Effects of Lactobacillus rhamnosus ATCC 7469 on Different Parameters Related to Health Status of Rainbow Trout (Oncorhynchus mykiss) and the Protection Against Yersinia ruckeri.

In the current study, we investigated the effect of a probiotic bacterium (Lactobacillus rhamnosus ATCC 7469) microencapsulated with alginate and hi-maize starch and coated with chitosan on improving growth factors, body composition, blood chemistry, and the immune response of rainbow trout (initial weight: 18.41 ± 0.32 g). Four experimental diets were formulated to feed fish for 60 days. They were control diet without any additive (C), diet added with beads without probiotic (E), a probiotic sprayed to the diet (L.r), and encapsulated probiotic supplemented diet (E-L.r). The results indicated that feeding with E-Lr significantly improved weight gain (84.98 g) and feed conversion ratio (0.95) compared to the other groups (P < 0.05). Also, fish fed E-Lr diet had a significantly higher value of whole-body protein (17.51%), total protein in the blood (4.98 g/dL), lysozyme (30.66 U/mL), alternative complement pathway hemolytic activity (134 U/mL), superoxide dismutase (203 U/mg protein), and catalase (528.33 U/mg protein) (P < 0.05) as compared to those fed the control diet. Similarly, a higher relative expression of immune-related genes such as interleukin-1 (Il-1) and tumor necrosis factor-alpha (TNF-1α) were reported in those fed E-L.r and L.r diets respectively. Interestingly, the fish fed dietary E-L.r had a significantly lower value of lipid in the whole body (4.82%) and cholesterol in the blood (160.67%) in comparison with those fed the control diet (P < 0.05). At the end of the experiment, all groups were challenged by Yersinia ruckeri where the survival rate of rainbow trout fed dietary E-L.r (70.36%) was statistically higher than that of the others (P < 0.05). Overall, the results suggested that encapsulated probiotic Lact. rhamnosus ATCC 7469 acted better than unencapsulated probiotic and has a potential to improve growth performance, flesh quality, and the immune response of rainbow trout.

Yersiniosis in Poland in 2014

OBJECTIVE: The aim of the study is to present the epidemiological situation of yersiniosis in Poland in 2014 and compare it with the situation in the previous years. MATERIAL AND METHODS: The evaluation was based on analysis of data from the annual bulletins "Infectious diseases and poisoning in Poland" for the period 2009-2014 (MP Czarkowski et al., National Institute of Hygiene and GIS ­ Chief Sanitary Inspectorate), interviews of individual yersiniosis cases, sent by the sanitary-epidemiological stations from the whole country and the data on deaths from the Department of Demographic Studies of the Central Statistical Office. RESULTS: In 2014 in Poland 244 cases of yersiniosis were recorded (0.63/100 000). Among them 241 infections were caused by Y. enterocolitica and 3 by Y. pseudotuberculosis. There were 215 cases of intestinal yersiniosis and 29 of extraintestinal. Hospitalization required 59.8% of patients. There were no deaths reported which cause was infection with Yersinia. Intestinal yersiniosis was manifested the mostly by symptoms as follow: diarrhea (88%, including 8% with blood in stool), fever (66%), abdominal pain (49%) and vomiting (22%). The most of the cases (131 - approx. 61%) of intestinal yersiniosis occurred among children in the age group 0-4 years . Number of extra intestinal Yersinia infections (20 cases) was higher than in 2013. The most frequent symptom of those cases was osteoarticular pain, which was observed in 79% of patients. As in 2013 most cases of intestinal yersiniosis were reported from the Mazowieckie voivodeship (104 cases). Serological type of Yersinia was determined only in 58 (24%) cases. This percentage was the lowest since the start of registration of yersiniosis in the country in the year 2006. The identified serotypes were O3 (88%) O8 (6.9%) and O9 (5.2%). In 2014, 4 cases of infection with "American" serotype O8 were identify. One family outbreak caused by Yersinia spp occurred in 2014. CONCLUSIONS: A significant decrease of serologically identified cases of yersinia observed in 2014. could be explained by the test for Yersinia not being reimbursed by routine health care insurance. Reporting cases of extraintestinal yersiniosis from only few voivodeships suggests that the real number of infections remains underreported. In 2014 significantly higher number of cases of Yersinia infection occurred during the second and third quarter of the year. Seasonality of yersiniosis in 2014 differs from seasonality in 2013. However, it was similar to the seasonality observed in previous years (2009-2012).

