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At least 19 recordsLinked to original sources
PubMed1989

Mechanisms involved in the pathogenesis of Yersinia infections.

Yersinia enterocolitica and Yersinia pseudotuberculosis are food-borne enterobacterial pathogens which may initiate rheumatoid diseases. By molecular genetic analysis of the pathogenicity of these species virulence gene loci could be identified on the chromosome and on a plasmid. Plasmid-encoded proteins mediate cell adherence, phagocytosis resistance, survival in serum, cytotoxicity, and collagen binding. Y. enterocolitica of serotype 0:8 is mouse-lethal and arthritogenic for Lewis rats. Mouse lethality is closely associated with the expression of a chromosome-encoded high-affinity iron transport system which enables the pathogen to acquire iron for growth in iron-deficient environments. The antibody response to virulence-associated antigens of arthritis-susceptible Lewis rats differed from that of arthritis-resistant Fisher rats: Lewis rats respond strongly to the collagen-binding protein Yop1 and weakly to the iron-transport receptor protein FyuA, whereas the reverse is found with Fisher rats. This specific antibody response of Lewis rats is suggested to be important for induction of arthritis.

Animals↗
PubMed2000

Yersinia enterocolitica invasin protein triggers differential production of interleukin-1, interleukin-8, monocyte chemoattractant protein 1, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha in epithelial cells: implications for understanding the early cytokine network in Yersinia infections.

Yersinia enterocolitica infection of epithelial cells results in interleukin-8 (IL-8) mRNA expression. Herein we demonstrate that besides IL-8, increased mRNA levels of five other cytokines, IL-1alpha, IL-1beta, monocyte chemoattractant protein 1 (MCP-1), granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor alpha (TNF-alpha), can be detected upon infection of HeLa cells with Yersinia. Yersinia-triggered cytokine production was not affected by blocking phosphatidylinositol-3-phosphate kinase with wortmannin, which inhibited bacterial invasion. Comparable cytokine mRNA responses were triggered by Escherichia coli expressing Yersinia inv, while no response was triggered by an inv-deficient Yersinia mutant. Moreover, cytokine responses were independent from metabolic activity of the bacteria, as killed bacterial cells were sufficient for triggering cytokine responses in HeLa cells. Semiquantitative reverse transcription-PCR analysis was used to assess the kinetics of cytokine mRNA expression in infected HeLa cells. IL-8, IL-1alpha, IL-1beta, MCP-1, GM-CSF, and TNF-alpha mRNA expression increased within 1 h postinfection, reached a maximum after 3 to 4 h, and then declined to preinfection levels within 3 h. IL-8, MCP-1, and GM-CSF were secreted by HeLa cells, whereas IL-1alpha and IL-1beta were not secreted and thus were found exclusively intracellularly. TNF-alpha protein could not be detected in cell lysates or supernatants. Stimulation of HeLa cells with IL-1alpha was followed by increased IL-8 mRNA expression, whereas stimulation with IL-8 did not induce cytokine production. Likewise, MCP-1 and GM-CSF did not induce significant cytokine responses in HeLa cells. Our results implicate that the initial host response to Yersinia infection might be sustained by IL-8, MCP-1, and GM-CSF produced by epithelial cells.

Adhesins, Bacterial↗
PubMed1981

Glomerulonephritis in infections with Yersinia enterocolitica O-serotype 3. II. The incidence and immunological features of Yersinia infection in a consecutive glomerulonephritis population.

In a consecutive series of 38 patients with acute glomerulonephritis (GN), 17 showed serological or immunological signs of current or previous yersiniosis. None of these 17 patients had raised antistreptolysin-o titres. Only half of these patients had had clinical symptoms of Yersinia infection. Light microscopic examination revealed that 12 of the 17 patients had proliferative and 4 epimembranous GN. In 8 out of 14 biopsy specimens, Yersinia antigen could be demonstrated by immunoglobulins and complement. Immunofluorescence microscopy examination of all biopsy specimens containing sufficient tissue for a valid analysis showed deposits of complement and immunoglobulin G, most specimens also immunoglobulins A and M. It is considered highly likely that Y. ent. O:3 may be, and frequently is, an etiological factor for development of acute GN. It would be advisable not only to investigate all patients with acute GN for streptococcal infections, but also to carry out serological and bacteriological tests for Y. eng. O:3 infection and to institute an active therapeutic approach to acute infections caused by this bacterium.

