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A hepatitis E-vírus (HEV) az egyik leggyakoribb, széklettel terjedő, hepatitist okozó ágens a fejlődő országokban. A fejlett országokban a vírus szórványos emberi megbetegedésekből és házisertésekből való kimutatása azonban felveti a HEV zoonosis útján való terjedését is. Célkitűzés: A hepatitis E-vírus kimutatása emberben, házi- (sertés, szarvasmarha) és vadon élő (vaddisznó, őz) állatokban, és a vírus molekuláris epidemiológiája hazánkban. Módszer: A szerzők a 2001 és 2006 között a szegedi városi kórház infektológiai osztályán ismeretlen eredetű hepatitisben szenvedő betegek szérummintáit HEV ELISA módszerekkel előszűrték, majd a HEV-IgM-pozitív szérummintákat és az állati bélsár-, máj-, valamint bélmintákat RT-PCR módszerekkel vizsgálták. Eredmények: Összesen 116 (9,6%) beteg szérummintája tartalmazott HEV-IgM ellenanyagot. Ötvenhárom HEV-IgM-pozitív szérummintából 13-ban (24,5%) a HEV is kimutatható volt RT-PCR és szekvenálási módszerekkel. A sertésmintákból 42 minta (bélsár: 22,7%, máj: 30,8%), az őzmintákból 11 (máj: 34,4%) és a vaddisznómintákból 9 minta (máj: 12,2%) mutatott RT-PCR-pozitivitást. Egy Indiából importált 1-es genotípusú HEV víruson kívül minden további HEV (12 humán, 19 sertés, 3 őz, 2 vaddisznó) a 3-as genotípusba tartozik. Genetikailag megegyező szekvenciájú HEV-et lehetett kimutatni őzből és egy emberi fertőzésből, továbbá két-két emberi fertőzésből. Megbeszélés: A HEV endémiásan jelen lévő kórokozó. A nyers vagy nem kellően hőkezelt hústermékek (házi és vadhús) elfogyasztása a legvalószínűbb forrása a hazai szórványos hepatitis E-fertőzéseknek. A 3-as genotípusú HEV-ek okozta endémiás humán fertőzések fajokon keresztüli zoonosisok, amelyek élelmiszerek közvetítésével terjednek hazánkban.
Bevezetés: Az inaktivált influenzavírus elleni védőoltás évente javasolt az immunszupprimált gyulladásos bélbetegek számára. Cél: A szerzők célja volt, hogy megvizsgálják a szezonális influenzavírus elleni védőoltás hatására kialakuló immunválasz mértékét immunszuppresszív terápiában részesülő gyulladásos bélbetegekben. Betegek és módszerek: Prospektív tanulmányukba 30, immunszuppresszív kezelésben részesülő, gyulladásos bélbetegségben szenvedő beteget vontak be. Az immunizációt (A/California/7/2009 [H1N1], A/Perth/16/2009 [H3N2], B/Brisbane/60/2008) megelőzően és egy hónappal később a betegektől vért vettek pre- és posztimmunizációs antitesttiter meghatározása céljából. A vírusspecifikus ellenanyagok kimutatása ELISA-módszerrel történt. Eredmények: A betegek oltási hajlandósága 53,3%-os volt. Mellékhatásként öt betegnél helyi, hét betegnél szisztémás tünetek jelentkeztek. Két betegnél jelentkeztek influenzaszerű tünetek, az antitesttiter-értékük nem szignifikáns mértékben emelkedett meg. Valamennyi betegben az influenzavírus elleni antitest-pozitivitás már az oltást megelőzően is kimutatható volt. Következtetések: Eredményeik valamennyi betegben megfelelő védettséget jelző antitesttiterszintet igazoltak az immunizációt megelőzően is. A védőoltás szignifikánsan nem befolyásolta a szeroprotekció mértékét és biztonságosnak bizonyult. Orv. Hetil., 2012, 153, 1870–1874.
