Transfusion-Transmitted Yersinia enterocolitica Infection: Protection Through Buffy Coat Removal and Failure of the Bacteria to Grow in Platelet-Rich or Platelet-Poor Plasma

In a previous study, removal of white blood cells (WBC), by filtration 5 h after deliberate contamination of whole blood with a type 0:3 strain of Yersinia enterocolitica, was shown to be an effective way of avoiding bacterial growth in red blood cells (RBC) during storage. In the present study the Opti-System technique was used to remove the buffy coat from whole blood, leaving 10–20% of the original number of WBC in the RBC preparation. In one series of experiments, all of 4 units of RBC suspension, from which buffy coats were removed 2 h after inoculation of 112 colony-forming units (cfu) per ml of Y. enterocolitica, became Yersinia-free, while abundant bacterial growth occurred in all of 4 units where RBC suspension and buffy coat had been recombined. In a second series of 10 experiments, with an inoculum of 80 cfu/ml, no growth was found in platelet-poor plasma stored for 42 days at 4°C. Five out of 10 RBC suspensions in SAGM additive solution remained Yersinia-free throughout a 6-week storage period; 4 of these 10 units showing growth of Yersinia after 4 weeks and 5 after 6 weeks. In the buffy coats bacterial growth was found in 1 out of 10 units after 1 week, 4 after 2 weeks, and in all of 10 units after 4 weeks. In 2 control experiments with WBC-reduced RBC inoculated with the same bacterial dose, growth started within 24 h and was abundant after 1 week. In platelet-rich plasma (PRP), prepared from 4 units of whole blood that had been inoculated with Y. enterocolitica (106 cfu/ml), no bacterial growth was found during 10 days of storage at 22°C. Also, after Y. enterocolitica inoculation (114 cfu/ml) directly into PRP, bacteria failed to grow. We conclude that removal of the buffy coat from whole blood that had been previously contaminated with a moderate inoculation of Y. enterocolitica partly protects the red cells from bacterial growth during storage. The risk of transmitting Y. enterocolitica with platelet-poor plasma, liquid stored at 4°C, seems minimal. This bacterial species shows very poor capacity to grow in PRP at 22°C.     

Yersinia enterocolitica infection complicated by intestinal perforation

Yersinia enterocolitica causes primarily ileocolitis in human beings, and is manifested by abdominal pain, diarrhea, and fever. Usually, it is a self-limiting disease. Local or systemic complications are rare. A 71-year-old man with Y enterocolitica colitis complicated by perforation and abscess formation is described. This complication is very rare, and the four other cases that have been reported in the literature are reviewed.     

Yersinia enterocolitica infection complicated by glomerulonephritis.

A case of mild glomerulonephritis in a 24-year-old man with clinical and immunohistological findings associated with Yersinia enterocolitica serotype 3 infection is described. The role of IgA in the pathogenesis of glomerulonephritis associated with mucosal infection is briefly discussed. Although attempts to demonstrate Y. enterocolitica 3 antigen in the biopsy specimen were unsuccessful, the glomerular deposits of immunoglobulins and complement suggest immune pathogenesis.     

小肠结肠炎耶氏菌诊断噬菌体(J+H)溶菌谱的进一步研究

从猪便分离的两株小肠结肠炎耶氏菌噬菌体,在临用时混合为J+H噬菌体,能裂解小肠结肠炎耶氏菌48个血清型标准株中的42个型;裂解498个地方株中的97％;裂解志贺氏菌属的0.5％,艾希氏菌属的2.2％,但不能裂解沙门氏菌属和枸橼酸杆菌属;裂解26株假结核耶氏菌中的1株。J+H混合噬菌体具有高度敏感性和特异性,是一种很理想的诊断噬菌体,很适用于菌株的初步鉴定。     

Adult Still's disease caused by Yersinia enterocolitica infection

Clinical and biologic features of adult Still's disease developed in a patient who had high antibody titers against Yersinia enterocolitica during his illness. Immunocomplexes containing antibodies against Yersinia antigens were isolated at the beginning of the disease. Yersinia was not isolated from blood or stool specimens probably because we observed the patient during the secondary phase of the disease.     

Collagenous Colitis and Yersinia enterocolitica Infection

Collagenous colitis is a rare clinical andpathological entity characterized by watery diarrhea anddeposition of collagen beneath the surface epithelium ofthe colon. Its etiology is unknown. We present a careful retrospective clinicopathologicalanalysis of six patients with collagenous colitisdiagnosed at our hospital during a three-year period.Three of the patients had had a Yersinia enterocolitica infection, detected by stool culture andelevated serum antibody titers, preceding the diagnosisof collagenous colitis. Four patients had duodenalvillous atrophy, which in two patients was refractory to a gluten-free diet. We propose that Yersiniaenterocolitica infection may be a triggering factor forthe development of collagenous colitis in some cases.Duodenal villous atrophy not responding to gluten withdrawal is common in association withcollagenous colitis.     