Acute Disease↗
PubMedDate not supplied

Yersinia infections in patients with homozygous beta-thalassemia associated with iron overload and its treatment.

Patients with homozygous beta-thalassemia are at increased risk of serious infections. Yersinia enterocolitica is an organism with a predilection for these and other iron-overloaded patients. Three young adult patients with beta-thalassemia who were chronically transfused and developed yersiniosis are reported. Iron overload and desferrioxamine use are predisposing factors, as supported by clinical, animal, and in vitro data. Iron excess both immunologically compromises the host and greatly enhances yersinial growth. Desferrioxamine may make host iron even more bioavailable to Yersinia. Recognition of this association and unusual manifestations in these patients such as an appendicitis-like syndrome may direct clinicians to earlier antiyersinial therapy and temporary cessation of chelation.

Adolescent↗
PubMed1999

Clinical and experimental evidence for persistent Yersinia infection in reactive arthritis.

The findings of bacterial antigens in the joint and persistent triggering infection elsewhere in the body are thought to be important in the pathogenesis of reactive arthritis (ReA). We describe a patient with clinical and laboratory features consistent with this. The initial presentation with erythema nodosum and periarthritis due to infection with Yersinia pseudotuberculosis IV was followed 13 months later by recurrent erythema nodosum with joint effusion. At that time, synovial fluid was shown to contain Yersinia antigens, and, surprisingly, Yersinia-specific 16S ribosomal RNA (rRNA) sequences were also identified by reverse transcriptase-polymerase chain reaction and sequencing. Since there was no serologic evidence of reinfection, we postulate that a silent persistent Yersinia infection was reactivated, leading to dissemination of organisms to the joint, with consequent induction of ReA. Although the finding of synovial Yersinia antigens years after the original infection in ReA has previously been reported, the presence of Yersinia 16S rRNA indicates that viable organisms were also able to reach the joint.

Antigens, Bacterial↗
PubMed1986

Urinary tract and renal findings in acute Yersinia infections.

We studied 71 patients with acute Yersinia infection for the occurrence of pathologic urinary and renal findings. Transient proteinuria and/or microhematuria was found in 17 patients (24%) and slightly elevated serum creatinine in seven patients (10%). Renal biopsy was done in two patients and revealed mild mesangial glomerulonephritis in both cases. One of these patients had IgA glomerulonephritis and Reiter's syndrome. Pyuria occurred in 16 patients (23%) and was frequently associated with Reiter's syndrome. Seventy-three patients with acute intrinsic renal failure were studied for the occurrence of acute Yersinia infection by determining Yersinia antibodies by ELISA. One out of 13 patients with acute glomerulonephritis but none of 60 patients with acute tubulointerstitial renal disease had acute Yersinia infection. Acute Yersinia infection seems to be rarely an etiologic factor in acute intrinsic renal failure. Our results indicate that transient proteinuria, microhematuria, pyuria or impaired renal function are frequent findings in patients with acute Yersinia infections. However, glomerulonephritis seems to be a rather infrequent and mild complication of acute Yersinia infection.

Acute Disease↗
PubMed1989

Seronegative arthritis associated with serological evidence of Yersinia infection in Australia.