High mobility group box 1 protein (HMGB-1), a nuclear protein is a critical cytokine that mediates the response to infection, injury and inflammation.The aim of our study was to elaborate a reliable in vitro model to investigate whether Mycobacterium bovis BCG is able to induce HMGB-1 secretion from the monocytic U-937 cells. Western blot technique was applied for the detection of HMGB-1 from supernatants of cells, following induction with LPS, Staphylococcus aureus , and Mycobacterium bovis BCG. HMGB-1 was subjected to MALDI-TOF mass and PSD analysis. Quantitation of the secreted HMGB-1 was performed by ELISA. The BCG strain induced higher amounts of secreted HMGB-1 than LPS or Staphylococcus aureus . The translocation of the HMGB-1 to the cytoplasm following infection of cells with BCG was demonstrated by immunofluorescence examinations.Conclusion: Our pilot experiments draw attention the to HMGB-1-inducing ability of Mycobacterium bovis . Assessment of the pathophysiological role of this late cytokine in mycobacterial infections demands further in vitro and in vivo examinations.
Hungarian cattle herds were surveyed for bovine herpesvirus 1 (BHV-1) infection by ELISA of milk and serum samples. In 1993, 75% of the large cattle herds (consisting of more than 50 cattle) and all small herds (small-scale producers' stocks), while in 1997 90% of the small herds were included in the survey. In the case of large herds, 79.3% of the herds and 64.1% of the samples tested were found to be positive. Of the small herds, 13.5% and 15.7% tested positive in 1993 and 1997, respectively. The majority of large herds were Holstein-Friesian dairy stocks. Small herds with an infection rate markedly exceeding the average were found in those counties where the small herds had been in close contact with the large-scale farms, or where new herds were established by using animals of uncontrolled infectious bovine rhinotracheitis (IBR) status originating from large farms. Attention is called to the importance of maintaining the IBR-free status of small herds that constitute one-third of the Hungarian cattle population.
Serum/plasma fructosamine (SeFa) concentration is a reliable indicator used in human diabetic control. Tests for monitoring the carbohydrate/energy metabolism of (farm) animals are less commonly performed in veterinary laboratories, since most of the reliable determinations, both automated and manual, are relatively expensive. The aim of this study was to develop a precise, money- (and time-) saving automated micro method for measuring SeFa. ELISA microplates (20 µL samples and 200 µL reagents) and an automatic microplate autoreader were used. The classical nitroblue tetrazolium (NBT) stain reagent solution of Johnson et al. (1982) was modified using a SIGMA reagent to render it stable for up to one year. SeFa concentrations measured by the new method in 30 human blood plasma samples were compared with values obtained by the standard (generally used) LaRoche kit procedure. Fifteen cow, 13 dog and 18 chicken plasma samples were assayed by the new automated ‘micro’ method as well as by the manual test tube ‘macro’ method commonly used earlier. The modified reagent was applied for both methods. The coefficient of correlation (r) between the results obtained by the two methods was consistently between 0.94 and 0.98 (p < 0.001).
The objective of this study was to investigate whether baboon females respond to an ovarian stimulation protocol incorporating pituitary suppression with a GnRH agonist (GnRHa) and either highly purified human FSH (hphFSH) or recombinant human FSH (rhFSH) with follicular development and oocyte maturation. A modified human ovulation induction protocol was applied to 5 adult female baboons with a history of regular menstrual cycles (33–34 days). A long-acting GnRHa implant containing goserelin acetate was placed subcutaneously (s.c.) on Days 22–24 of their menstrual cycle. Concentrations of serum oestradiol (E2), progesterone (P4) and human FSH were obtained by ELISA. Menses occurred ∼ 10 days after GnRHa implantation. Daily hphFSH or rhFSH (75 IU i.m.) treatments were started ∼ 10 days following menses. When the majority of follicles were ≥ 5 mm in diameter and the E2 levels had reached a maximum, hCG (2000 IU i.m.) was administered to induce final maturation of oocytes and ovulation. Thirty to 34 h after hCG administration, transabdominal follicular aspiration was performed using a variable frequency transvaginal transducer with ultrasound. A total of 71 oocytes were collected from 4 animals (average: 17). The meiotic maturity of oocytes was evaluated 3 h after retrieval. Ninety-one percent of oocytes were in metaphase 2 and of grades I and II which are appropriate for in vitro insemination.
