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Apart from the efficiency of coumaphos against Varroa mites, its impact on the oxidative status and survival of the honey bee (Apis mellifera) was assessed. The research was conducted on hives from the same apiary, equalised regarding the number of bees, brood area and food storage. Based on Varroa infestation the hives were allotted to two groups: non-infested (N) and infested (I). Both groups were either treated (T) – NT and IT, or untreated (U) – NU and IU. The treatment of infested bees was controlled with a follow-up treatment with amitraz. The efficiency of coumaphos was 96-97%. This organophosphate had a negligible effect on bee survival, but it significantly affected their oxidative status: superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) activities, and the concentrations of malonyl dialdehyde (MDA). Coumaphos significantly (p˂0.0001) decreased SOD activity in non-infested bees, but increased it in those infested. By contrast, both CAT and GST activities, as well as MDA concentrations significantly increased (from p˂0.05 to p˂0.0001) after treatment in all groups, with the exception of IT, where it declined. Coumaphos in non-infested hives caused oxidative stress per se, not unlike varroa in infested colonies. However, in infested colonies it decreased oxidative stress, owing to its efficacy against Varroa mites and contributed to the recovery of bee colonies. In spite of its certain downsides, coumaphos remains an effective anti-varroa substance, but should be used with precaution, not to add to the effects of environmental factors which may cause red-ox misbalance.

The hygienic behavior in honey bees is a dominant natural defense mechanism against brood diseases. In this study, the influence of sugar dusting treatments on hygienic behavior was evaluated in 44 strong honey bee colonies. Three doses of pulverized sugar, 20, 30 and 40 g, each applied at three-, seven- and fourteen-day intervals were tested. The percentage of cleaned cells (PCC) in the total number of those with pin-killed brood served as a measure of the hygienic potential. The effect was dependent on the frequency of treatments: all doses applied every third and seventh day significantly (p

The influence of various diets on the quality of Apis mellifera queens was assessed. Colonies intended for queen cell production were assigned to four groups fed on (1) sugar-only, (2) mix of sugar, honey and fresh pollen, (3) sugar and pollen substitute (FeedBee®), and (4) natural sources. In addition, a fifth group had queen cells obtained naturally, by swarming. Sugar-only diet exerted a significant (p < 0.05) stimulating effect on the acceptance of queen cells and the weight of newly emerged queens, not affecting mated queens. Among mated queens those raised by bees fed on the mix of sugar, honey and fresh pollen had significantly (p < 0.05) larger numbers of ovarioles in comparison with all the others. Their weight was significantly higher than that of the queens from groups given FeedBee® and swarming queens. Compared to the latter, they had significantly wider spermatheca. Given the parameters monitored, FeedBee® proved not to be advantageous for queens. [ABSTRACT FROM AUTHOR]

Eight lovebirds of both sexes and different age were admitted showing alterations in behaviour and apathy. During the initial examination delamination of the beak was noted in all birds and discrete areas of alopecia in three of eight birds. Based on clinical experience, molecular diagnostic on PBFD, sequencing of obtained amplicons, and histopathological examination were performed. All birds tested positive on the presence of PBFD virus, despite the fact they did not exhibit expected clinical signs for PBFD. Sequencing results showed 100% match with sequences previously isolated from parrots with PBFD exhibiting classical PBFD manifestation. Histopathological examination showed similar findings as in previously described cases of PBFD in parrots. Other studies on psittacine birds correlate clinical manifestations and nucleotide variations with geographic localization. Our results indicate that the clinical manifestation of the disease is more dependent on bird species than on the genetic variation of the virus or the geographical distribution.

Colony losses, including those induced by the colony collapse disorder, are an urgent problem of contemporary apiculture which has been capturing the attention of both apiculturists and the research community. CCD is characterized by the absence of adult dead bees in the hive in which few workers and a queen remain, the ratio between the brood quantity and the number of workers is heavily disturbed in favor of the former, and more than enough food is present. Robbing behavior and pests usually attacking the weakened colony do not occur. In the present paper, the causes of the emergence of this problem are discussed, as well as the measures of its prevention.

Commercial feed intended for dogs and cats is an almost unrecognised source of human infection with various serovars of Salmonella enterica. However, people may catch the infection both via direct contact with contaminated pet feed and by contact with pets, which usually shed Salmonella without signs of infection. A relatively new trend of feeding dogs and cats with raw feed is considered to be a special risk owing to the fact that it usually contains foodborne pathogens, such as Salmonella spp., Escherichia coli and Campylobacter spp. Nonetheless, the epidemiological data do not support this idea. In the current review relevant data on the significance of pet feed in the outbreak of human salmonellosis are discussed and the recommendations for the prevention of the infection originating from these sources are suggested.

