ng/mL (reference range < 0.5 ng/mL), suggesting possible bacterial coinfection. Given the severity of pneumonia (with type I respiratory failure) and life-threatening hemolytic anemia, the patient was transferred to the intensive care unit. Management included the transfusion of saline-washed, warm (37°C), Coombs-compatible packed red blood cells through a blood warmer to prevent the exacerbation of cold-induced hemolysis. High-dose intravenous methylprednisolone (80 mg daily for 3 days, then tapered to 40 mg daily) was initiated for the cold agglutinin disease. Treatment Targeted antimicrobial therapy with intravenous clarithromycin (1000 mg daily for 5 days) was started for the Mycoplasma pneumoniae infection, then transitioned to oral levofloxacin (750 mg daily for an additional 7 days, totaling 12 days of antibiotic therapy). Supplemental oxygen was required but was successfully weaned over four days as the patient's respiratory status improved. Additional workup ruled out other infections (negative HIV, hepatitis B and C serologies) and autoimmune disorders (negative antinuclear antibodies and antineutrophil cytoplasmic antibodies). The patient showed remarkable clinical improvement within 48 hours of initiating targeted therapy. The methylprednisolone was transitioned to oral prednisolone (50 mg daily) and gradually tapered over 10 days before complete discontinuation. By the time of discharge, the patient's hematological parameters had significantly improved with hemoglobin stabilizing at 8.6 g/dL, the white blood cell count normalizing to 9,350 cells/µL, and platelet count remaining elevated at 560,100 cells/µL. The patient was discharged with close outpatient follow-up arranged with both hematology and pulmonology specialists to monitor for potential recurrence of hemolysis or respiratory complications. Discussion This case demonstrates a rare combination of M. pneumoniae pneumonia with severe cold agglutinin hemolysis and persistent leukocytosis. This infection, although primarily a respiratory pathogen, can trigger a spectrum of rare but serious extrapulmonary complications, including cold agglutinin-mediated hemolytic anemia, central nervous system involvement (such as encephalitis or meningitis), glomerulonephritis, acute kidney injury secondary to intravascular hemolysis, myositis, and subclinical hemolysis[ 1 ]. Among these manifestations, the simultaneous occurrence of severe hemolytic anemia and neurological manifestations is rare [ 3 ]. Cold agglutinin-induced autoimmune hemolytic anemia is relatively rare, accounting for only 10–20% of cases, and is often associated with infections by pathogens such as Mycoplasma pneumoniae , Epstein-Barr, and cytomegalovirus, among others[ 2 ].The pathogenesis of IgM Anti-I mediated cold agglutinin disease follows a characteristic cascade beginning with exposure to cold temperatures (< 30°C), which triggers IgM autoantibodies to bind specifically to I antigens abundantly expressed on adult RBC membranes[ 4 ]. This antigen-antibody interaction initiates complement activation through the classical pathway (C1q binding), progressing to C3b deposition, which marks RBCs for opsonization and subsequent extravascular hemolysis via liver macrophages. In severe cases, full complement cascade activation leads to membrane attack complex (C5-C9) formation causing intravascular hemolysis. Clinically, this manifests through two hallmark phenomena: temperature-dependent agglutination (reversible RBC clumping in cold extremities) and complement-mediated hemolysis, resulting in anemia, acrocyanosis, hemoglobinuria, and Raynaud-like symptoms. Diagnostic confirmation requires demonstration of high-titer cold agglutinins (> 1:64 at 4°C) and a positive direct antiglobulin test (DAT) showing the C3d coating of RBCs, whereas IgM itself is rarely detected on erythrocytes due to elution during warming. The entire process underscores the temperature-sensitive nature of anti-I antibodies and their capacity to bridge benign respiratory infections with potentially severe hematologic complications. Thus, this case report aligns with other studies in which the proportion of female M . Pneumoniae infections was relatively high in both children and adults, which is consistent with previous research[ 5 ], [ 6 ], [ 7 ], [ 8 ]. The occurrence of chronic cold agglutinin syndrome (CAS) associated with lymphoproliferative disorders is another rare finding observed in this case. The typical nature of rare disease conditions, such as this case, lies in the absence of a definitive treatment plan thus, the optimal management strategy remains