Needlestick and occupational exposure to infections: a compendium of current guidelines.

Needlestick and occupational exposure to infections is a constant threat in dental practice. Many blood-borne infections, including human immunodeficiency virus (HIV) infection, hepatitis B and hepatitis C, may be contracted through this route. We provide here a useful compendium for dental practitioners on current guidelines available to obviate such threats, as well as a simple flowchart on prophylactic measures that could be taken after an accidental exposure.

Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis.

Dendritic cells (DCs) as professional antigen-presenting cells play an important role in the initiation and modulation of the adaptive immune response. However, their role in the innate immune response against bacterial infections is not completely defined. Here we have analyzed the role of DCs and their impact on the innate anti-bacterial host defense in an experimental infection model of Yersinia enterocolitica (Ye). We used CD11c-diphtheria toxin (DT) mice to deplete DCs prior to severe infection with Ye. DC depletion significantly increased animal survival after Ye infection. The bacterial load in the spleen of DC-depleted mice was significantly lower than that of control mice throughout the infection. DC depletion was accompanied by an increase in the serum levels of CXCL1, G-CSF, IL-1α, and CCL2 and an increase in the numbers of splenic phagocytes. Functionally, splenocytes from DC-depleted mice exhibited an increased bacterial killing capacity compared to splenocytes from control mice. Cellular studies further showed that this was due to an increased production of reactive oxygen species (ROS) by neutrophils. Adoptive transfer of neutrophils from DC-depleted mice into control mice prior to Ye infection reduced the bacterial load to the level of Ye-infected DC-depleted mice, suggesting that the increased number of phagocytes with additional ROS production account for the decreased bacterial load. Furthermore, after incubation with serum from DC-depleted mice splenocytes from control mice increased their bacterial killing capacity, most likely due to enhanced ROS production by neutrophils, indicating that serum factors from DC-depleted mice account for this effect. In summary, we could show that DC depletion triggers phagocyte accumulation in the spleen and enhances their anti-bacterial killing capacity upon bacterial infection.

Protective roles for fibrin, tissue factor, plasminogen activator inhibitor-1, and thrombin activatable fibrinolysis inhibitor, but not factor XI, during defense against the gram-negative bacterium Yersinia enterocolitica.

Septic infections dysregulate hemostatic pathways, prompting coagulopathy. Nevertheless, anticoagulant therapies typically fail to protect humans from septic pathology. The data reported in this work may help to explain this discrepancy by demonstrating critical protective roles for coagulation leading to fibrin deposition during host defense against the Gram-negative bacterium Yersinia enterocolitica. After i.p. inoculation with Y. enterocolitica, fibrinogen-deficient mice display impaired cytokine and chemokine production in the peritoneal cavity and suppressed neutrophil recruitment. Moreover, both gene-targeted fibrinogen-deficient mice and wild-type mice treated with the anticoagulant coumadin display increased hepatic bacterial burden and mortality following either i.p. or i.v. inoculation with Y. enterocolitica. Mice with low tissue factor activity succumb to yersiniosis with a phenotype similar to fibrin(ogen)-deficient mice, whereas factor XI-deficient mice show wild-type levels of resistance. Mice deficient in plasminogen activator inhibitor-1 or thrombin-activatable fibrinolysis inhibitor display modest phenotypes, but mice deficient in both plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor succumb to yersiniosis with a phenotype resembling fibrin(ogen)-deficient mice. These findings demonstrate critical protective roles for the tissue factor-dependent extrinsic coagulation pathway during host defense against bacteria and caution that therapeutics targeting major thrombin-generating or antifibrinolytic pathways may disrupt fibrin-mediated host defense during Gram-negative sepsis.

[Chronic Yersinia infections as a therapeutic problem].

Physicians of any specialty encounter the chronic course of yersiniasis, the clinical manifestations of which are polymorphic and similar to the symptoms of other diseases, including autoimmune ones. The long interval of an evolving pathological condition after the acute period of the disease leads to the fact that the clinical and laboratory manifestations of chronic yersiniasis are wrongly regarded as an independent nosological entities unassociated with the persistence of Yersinia. Dynamic blood tests for specific IgA to the Yersinia enterocolitica virulence factors that are an indirect sign of on-going pathogen persistence in the body are required to elaborate the tactics for the examination, treatment, and follow-up of patients.

