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Background:Four countries are free from the porcine reproductive and respiratory syndrome virus (PRRSV) in Europe, a virus that causes severe economic losses worldwide. A number of countries have initiated eradication programmes against the disease. Among the applied methods, complete depopulation-repopulation is the safest and fastest but at the same time the most expensive process. Another possible way of heard eradication is to replace the infected breading stock by gilts reared PRRSV free on the infected farm. This way maintaining continued farm production. In this paper, the authors present a successful complex method of eradication (including the application of an inactivated vaccine and segregated rearing of offspring) in a Hungarian large scale pig farm. Case presentation:A farm of 1475 sows (Farm A) was infected with PRRSV and the clinical signs of reproductive failure were eliminated by using an inactivated vaccine (Progressis®, Ceva). At the beginning of eradication, gilts selected for breeding were vaccinated at 60 and 90–100 days of age, respectively. The subsequent vaccinations of breeding animals were applied at 6 months of age, on the 60–70th day of pregnancy and at weaning. The 7weeks-old piglets of the vaccinated sows, approximately 1200 piglets were transported in groups of 300 animals to a closed, empty farm (Farm B) after a testing negative with PCR, and they were reared here until 14 weeks of age. These seronegative gilts were subsequently transported to a third, closed, empty farm (Farm C), and (having reached the breeding age) they were inseminated here after a negative serological test (ELISA). At the same time, Farm A was depopulated, cleaned and disinfected. All pregnant gilts were transported from Farm C to Farm A after being tested negative with ELISA, where follow-up was performed after farrowing by two serological tests with an interval of six months. Based on the subsequent negative test results, the competent authority declared the herd PRRSV free. Conclusions:The farm presented in this study was the first in the course of the National PRRS Eradication Programme to eradicate PRRSV successfully by vaccinating the sows with an inactivated vaccine and performing segregated rearing of the offspring. Production was almost continuous during the whole process of the population replacement. Testing for monitoring purposes was also cheaper and simpler because of the use of an inactivated vaccine.

Ochratoxin-A (OTA) is a carcinogenic and nephrotoxic mycotoxin, which may cause health problems in humans and animals, and it is a contaminant in foods and feeds. The purpose of the present study is to evaluate the effect of oral OTA exposure on the antioxidant defense and lipid peroxidation in the kidney. In vivo administration of OTA in CD1, male mice (1 or 10 mg/kg body weight in a single oral dose for 24 h and repeated daily oral dose for 72 h or repeated daily oral dose of 0.5 mg/kg bodyweight for 21 days) resulted in a significant elevation of OTA levels in blood plasma. Some histopathological alterations, transcriptional changes in the glutathione system, and oxidative stress response-related genes were also found. In the renal cortex, the activity of the glutathione-system-related enzymes and certain metabolites of the lipid peroxidation (conjugated dienes, trienes, and thiobarbituric reactive substances) also changed.

Infectious laryngotracheitis is an economically significant viral disease of chickens, that mainly affects the upper respiratory tract, and is present worldwide. This case reports the first outbreak of infectious laryngotracheitis in a four-week-old organic broiler farm and surrounding flocks in Greece, with typical clinical symptoms and lesions, allegedly provoked by a wild strain of infectious laryngotracheitis virus. Our findings contradict the general perception indicating that the disease appears mainly in older birds and that vaccine strains are the primary cause of infectious laryngotracheitis outbreaks in most continents. A recombinant vectored vaccine was administered, supplementary to biosecurity measures, containing the viral spread. The responsible strain was potentially circulating in the area; therefore, an industry-wide holistic approach was applied, including the vaccination of neighboring broilers and breeders with the same vaccine, the rapid molecular diagnosis of the disease, and strict biosecurity protocols. The results of this holistic effort were effective because, following the application of vaccine and management protocols, manifestations of the disease in regional flocks dropped significantly, and there was no recurrence to date. These findings suggest that vaccination protocols should be modified, especially for organic broilers, to include vaccination against infectious laryngotracheitis.

