Health in relation to tail-biting behaviour was investigated on a problem farm. Quartets (n 5 16) of age-and gender-matched fattening pigs including a tail biter (TB, n 5 16), a victim (V, n 5 16), a control in the same pen (C tb , n 5 10) and a control in a pen where no tail biting was observed (C no , n 5 14) were chosen by direct behavioural observation. Haematological and clinicochemical analyses, autopsy and histological examination of 16 different tissues were carried out. Tail lesion severity was evaluated both macroscopically, on the basis of inspection, and histologically, in the sagittally cut tail. Category effects were tested using Friedman's ANOVA by Ranks, Cochran's Q or a repeated-measure GLM and, if significant, pair-wise tests were conducted using Wilcoxon Signed Ranks or McNemar's Test. The number of received tail bites correlated better with histological than with macroscopic tail lesion scoring because of deep inflammation beneath healthy skin in some cases. Most individuals had mild inflammatory lesions in internal organs suggestive of generalized activation of the immune system, and 30% of the animals were anaemic, possibly because of systemic spread of infectious agents. V had more severe respiratory organ lesions and higher serum protein concentrations than all other categories of pigs. Liver-and muscle-specific enzymes (alanine aminotransferase, alkaline phosphatase and creatine kinase) differed between categories. In conclusion, most animals had signs of generalized activation of the immune system, possibly because of systemic spread of infectious agents. V pigs suffered from more severe inflammatory lesions than TB, C tb or C no . Deep infections may exist under healthy skin in the tail of bitten pigs.

Three subgroups of the Finnish cat population underwent investigation for different aspects of feline toxoplasmosis. Blood samples of 445 purebred pet cats and 45 shelter cats were screened for Toxoplasma gondii-specific immunoglobulin G antibodies with a direct agglutination test. The overall seroprevalence was 48.4%; older cats and cats receiving raw meat in their diet were more often seropositive. Fecal samples were obtained from 131 shelters cats; 2 of the cats were found shedding T. gondii-like oocysts, and the oocysts shed by 1 of the 2 were confirmed as T. gondii with polymerase chain reaction. Among 193 cats submitted for necropsy during a 3.5-year period, 6 (3.1%) had been diagnosed with generalized toxoplasmosis and were retrospectively further investigated. The main pathological lesions included acute interstitial pneumonia, acute necrotizing hepatitis, and nonsuppurative meningoencephalitis with glial granulomas. Immunohistochemical staining demonstrated a mild to massive parasite burden in tissues with pathological lesions as well as in unaffected tissues. The results of the direct multilocus genotyping of T. gondii parasites detected were consistent with endemic genotype II, and the causative parasite strains were isolated from 2 of the generalized toxoplasmosis cases. The results indicate that cats in Finland commonly encounter T. gondii and contribute to the environmental oocyst burden, while the endemic genotype II can also prove fatal to the parasite's definitive host. Preventing feline T. gondii infections is not only of public health importance but also a welfare issue for the cats themselves.

This is the first study describing an experimental mastitis model using transgenic cows expressing recombinant human lactoferrin (rhLf) in their milk. The aim of the study was to investigate the concentrations in milk and protective effects of bovine and recombinant human lactoferrin in experimental Escherichia coli mastitis. Experimental intramammary infection was induced in one udder quarter of seven first-lactating rhLf-transgenic cows and six normal cows, using an E. coli strain isolated from cows with clinical mastitis and known to be susceptible to Lf in vitro. Clinical signs were recorded during the experimental period, concentrations of human and bovine Lf and indicators of inflammation and bacterial counts were determined for milk, and concentrations of acute-phase proteins and tumor necrosis factor alpha were determined for sera and milk. Serum cortisol and blood hematological and biochemical parameters were also determined. Expression levels of rhLf in the milk of transgenic cows remained constant throughout the experiment (mean, 2.9 mg/ml). The high Lf concentrations in the milk of transgenic cows did not protect them from intramammary infection. All cows became infected and developed clinical mastitis. The rhLf-transgenic cows showed milder systemic signs and lower serum cortisol and haptoglobin concentrations than did controls. This may be explained by lipopolysaccharide-neutralizing and immunomodulatory effects of the high Lf concentrations in their milk. However, Lf does not seem to be a very efficient protein for genetic engineering to enhance the mastitis resistance of dairy cows.