Spondylodiscitis of the lumbar spine in a non-immunocompromised host caused by Yersinia enterocolitica O:9.

Here presented is an extremely rare case of a spinal osteomyelitis (L5-S1) with epidural empyema in a non-immunocompromised 62-year-old man caused by Yersinia enterocolitica O:9. The infection occurred acutely and required immediate surgical treatment. Y. enterocolitica was cultured from the empyema fluid, wound swabs of the intervertebral disc L5-S1 and stool cultures. Following the surgical decompression and antibiotic treatment, the patient recovered completely, without neurological deficits. A review of the literature revealed only sparse cases of spondylodiscitis due to other Y. enterocolitica serogroups. To our knowledge, we report here the first case of a spondylodiscitis of the lumbar spine caused by Y. enterocolitica serovar O:9 in a non-immunocompromised patient.

Importância de Yersinia enterocolitica em microbilogia médica / Importance of Yersinia enterocolitica in medical microbiology

Y.enterocolitica é um enteropatógeno invasivo de humanos que provoca uma série de sintomas clínicos intestinais e extra-intestinais que variam desde uma gastrenterite branda a uma linfadenite mesentérica que mimetiza apendicite e em casos raros pode evoluir para uma septicemia.A infecção causada por Y.enterocolitica pode levar a seqüelas imunológicas, incluindo artrite, eritema nodoso e glomerulonefrite.Amostras patogênicas de Y.enterocolitica são associadas a determinados sorogrupos e biotipos e a uma variedade de características fenotípicas relacionadas a virulência.Estudos de genética molecular demonstraram a importância do plasmídio pYV que codifica vários genes de virulência, bem como a importância de vários genes de virulência cromossomais na patogênese dessa bactéria.As infecções intestinais causadas por Y.enterocolitica são normalmente auto-limitadas não havendo usualmente a necessidade de antibioticoterapia.A ocorrência de infecções por Y.enterocolitica no Brasil não é tão freqüente como em países europeus, Japão e Estados Unidos.Essa revisão enfoca as características gerais, a patogênese, os sintomas clínicos, mecanismos de virulência, tratamento e susceptibilidade a antibióticos de amostras de Y.enterocolitica isoladas no Brasil e ao redor do mundo.

A palpable right lower abdominal mass due to Yersinia mesenteric lymphadenitis.

Infection by Yersinia pseudotuberculosis has become of increasing pathological importance. This report describes the case of a 12-year-old female with mesenteric lymphadenitis due to Yersinia pseudotuberculosis. The patient presented with fever, abdominal pain, and a palpable right abdominal mass. Abdominal ultrasonic imaging and computerized axial tomography (CT) revealed a mass. An exploratory laparotomy was performed, followed by appendectomy and mesenteric lymph node biopsy. The diagnosis of Yersinia infection was confirmed by serology and bacterial culture of the biopsy material. This condition should be considered in patients with a right lower abdominal mass and symptoms similar to those of appendicitis.

Spontaneous pleural empyema due to Yersinia enterocolitica.

Yersinia enterocolitica is a well-known cause of enterocolitis. Although focal extraintestinal manifestations and disseminated disease have been described, usually in immunosuppressed patients, infection in the chest seems to be rare. We report the case of an alcoholic man who had spontaneous pleural empyema due to Y. enterocolitica.

Yersinia enterocolitica: overview and epidemiologic correlates.

Yersinia enterocolitica comprises both pathogenic and nonpathogenic members. Distinguished by biogrouping, serogrouping, and ecological distribution, commonly occurring pathogenic serobiogroups, e.g., O:3/4; O:5,27/2; O:8/1b; O:9/2, possess both chromosomal and plasmid-mediated virulence traits. Studies have revealed several (oral, blood transfusion) modes of acquisition, elucidated the putative role of chromosomal and plasmid-encoded virulence factors in the pathogenesis of human infection, and have identified major animal reservoirs, e.g., the pig. Diagnosis has been refined though use of selective media, monoclonal antibodies directed against outer membrane proteins, and of purified yersiniae outer membrane proteins for antibody detection. Epidemiological investigations of foodborne outbreaks have been advanced through the use of molecular biology techniques such as ribotyping and pulsed-field gel electrophoresis.

