A survey of acute and chronic disease associated with Yersinia enterocolitica infection. A Norwegian 10-year follow-up study on 458 hospitalized patients.

The aim of the present study was to further elucidate acute and chronic manifestations of Yersinia enterocolitica infection. During the period 1974-83, 458 hospitalized patients were diagnosed by antibody response and/or isolation of the microorganism. 64 patients had suffered from chronic conditions as rheumatic disease, inflammatory bowel disease, hepatitis, nephritis or thyroid disease for some time. Acute hepatic, renal, cardiac, pulmonary, pancreatic or neurologic involvement were observed in a substantial portion of patients; several had multiorgan disease. Acute insulin-dependent diabetes was seen in 2 patients, malignant mesothelioma in 2, and specific lymph node inflammation in 1. The patients were followed for 4-14 years (1987). 36/160 readmitted patients had abdominal pain and 26 had diarrhea; chronic colitis was demonstrated in 4. Some patients developed rheumatic conditions; others developed chronic disease of liver, kidneys, heart, pancreas, thyroid or nervous system. Chronic liver disease, in 22 patients, was correlated with positive tests for antinuclear antibody and rheumatoid factor; and might influence development of malignant disease, and mortality. A variety of acute and chronic clinical pictures may be associated with Y. enterocolitica infection, and further clinical research is required in this field.     

Survival and causes of death among patients with Yersinia enterocolitica infection. A Norwegian 10-year follow-up study on 458 hospitalized patients.

The aim of the present study was to elucidate the possible influence of the Yersinia enterocolitica infection on long-time survival, and to describe clinical conditions associated with a fatal issue. During the period 1974-83, Y. enterocolitica infection was diagnosed in 458 hospitalized patients by antibody response or isolation of the microorganism. The patients were followed for 4-14 years (until 1987). The observed cumulative survival rates for female patients, and for the whole material, deviated significantly from the expected rates for 10 and 8 years. Two patients died in association with the acute infection, and 2 died from malignant mesothelioma during the first year of observation. 4/42 other patients died during the follow-up period from chronic multiorgan disease, 9 from malignant disease, and 2 died from hematological disorders. A very high mortality (10/22) was observed among patients who had developed chronic liver disease subsequently to the infection. We conclude that chronic conditions associated with the Y. enterocolitica infection may exert a substantial impact on long-time survival.     

Acute and chronic liver disease associated with Yersinia enterocolitica infection: a Norwegian 10-year follow-up study of 458 hospitalized patients.

During the period 1974-1983, Yersinia enterocolitica infection was diagnosed in 458 hospitalized patients by antibody response or isolation of the micro-organism. A total of 54 (11.9%) patients had acute liver infection, with significantly elevated serum levels (greater than or equal to 2-fold) of bilirubin and/or enzyme levels. Serious liver disease with cellular necrosis was observed in biopsy specimens from two of 12 patients examined; six had unspecific changes. The patients were followed up for 4-14 years (until 1987). A total of 22 (4.9%) patients were readmitted with chronic liver disease; in one case non-specific microscopic changes developed into granulomatous hepatitis over a period of 3 years. In both the acute and chronic stages of disease, liver involvement was associated with involvement of other organ systems, and some patients developed multi-organ disease. Chronic liver disease was associated with positive tests for antinuclear antibody and rheumatoid factor, and with a high mortality.     

Acute and chronic pancreatic disease associated with Yersinia enterocolitica infection: a Norwegian 10-year follow-up study of 458 hospitalized patients.

During the period 1974-1983, Yersinia enterocolitica infection was diagnosed in 458 hospitalized patients by antibody response or isolation of the micro-organism. Eight (1.75%) patients showed signs of acute pancreatitis with elevated serum or urine levels of amylase; two patients had acute insulin-dependent diabetes. The patients were followed up for 4-14 years (until 1987). Four patients were readmitted with chronic pancreatitis, and one with acute pancreatitis. Diabetes developed in two males and nine females; in seven cases this was associated with chronic conditions of possible autoimmune aetiology. In 1987 a significantly higher than expected prevalence of diabetes was demonstrated among female subjects aged 30-54 years. Yersinia enterocolitica infection constitutes a differential diagnosis in acute pancreatitis, and might be related to the development of chronic pancreatitis and diabetes.     

