Effects of a tributyrin and monolaurin blend compared to high ZnO levels on growth performance, faecal microbial counts, intestinal histomorphometry and immunohistochemistry in weaned piglets: A field study in two pig herds.

The objective of the present study was to evaluate the effects of a tributyrin and monolaurin blend compared to high ZnO levels in weaned piglets under field conditions. In Trial 1, piglets (n = 168) were assigned to 1 of 2 treatments: 1) control (CON; diet supplemented with 3000 g ZnO/t of feed; n = 8 replicates); 2) tributyrin and monolaurin blend - Porcestin™ (PR; diet supplemented with basal level of ZnO at 150 g/t and with the tested blend at 5 kg/t of feed; n = 8 replicates). In Trial 2, piglets (n = 244) were assigned to the same two treatments (n = 10 replicates). The study duration was 4 (Trial 1) and 6 (Trial 2) weeks post-weaning. In both trials, growth performance was similar between treatments (P > 0.05). In Trial 1, faecal counts of Lactobacillus spp. increased in pigs of PR group (P < 0.05). In both trials, histomorphometrical analysis of jejunum and ileum samples showed a thicker intestinal mucosa in favor of the PR treatment (P < 0.01), and Foxp3-positive regulatory T cells increased together with a concomitant decrease of MPO-positive granulocytes in jejunal mucosa of piglets from the PR treatment (P < 0.01). Overall, supplementation of monolaurin and tributyrin blend compared to high ZnO levels resulted in similar growth performance. Moreover, beneficial effects on small intestinal morphometry and immune cells responses indicate its ability to attenuate inflammatory processes. Further research is necessary to optimize the use of tested product.

Inflammation-induced colon cancer in uPA-deficient mice is associated with a deregulated expression of Notch signaling pathway components.

Notch is an evolutionarily conserved signaling pathway with an important role in development and cell fate determination. Deregulation of Notch signaling has been associated with several pathological conditions, including cancer. Acting as an oncogene in some types of cancers and as a tumor suppressor in other, Notch effects seem to be highly context-dependent in solid tumors. In the present study, we aimed to investigate gene expression levels of Notch pathway constituents, including ligands, receptors, and target genes, during the early stages of inflammation-associated intestinal carcinogenesis. To achieve so, we used our recently developed mouse model, in which colon cancer arises in the absence of urokinase-type plasminogen activator (uPA) due to colitis induced by dextran sodium sulfate (DSS) treatment. Among the cell surface components, ligands Jag1/Jag2 and receptors Notch1/Notch2 were found to be significantly upregulated in the uPA-deficient protumorigenic inflammatory microenvironment. Moreover, several intracellular Notch modulators, i.e. Hes1, Hey1, and Klf4, were also shown to be deregulated with inflammation, yet irrespective of uPA status. Sox9 transcription factor, however, was significantly downregulated in the uPA-deficient/DSS-treated mice that developed colon adenomas as compared to the wild-type/DSS-treated group with no neoplasia identified. The latter finding supports a tumor suppressive role of Sox9 in intestinal carcinogenesis. Our results point towards an early activation of Notch signaling pathway at the receptor-ligand level in inflammation-associated colon neoplasmatogenesis developed in the absence of uPA. Interestingly, such activation may not be accompanied by deregulation of downstream Notch-target genes, possibly due to the effects of other inter-related signaling pathways.

Pyogranulomatous pneumonia in goats caused by an undescribed Porphyromonas species, "Porphyromonas katsikii".

A yet-undescribed bacterial species, tentatively named "Porphyromonas katsikii," was isolated from individuals of a small goat herd with pyogranulomatous pneumonia during an outbreak of acute respiratory disease. The isolated bacteria grew in the form of black-pigmented colonies after 14 days of incubation under anaerobic conditions at 37°C on a tryptic soy blood agar medium. The bacteria were identified as a yet-undescribed Porphyromonas species by determination of the nucleotide sequence of the rrs 16S rRNA gene, and this species was tentatively named Porphyromonas katsikii. PCR amplification with specific primers for this yet-undescribed species revealed the presence of P. katsikii in the lung tissue of all affected animals, while no PCR signals were evidenced from the lungs of healthy goats or from goats with pasteurellosis caused by Mannheimia haemolytica. These data indicate P. katsikii as the causative agent of acute respiratory distress. P. katsikii is phylogenetically related to Porphyromonas somerae and Porphyromonas levii, which cause pathologies in humans and animals, respectively. P. katsikii was not detected by PCR from samples of the gingival pockets or of the faces of healthy goats.