Clostridium perfringens is a Gram-positive, endospore-forming, anaerobic rod, ubiquitous in nature. C. perfringens strains can produce about 17 toxins. Many of them can lead to miscellaneous diseases, among which the enteric ailment may be the most common and is of utmost importance. In the present work 34 strains of C. perfringens isolated from feed and one from a cow suspected to have died of clostridial infection were subjected to molecular analysis. In order to detect the genotypes, the following genes coding for toxins were targetted: cpa, cpb, cpb2, cpe, etx and iap. The multiplex PCR assay revealed that all C. perfringens isolates from animal feed were of type A and b2-toxinogenic type A strains, possessing only the cpa (n=21), or both the cpa and the cpb2 genes (n=13). The importance of C. perfringens toxins α and β-2 in the pathogenesis of enterotoxemia is discussed and the regulation on the detection of this bacteria in animal feed questioned. The use of PCR in practise could enable the toxin-genotyping of C. perfringens isolates and, thus, provide a real basis for the establishment of maximum acceptable limits of this bacteria in feed.

The aim of this research was to test the CHD gene ( Chromo Helicase DNA-binding gene) as a universal molecular marker for sexing birds of relatively distant species. The CHD gene corresponds to the aim because of its high degree of conservation and different lengths in Z and W chromosomes due to different intron sizes. DNA was isolated from feathers and the amplification of the CHD gene was performed with the following sets of polymerase chain reaction ( PCR) primers: 2550 F/2718 R and P2/ P8. Sex determination was attempted in 284 samples of 58 bird species. It was successful in 50 bird species; in 16 of those ( Alopochen aegyptiacus, Ara severus, Aratinga acuticaudata, Bucorvus leadbeateri, Cereopsis novaehollandiae, Columba arquatrix, Corvus corax, C. frugilegus, Cyanoliseus patagonus, Guttera plumifera, Lamprotornis superbus, Milvus milvus, Neophron percnopterus, Ocyphaps lophotes, Podiceps cristatus, and Poicephalus senegalus), it was carried out for the first time using molecular markers and PCR. It is reasonable to assume that extensive research is necessary to define the CHD gene as a universal molecular marker for successful sex determination in all bird species (with exception of ratites). The results of this study may largely contribute to the aim. Zoo Biol 32:269-276, 2013. © 2012 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Posthodiplostomatosis (black spot disease) is a disease of young freshwater fish species of families Cyprinidae and Cobitidae, resulting from infection with metacercaria, which is the penultimate developmental stage of Posthodiplostomum cuticola. Metacercaria give rise to black cysts located primarily in the skin, muscles and on the fins. The disease caused by P. cuticola in certain fish species is first detected in a fishpond in Serbia, as presented in the current work, whilst in natural waters it has been existing for many years. Diagnosis of the infection in the grass carp (Ctenopharyngodon idella) and the bighead carp (Aristichthys nobilis) was based on the occurrence of dark discolorations and cysts of the parasite on the fins. Cysts measured approximately 1 mm in diameter, were confirmed by histopathological means. Posthodiplostomatosis occurred in fishponds in which preventive measures were not implemented, i.e. where the nurseries were not dried up and mechanically cleaned.

Objective: To determine the role of prostacyclin (PGI2) in protecting endothelial cells (ECs) from apoptosis and elucidate the protective mechanism., Methods and Results: To evaluate the effect of PGI2 on EC survival, we treated ECs with Ad-COX1/PGIS (Ad-COPI), which augmented selectively PGI2 production or carbaprostacyclin (cPGI2) followed by H2O2 for 4 hours. Ad-COPI inhibited annexin V-positive cells and blocked caspase 3 activation. cPGI2 inhibited apoptosis in a concentration-dependent manner. L-165041 had a similar effect, suggesting the involvement of peroxisome proliferator-activated receptor-delta (PPARdelta). ECs expressed functional PPARdelta. PPARdelta overexpression enhanced whereas PPARdelta knockdown by small interfering RNA abrogated the antiapoptotic action of cPGI2 and L-165041. Our results show for the first time that PGI2 stimulated 14-3-3alpha expression via PPARdelta activation. cPGI2 and L-165041 induced binding oaf PPARdelta to PPAR response elements located between -1426 and -1477 of 14-3-3alpha promoter region, thereby activating 14-3-3alpha promoter activity and protein expression. Upregulation of 14-3-3alpha proteins resulted in an increase in Bad binding to 14-3-3alpha and a reduction in Bad translocation to mitochondria., Conclusions: PGI2 protects ECs from H2O2-induced apoptosis by inducing PPARdelta binding to 14-3-3alpha promoter, thereby upregulating 14-3-3alpha protein expression. Elevated 14-3-3alpha augments Bad sequestration and prevents Bad-triggered apoptosis.