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ysis tools (SeqSero-1.2, MLST 2.0, ResFinder 4.1, andPlasmidFinder 2.1) available at Center for Genomic Epidemiology (http:// genom icepi demio logy. org/). Genomebased serotyping assigned the strain to S. Livingstonewith an antigenic profile of 7:d:l,w (O antigen, O-7; H1antigen, d; H2 antigen, l,w). Its draft genome sequencehas been deposited in GenBank under accession no. JAGHKU000000000. The strain belongs to sequence type 543(allele profile, 62-162-38), carries a single antimicrobial resistance gene, aac(6′)-Iaa, mediating resistance toaminoglycosides, and has a single known plasmid replicon Col(pHAD28) 1 KU674895. Virulence factors ofthe strain was predicted by querying the Virulence Factors of Pathogenic Bacteria (VFDB, http:// www. mgc. ac. cn/ cgi- bin/ VFs/ v5/ main. cgi). The strain carried multiplevirulence factors including fimbrial adherence determinants csg, bcf, fim, saf, stb, stc, std, ste, stf, sth, sti and stk,macrophage inducible gene mig-14, magnesium transport genes mgtB and mgtC, nonfimbrial adherence determinants misL, ratB, shdA and sinH, genes for SP1- andSP2-encoding type III secretion systems (hil, iac, inv, org,prg, sic, sip, sop, spa, spi, sprB, spv, ssa, ssc, sse, ssr), andafimbrial adhesin-encoding afaB and afaC (Additionalfile 2: Table S1). The strain was susceptible to third-generation cephalosporins, carbapenems and fluoroquinolones as determined using Vitek II (bioMérieux). Splenicabscess due to splenic cyst with S. Livingstone infectionwas diagnosed.He received imipenem (500 mg every 8 h) for 10 daysand then cefperazone-sulbactam (3 g every 8 h) for30 days. About 500 mL bloody pus was drained fromthe splenic abscess daily. One month later, the spleendrainage tube was removed since no drainage fluid hadbeen observed for 1 week. The abscess had significantlydecreased according to the abdominal CT taken 42 dayslater (Fig. 2b). The patient recovered well and had norecurrent symptoms during the follow-up.Discussion and conclusionsSalmonellosis due to S. Livingstone in human is uncommon and giant splenic cysts complicated with S. Livingstone infection have not been previously reported. Themost common clinical presentation of S. Livingstoneinfection was gastroenteritis [11]. S. Livingstone did notcause bacteremia due to the absence of the spv genes butcould invade the adjacent organs from the intestine [14].For splenic abscess, the most common clinical manifestations are fever, abdominal pain, left upper abdominaltenderness and splenomegaly [15], as seen in this case.Splenic cysts may act as a predisposing factor for splenicabscess. Many previous studies have shown that congenital epidermoid and mesothelial cysts are associated withincreased CA-199 [1]. We did not have histopathological confirmation of splenic epithelioid cyst in this case.However, in light of his age, history, and significantlyelevated serum CA-199, the most likely diagnosis wassplenic abscess due to epidermoid cyst with S. Livingstone infection.Like most NTS, S. Livingstone causes diseases mainlyin individuals with underlying factors such as theimmunocompromised status [16]. Patients with HIVinfection, malnutrition, malaria, or inherited immunodeficiencies including chronic granulomatous diseases, sickle-cell diseases and B-cell deficiencies are atincreased risks for invasive NTS (iNTS) diseases suchas bacteremia and meningitis [17–19]. Host susceptibility to iNTS diseases varies significantly among individuals, and currently-available studies have focused onprimary immunodeficiencies. The innate and acquired

Qu and Zong BMC Infectious Diseases(2022) 22:557immune systems help the host to control of invasiveSalmonella infection [20–23]. In addition, genetic variations may lead to susceptibility to different Salmonellaspecies [20]. Although our patient did not have apparent immune deficiency, it cannot be excluded that hehad genetic factors predisposing to the NTS infection.Splenectomy was previously considered the gold standard for the treatment of splenic abscess [24]. However,recent studies have shown that percutaneous drainagecombined with antimicrobial agents could be a bettertreatment option. Therapeutic splenectomy was requiredin only about 20% of patients [25, 26]. Splenectomy maylead to presumptive immune deficiency and increasethe risk of bacterial infections and therefore should beavoided, especially in children. Percutaneous imageguided splenic intervention has also been found saferthan splenectomy [27]. Splenic abscess could be single ormultiple, with