unclear. Supportive care should focus on keeping the patient warm, and if transfusion is necessary, it should be administered through a blood warmer. Glucocorticoid treatment has been shown to be beneficial in the treatment of CAS, but its role in specific therapeutic interventions for cold agglutinin hemolysis remains unclear, as no standardized treatment approach has been firmly established. Management is often individualized, and guided by clinical presentation and severity[ 9 ]. Among nine well-documented cases of Mycoplasma pneumoniae -associated hemolysis, glucocorticoid therapy was administered to four patients. Notably, two of these individuals showed significant clinical improvement following treatment, suggesting a potential, although not definitive, benefit[ 10 ].Signs of reduced hemolysis were present in our patient on day three after glucocorticoid treatment-initiation with a steady decrease of LDH, and normalized within a week. In cases where the hemolysis worsens despite supportive therapy and antibodies it seems reasonable to administer glucocorticoids. Glucocorticoid therapy in M . Pneumonia- Pneumonia without hemolysis is sometimes advocated but beneficial effects have not been well established and its use remains controversial. Antibiotics are generally recommended but probably play a limited role in the treatment of hemolysis. Theoretically, a faster clearance of the pathogen by antibiotic treatment could limit the production of cold agglutinins and their hemolytic effect. Mycoplasma pneumonia usually does not cause marked leukocytosis since it usually indicates another bacterial etiology other than M. pneumoniae [ 11 ] Our patient developed marked thrombocytosis. More frequently, thrombocytopenia has been reported in association with M. pneumoniae infection, in some cases leading to fatal complications [ 12 ]. Our patient’s rapid improvement with corticosteroids suggests an immune-mediated component beyond infection alone. Persistent leukocytosis in M. pneumoniae is unusual and may reflect inflammatory stress or bacterial coinfection. Updated management emphasizes pathogen-directed therapy (macrolides or fluoroquinolones), temperature control, and supportive transfusion strategies using warmed blood[ 13 ]. This case illustrates several important clinical teaching points. First, it reveals the potentially severe hematological complications (cold agglutinin-mediated hemolytic anemia) that can accompany Mycoplasma pneumoniae infection, even in previously healthy individuals. Second, it highlights the critical importance of proper blood bank techniques (warm washing, use of blood warmers) in managing patients with cold agglutinin disease. Third, the findings underscore the value of early corticosteroid therapy in severe cases of cold agglutinin-mediated hemolysis. Finally, these finding indicates that Mycoplasma pneumoniae infection can cause significant pulmonary disease in adults, sometimes requiring intensive care management, and that macrolides remain first-line therapy despite increasing resistance patterns. The rapid clinical response to appropriate antimicrobial and immunomodulatory therapy in this case was particularly noteworthy and reinforces the importance of timely diagnosis and intervention in such cases. Conclusion This case underscores the rare but serious potential of Mycoplasma pneumoniae to induce cold agglutinin hemolysis—a complication that, while uncommon, can be life-threatening and diagnostically challenging. The clinical course highlights the importance of maintaining a broad differential diagnosis in patients presenting with severe hemolysis and respiratory symptoms. In the absence of established therapeutic protocols for M. pneumoniae -associated hemolysis, a multidisciplinary approach involving timely diagnosis, supportive care with warmed transfusions, appropriate antimicrobial therapy, and judicious corticosteroid use has proven effective. Patient recovery illustrates the potential value of conservative management tailored to clinical presentation. This case adds to the limited literature on this rare complication and reinforces the need for continued vigilance and further investigation into evidence-based treatment strategies for atypical presentations of Mycoplasma pneumoniae infection. Declarations Author Contribution Thanks to Dr Vigneshwaran V and Dr Nanda Kumar R for explaning the case and helped Pravin Selvi Saravanan to write the main manuscrpt under the guidance of Sarumathy S Informed Patient Consent: Complete informed consent was obtained from the patient for the publication of this study and any accompanying images. Declaration of competing interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. References Georgakopoulou V, Lempesis I, Tarantinos K, Sklapani P, Trakas N, Spandidos D (Sep. 2024) Atypical pneumonia (Review). Exp Ther Med 28(5):424. 