The effects of brain ischemia and reperfusion on smooth muscle function in remote cerebral and peripheral arteries are hardly known. Maximum vasoconstrictions (Emax) caused by 120 mmol/l KCl and 5-HT in endothelium-denuded ring preparations were measured in ischemic and control cerebral arteries of rats after a 1-h right middle cerebral artery occlusion followed by 0-min (I/NR) or 2–3-min (I/SR) reperfusion, and in peripheral arteries after I/SR. Surprisingly, vasoconstrictions to 5-HT and 120 mmol/l K+ were attenuated in remote brain vessels after I/SR, i.e. in the contralateral middle cerebral artery and the basilar artery, while I/NR depressed Emax of 5-HT and high KCl only in the ischemic middle cerebral artery. Pretreatment with N-(2-mercaptopropionyl) glycine (MPG, 100 mg/kg i.p.), a free radical scavenger, fully prevented the impairment of vasomotor function in the middle cerebral artery on both sides after I/SR. Moreover, vasomotor functions were normal in the coronary, renal and pulmonary arteries after I/SR. In conclusion, focal cerebral ischemia and reperfusion impaired vasoconstrictor responses in remote brain arteries of rats by a mechanism involving free radicals. The lack of similar effects in peripheral vessels indicates poor defence of brain arteries against remote injury caused by reactive oxygen species-dependent mechanisms.

Background Detection of acute kidney injury (AKI) is still a challenge if conventional markers of kidney function are within reference range. We studied the sensitivity and specificity of NGAL as an AKI marker at different degrees of renal ischemia. Methods Male C57BL/6J mice were subjected to 10-, 20- or 30-min unilateral renal ischemia, to control operation or no operation, and AKI was evaluated 1 day later by histology, immunohistochemistry, BUN, creatinine, NGAL (plasma and urine) and renal NGAL mRNA expression. Results A short (10-min) ischemia did not alter BUN or kidney histology, but elevated plasma and urinary NGAL level and renal NGAL mRNA expression although to a much smaller extent than longer ischemia. Surprisingly, control operation elevated plasma NGAL and renal NGAL mRNA expression to a similar extent as 10-min ischemia. Further, the ratio of urine to plasma NGAL was the best parameter to differentiate a 10-min ischemic injury from control operation, while it was similar in the non and control-operated groups. Conclusions These results suggest that urinary NGAL excretion and especially ratio of urine to plasma NGAL are sensitive and specific markers of subclinical acute kidney injury in mice.

Materials and methods The CA3 neurons were chemically lesioned by intracerebrally administration of NaN3 in doses of 8 and 16 mg/ml. To examine learning functions Morris maze was used. During acquisition trials animals had to find a black platform within 120 s. We measured the “escape latency"(msec). Detailed histopathology of brain was performed at the termination of the study. Learning function was measured after 7 days of ic. treatment.

2,3,5-Triphenyltetrazolium chloride (TTC) staining measures tissue viability used to evaluate infarct size. The goal of this study was to compare viability of neuronal tissue during the early phases of ischemia-reperfusion assessed either by perfusion of the brain with TTC solution transcardially, in vivo, or by staining brain slices, in vitro.The middle cerebral artery was occluded for 1 h in male SPRD rats and then reperfused for 0, 1, 4, 8, 16 and 24 h. Ischemic damage was evaluated by TTC staining, in vivo and in vitro, and by histology (Luxol Fast Blue and Fluoro-Jade staining, electron microscopy).Core volume of tissue injury measured in vivo was large at 0 h and steadily decreased by 50% (p0.001) up to 16 h, but substantially increased from 16 to 24 h of reperfusion. In contrast, a significant core volume appeared at 4 h only, in vitro, and gradually increased up to 24 h. Core volume was larger in vivo than in vitro at all times except at 16 h when the opposite was observed. Evans blue administered intracardially stained TTC-negative areas at 1 and 24 h. Histology covered the evolution of serious tissue injury but also demonstrated some morphologically preserved neurons in the infracted area at 24 h.Formation of formazan from TTC can depend on both the staining method and the metabolic burden of the brain tissue causing uncertainties in the volume of ischemia-induced brain injury measured by TTC staining.