Infection due to yersinia enterocolitica is a common antecedent illness in patients with reactive arthritis in Scandinavia, but appears to be less frequent in other countries. In order to examine the frequency of yersinia infection in patients with seronegative arthritis in Australia we examined 22 patients, 15 with ankylosing spondylitis (AS) and seven with Reiter's syndrome (RS). A sensitive ELISA assay was used to detect serum antibodies to the most common serotypes. Six patients (29%) had positive yersinia serology, all were HLA B27 and four had a history of diarrhea preceding the onset of their disease. Four patients with positive yersinia serology had AS and two had RS. Antibodies were directed against Y. enterocolitica biotype 0:3 in three cases, Y. enterocolitica 0:9 in two cases and Y. enterocolitica 0:8 in one subject. Twenty-nine control subjects (13 HLA B27) had no serum antibodies to yersinia. The results of this study indicate that preceding yersinia infection occurs in a significant (p less than 0.05; compared to controls) proportion of patients with HLA B27 related seronegative arthropathies.

Adult↗
PubMed1998

Role of YopP in suppression of tumor necrosis factor alpha release by macrophages during Yersinia infection.

The Yersinia plasmid-encoded Yop virulon enables extracellular adhering bacteria to deliver toxic effector proteins inside their target cells. It includes a type III secretion system (Ysc), at least two translocator proteins (YopB, YopD), and a set of intracellular Yop effectors (YopE, YopH, YopO, YopM, and YopP). Infection of macrophages with a wild-type strain leads to low levels of tumor necrosis factor alpha (TNF-alpha) release compared to infection with plasmid-cured strains, suggesting that the virulence plasmid encodes a factor impairing the normal TNF-alpha response of infected macrophages. This effect is correlated with the inhibition of the macrophage mitogen-activated protein kinase (MAPK) activities. To identify the Yop protein responsible for the suppression of TNF-alpha release, we infected J774A.1 and PU5-1.8 macrophages with a battery of knockout Yersinia enterocolitica mutants and we quantified the TNF-alpha released. Mutants affected in secretion (yscN), in translocation (yopB and yopD), or in synthesis of all the known Yop effectors (yopH, yopO, yopP, yopE, and yopM polymutants) were unable to block the TNF-alpha response of the macrophages. In contrast, single yopE, yopH, yopO, and yopM mutants behaved like the wild-type strain. A yopP mutant elicited elevated TNF-alpha release, and complementation of the yopP mutant or the yop effector polymutant strain with yopP alone led to a drop in TNF-alpha release. In addition, YopP was also responsible for the inhibition of the extracellular signal-regulated kinase2 (ERK2) and p38 MAPK activities. These results show that YopP is the Yop effector responsible for the Yersinia-induced suppression of TNF-alpha release by infected macrophages.

Animals↗
PubMed1982

[Liver diseases associated with Yersinia infections (author's transl)].

Yersinia infections are exceptionally responsible for liver damage, the hepatic diseases most commonly encountered being liver abscess consecutive to Y. enterocolitica or Y. pseudo-tuberculosis septicaemia or, more rarely, hepatic granulomata or hepatitis with necrosis and cholestasis. Two new cases are reported. One patient had hepatic granulomata caused by Y. pseudo-tuberculosis and the other, necrotizing hepatitis caused by y. enterocolitica. The course of the disease was favourable in both cases.

Adult↗
PubMedDate not supplied

In vitro lymphoproliferative response to Yersinia: depressed response in arthritic patients years after Yersinia infection.

The persistence of lymphocyte transformation response to Yersinia was studied three to six years after Yersinia infection in subjects who had or had not suffered from reactive arthritis. In persons who had had arthritis, significantly weaker response to Yersinia was found than in those who had recovered without developing arthritis. The same held true also for the response to Klebsiella. These results support and extend our earlier observations of a depressed lymphocyte transformation response to Yersinia during the course of Yersinia arthritis. This phenomenon may be linked to the individual's susceptibility to arthritic complications after Yersinia infection.

Arthritis, Infectious↗
PubMed1980

Reactive arthritis following asymptomatic yersinia infection.

A case of an acute asymmetrical polyarthritis occurring in a teenage boy is described. This was shown by serological tests to be secondary to a recent infection with Yersinia enterocolitica. Reactive arthritis following infection by this organism is well recognised in Scandinavia. Only recently have two cases been reported in the U.K. (1,2). This is the first reported case in Scotland and is unusual in that the initial infection was asymptomatic. Clinical improvement was associated with falling Y. enterocolitica titres and a reduction in the E.S.R. The patient was HLA B27 positive. It is suggested that all patients presenting with an acute asymmetrical polyarthritis predominantly affecting the lower limbs should be screened by stool culture and serology for recent Y. enterocolitica infection.