10.3892/etm.2024.12713 Cuzco Macias LG, Cuzco Macias AC, Simancas-Racines D, Parise-Vasco JM (2025) Cryoagglutinin autoimmune hemolytic anemia secondary to Mycoplasma pneumoniae infection in patient with pernicious anemia: A case report, Medwave, vol. 25, no. 08, pp. e3039–e3039, Sep. 10.5867/medwave.2025.08.3039 Khan FY, yassin MA (Feb. 2009) Mycoplasma pneumoniae associated with severe autoimmune hemolytic anemia: case report and literature review. Braz J Infect Dis 13(1):77–79. 10.1590/s1413-86702009000100018 Donham JA, Denning V (1985) Cold agglutinin syndrome: nursing management., Heart Lung, vol. 14, no. 1, pp. 59–67, Jan Lv Y-T, Sun X-J, Chen Y, Ruan T, Xu G-P, Huang J-A (Oct. 2022) Epidemic characteristics of Mycoplasma pneumoniae infection: a retrospective analysis of a single center in Suzhou from 2014 to 2020. Ann Transl Med 10(20):1123. 10.21037/atm-22-4304 Yan C, Sun H, Zhao H (May 2016) Latest Surveillance Data on Mycoplasma pneumoniae Infections in Children, Suggesting a New Epidemic Occurring in Beijing. J Clin Microbiol 54(5):1400–1401. 10.1128/JCM.00184-16 Zhao H et al (2014) Surveillance of Mycoplasma pneumoniae infection among children in Beijing from 2007 to 2012. Chin Med J (Engl) 127(7):1244–1248 Foy HM, Kenny GE, Cooney MK, Allan ID (1979) Long-term epidemiology of infections with Mycoplasma pneumoniae., J Infect Dis, vol. 139, no. 6, pp. 681–7, Jun. 10.1093/infdis/139.6.681 Petz LD (2001) Treatment of autoimmune hemolytic anemias, Curr Opin Hematol, vol. 8, no. 6, pp. 411–416, Nov. 10.1097/00062752-200111000-00016 Cherry JD, Supplement_1 (1993) S47–S51 doi: 10.1093/clinids/17.Supplement_1.S47 Waites KB, Xiao L, Liu Y, Balish MF, Atkinson TP (2017) Mycoplasma pneumoniae from the Respiratory Tract and Beyond, Clin Microbiol Rev, vol. 30, no. 3, pp. 747–809, Jul. 10.1128/CMR.00114-16 Gouveia C, Evangelista V, Almeida R, Baptista AM (2018) Immune Thrombocytopenia Associated with Mycoplasma pneumoniae Infection, Eur J Case Rep Intern Med, no. LATEST ONLINE, p. 1, Jan. 10.12890/2018_000817 Guo Z, Gu S, Tian Z, Du B (2024) Corrigendum: A comprehensive review of Mycoplasma pneumoniae infection in chronic lung diseases: recent advances in understanding asthma, COPD, and bronchiectasis, Front Med (Lausanne), vol. 11, Nov. 10.3389/fmed.2024.1512825 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Revision requested 16 Dec, 2025 Reviews received at journal 15 Dec, 2025 Reviewers agreed at journal 05 Dec, 2025 Reviews received at journal 05 Dec, 2025 Reviewers agreed at journal 04 Dec, 2025 Reviewers invited by journal 04 Dec, 2025 Editor assigned by journal 20 Nov, 2025 Submission checks completed at journal 19 Nov, 2025 First submitted to journal 17 Nov, 2025 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. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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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-8131850","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":555758900,"identity":"32608934-5e8f-4ea5-8b8f-fc6dd17c2486","order_by":0,"name":"Vigneshwaran V","email":"","orcid":"","institution":"SRM Institute of Science and Technology","correspondingAuthor":false,"prefix":"","firstName":"Vigneshwaran","middleName":"","lastName":"V","suffix":""},{"id":555758901,"identity":"a4122a97-8315-404f-9441-e8524bfd3f34","order_by":1,"name":"Nanda Kumar R","email":"","orcid":"","institution":"SRM Institute of Science and 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SCAN OF CHEST (PLAIN): Patchy areas of consolidation involving right upper lobe and middle lobe. Geographic areas of consolidation in anterior and medial segment of right lower lobe with adjacent ground glassing. Patchy atelectasis in posterobasal\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8131850/v1/4efeeb6677f0e0602ae1be7b.png"},{"id":97744925,"identity":"379cb264-582c-4694-b1af-b44e39c43bd3","added_by":"auto","created_at":"2025-12-09 00:23:32","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":773510,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8131850/v1/dd9f3a6a-5589-45d2-8a93-006ded9c4244.