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January 14, 2026, 02:03

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Commentary: Clinical Considerations in Immunocompromised Patients With Edwardsiella tarda–Associated Spontaneous Bacterial Peritonitis The case report by Usuda et al., recently published in the World Journal of Clinical Cases, represents a notable contribution to clinical microbiology by documenting, to the best of current knowledge, the first reported case of spontaneous bacterial peritonitis (SBP) caused by Edwardsiella tarda in an immunocompromised patient undergoing dialysis [1].This report substantially expands the recognized infectious spectrum in patients with end-stage renal disease (ESRD) and underscores the need for heightened clinical awareness of atypical and opportunistic pathogens in this vulnerable population. One particularly commendable aspect of this report is the authors’ detailed discussion of the virulence mechanisms of E. tarda. The organism’s capacity to survive and replicate within macrophages plays a pivotal role in its pathogenicity, especially in hosts with compromised cellular immunity [2,3]. In the present case, the coexistence of diabetic nephropathy and long-term dialysis likely created a permissive immunological milieu that facilitated this opportunistic infection. Such intracellular persistence provides a plausible explanation for the severe and insidious clinical course observed, even in the absence of classical epidemiological exposures such as raw seafood consumption or contact with freshwater environments. Equally noteworthy is the authors’ adherence to principles of antimicrobial stewardship. The stepwise transition from empirical broad-spectrum therapy with cefmetazole to targeted, de-escalated treatment using cefalexin—guided by comprehensive antimicrobial susceptibility testing (Table 3)—offers a valuable therapeutic reference for clinicians managing similarly rare infections. Nevertheless, building on the authors’ insightful acknowledgment of the limitations surrounding “ascites culture conversion,” I would like to propose a more structured and rigorous framework for defining treatment endpoints in such high-risk cases. While clinical and symptomatic improvement remains an essential marker of response, it may be insufficient when dealing with pathogens such as E. tarda, which possess the ability to persist intracellularly [4,5]. Accordingly, I suggest an integrated “imaging-to-microbiology” strategy prior to antibiotic discontinuation. First, advanced imaging modalities—such as abdominal computed tomography or high-resolution ultrasonography—should be systematically incorporated to objectively assess the resolution of ascites. Complete radiological absorption of ascitic fluid would substantially strengthen the clinical justification for treatment cessation. Conversely, if residual ascites is detected, even in minimal or loculated forms, reliance on systemic inflammatory markers such as C-reactive protein or leukocyte counts alone may be misleading. Given the organism’s persistence potential [3], repeat diagnostic paracentesis should be strongly considered to confirm microbiological eradication. This dual confirmation—radiological and microbiological—would provide a more robust and evidence-based rationale for terminating antimicrobial therapy [6], thereby reducing the risk of relapse in immunocompromised patients. In conclusion, while this case report fills an important gap in the current literature, it also highlights the need to refine discharge and treatment-completion criteria for rare causes of SBP. Adoption of an imaging-guided microbiological confirmation strategy may enhance the precision of clinical decision-making and ultimately improve long-term outcomes in patients with complex comorbidities. 参考文献 [1]Usuda D , Furukawa D, Imaizumi R et al. Spontaneous bacterial peritonitis due to Edwardsiella tarda in an immuno-compromised dialysis patient: A case report and review of literature. World J Clin Cases 2026,6; 14(1): 115102. [2][2]Qin L, Li F, Wang X, Sun Y, Bi K, Gao Y. Proteomic analysis of macrophage in response to Edwardsiella tarda-infection. Microb Pathog, 2017; 111: 86-93 [RCA] [PMID: 28826764 DOI: 10.1016/j.micpath.2017.08.028] [3]Zhang L, Ni C, Xu W, Dai T, Yang D, Wang Q, Zhang Y, Liu Q. Intramacrophage Infection Reinforces the Virulence of Edwardsiella tarda. J Bacteriol 2016; 198: 1534-1542 [RCA] [PMID: 26953340 DOI: 10.1128/JB.00978-15] [4]An L, Chan JL, Nguyen M, Yang S, Deville JG. Case Report: Disseminated Edwardsiella tarda infection in an immunocompromised patient. Front Cell Infect Microbiol 2023; 13: 1292768 [RCA] [PMID: 38053529 DOI: 10.3389/fcimb.2023.1292768] [5]Matsukawa H, Usuda D, Takami H, Nomura T, Sugita M. A Case of Edwardsiella tarda Infection With Iliopsoas Abscess Following Acute Pyelonephritis. Cureus 2024; 16: e58868 [RCA] [PMID: 38800258 DOI: 10.7759/cureus.58868] [6]A Rimola , G García-Tsao, M Navasa, L J Piddock, R Planas, B Bernard, J M Inadomi. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document. International Ascites Club. J Hepatol, 2000; 32(1):142-53[RCA][PMID: 10673079 DOI: 10.1016/s0168-8278(00)80201-9]

Replied on January 21, 2026, 16:03

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