diameters ranging from 1 to 23 cm [28, 29].Percutaneous aspiration and drainage have usually beenperformed in patients with a splenic abscess less than10 cm in diameter [25, 30], while percutaneous drainage was successfully treated in this case with a spleenabscess of 21 cm in diameter. The most common complication of splenic intervention is hemorrhage [27]. Thepurulent and bloody drainage was initially drained fromthe splenic abscess of this case, which may reflect hemorrhage. Nonetheless, his drainage fluid became purulent and he had no bloody fluid after 10 days of drainage.Therefore, large unruptured splenic abscesses may betreated with percutaneous aspiration and drainage, whilesalvage splenectomy could be considered if other treatments fail. As for splenic cysts, different managementapproaches can be selected according to the clinical situation of the patient in the future, including percutaneousdrainage, partial splenectomy, splenectomy, total cystectomy, laparoscopic decapsulation, marsupialization orcyst unroofing [4, 31]. Preserving splenunculus therapy,rather than splenectomy, may be preferred due to theimmune function of the spleen.In conclusion, splenic cyst can be complicated with S.Livingstone infection, resulting in splenic abscess, evenin previously healthy adolescents. Percutaneous drainage and appropriate antimicrobial therapy can be usedto treat large splenic abscess. This case of a previouslyhealthy adolescent may help clinicians to raise awarenessof splenic abscess and highlights the importance of drainage and antimicrobial agents to avoid splenectomy.AbbreviationsAFP: Alpha fetoprotein; CA: Carbohydrate antigen; CEA: Carcinoma embryonicantigen; CRP: C-reactive protein; CT: Tomography; HIV: Human immunodeficiency virus; iNTS: Invasive non-typhoidal Salmonella; NTS: Non-typhoidSalmonella; PCT: Procalcitonin; WBC: White blood cell.Page 4 of 5Supplementary InformationThe online version contains supplementary material available at https:// doi. org/ 10. 1186/ s12879- 022- 07529-6.Additional file 1: Figure S1. Chest CT on admission showed consolidation of lower lobes of both lungs (Panel a). Chest CT was normal after20 days of antibacterial therapy (Panel b).Additional file 2: Table S1. Virulence factors of the strain.AcknowledgementsWe are grateful for Lina Liu and Yu Feng, West China Hospital, Sichuan University for performing genome sequencing and analysis.Author contributionsZZ and JQ designed the study. JQ collected and interpreted the clinical dataand drafted the manuscript. ZZ revised the manuscript. All authors read andapproved the final manuscript.FundingThe work was supported by a grant from West China Hospital of Sichuan University (1.3.5 project for disciplines of excellence, project no. ZYYC08006; andGrant No. 312190022). The funders had no role in study design, data collectionand analysis, decision to publish, or preparation of the manuscript.Availability of data and materialsDraft genome sequence of the strain has been deposited in GenBank underaccession no. JAGHKU000000000. All other data are available in the text.DeclarationsEthics approval and consent to participateThe investigation was approved by the Ethics Committee of West ChinaHospital, Sichuan University.Consent for publicationThe authors declare that the written informed consent for publication hasbeen obtained from the patient’s guardian.Competing interestsThe authors declare no conflict of interest.Author details1Center of Infectious Disease, West China Hospital (Huaxi), Sichuan University,Guoxuexiang 37, Chengdu 610041, China. 2 Center for Pathogen Research,West China Hospital, Sichuan University, Chengdu, China.Received: 29 June 2021 Accepted: 10 June 2022References1. Bresadola V, Pravisani R, Terrosu G, Risaliti A. Laparoscopic splenectomy asthe definitive investigation for differential diagnosis of elevated serum CA19-9 levels associated with a splenic cyst: case report and review of theliterature. J Surg. 2013;1(1):6.2. Morgenstern L. Nonparasitic splenic cysts: pathogenesis, classification,and treatment. J Am Coll Surg. 2002;194(3):306–14.3. Garg M, Kataria SP, Sethi D, Mathur SK. Epidermoid cyst of spleen mimicking splenic lymphangioma. Adv Biomed Res. 2013;2:49.4. Ingle SB, Hinge Ingle CR, Patrike S. Epithelial cysts of the spleen: a minireview. World J Gastroenterol. 2014;20(38):13899–903.5. Ooi LL, Leong SS. Splenic abscesses from 1987 to 1995. Am J Surg.1997;174(1):87–93.6. Liu YH, Liu CP, Lee CM. Splenic abscesses at a tertiary medical center innorthern Taiwan. J Microbiol Immunol Infect. 2014;47(2):104–8.