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Mycoplasma Pneumonia Infection Complicated with Hemolytic Anemia and Persistent Leukocytosis in a Middle-Aged Woman: A Case- Report.","fulltext":[{"header":"Introduction","content":"\u003cp\u003eThis case report adds to \u003cem\u003eMycoplasma pneumonia\u003c/em\u003e, a form of CAD, caused by \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e, which is one of the major causative organisms of CAD and infection indeed manifests in two main ways namely respiratory tract infections and extrapulmonary diseases ranging from mild upper respiratory symptoms to severe pneumonia. The reported detection rates of atypical pneumonia range from 20\u0026ndash;28% [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Cold agglutinin hemolysis which is linked to an IgM mediated complementary cascade mechanism causes extravascular hemolysis and intravascular hemolysis (less common) in patients after one to two weeks after infection[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Severe anemia is typically described in pediatric patients or in patients with sickle cell disease This case describes an unusual triad of severe hemolysis, persistent leukocytosis, and thrombocytosis in a middle-aged woman.\u003c/p\u003e"},{"header":"Case Report","content":"\u003cp\u003eA 44-year-old woman presented to the emergency department with a 10-day history of persistent high fever (up to 102\u0026deg;F/38.9\u0026deg;C), progressive generalized fatigue, and persistent headache with no significant medical history. Five days prior to admission, she sought care at an outside facility where she was empirically treated with intravenous ceftriaxone (dose not specified) and oral chloroquine (dose not specified) without any clinical improvement. Upon presentation to our institution, the patient appeared acutely ill with marked respiratory distress. Vital signs revealed tachycardia (heart rate of 110 beats per minute), tachypnea (respiratory rate of 28 breaths per minute), borderline hypertension (blood pressure of 140/90 mmHg), and significant hypoxemia (oxygen saturation of 88% on room air). The physical examination revealed bilateral inspiratory crackles on lung auscultation, but neurological examination was completely normal with a GCS score of 15 and no focal neurological deficits.\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\u003eBlood parameters on the first and second days of admission followed by the last day\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"5\"\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\u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003eParameter\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eDay \u0026minus;\u0026thinsp;1\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003eDay \u0026ndash; 2\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c4\"\u003e\u003cp\u003eDay \u0026minus;\u0026thinsp;6\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c5\"\u003e\u003cp\u003eNormal Range\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eHemoglobin (Hb)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e5.3 g/dL\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e4.6 g/dL\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e8.6 g/dL\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e12\u0026ndash;15 g/dL\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eWhite Blood Cell (WBC) Count\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e42,000 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e36,390 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e9,350 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e4,000\u0026ndash;11,000 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003ePlatelet Count\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e564,000 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e488,400 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e560,100 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e150,000\u0026ndash;450,000 cells/\u0026micro;L\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003eInvestigations\u003c/h2\u003e\u003cp\u003eInitial laboratory investigations revealed profound hematological abnormalities including severe normocytic anemia, marked leukocytosis, and thrombocytosis as represented in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e. The peripheral blood smear rrevealed a strikingly reduced red blood cell count (1.60\u0026nbsp;million/\u0026micro;L, reference range 3.9\u0026ndash;5.1\u0026nbsp;million/\u0026micro;L) with evidence of hemolysis including polychromasia and occasional schistocytes. Biochemical markers revealed elevated serum iron (325 \u0026micro;g/dL, reference range 50\u0026ndash;170 \u0026micro;g/dL), extremely elevated erythrocyte sedimentation rates (140 mm/hr, reference range 