Yersinia enterocolitica abscess of the transverse colon

Yersinia enterocolitica abscess of the bowel is a rare entity. Only five cases have previously been reported--none in the surgical literature. A unique presentation for Yersinia infection, abscess of the transverse colon, is described, and the literature of Y. enterocolitica intestinal perforation and abscess is reviewed.     

Interstitial pneumonia and sepsis caused by Yersinia enterocolitica serotype 3

Micronodular pneumonia and persistent sepsis with mild symptoms caused by Yersinia enterocolitica serotype 3 is described. Two of 4 patients had pneumonia as their only clinical manifestation, while the others had diarrhea as well. Pneumonic changes disappeared quickly during antimicrobic therapy. The course of the disease was fundamentally different from septicaemias caused by other gram-negative bacteria.     

Persistence of Yersinia enterocolitica in man

Summary Ten patients with chronicYersinia enterocolitica infections are described. The initial diagnosis was made by culture, significant agglutinin titres and indirect immunofluorescence (IF) on biopsies. During the chronic phase, culture and agglutinin titres were negative, but specific serum IgA and IgG antibodies reactive with at least two, i.e. the 36 kDa and the 46 kDa, virulence-associated released proteins were demonstrated in nine patients by immunoblot techniques. One patient had only IgG antibodies. The chronically elevated IgA production was the result of chronic stimulation of the gut-associated lymphoid tissue by virulent persistentYersinia antigen, which was identified by IF with O-specific antiserum and monospecific antiserum to the 46 kDa released protein in biopsies. VirulentYersinia bacilli were demonstrated in the intestinal mucosa and in the lymphoid tissue of the submucosa associated with macrophages in patients with chronic ileitis and arthritis, in granulomatous centres of lymph nodes in patients with chronic lymphadenopathy and in portal infiltrates in a patient with chronic hepatitis. Recognition of persistentYersinia infections may have therapeutic implications.

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Persistenz von Yersinia enterocolitica bei Menschen

Zusammenfassung Zehn Patienten mit chronischerYersinia enterocolitica-Infektion werden beschrieben. Die Anfangsdiagnose war mittels positiver Kulturen, signifikanter Agglutinationstiter und immunhistologischem (IF) Yersinia-Nachweis in menschlichem Biopsiematerial gestellt worden. Während der chronischen Phase waren Kultur und Agglutinationstiter negativ, aber im Serum von neun Patienten waren mit Immunoblot spezifische IgA- und IgG-Antikörper gegen mindestens zwei, d. h. die 36 kDa und 46 kDa Virulenz-assoziierten Proteine nachzuweisen. Ein Patient hatte nur IgG-Antikörper. Die chronisch erhöhte IgA-Produktion war verursacht durch chronische Stimulierung des intestinalen lymphatischen Gewebes durch virulente, persistierendeYersinia-Antigene, die mittels IF mit O-spezifischem Antiserum und monospezifischem Antiserum gegen das 46 kDa Virulenz-Protein in Biopsiematerial identifiziert werden konnten. VirulenteYersinia-Bazillen lagen in Biopsien von Patienten mit chronischer Ileitis und Arthritis tief in der Darmmukosa und im lymphoiden Gewebe der Submukosa, assoziiert mit Makrophagen. Sie wurden auch in Lymphknoten von Patienten mit chronischer Lymph-adenopathie nachgewiesen und in portalen Infiltraten eines Patienten mit chronischer Hepatitis. Der Nachweis persistierenderYersinia-Infektionen kann therapeutische Konsequenzen haben.

     

1例小肠结肠炎耶尔森菌人畜感染情况研究

目的 研究小肠结肠炎耶尔森菌(Y.e)人畜感染情况,探索传染来源。方法 采集腹泻病人粪便标本和猪咽拭子进行Y.e常规分离鉴定。对分离株进行血清学分型,用PCR方法检测毒力基因,用脉冲场凝胶电泳(PFGE)进行分子分型。结果 从150例腹泻病人中分离到Y.e 3株,其中1株血清型为O∶3;从该O∶3株病患老家采集的222份猪咽拭子分离到Y.e 14株,都为O∶3血清型;PFGE分子分型显示病人体内分离到的致病Y.e与家猪分离株有较高的同源性。结论 证实1例小肠结肠炎耶尔森菌从家猪传染人的病例,并发现Y.e在治愈病人体内至少存在了2个月。     

Perforation of the Ileum in Yersinia enterocolitica Infection

A 69-year-old woman with a 5-wk history of diarrhea and abdominal pain was found to have multiple perforations of the terminal ileum. Blood cultures and cultures of the fistulae and mesenteric lymph nodes were positive for Yersinia enterocolitica infection. This is believed to be the first documented case of perforation of the intestinal tract with this disease.     

