BackgroundThe grey partridge is an important game bird in Europe that has declined considerably over the last decades. The production and release of farm-bred birds can be threatened by infectious agents. The objective of this study was to describe the outbreak, pathology, and blood and tissue biochemical responses in a flock of grey partridges naturally infected with Mycoplasma gallisepticum.ResultsMorbidity and mortality rates were 100% and 60%, respectively. Necropsy revealed an accumulation of caseous exudate within the infraorbital sinuses, tracheitis, pneumonia and airsacculitis. There were significant increases in activities of lactate dehydrogenase, creatine kinase and amylase, and levels of total protein and glucose in Mycoplasma-infected birds when compared to control. Catalase showed significantly lower activity in the heart, lungs, liver and gonads of Mycoplasma-infected birds. Glutathione-S-transferase activity was elevated in the eye and the associated infraorbital sinus and kidneys, and decreased in the liver. Decreased levels of reduced glutathione were found in the heart, kidneys, liver and gonads. The activity of glutathione reductase was lower only in the lungs. Compared to healthy birds, mycoplasmosis in the grey partridge caused significant differences in the level of lipid peroxidation in lungs and plasma (p < 0.05), while the ferric reducing antioxidant power was lower in the heart and kidneys (p < 0.01). Significant correlations among responses of the antioxidant parameters were found namely in the heart, lungs, spleen, liver and plasma. There were also numerous significant inter-tissue correlations of all the studied antioxidant parameters.ConclusionsThe present study demonstrates the high susceptibility of grey partridges to natural infection by M. gallisepticum, the severity of the disease based on histopathology, and the modulation of blood chemical profiles and oxidative stress-associated parameters in the avian hosts, thus enhancing the understanding of the pathogenesis of mycoplasmosis in birds. Moreover, the reported reference values can be useful for the evaluation of the state of health in grey partridges.

BackgroundLead, a serious threat for raptors, can hamper the success of their conservation. This study reports on experience with accidental lead intoxication and responses to chelation therapy in captive Cinereous (Aegypius monachus) and Egyptian (Neophron percnopterus) Vultures.ResultsSoil contamination by lead-based paint sanded off the steel aviary resulted in poisoning of eight Cinereous and two Egyptian Vultures. A male Egyptian Vulture developed signs of apathy, polydipsia, polyuria, regurgitation, and stupor, and died on the next day. Liver, kidney and blood lead concentrations were 12.2, 8.16 and 2.66 μg/g, respectively. Laboratory analyses confirmed severe liver and kidney damage and anaemia. Blood Pb levels of Pb-exposed Cinereous Vultures were 1.571 ± 0.510 μg/g shortly after intoxication, decreased to 0.530 ± 0.165 μg/g without any therapy in a month and to 0.254 ± 0.097 μg/g one month after CaNa2EDTA administration. Eight months later, blood lead levels decreased to close to the background of the control group. Blood parameters of healthy Pb-non-exposed Cinereous Vultures were compared with those of the exposed group prior to and after chelation therapy. Iron levels in the lead-exposed pre-treatment birds significantly decreased after chelation. Haematocrit levels in Pb-exposed birds were significantly lower than those of the controls and improved one month after chelation. Creatine kinase was higher in pre-treatment birds than in the controls but normalised after therapy. Alkaline phosphatase increased after chelation. A marked increase in the level of lipid peroxidation measured as thiobarbituric acid reactive species was demonstrated in birds both prior to and after chelation. The ferric reducing antioxidant power was significantly lower in pre-treatment vultures and returned to normal following chelation therapy. Blood metallothionein levels in lead-exposed birds were higher than in controls. Reduced glutathione dropped after CaNa2EDTA therapy, while oxidised glutathione was significantly lower in both pre- and post-treatment birds. A chick in an egg produced by a Cinereous Vulture female two months after lead toxicosis died on day 40 of artificial incubation. Lead concentrations in foetal tissues were consistent with levels causing avian mortality.ConclusionsThe reported blood parameters and reproduction impairment in captive birds may have implications for professionals dealing with lead exposure in wild birds.

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Responses of wildlife to multiple stressors fit in the ecological concept of trade-off. While toxicity of non-steroidal anti-inflammatory drugs and heavy metals for free-ranging birds has been shown in single exposures, the present study aims to evaluate oxidative stress, and liver and kidney damage caused by single and combined effects of diclofenac and lead in the Japanese quail. Forty Japanese quail (Coturnix coturnix japonica) were divided into equal groups of controls, diclofenac, Pb, and Pb+diclofenac exposures. The birds were exposed to the respective chemicals through insertion of lead shots (1.5 g) into the crop on day 0 of the experiment and/ or administration of 5 mg/kg of diclofenac intramuscularly in two treatments on days 0 and 5. Groups in liver and kidney tissues of birds were then compared after 10 days using histopathology and biochemistry markers such as glutathione reductase (GR), ferric reducing antioxidant power (FRAP), and lipid peroxidation measured as total thiobarbituric acid reactive species (TBARS). The liver damage score gradient was Pb+diclofenac exposure group > Pb exposure group > diclofenac exposure group and hepatic TBARS values were significantly increased in the group of birds exposed to a combination of diclofenac and lead compared to the healthy control group. The study has shown that, apart from the reported nephrotoxicity of diclofenac, hepatic toxicity should also be considered. Avian clinicians should be cautious when selecting drugs for therapy of wild birds with unknown history of exposure to toxic substances. Total antioxidant capacity, lipid peroxidation, non-steroidal anti-inflammatory drugs, heavy metals, Japanese quail

In previous work, we found significant associations of horse chromosome 15 (ECA15) microsatellite markers HMSO1 and HTG06 with two horse infections, Rhodococcus equi and Lawsonia intracellularis, respectively. Interleukin-1 beta subunit and interleukin-1 receptor antagonist encoding genes (IL1B and IL1RN) could be considered as candidate genes underlying the associations reported. Therefore, we identified single nucleotide polymorphisms (SNPs) within three interleukin-1 beta functionally related genes: IL1B, IL1RN and Casp1 (interleukin-1 beta converting enzyme/caspasel encoding gene). Using appropriate restriction fragment length polymorphism (PCR-RFLP) and/or single strand conformation polymorphism (PCR-SSCP) markers, their associations with the two infections by genotyping foals from the original study were tested. In addition, the physical localization of one of the two closely located genes, IL1RN, was re-assessed by fluorescence in-situ hybridization (FISH). A statistically significant association between an intronic SNP of the Casp1 gene with R. equi infection was found. The IL1RN gene was localized to 15q13-q14 in agreement with its originally reported physical position.