Background Alpha-chloralose (AC) is a compound known to be toxic to various animal species and humans. In 2018 and 2019 an increase in suspected cases of AC poisoning in cats related to the use of AC as a rodenticide was reported to national veterinary and chemical authorities in Finland, Norway and Sweden by veterinarians working in clinical practices in respective country. The aims of this study were to prospectively investigate AC poisoning in cats, including possible secondary poisoning by consuming poisoned mice, and to study metabolism and excretion of AC in cats through analysis of feline urine. Methods Data on signalment, history and clinical findings were prospectively collected in Finland, Norway and Sweden from July 2020 until March of 2021 using a questionnaire which the attending veterinarian completed and submitted together with a serum sample collected from suspected feline cases of AC-poisoning. The diagnosis was confirmed by quantification of AC in serum samples. Content of AC was studied in four feline urine samples, including screening for AC metabolites by UHPLC-HRMS/MS. Bait intake and amount of AC consumed by mice was observed in wild mice during an extermination of a rodent infestation. Results In total, 59 of 70 collected questionnaires and accompanying serum samples were included, with 127 to 70 100 ng/mL AC detected in the serum. Several tentative AC-metabolites were detected in the analysed feline urine samples, including dechlorinated and oxidated AC, several sulfate conjugates, and one glucuronic acid conjugate of AC. The calculated amount of AC ingested by each mouse was 33 to 106 mg with a mean of 61 mg. Conclusions Clinical recognition of symptoms of AC poisoning in otherwise healthy cats roaming free outdoors and known to be rodent hunters strongly correlated with confirmation of the diagnosis through toxicological analyses of serum samples. The collected feline exposure data regarding AC show together with the calculation of the intake of bait and subsequent AC concentrations in mice that secondary poisoning from ingestion of mice is possible. The results of the screening for AC metabolites in feline urine confirm that cats excrete AC both unchanged and metabolized through dechlorination, oxidation, glucuronidation and sulfatation pathways.

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A 3-year-old Cairn Terrier dog that had been in contact with sea water containing cyanobacteria (blue-green algae) was euthanized because of acute hepatic failure and anuria after a 5-day illness. Histologic findings included lytic and hemorrhagic centrilobular hepatocellular necrosis and renal tubular necrosis. The cyanotoxin nodularin was detected in liver and kidney by highperformance liquid chromatography-mass spectrometry. Nodularin is a potent hepatotoxin produced by the algal species Nodularia spumigena. The intensity of algal blooms has increased during the past decades in the Baltic Sea region, thus increasing the risk for intoxications in domestic and wild animals. The authors describe the pathologic findings of cyanobacterial toxicosis in a dog with direct identification of the toxin from organ samples.Keywords cyanobacterium, dog, hepatic necrosis, kidney, liquid chromatography-mass spectrometry, liver, nodularin, renal tubular necrosis Hepatic necrosis due to toxins produced by blue-green algae (cyanobacteria) is a well-known cause for acute hepatic failure and death in wild and domestic animals. Although at least 40 species of cyanobacteria, with worldwide distribution, can synthesize a range of hepatotoxins, neurotoxins, and dermatotoxins, the threat of cyanotoxin-contaminated water is often ignored. 3,24Blooming of blue-green algae, especially the toxigenic species Nodularia spumigena, occurs annually in the Baltic Sea region, presenting a threat for animals exposed to contaminated water. Previously, the identification of blue-green algal toxin was laborious, requiring water samples and the use of experimental animals; 5,6,10,16,25,26 algal toxins have not been analyzed routinely from animal tissues in diagnostic cases. In this report, blue-green algal toxicosis was confirmed by direct toxin analysis from organ samples. Case HistoryA 3-year-old female Cairn Terrier weighing 9.6 kg was exposed to sea water containing blue-green algae in the Finnish southwest coastal region of the Baltic Sea. The exact route of exposure is uncertain; the dog was not seen swimming in the sea but may have consumed algal scum or drunk contaminated water. Subsequently, the dog became acutely lethargic with vomiting and inappetence. Initially, it was treated supportively with antiemetics and fluid therapy. Three days after the onset of clinical signs, the dog was admitted to the university hospital because of further clinical deterioration.Upon physical examination, the dog was lethargic, dehydrated, and icteric. Abnormal hematologic findings included mild nonregenerative anemia (packed cell volume, 32%; reference range, 38%-57%; mean corpuscular volume and hemoglobin within reference ranges) with normal leukocyte count (14.0 Â 10 9 /liter; reference range, 5.4-17.4 Â 10 9 /liter). Serum biochemistry profile abnormalities included elevated alanine aminotransferase (6211 U/liter; reference range, 18-77 U/liter), alkaline phosphatase (392 U/liter; reference range, 33-215 U/liter), total bilirubin (272.5 mmol/liter...

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