Collagenous duodeno-ileo-colitis with transient IgG deficiency preceded by Yersinia enterocolitica intestinal infection: case report and review of literature

A case-report of a man with chronic diarrhoea is presented. After an unsuccessful treatment of an intestinal yersioniosis, the diagnosis of collagenous intestinal disease affecting duodenum, ileum and colon was made. In addition, a IgG transient deficiency was observed. The literature about gastrointestinal involvement, concomintant infection by Yersinia and IgG deficiency in collagenous colitis is reviewed.     

Yersinia enterocolitica O:3 infection of a prosthetic knee joint related to recurrent hemarthrosis

Yersinia enterocolitica was isolated in joint fluid containing blood extracted from the knee of an 80-y-old woman with a 10-y history of total knee arthroplasty. Recurrent hemarthrosis had previously occurred in this knee. It appeared that the effusion of blood led to the deposition of iron on the joint, which may have contributed to the development of infection.     

Yersinia enterocolitica invasin: a primary role in the initiation of infection.

The ability to invade the intestinal epithelium of mammals is an essential virulence determinant of Yersinia enterocolitica. The chromosomally encoded Y. enterocolitica 8081v invasion gene, inv, was disrupted to assess its role in pathogenesis. The inv mutant (JP273v) was approximately 80-fold less invasive than wild type for cultured epithelial cells. When mice were infected intragastrically, up to 10(7) fewer JP273v were recovered from Peyer's patches early (6-18 hr) after infection compared with wild type. Analysis of the course of infection revealed that the inv mutant had distinct differences relative to wild type in the distribution of visible infectious foci and in tissue colonization; however, the mutant and wild-type strains had similar LD50 values for both orally and intraperitoneally infected mice. The invasion defect of the inv mutant was fully complemented in vitro and in vivo by introduction of the wild-type inv gene in trans. The inv gene product, invasin, appears to play a vital role in promoting entry during the initial stage of infection. During the subsequent establishment of a systemic infection, invasin may be of secondary importance, since the Y. enterocolitica inv mutant was as proficient as wild type at causing a fatal infection in mice. Based on these data, we discuss the role of invasin in a naturally occurring Y. enterocolitica infection.     

Yersinia enterocolitica O:3: an emerging cause of pediatric gastroenteritis in the United States. The Yersinia enterocolitica Collaborative Study Group

After an outbreak of Yersinia enterocolitica infections among black children in Atlanta, a seven-hospital study was conducted to determine the importance of this pathogen in other communities with large black populations. Of 4841 stool specimens from patients with gastroenteritis examined between November 1989 and January 1990, Y. enterocolitica, Shigella, Campylobacter, and Salmonella were identified in 38, 49, 60, and 98 specimens, respectively; 34 (92%) of 37 Y. enterocolitica isolates were serotype O:3. Of the 38 patients with yersiniosis, 37 (97%) were children. Illnesses were clustered around the holidays, and 20 (62%) of 32 patients had been exposed to raw pork intestines in the 2 weeks before onset. Exposure was significantly associated with illness in a case-control study of eight patients identified at one hospital (P = .004). Infants less than or equal to 6 months old with yersiniosis were more likely to have immature-to-total neutrophil ratios greater than 0.50 than were infants of comparable age with salmonellosis (P = .02). Infrequently isolated in the past, Y. enterocolitica O:3 is emerging as an important enteric pathogen in this country, particularly among black children.     