0\u0026ndash;20 mm/hr), and significantly increased C-reactive protein levels (34.2 mg/L, reference range\u0026thinsp;\u0026lt;\u0026thinsp;5 mg/L). Renal function remained normal (serum creatinine 0.6 mg/dL, reference range 0.5\u0026ndash;1.2 mg/dL). Initial chest radiography revealed a right-sided mild pleural effusion without obvious parenchymal infiltrates. The patient was promptly administered broad-spectrum intravenous antibiotics (piperacillin-tazobactam 4.5g every 8 hours) and aggressive fluid resuscitation. However, computed tomography of the chest performed within 24 hours of admission revealed bilateral multifocal pneumonic infiltrates as presented in Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e that were not apparent on the initial chest X-ray. By the second visit at the hospital, the patient's condition had deteriorated hematologically with further decrease in hemoglobin, persistent leukocytosis, and thrombocytosis as represented in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e. Additional laboratory tests confirmed ongoing hemolysis with markedly elevated lactate dehydrogenase (1329 U/L, reference range 140\u0026ndash;280 U/L) and undetectable serum haptoglobin levels (\u0026lt;\u0026thinsp;0.072 g/L, reference range 0.3-2.0 g/L).\u003c/p\u003e\u003cp\u003eImmunohematological workup revealed a blood group discrepancy due to autoagglutination that resolved when testing was performed at 37\u0026deg;C, ultimately confirming that the patient's blood group was O-positive. Direct antiglobulin testing was strongly positive (4+) for IgM, with a weakly positive indirect antiglobulin test (2+). Cold agglutinin testing revealed no reactivity with neonatal O-positive red blood cells (excluding anti-i specificity) but strong agglutination with adult O-positive red blood cells at 4\u0026deg;C with a titer of 1:256, which is consistent with anti-I IgM-mediated cold agglutinin disease. Serological testing confirmed acute \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e infection with elevated IgM antibodies (727 AU/mL) and IgG antibodies (197 AU/mL). The procalcitonin level was mildly elevated at 0.33 ng/mL (reference range\u0026thinsp;\u0026lt;\u0026thinsp;0.5 ng/mL), suggesting possible bacterial coinfection. Given the severity of pneumonia (with type I respiratory failure) and life-threatening hemolytic anemia, the patient was transferred to the intensive care unit. Management included the transfusion of saline-washed, warm (37\u0026deg;C), Coombs-compatible packed red blood cells through a blood warmer to prevent the exacerbation of cold-induced hemolysis.\u003c/p\u003e\u003cp\u003eHigh-dose intravenous methylprednisolone (80 mg daily for 3 days, then tapered to 40 mg daily) was initiated for the cold agglutinin disease.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003eTreatment\u003c/h3\u003e\n\u003cp\u003eTargeted antimicrobial therapy with intravenous clarithromycin (1000 mg daily for 5 days) was started for the \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e infection, then transitioned to oral levofloxacin (750 mg daily for an additional 7 days, totaling 12 days of antibiotic therapy). Supplemental oxygen was required but was successfully weaned over four days as the patient's respiratory status improved.\u003c/p\u003e\u003cp\u003eAdditional workup ruled out other infections (negative HIV, hepatitis B and C serologies) and autoimmune disorders (negative antinuclear antibodies and antineutrophil cytoplasmic antibodies). The patient showed remarkable clinical improvement within 48 hours of initiating targeted therapy. The methylprednisolone was transitioned to oral prednisolone (50 mg daily) and gradually tapered over 10 days before complete discontinuation. By the time of discharge, the patient's hematological parameters had significantly improved with hemoglobin stabilizing at 8.6 g/dL, the white blood cell count normalizing to 9,350 cells/\u0026micro;L, and platelet count remaining elevated at 560,100 cells/\u0026micro;L. The patient was discharged with close outpatient follow-up arranged with both hematology and pulmonology specialists to monitor for potential recurrence of hemolysis or respiratory complications.