冷冻食品中小肠结肠炎耶尔森氏菌的分离和鉴定

<正> 小肠结肠炎耶尔森氏菌广泛分布于自然界,是一种人畜共患的病原菌。食品和饮水受到耶氏菌的污染是爆发胃肠炎型结肠炎耶氏菌病的重要原因,已从各种食品中分离到本菌,但目前国内尚未见从冷冻食品中分离出耶氏菌的报导。本文报告从557份冷冻食品中分出26株耶氏菌,其血清群和人体分离株相符,具有流行病学意义。     

32株小肠结肠炎耶尔森菌病原学特征

目的了解徐州地区小肠结肠炎耶尔森菌的分布及病原学特征。方法常规方法在腹泻患者粪便、家禽家畜粪便、苍蝇、肉食品中分离小肠结肠炎耶尔森菌，用血清学、生物学方法分型及抗菌耐药性分型。并通过PCR技术进行毒力基因检测，同时对检出的国内主要流行血清型O：3和O：9菌株进行脉冲场凝胶电泳分析。结果2014份标本中共检出32株（分为17个血清型）小肠结肠炎耶尔森菌，总检出率为1．59％，其中O：3和O：9血清型的检出率分别为9．4％，且耐药模式相同。32株小肠结肠炎耶尔森菌分别携带ail、ystA、yadA、virF和all、ystA毒力基因的各占9．4％，只携带ystB基因的占21．8％，不携带以上任何基因的占59．4％。32株小肠结肠炎耶尔森菌分为3个生物型别，其中1A型为78．1％，3型为18．8％，2型为3．1％。本地区分离的2株O：3血清型小肠结肠炎耶尔森菌的脉冲场凝胶电泳带型相同，是我国O：3血清型小肠结肠炎耶尔森菌的主要克隆系。结论徐州地区存在致病性小肠结肠炎耶尔森菌O：3和O：9血清型及由此引起的腹泻疾病，应引起高度重视。     

Induction of autoimmune colitis by Yersinia enterocolitica 60-kilodalton heat-shock protein

BACKGROUND: Many investigations of the relationship between ulcerative colitis (UC) and heat-shock protein (Hsp) 60 have been reported. We have already established an animal model exhibiting UC-like lesions caused by administration of Escherichia coli expressing Yersinia enterocolitica Hsp60. In this study, we therefore attempted to induce mouse colitis by purified Y. enterocolitica Hsp60. METHODS: Purified Y. enterocolitica Hsp60 was injected intraperitoneally into B10A/SgSn mice at a dose of 3 microg/0.2 ml once a week for 2 months, and morphological changes in the intestine were examined by light and electron microscopical analysis. Autoimmune responses were also examined. RESULTS: The mice treated with Y. enterocolitica Hsp60 exhibited immune reaction between large intestine and autologous serum. Light and electron microscopically, degradation of glandular ducts, erosions, ulceration, crypt abscess-like formation, infiltration of inflammatory cells and absence of perivascular reticular fibers in lamina propria mucosae and subepithelial reticular layer were observed. CONCLUSIONS: These findings indicate that administration of Y. enterocolitica Hsp60 induces UC-like lesions with autoimmune responses.     

Induction of Autoimmune Colitis by Yersinia enterocolitica 60-kilodalton Heat-Shock Protein

We investigated changes in the concentrations of thrombin-antithrombin III complex (TAT) and plasmin-α₂ plasmin inhibitor complex (PIC) after the intravenous administration of 4000 units of antithrombin III (AT III) concentrate to patients with fulminant hepatic failure (FHF), subacute hepatitis (SH), or liver cirrhosis (LC). FHF patients showed shortening of the initial half-life of exogenous AT III. In addition, a marked rise in plasma TAT was noted 3 to 6h after the intravenous administration of AT III, even in patients who had a normal plasma TAT level before AT III therapy. In contrast, SH and LC patients showed no marked changes of plasma TAT levels after AT III administration. No marked changes were observed in the PIC concentration in any of the patients. These findings suggest that thrombin formation is increased in FHF and that simple measurement of the plasma TAT concentration is not an adequate method for assessing thrombin formation in FHF patients who have suspected disseminated intravascular coagulation associated with an apparent decrease in AT III synthesis. Instead, it seems necessary to measure the plasma TAT concentration in FHF patients after replacement therapy with AT III concentrate has been performed, to evaluate their hypercoagulability more accurately.     

携带ystB基因小肠结肠炎耶尔森菌分子流行病学研究

目的了解我国携带ystB基因小肠结肠炎耶尔森菌的分子流行病学特征。方法通过PCR扩增ystB基因;通过血清凝集实验和生化反应分析其血清型及生物型;使用脉冲场凝胶电泳(PFGE)对其进行分子分型,并将带型进行聚类分析;ATBG-5试剂条测定菌株的耐药情况。结果所分析250株小肠结肠炎耶尔森菌均为生物1A型;包括至少23种血清型;通过PFGE分型,250株细菌共产生167个型别;多数菌株对阿莫西林、头孢噻吩、替卡西林等抗生素耐药,所有菌株对环丙沙星以及阿米卡星敏感。结论ystB基因仅出现在生物1A型小肠结肠炎耶尔森菌中;多数菌株对阿莫西林和部分头孢菌素类抗生素高度耐药,可能与这些菌株表达β-内酰胺酶有关;PFGE不能对携带ystB基因小肠结肠炎耶尔森菌进行有效的分子分型。