蟑螂携带小肠结肠炎耶氏菌的调查研究

<正> 蟑螂能携带多种病原体和寄生虫卵,传播许多疾病,危害严重。前文报道,人工感染试验证明小肠结肠炎耶氏菌(简称耶氏菌),在它的体内至少可保存30天。但自然界的蟑螂有否携带耶氏菌尚未见有国内外文献报道。我们于今年4～5月间在建瓯县捕捉蟑螂进行调查,现将结果报告如下。     

Too early to dismiss Yersinia enterocolitica infection in the aetiology of Graves' disease: evidence from a twin case-control study

Background Yersinia enterocolitica (YE) infection has long been implicated in the pathogenesis of Graves’ disease (GD). The association between YE and GD could, however, also be due to common genetic or environmental factors affecting the development of both YE infection and GD. This potential confounding can be minimized by investigation of twin pairs discordant for GD. Aim To examine whether YE infection is associated with GD. Design We first conducted a classical case–control study of individuals with (61) and without (122) GD, and then a case–control study of twin pairs (36) discordant for GD. Methods Immunoglobulin (Ig)A and IgG antibodies to virulence‐associated Yersinia outer membrane proteins (YOPs) were measured. Main outcome measures The prevalence of YOP IgA and IgG antibodies. Results Subjects with GD had a higher prevalence of YOP IgA (49%vs. 34%, P = 0·054) and YPO IgG (51%vs. 35%, P = 0·043) than the external controls. The frequency of chronic YE infection, reflected by the presence of both IgA and IgG YOP antibodies, was also higher among cases than controls (49%vs. 33%, P = 0·042). Similar results were found in twin pairs discordant for GD. In the case–control analysis, individuals with GD had an increased odds ratio (OR) of YE infection: IgA 1·84 (95% CI 0·99–3·45) and IgG 1·90 (95% CI 1·02–3·55). In the co‐twin analysis, the twin with GD also had an increased OR of YE infection: IgA 5·5 (95% CI 1·21–24·81) and IgG 5·0 (95% CI 1·10–22·81). Conclusion The finding of an association between GD and YE in the case–control study and within twin pairs discordant for GD supports the notion that YE infection plays an aetiological role in the occurrence of GD, or vice versa. Future studies should examine the temporal relationship of this association in more depth.     

Effects of Yersinia enterocolitica infection on rabbit intestinal and colonic goblet cells and mucin: morphometrics, histochemistry, and biochemistry.

The effects of Yersinia enterocolitica on intestinal goblet cells were investigated in New Zealand white rabbits. Animals infected with Y enterocolitica were compared with weight matched and pair fed controls. Goblet cell hyperplasia developed in the distal small intestine of infected rabbits on day 1, in the mid small intestine on day 3, and in the upper small intestine on day 6. In all regions hyperplasia persisted throughout the 14 day study. The degree of hyperplasia was greater in the distal small intestine than the upper and mid regions. Goblet cells in the proximal colon of infected animals seemed to respond as those in the distal small intestine. Thus goblet cell hyperplasia developed more rapidly and to a greater extent in the ileocaecal region where mucosal injury was most severe. These changes resulted directly from Y enterocolitica infection since goblet cell numbers did not increase in pair fed controls. Histochemically, goblet cell mucins from infected rabbits were unchanged at either six or 14 days. Biochemical analysis, however, established that purified mucins from animals on day 6 after infection were less sialylated (in the small intestine) and more sulphated (in the small intestine and proximal colon). In addition, mucins from the distal small intestine and the proximal colon seemed to contain fewer but longer oligosaccharide chains.     

Bacterial resistance to complement killing mediated by the Ail protein of Yersinia enterocolitica.

Ail is a 17-kDa outer membrane Yersinia protein that mediates bacterial attachment to, and invasion of, cultured epithelial cells. We report here an alternative role for Ail in the pathogenesis of Yersinia infection. We found that Escherichia coli HB101 harboring the 4-kilobase recombinant ail clone pVM102 were highly resistant to killing in up to 50% normal human serum. A 674-base-pair fragment of DNA from pVM102, which encodes the ail gene, was inserted into pUC18 and shown to promote full resistance to complement killing in E. coli HB101. Cellular attachment and resistance to complement killing in a plasmid-cured inv- strain of Yersinia enterocolitica (0:8) was correlated with the thermoinduced expression of Ail at 37 degrees C. Insertional inactivation of ail in Y. enterocolitica resulted in loss of both thermoinduced bacterial properties. Cellular attachment and serum resistance were restored by complementation of the defect by plasmid-encoded ail. Complementation of cell attachment activity required bacterial growth at 37 degrees C, indicating that an additional thermoinduced factor is required for this Ail function. In addition, these studies reveal that functional homology exists between Ail and the structurally related protein Rck, which promotes resistance to complement killing in Salmonella typhimurium.     

