Strongyloides permission [7]. 

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... eosinophilia is the presence of >10% of the white blood cell (WBC) differential in dialysate being eosinophils ( Table 1). It is typically associated with sterile (idiopathic) peritonitis and culture-positive microbial peritonitis [1]. Since microbial peritonitis accompanied by dialysate eosinophilia is unusual but not rare, we report a case illustrating subtle features of infection and the host response to it. A 59-year-old Laotian male developed multiple myeloma in 2002, was treated with thalidomide/dexamethasone in 2006 and began peritoneal dialysis (PD) in 2007. In De- cember 2011, he presented with abdominal pain. Abnor- mal labs included a peripheral WBC 11 × 10 9 /L 11 000/ μ L (4% eosinophils) and a dialysate WBC 9.05 × 10 8 /L (905/ μ L) (77% eosinophils, 2% neutrophils). The dialysate was cultured and PD continued with empiric intraperitoneal ceftazidime and vancomycin. He responded well and was discharged the next day with a dialysate WBC of 5.3 × 10 7 /L (53/ μ L) (70% eosinophils). The working diagnosis was a bacterial infection characterized by an eosinophilic response. Three days later he returned with recurrent abdominal pain, constipation, vomiting, and his peripheral WBC was 17 × 10 9 /L (17 000/ μ L) (23% eosinophils). Dialysate culture remained negative. Nine years earlier he had an unexplained absolute peripheral eosinophilia of 1.080 × 10 9 /L (1080 cells/ μ L). In 2011, microscopy of the ef fl uent using wet mount and iodine stain did not reveal the presence of fi laform larvae, but only atypical, reactive mesothelial cells. Serum Strongyloides IgG was detected. After two oral doses of ivermectin (200 μ g/kg), he dra- matically improved and stool yielded Strongyloides stercoralis larvae. He was discharged with a dialysate WBC of 1.1 × 10 7 /L (11/ μ L) (35% eosinophils), his last documented ef fl uent count. Five months later, his myeloma required treatment and he started hemodialysis. In retrospect, his myeloma was probably relapsing during the Strongyloides infection. Albeit unusual, microbial peritonitis may be accompanied with dialysate eosinophilia [1]. A retrospective observa- tional report purposefully excluded episodes of transient noninfectious peritoneal eosinophilia occurring at the start of PD and uncovered 42 cases of peritoneal eosinophilia: 22 with microbial organism-related peritonitis and 20 cases of idiopathic (noninfectious) eosinophilic peritonitis [1]. Fifteen of the 20 idiopathic cases had been on PD <3 months, whereas only 3 of the 22 infection cases occurred in the fi rst 3 months (P < 0.001) [1]. Patients in the infection group had been on PD for 30 months compared with the idiopathic group on PD for only 14 months. Peripheral eosinophilia of >500/ μ L was seen in almost half the patients in the idiopathic group and not at all in the infection group (P < 0.02) [1]. Furthermore, a third of the patients in the infection group had blood leukocytosis >10 × 10 9 /L (10 000/ μ L). Dialysate cell counts were higher in the infection group, but the fraction of eosinophils was higher in the idiopathic group. The microbiology of eosinophilic peritonitis was similar to non-eosinophilic peritonitis, except for more Staphylococ- cus aureus and fungal peritonitis and overall fewer Gram- positive organisms in the eosinophilic group. In the Spanish center, the most frequent cause of overt eosinophilic peritonitis was microbial infection. Hypersensitivity to PD materials have been suggested as an etiology of idiopathic eosinophilic peritonitis devel- oping within weeks after initiation. Humayun et al . found that one-third of the newly initiated patients developed peritoneal fl uid eosinophilia within 2 weeks of catheter insertion and PD initiation [2]. Implicated triggers include plasticizers, additives, heparin, fi brin, blood, iodine or mechanical irritation from the catheter or the distension of the abdomen (Table 2). Dialysate eosinophilia has been identi fi ed with intraperitoneal air exposure during exchanges [3]. Interleukin-5, interleukin-3 and granulo- cyte/monocyte colony-stimulating factor released into in fl amed peritoneum may recruit eosinophils [1]. The pro- totypical presentation includes an intermittently cloudy ef fl uent without associated nausea, vomiting or abdominal pain, which helps us to differentiate the idiopathic variant from the quite symptomatic microbial peritonitis. The idiopathic variant of peritoneal eosinophilia has similarities to an allergy. Typical microbial infections com- plicating PD on occasion are accompanied by an unusual presence of peritoneal eosinophils. Microbial peritonitis associated with peritoneal eosinophilia may also be sec- ondary to atypical infections like tuberculosis [4, 5]. A third category of peritoneal eosinophilia is that of infections caused by microbial agents or parasites that are known to provoke an eosinophilic reaction. Our institution reported a patient with a rejected renal transplant who developed E. coli PD-associated peritonitis [6]. She relapsed following initial improvement with antibiotics. Strongyloides stercoralis larvae were detected in the dialysate. In another report, larvae were seen in the peritoneal dialysate sediment (Figure 1) [7]. The considered mechanisms of Strongyloides in fi ltration were transmural migration or touch contamination. In our case, larvae were not detected in the dialysate nor was there any culture evidence that larvae tracked bacteria into the dialysate. Was peritoneal eosinophilia a reaction to the underlying bowel pathology, simply eosinophilic ascites related to Strongyloides infection, incidental to PD? Eosinophilic ascites in the absence of peritonitis was described with Toxocara canis infection in a patient not on dialysis, where the ascites may have resulted from larval invasion of the peritoneal cavity after excysting in the small bowel creating a local reaction [8]. Eosinophilic ileitis in a patient not on dialysis was also associated with peritoneal eosinophilia [9]. Strongyloides larvae burrow into duodenal and proximal jejunal mucosa; some mature and subsequently invade the bowel wall. This insult may cause an acute neighborhood reaction resulting in peritoneal eosinophilia. Several risk factors have been identi fi ed for Strongyloides infections, including having lived in Laos [10]. In the United States corticosteroids, acting as a larval growth factor, are most commonly associated with Strongyloides infection [6]. Furthermore, an underlying hematologic malignancy may also increase the risk of Strongyloides infection [11, 12]. Our patient had not received corticosteroids in the 4 years prior to his Strongyloides infection, but in retrospect may have been immunocompromised by his subtle myeloma relapse. Failing to adequately treat the speci fi c etiology of peritonitis can result in signi fi cant morbidity and mor- tality. In PD patients with overt signs of peritonitis, empiric treatment for bacterial peritonitis is appropriate. While exposure to corticosteroids does not predispose patients to typical peritonitis, if there is a history of parasitic contact exposure, immunocompromised or immunosuppressive agents, one must consider parasites as the infectious agent ...