Adolescent↗
PubMed1982

[Differential diagnosis of enteral Yersinia infection (author's transl)].

Two case reports are given of patients suffering from Yersinia infection; one of these showed symptoms of enteritis, the other one symptoms of appendicitis. Both cases would have been misdiagnosed as Crohn's disease, had there not been the serological prove of Yersinia infection. The disease entity of Yersinia infection and the diagnostic approach are described.

Adult↗
PubMed1987

Yersinia infection and acute abdominal pain.

In 194 patients presenting with acute abdominal pain from whom sequential serum samples were taken, the frequency of yersiniosis, established serologically, was significantly higher (23%) than in 320 control subjects (2%). Yersiniosis occurred in 31% of patients with acute appendicitis. Acute-phase serum samples only, obtained in a further 307 patients, yielded a falsely low frequency of yersiniosis (4%). Y pseudotuberculosis was five times more common than Y enterocolitica, and Y pseudotuberculosis type IV was the most common serotype, accounting for 43% of Yersinia infections. Yersinia may play a more important part in the aetiology of acute abdominal pain, and particularly acute appendicitis, than has been previously appreciated. Antibody titres to both Y enterocolitica and Y pseudotuberculosis frequently rise late in infections causing abdominal pain. Consequently analysis of acute-phase serum samples alone leads to underdiagnosis of yersiniosis.

Abdomen↗
PubMed1990

[Acute appendicitis in patients with Yersinia infection].

The article is the result of the joint work of a surgeon and a specialist in infectious diseases and is based on the results of treatment of 307 patients with the abdominal form of Yersinia infection Acute appendicitis was diagnosed in 73 (23.8%) of them. The abdominal form of Yersinia infection is encountered frequently among children. The authors analyse the clinical picture of acute appendicitis in patients with Yersinia infection, the time between the onset of the disease and the patient's call for the doctor, the dependence of the histologic findings in the examined removed vermiform processes on the duration of the disease, and the results of surgery. The difficulties in making the diagnosis of acute appendicitis in patients with yersinosis and concomitant mesadenitis and terminal ileitis are discussed. It is concluded that laparoscopy is advisable in doubtful clinical signs of acute appendicitis in patients with Yersinia infection due to the high frequency of destructive forms (77.9%). The average duration of in-patient treatment of persons with acute appendicitis and Yersinia infection was 4.8 days. The positive results of treatment are attributed to timely prescription of specific antibacterial therapy--the prescription of chloramphenicol from the moment that the diagnosis of yersinosis was established.

Acute Disease↗
PubMed1996

[Yersinia infections].

The genus Yersinia contains three pathogenic species: Y. pestis, Y. enterocolitica and Y. pseudotuberculosis. All pathogenic strains contain a 70 kb plasmid coding for a number of virulence factors, of which outer membrane proteins including an adhesin are the most important. In 65% of the patients the infection is self-limiting, but in the others a chronic local inflammation develops. Persistence of the infection has been associated with the immune status and the HLA-B27 antigen. Y. enterocolitica leads to abdominal complaints in young children that usually subside spontaneously. The infection is more serious with increasing age, and in people older than 30 years may involve a septicaemic form with multiple abscesses in various organs, or a lymphadenopathic form with generalized lymphadenitis mimicking a haematologic malignancy. Yersinia can be easily isolated during the acute phase by culture; during the chronic and persistent phase it is not cultivable anymore. Then serology should be performed, anti-Yop serology being the most reliable. Yersinia is susceptible to most antibiotics, except penicillins. Local penetration of the antibiotic may be a problem, however. First-choice antibiotics are cotrimoxazole, tetracyclines, chloramphenicol and fluoroquinolones. Systemic extra-mesenteric infections should always be treated with antibiotics.

Arthritis, Infectious↗