An outbreak of caprine meningoencephalitis due to Escherichia coli O157:H7.

Five 1-month-old kid goats from a local herd in Kozani (northwest Greece) developed neurological disorders characterized by decreased appetite, ataxia, and head pressing. The animals received a 3-day course of treatment with intramuscular administration of enrofloxacin and ketoprofen. However, no significant clinical improvement was achieved, and 2 kids died. The remaining 3 animals were euthanized, and a necropsy was performed within 1 hr. Macroscopic lesions were confined to the central nervous system, with congestion and petechiae in the meninges. Microscopic lesions in all 3 animals revealed multifocal acute meningoencephalitis characterized by infiltrations composed of mononuclear inflammatory cells, lesser numbers of lymphocytes, and occasionally neutrophils and eosinophils. Additionally, in the kidney, there was multifocal expansion of the glomerular tufts by eosinophilic amorphous material, multifocal interstitial hemorrhages, and multifocal glomerular hypercellularity. The above noted lesions are consisted with an acute ongoing nephropathy indicative of a septicemic-toxemic procedure at its primary stages. Small, gray bacterial colonies, 3-4 mm in diameter, were obtained in pure culture from the brain of all 3 necropsied animals and were confirmed as Escherichia coli O157:H7 by use of phenotypic and genotypic methods. The isolates were sensitive to cefuroxime, ceftazidime, and gentamicin. In contrast, resistance to enrofloxacin, trimethoprim-sulfamethoxazole, and tetracycline was displayed. Additionally the bacterial isolates were found to carry a plasmid that harbored qnrS, sulII, and tetB genes that contribute to high-level resistance to fluoroquinolones, co-trimoxazole, and tetracycline, respectively.

Stenotrophomonas maltophilia as a causal agent of pyogranulomatous hepatitis in a buffalo (Bubalus bubalis).

A 7-year-old female buffalo (Bubalus bubalis) from a local herd in Serres, northern Greece, was presented to a private veterinary clinic with a chronic loss of appetite for 15 days. The clinical examination revealed high fever (41.5 degrees C), lethargy, yellow discoloration of skin and mucous membranes, an abdomen that appeared to be empty, hyperactive rumen motility, and tachypnea. A biochemical profile revealed an elevated total bilirubin concentration and hepatic enzyme activities, whereas globulin, creatinine, and glucose concentrations were within the reference intervals. The animal received a 12-day course of treatment with intramuscular administration of ampicillin and corticosteroids. However, no significant clinical improvement was achieved, and the buffalo was euthanized. Gross necropsy lesions included serous atrophy of adipose tissue and hepatomegaly. Microscopic lesions included necrotizing pyogranulomatous hepatitis with thrombosis, hemorrhages, edema, and fibrosis. Small, nonpigmented, bacterial colonies were harvested in pure culture from the liver and were confirmed as Stenotrophomonas maltophilia by polymerase chain reaction. The bacterium was sensitive to ciprofloxacin, enrofloxacin, colistin, polymyxin, trimethoprim/sulfamethaxazole, and chloramphenicol. In contrast, resistance to ticarcillin, piperacillin, imipenem, ceftazidime, amikacin, gentamicin, tobramycin, and tetracycline was displayed. The bacterial strain carried the L1 metallo-beta-lactamase (L1) and tet35 genes, which contribute to high-level resistance to beta-lactams and tetracycline, respectively. Although S. maltophilia is widely believed to be a contaminant, the present report suggests that the isolation, identification, and susceptibility testing of this multidrug-resistant bacterium may be of clinical importance in diagnostic samples.