The 19 kDa protein of Yersinia enterocolitica O:3 is recognized on the cellular and humoral level by patients with Yersinia induced reactive arthritis.

OBJECTIVE: Gastrointestinal infections with Yersinia enterocolitica O:3 (YE O:3) can trigger reactive arthritis (ReA). The cellular immune response seems to be of pathogenic importance in ReA, since synovial fluid mononuclear cells (SFMC) of patients with ReA have been shown to recognize YE O:3 antigens. One of these, a 19 kDa protein identified as the beta-urease subunit of YE, has been identified as a target of SFMC. We investigated the humoral immune response to this antigen. METHODS: Sera of 32 patients with SFMC proliferation to YE O:3 diagnosed as having ReA (n = 16) and undifferentiated oligoarthritis (UOA, n = 16), and of patients with other rheumatic diseases (n = 32) and healthy persons (n = 12) were investigated for the humoral response to the biochemically purified 19 kDa protein of YE. Anti-19 kDa antibodies (ab) were identified by immunoblotting; ab to the Yersinia outer membrane protein (YOP) antigen were detected by ELISA. Proliferation of SFMC to 19 kDa and other YE O:3 antigens was tested in 12 patients in parallel. RESULTS: SFMC of all 32 patients with ReA and UOA showed the highest proliferation to YE O:3 (13.7+/-7.5), and 10/12 of these patients had the highest stimulation index to the 19 kDa (14.9+/-6.4). Anti-19 kDa IgG ab were detected in 93% and 55% and anti-19 kDa IgA ab in 56% and 36% of the ReA and UOA patients, respectively, compared to 26% (p = 0.002) and 8% (p = 0.001) in controls. IgG ab to the 19 kDa were sensitive (93%) and IgA ab specific (92%) to detect patients with a synovial cellular response to YE. IgG ab to YOP were found in 62% and IgA ab in 46% of the ReA patients and in 32% (p = 0.002) and 13% (p = 0.004) of the controls. CONCLUSION: This study provides evidence of a cellular and a significant humoral immune response to the 19 kDa protein in Yersinia triggered arthritis. Detection of IgG antibodies to the 19 kDa correlates with a synovial cellular immune response in YE induced arthritis. These antibodies can be used as a screening system for research and possibly also for clinical purposes, since absence of such antibodies seems to negatively predict YE O:3 directed immune reactivity.     

Undernournishment and Yersinia enterocolitica enterocolitis alter intestinal contractility in the rabbit: role of smooth muscle contractile protein content.

Previous studies have demonstrated that the longitudinal smooth muscle of rabbits infected with Yersinia enterocolitica and undernourished because of reduced food intake exhibit a significantly reduced ability to develop tension in response to carbachol compared with pair-fed animals, which are uninfected but equivalently undernourished. To determine whether the alteration in smooth muscle contractility results from changes in cell number (hypo- or hyperplasia), or in contractile protein content or isoform distribution, New Zealand White rabbits (600 to 1000 g) were randomly assigned to one of three treatment groups: infected, pair-fed or control. Tissue contractility was measured, morphometric studies were performed and immunoassays were developed for the measurement of total actin, gamma-enteric and alpha-vascular isoactins, and myosin heavy chain. Consistent with what was found in previous reports, the contractility of longitudinal smooth muscle in response to carbachol was found to increase in pair-fed animals and to decrease in Y enterocolitica-infected animals. There was no significant change in the proportional thickness of the ileal longitudinal smooth muscle coat, and the number of cross-sectioned longitudinal smooth muscle cells/mm2 was not significantly different in infected, pair-fed or control tissues. Immunoassay indicated that the proportion of each specific contractile protein, relative to total protein content in the muscularis propria, was unaffected by Y enterocolitica infection or by pair-feeding. Thus, the alterations in intestinal longitudinal smooth muscle function observed after Y enterocolitica infection were concluded not to be associated with tissue hypo- or hyperplasia, or changes in the total content or isoform distribution of contractile proteins in the muscularis propria.     