[Development of studies on problem of infectious arthritis at the Institute of RHeumatology, Russian Academy of Medical Sciences in 1970 to 1990]. / Razvitie issledovanii po probleme sviazannykh s infektsiiami artritov v Institute Revmatologii RAMN v 70-90-kh godakh.

The paper presents information on the studies on the elucidation of the etiopathogenetic role of Chlamydia and Yersinia infections in reactive arthritis, which have been made at the Institute in the past decades. Among them it mentions the first experiments and subsequent findings of detection of both Chlamydia and DNA in joint tissues in urogenic arthritis, those of identification of altered minor forms of this microbe in chronic types, which mimic in vitro persistent Chlamydia infection. The clinical experience gained by the Institute in treating Chlamydia-induced urogenic arthritis with high-dose antibiotics is reported. In addition to detailed studies of the clinical manifestations and outcomes of Yersinia-induced arthritis, long-term follow-ups have examined an association of clinical and serological manifestations with HLA B27 carriage; it is suggested that there is a partial similarity between this antigen and Yersinia antigens. Pronounced changes have been found in the mucosa of the intestine and its microflora in enterogenous reactive arthritis and a treatment with bifidum-containing drugs proposed. A variety of clinical and serological manifestations of Lyme borreliasis detected in the endemic areas of Russia is described. The specific features of rheumatological manifestations of this disease are comparable with those observed in the USA and Europe.

Tumor necrosis factor-alpha expression induced by anti-YopB antibodies coincides with protection against Yersinia enterocolitica infection in mice.

Previous studies have suggested that virulence of pathogenic Yersiniae is associated with a suppression of the local cytokine response. In this context, the plasmid-encoded 41-kDa Yersinia outer protein B (YopB) has been implicated with the lack of tumor necrosis factor-alpha (TNF-alpha) expression in Peyer's patches (PP), following oral infection of mice with the enteropathogenic Yersinia enterocolitica. The present study was performed to further evaluate the relationships between YopB-induced suppression of TNF-alpha and bacterial survival in host tissue. Results are presented to show the ability of purified YopB to suppress the release of TNF-alpha by macrophages, the effect of which was neutralized by monospecific anti-YopB antiserum. In mice orally infected with Y. enterocolitica, anti-YopB treatment on days 3 and 5 postinfection, significantly decreased the recovery of live bacteria from PP. This observation correlated with a strong increase in TNF-alpha expression, as determined by reverse transcription-polymerase chain reaction and measuring the levels of TNF activity in homogenates of PP. Moreover, treatment of mice with a combination of anti-YopB and anti-TNF-alpha antiserum, completely abrogated the beneficial effect of the anti-YopB antiserum. In controls, expression of other proinflammatory cytokines such as interleukin-1 remained unaffected by either treatment. Therefore, the results indicate that endogenous TNF-alpha is required for eradication of Y. enterocolitica from host tissue, and further imply that YopB significantly contributes to suppression of the local TNF-alpha response in PP.

Treatment of arthritis in Lewis rats by a monoclonal antibody against alpha beta T cell receptor: differential sensitivity of Yersinia-induced arthritis versus adjuvant arthritis.

Lewis rats experimentally infected with Yersinia enterocolitica develop sterile arthritis similar to Yersinia-associated reactive arthritis in humans. To investigate the putative role of alpha beta T cells in the pathogenesis of Yersinia-induced arthritis (YIA) rats were treated with the monoclonal antibody (mAb) R73 mAb directed against the rat alpha beta T cell receptor. In spite of reduction of alpha beta T cells in peripheral blood and in liver lesions of Yersinia-infected rats this serotherapy had no suppressive effect on YIA. Moreover, R73 mAb treatment had no influence on the number of alpha beta T cells in the inflammed synovial tissue. In contrast, R73 mAb serotherapy in Mycobaterium tuberculosis-immunized rats blocked development of adjuvant arthritis (AA) and suppressed the presence of alpha beta T cells in the synovial tissue. These results suggest fundamental differences between the immunopatho-mechanism of YIA caused by bacterial infection and AA induced by bacterial immunization and known to be T cell mediated. These data might have consequences for putative serotherapy of arthritis in humans.