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis case demonstrates a rare combination of \u003cem\u003eM. pneumoniae\u003c/em\u003e pneumonia with severe cold agglutinin hemolysis and persistent leukocytosis. This infection, although primarily a respiratory pathogen, can trigger a spectrum of rare but serious extrapulmonary complications, including cold agglutinin-mediated hemolytic anemia, central nervous system involvement (such as encephalitis or meningitis), glomerulonephritis, acute kidney injury secondary to intravascular hemolysis, myositis, and subclinical hemolysis[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Among these manifestations, the simultaneous occurrence of severe hemolytic anemia and neurological manifestations is rare [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Cold agglutinin-induced autoimmune hemolytic anemia is relatively rare, accounting for only 10\u0026ndash;20% of cases, and is often associated with infections by pathogens such as \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e, Epstein-Barr, and cytomegalovirus, among others[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].The pathogenesis of IgM Anti-I mediated cold agglutinin disease follows a characteristic cascade beginning with exposure to cold temperatures (\u0026lt;\u0026thinsp;30\u0026deg;C), which triggers IgM autoantibodies to bind specifically to I antigens abundantly expressed on adult RBC membranes[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. This antigen-antibody interaction initiates complement activation through the classical pathway (C1q binding), progressing to C3b deposition, which marks RBCs for opsonization and subsequent extravascular hemolysis via liver macrophages. In severe cases, full complement cascade activation leads to membrane attack complex (C5-C9) formation causing intravascular hemolysis. Clinically, this manifests through two hallmark phenomena: temperature-dependent agglutination (reversible RBC clumping in cold extremities) and complement-mediated hemolysis, resulting in anemia, acrocyanosis, hemoglobinuria, and Raynaud-like symptoms. Diagnostic confirmation requires demonstration of high-titer cold agglutinins (\u0026gt;\u0026thinsp;1:64 at 4\u0026deg;C) and a positive direct antiglobulin test (DAT) showing the C3d coating of RBCs, whereas IgM itself is rarely detected on erythrocytes due to elution during warming. The entire process underscores the temperature-sensitive nature of anti-I antibodies and their capacity to bridge benign respiratory infections with potentially severe hematologic complications. Thus, this case report aligns with other studies in which the proportion of female \u003cem\u003eM\u003c/em\u003e. \u003cem\u003ePneumoniae\u003c/em\u003e infections was relatively high in both children and adults, which is consistent with previous research[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e], [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e], [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e], [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. The occurrence of chronic cold agglutinin syndrome (CAS) associated with lymphoproliferative disorders is another rare finding observed in this case. The typical nature of rare disease conditions, such as this case, lies in the absence of a definitive treatment plan thus, the optimal management strategy remains unclear. Supportive care should focus on keeping the patient warm, and if transfusion is necessary, it should be administered through a blood warmer. Glucocorticoid treatment has been shown to be beneficial in the treatment of CAS, but its role in specific therapeutic interventions for cold agglutinin hemolysis remains unclear, as no standardized treatment approach has been firmly established. Management is often individualized, and guided by clinical presentation and severity[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. Among nine well-documented cases of \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e-associated hemolysis, glucocorticoid therapy was administered to four patients. Notably, two of these individuals showed significant clinical improvement following treatment, suggesting a potential, although not definitive, benefit[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].Signs of reduced hemolysis were present in our patient on day three after glucocorticoid treatment-initiation with a steady decrease of LDH, and normalized within a week. In cases where the hemolysis worsens despite supportive therapy and antibodies it seems reasonable to administer glucocorticoids. Glucocorticoid therapy in \u003cem\u003eM\u003c/em\u003e. \u003cem\u003ePneumonia-\u003c/em\u003ePneumonia without hemolysis is sometimes advocated but beneficial effects have not been well established and its use remains controversial. Antibiotics are generally recommended but probably play a limited role in the treatment of hemolysis. Theoretically, a faster clearance of the pathogen by antibiotic