Protection against infection with Vibrio cholerae by passive transfer of monoclonal antibodies to outer membrane antigens

Ten monoclonal antibodies (MAbs), produced by hybridomas obtained through the cell fusion of mouse myeloma cells and spleen cells from mice immunized with outer membrane antigens of Vibrio cholerae, were mixed with suspensions of V. cholerae and administered orally to infant rabbits. Six of these MAbs, each one recognizing a different outer membrane antigen, did not confer protection from fatal V. cholerae infection. Four MAbs that reacted with the 18-kDa antigen, also called the cholera protective antigen, were highly protective against infection with V. cholerae.     

Analysis of circulating immune complexes (CICs) in childhood tuberculosis: levels of specific antibodies to glycolipid antigens and relationship with serum antibodies.

BACKGROUND: The presence of specific antiglycolipid antibodies in serum and circulating immune complexes (CIC) in children with tuberculosis was detected in order to evaluate their contribution to the value of serodiagnosis of tuberculosis, as has already been shown in adults. METHODS: ELISAs using the three glycolipids LOS, DAT and PGLTb1 were performed in whole serum and immune complexes from 20 children with tuberculous disease or infection, in seven child contacts, and in 26 children with non-tuberculous disease. The contribution of complexed IgG antibody to the diagnostic values was established for each group. RESULTS: The antibody levels in free serum were higher (P < 0.01) in children with tuberculous disease or infection and in contacts than in controls. By contrast, except for PGLTb1, the IgG antibody levels were higher (P < 0.02) in children with tuberculous disease than in the other groups. The highest contribution of IgG antibody against LOS to the predictive values was shown in children with pulmonary tuberculosis (positive predictive value 1,000, negative predictive value 1,000). In paucibacillary tuberculosis (extra-pulmonary and tuberculous infection) and in contacts, the IgG antibody did not contribute to the sensitivity of the serodiagnosis, where the combination of antigens tested in serum increased the diagnostic yield. The very low levels of IgG antibody in these settings may indicate a different B cell response. CONCLUSION: The detection of immune complexes and IgG antibodies against the three glycolipid antigens is useful as a complementary technique for the serodiagnosis of children with a high probability of pulmonary tuberculosis.     

Immunoblot analysis of IgM, IgG, and IgA responses to plasmid encoded released proteins of Yersinia enterocolitica in patients with or without yersinia triggered reactive arthritis.

The IgM, IgG, and IgA antibody responses of patients with Yersinia enterocolitica O:3 infection were studied by immunoblotting with plasmid encoded released proteins of Y enterocolitica as the antigens. The results indicate that antibodies of all three classes are most consistently directed against the proteins of molecular weights 25,000 and 36,000. Less than two months after the onset of infection 18 of the 19 patients with yersinia triggered reactive arthritis had IgA class antibodies against the released protein of mol. wt 36,000, whereas only eight of the 17 patients with non-arthritic yersiniosis had these antibodies. The same difference between the arthritic and non-arthritic patients was observed also 8-12 months after the onset of infection.     

New monoclonal antibodies specific to HLA class I and their application in the study of acid treatment effect on cell surface antigens.

New monoclonal antibodies (mAbs) against HLA class I antigens were prepared and characterized. Three mAbs (CLI-1, CLI-2, CLI-3) were directed to the heavy chain of HLA class I molecules and one mAb (B2M-1) is specific to beta 2-microglobulin. Using these mAbs, it was confirmed that acid treatment selectively eliminated cell surface HLA class I antigenicity. The treatment with citric acid solution resulted in preparation of cells with lower residual HLA class I surface molecules than was seen after the treatment with glycine buffer.