Ghrelin is a gut hormone shown to have protective effects throughout the gastrointestinal tract. This study aims to investigate its protective effect in celiac disease induced in rats. Twenty-four rat pups were divided into 4 groups as follows: control, disease (1.5 mg/g intragastric gliadin), co-treatment (50 ng/g intraperitoneal ghrelin after gliadin gavage) and pretreatment (50 ng/g intraperitoneal ghrelin before gliadin gavage). Animals’ weight gain was charted. Histological features assessed include villus length, villus width, crypt depth and number of intraepithelial lymphocytes. Tissue interferon-gamma was quantified by ELISA. ANOVA was used to compare results statistically. Results showed that villi were shortened in the diseased group, but were as long as the control in pretreatment and co-treatment groups. Crypt depth had increased in disease group, but turned to normal in co-treatment group. Number of intraepithelial lymphocytes was significantly higher in disease group than the control, while no difference was observed between co-treatment and control groups. Disease and control animals weighed equally at the end of the experiment, but ghrelin-treated animals had significantly gained more weight than these two. Interferon-gamma measurement revealed no significant difference among groups. We concluded administration of ghrelin led to histological improvement of celiac disease which was more obvious if administered after exposure to gliadin.
ST2 is a member of IL-1 receptor family expressed on Th2 cells and regulates Th2 responces. The gene of ST2 encodes soluble ST2 (sST2) and the transmembrane ST2 (ST2L) isoforms through alternative mRNA splicing. The discovery of IL33/ ST2 signaling pathway, has drawn a great scientific attention to this system. sST2 has been shown to be an indacating factor in various infl ammatory conditions. This study aims to evaluate serum sST2 levels in HTLV-1 infected patients. This study included 49 HTLV-1 seropositive cases of which 14 were sympthomatic. Controls consisted of 30 healthy volunteers. sST2 level was measured using a quantitative ELISA assay and the results of the study groups were compared. Corroborating the previous reports, sST2 was lower in females (P = 0.003). The sST2 levels was slightly increased in HTLV-1 patients, though such increase was not statistically significant (P = 0.91), in addition sST2 level did not correlate significantly to the disease duration (P = 0.78). Despite some other chronic viral infection, HTLV-1 seems not to induce high serum sST2. However owing to relatively high normal variation of sST2 levels and rather small sample size, we stongly recommend further reseach with preferably larger sample size to evalute sST2 in HTLV-1 infected patients.
We describe a rare case of Lyme disease complicated by unilateral neuroretinitis in the right eye. We report a case of a 27-year-old woman with blurred vision on her right eye. Because of the suspicion of optic neuritis (multiplex sclerosis) neurological examination was ordered. Surprisingly, computer tomography of the brain revealed incomplete empty sella, which generally results not monocular, but bilateral optic nerve swelling. Opthalmological examination (ophthalmoscopy and optical coherence tomography) indicated not only monocular optic nerve, but retinal oedema next to the temporal part of the right optic disk. Visual evoked potentials (VEP) demonstrated no P100 latency delay and mild differences between the amplitudes of the responses of the left and right eye. Optical coherence tomography (OCT) demonstrated the swelling of the optic nerve head and oedematous retina at the temporal part of the disk. Suspicion of an inflammatory cause of visual disturbance blood tests was ordered. Doxycycline treatment was ordered till the result of the blood test arrived. The Western blot and ELISA test were positive for Borrelia burgdorferi sensu lato. Following one week corticosteroide and ceftriaxone treatments, the patient displayed a clinical improvement. Unilateral neuroretinitis with optic disk swelling due to neuroborreliosis is a rare complication and in many cases it is difficult to distinguish between inflammatory and ischemic lesions. Further difficulty in the diagnosis can occur when intracranial alterations such as empty sella is demonstrated by CT examination.
The aim of the present study was to investigate the serum and cerebrospinal fluid (CSF) concentrations of tumor necrosis factor alpha (TNF-alpha) and soluble vascular cell adhesion molecule-1 (sVCAM-1) in patients with primary progressive form of multiple sclerosis (MS) and in patients with connective tissue diseases (CTDs) complicated with central nervous system (CNS) involvement. Stimulation of sVCAM-1 release by TNF-alpha was demonstrated on endothelial cells of brain vessels. We intended to present the TNF-alpha stimulated elevation of sVCAM-1 in the serum and CSF in any cases of CNS lesion. Fifty patients with several CTDs complicated with neuropsychiatric symptoms and 25 MS patients with primary chronic progressive form of the disease were selected. Determinations of TNF-alpha and sVCAM-1 were performed using ELISA methods. TNF-alpha and sVCAM-1 concentrations were elevated in the CSF of all patients, intrathecal synthesis of sVCAM-1 was demonstrated in MS patients. The changes in the TNF-alpha and sVCAM-1 concentrations were independent from the clinical manifestations, immunoserological changes and quality of neuropsychiatric symptoms of the CTDs. The stimulatory effect of TNF-alpha was more pronounced in the CSF of MS patients.