treatment could limit the production of cold agglutinins and their hemolytic effect. \u003cem\u003eMycoplasma\u003c/em\u003e pneumonia usually does not cause marked leukocytosis since it usually indicates another bacterial etiology other than \u003cem\u003eM. pneumoniae\u003c/em\u003e[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e] Our patient developed marked thrombocytosis. More frequently, thrombocytopenia has been reported in association with \u003cem\u003eM. pneumoniae\u003c/em\u003e infection, in some cases leading to fatal complications [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Our patient\u0026rsquo;s rapid improvement with corticosteroids suggests an immune-mediated component beyond infection alone. Persistent leukocytosis in \u003cem\u003eM. pneumoniae\u003c/em\u003e is unusual and may reflect inflammatory stress or bacterial coinfection. Updated management emphasizes pathogen-directed therapy (macrolides or fluoroquinolones), temperature control, and supportive transfusion strategies using warmed blood[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. This case illustrates several important clinical teaching points. First, it reveals the potentially severe hematological complications (cold agglutinin-mediated hemolytic anemia) that can accompany \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e infection, even in previously healthy individuals. Second, it highlights the critical importance of proper blood bank techniques (warm washing, use of blood warmers) in managing patients with cold agglutinin disease. Third, the findings underscore the value of early corticosteroid therapy in severe cases of cold agglutinin-mediated hemolysis. Finally, these finding indicates that \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e infection can cause significant pulmonary disease in adults, sometimes requiring intensive care management, and that macrolides remain first-line therapy despite increasing resistance patterns. The rapid clinical response to appropriate antimicrobial and immunomodulatory therapy in this case was particularly noteworthy and reinforces the importance of timely diagnosis and intervention in such cases.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case underscores the rare but serious potential of \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e to induce cold agglutinin hemolysis\u0026mdash;a complication that, while uncommon, can be life-threatening and diagnostically challenging. The clinical course highlights the importance of maintaining a broad differential diagnosis in patients presenting with severe hemolysis and respiratory symptoms.\u003c/p\u003e\u003cp\u003eIn the absence of established therapeutic protocols for \u003cem\u003eM. pneumoniae\u003c/em\u003e-associated hemolysis, a multidisciplinary approach involving timely diagnosis, supportive care with warmed transfusions, appropriate antimicrobial therapy, and judicious corticosteroid use has proven effective. Patient recovery illustrates the potential value of conservative management tailored to clinical presentation. This case adds to the limited literature on this rare complication and reinforces the need for continued vigilance and further investigation into evidence-based treatment strategies for atypical presentations of \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e infection.\u003c/p\u003e"},{"header":"Declarations","content":"\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eThanks to Dr Vigneshwaran V and Dr Nanda Kumar R for explaning the case and helped Pravin Selvi Saravanan to write the main manuscrpt under the guidance of Sarumathy S\u003c/p\u003e\n\u003ch3\u003eInformed Patient Consent:\u003c/h3\u003e\n\u003cp\u003e Complete informed consent was obtained from the patient for the publication of this study and any accompanying images.\u003c/p\u003e\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\u003ch2\u003eDeclaration of competing interests:\u003c/h2\u003e\u003cp\u003eThe authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.\u003c/p\u003e\u003c/div\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eGeorgakopoulou V, Lempesis I, Tarantinos K, Sklapani P, Trakas N, Spandidos D (Sep. 2024) Atypical pneumonia (Review). 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LATEST ONLINE, p. 1, Jan. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.12890/2018_000817\u003c/span\u003e\u003cspan address=\"10.12890/2018_000817\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGuo Z, Gu S, Tian Z, Du B (2024) Corrigendum: A comprehensive review of Mycoplasma pneumoniae infection in chronic lung diseases: recent advances in understanding asthma, COPD, and bronchiectasis, Front Med (Lausanne), vol. 11, Nov. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.3389/fmed.2024.1512825\u003c/span\u003e\u003cspan address=\"10.3389/fmed.2024.1512825\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"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":"the-egyptian-journal-of-bronchology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [The Egyptian Journal of Bronchology](https://ejb.springeropen.com/)","snPcode":"43168","submissionUrl":"https://submission.nature.com/new-submission/43168/3","title":"The Egyptian Journal of Bronchology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Mycoplasma pneumonia, cold agglutinin hemolysis, lymphoproliferative disorders, IgM anti-I mediated cold agglutinin disease","lastPublishedDoi":"10.21203/rs.3.rs-8131850/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8131850/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground: \u003cem\u003eMycoplasma pneumonia\u003c/em\u003e is one of the causes of community-acquired pneumonia (CAD) with rare extrapulmonary complications, including hemolytic anemia, persistent leukocytosis, Stevens-Johnson syndrome, meningoencephalitis. While these conditions are most common in children and young adults, typically those aged 5 to 20 years, this case report covers \u003cem\u003eMycoplasma pneumonia \u003c/em\u003ewith the very rare complication of hemolytic anemia and persistent leukocytosis in a middle-aged woman.\u003c/p\u003e\n\u003cp\u003eCase Presentation: A 44-year-old woman with a history of high-grade fever for 10 days, fatigue, and headache came to the emergency medicine. Laboratory evaluation revealed severe normocytic anemia (Hb 5.3 g/dL), leukocytosis (42,000/μL), and thrombocytosis (564,000/μL). Cold agglutinin testing confirmed anti-I IgM–mediated disease with high titers (1:256), and serology was positive for \u003cem\u003eM. pneumoniae\u003c/em\u003e IgM and IgG antibodies. She was treated with warmed red cell transfusions, intravenous methylprednisolone, and clarithromycin, followed by oral levofloxacin. Her condition improved significantly.\u003c/p\u003e\n\u003cp\u003eRationale: This case highlights the diagnostic complexity in a woman patient with rare hemolytic anemias in the context of atypical infections and the approach for their diagnosis and appropriate treatment. The coexistence of IgM-mediated autoimmune hemolytic anemia and leukocytosis poses diagnostic and therapeutic challenges that are relevant to clinical practice. This case underscores the diagnostic and therapeutic challenges of cold agglutinin hemolysis secondary to \u003cem\u003eM. pneumoniae\u003c/em\u003e infection.\u003c/p\u003e","manuscriptTitle":"Mycoplasma Pneumonia Infection Complicated with Hemolytic Anemia and Persistent Leukocytosis in a Middle-Aged Woman: A Case- Report.","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-09 00:23:09","doi":"10.21203/rs.3.rs-8131850/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-12-16T20:47:09+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-12-15T10:06:47+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"172614436661044628469531128453233994597","date":"2025-12-05T11:06:24+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-12-05T06:39:23+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"145679249192353916564027881033628048816","date":"2025-12-05T03:43:30+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-12-04T22:51:39+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-11-20T05:58:13+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-11-19T09:14:56+00:00","index":"","fulltext":""},{"type":"submitted","content":"The Egyptian Journal of Bronchology","date":"2025-11-17T06:37:13+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"the-egyptian-journal-of-bronchology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [The Egyptian Journal of Bronchology](https://ejb.springeropen.com/)","snPcode":"43168","submissionUrl":"https://submission.nature.com/new-submission/43168/3","title":"The Egyptian Journal of Bronchology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"56eaf77a-f126-4f7a-9f83-f789ef733579","owner":[],"postedDate":"December 9th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-05-12T19:23:24+00:00","versionOfRecord":[],"versionCreatedAt":"2025-12-09 00:23:09","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8131850","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8131850","identity":"rs-8131850","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}