Mycobacteriosis is a significant disease of companion and wild birds which causes emaciation and widely distributed lesions, as well as being a potential zoonosis. Its primary aetiological agents in birds are Mycobacterium avium subsp. avium and the fastidious Mycobacterium genavense. This study monitored the therapy of birds naturally infected with Mycobacterium genavense to gain understanding of its effectiveness and the interrelation of co-infections with the disease course and pharmacotherapy. Five Atlantic canaries (Serinus canaria) and one Bengalese finch (Lonchura striata) with tentative diagnoses of mycobacteriosis resulting from M. genavense infection were treated twice daily with clarithromycin at 40 mg/kg, ethambutol at 30 mg/kg, and moxifloxacin at 10 mg/kg for 6 months. Two canaries were also found to be carriers of Cryptosporidium galli. Mycobacteria in faecal samples of all birds were investigated by bacterioscopy and quantitative PCR. Molecular tests yielded positive results for up to four months after treatment initiation for M. genavense and Cryptosporidium, but microscopy failed to detect the latter after four weeks in specimens from one canary. Co-infections with polyomavirus (in all birds) and circovirus and bornavirus (in canaries) were diagnosed. Two birds died during treatment and one was euthanised because of other disease, 1 month after treatment completion. Three canaries were in relatively good health a year after treatment. Canary circovirus and polyomavirus co-infection may suppress the immune system and this may facilitate the development of mycobacteriosis. The set of drugs used led to the complete cure of mycobacteriosis in three canaries. In one bird the disease returned. Clarithromycin was the active drug against C. galli. Molecular methods serve well to monitor mycobacteriosis therapy and identify M. genavense and C. galli carriage.

Introduction: Breed predisposition to cutaneous mast cell tumours (MCT) in a population of dogs in Poland affected by various skin tumours was assessed, and the distribution of MCT characteristics such as histological grading, sex, age, and location, in predisposed breeds was evaluated. Material and Methods: The retrospective epidemiological study included 550 dogs affected by cutaneous MCTs with a reference group of 2,557 dogs diagnosed with other skin tumours. Results: A univariable logistic regression analysis was performed to determine the odds ratios (ORs) with 95% confidence intervals. The risk of high-grade MCTs was the highest for Shar-Peis (OR: 26.394) and American Staffordshire Terriers (OR: 2.897). Boxers (OR: 6.619), Labrador Retrievers (OR: 2.630), French Bulldogs (OR: 2.050), Golden Retrievers (OR: 1.949), and American Staffordshire Terriers (OR: 2.592) were mainly affected by low-grade MCTs. The high risk of MCT was calculated to be at the age of 4–6 years for Labrador Retrievers (OR: 2.686) and 7–10 years for Boxers (OR: 2.956) and French Bulldogs (OR: 9.429). MCTs were significantly more often located on the trunk in French Bulldogs (OR: 4.680), American Staffordshire Terriers (OR: 2.520), and Labrador Retrievers (OR: 1.948). There was no statistically significant correlation between gender and the occurrence of MCTs in the breeds. Conclusions: The breed-predicated differences in the clinical course of MCTs suggest a genetic background for the tumours.

Avian reticuloendotheliosis (RE) represents an important immunosuppressive disease of poultry. The occurrence of RE in both chickens and turkeys has an immunosuppressive effect and may lead to vaccination failures. Avian reticuloendotheliosis virus (REV) is widely distributed in different kinds of birds, causing subclinical infections. Another important issue adhering to this disease is contamination of vaccines against fowl pox (FP) and Marek’s disease (MD) with REV. The capability of REV to integrate into the genome of other larger DNA viruses complicates its diagnosis and prevention. There are no efficient vaccines against RE nor treatment, which also complicates how to limit its impact on poultry farming. This paper reviews the current state of knowledge of this important immunosuppressive agent of poultry emphasising the importance of this problem in terms of diagnosis of RE.

Avian reticuloendotheliosis (RE) represents an important immunosuppressive disease of poultry. The occurrence of RE in both chickens and turkeys has an immunosuppressive effect and may lead to vaccination failures. Avian reticuloendotheliosis virus (REV) is widely distributed in different kinds of birds, causing subclinical infections. Another important issue adhering to this disease is contamination of vaccines against fowl pox (FP) and Marek’s disease (MD) with REV. The capability of REV to integrate into the genome of other larger DNA viruses complicates its diagnosis and prevention. There are no efficient vaccines against RE nor treatment, which also complicates how to limit its impact on poultry farming. This paper reviews the current state of knowledge of this important immunosuppressive agent of poultry emphasising the importance of this problem in terms of diagnosis of RE.

Introduction: The functions and mechanisms of prion proteins (PrPC) are currently unknown, but most experts believe that deformed or pathogenic prion proteins (PrPSᶜ) originate from PrPC, and that there may be plural main sites for the conversion of normal PrPC into PrPSᶜ. In order to better understand the mechanism of PrPC transformation to PrPSᶜ, the most important step is to determine the replacement or substitution site. Material and Methods: BALB/c mice were challenged with prion RML strain and from 90 days post-challenge (dpc) mice were sacrificed weekly until all of them had been at 160 dpc. The ultra-structure and pathological changes of the brain of experimental mice were observed and recorded by transmission electron microscopy. Results: There were a large number of pathogen-like particles aggregated in the myelin sheath of the brain nerves, followed by delamination, hyperplasia, swelling, disintegration, phagocytic vacuolation, and other pathological lesions in the myelin sheath. The aggregated particles did not overflow from the myelin in unstained samples. The phenomenon of particle aggregation persisted all through the disease course, and was the earliest observed pathological change. Conclusion: It was deduced that the myelin sheath and lipid rafts in brain nerves, including axons and dendrites, were the main sites for the conversion of PrPC to PrPSᶜ, and the PrPSᶜ should be formed directly by the conversion of protein conformation without the involvement of nucleic acids.

Introduction: The aim of this study was to carry out a genetic analysis of Babesia canis isolates detected in dogs in eastern Poland and to study the correlation of the protozoa variant with a specific geographical region. Material and Methods: PCR was used to identify strains of B. canis from naturally infected animals (240 dogs from four provinces: Mazowieckie, Lublin, Podlasie, and Podkarpacie) by amplifying and sequencing a fragment of the 18S rRNA gene. Results: Sequencing the PCR products led to the identification of four variants of B. canis. Two previously described protozoa variants (18S rRNA-A and 18S rRNA-B) were observed in all provinces. Additionally, in the Mazowieckie and Lublin provinces a B. canis variant which contributed to the development of acute or atypical babesiosis was observed. The fourth variant of B. canis was detected only in dogs from the Lublin province, and the course of the disease was subclinical in all dogs infected with this variant. Conclusion: These results indicate the appearance of a new fourth B. canis genotype in Poland and confirm that it is still necessary to study the relationships between the genetic structure of protozoa, geographical distribution of the parasites, and clinical course of the disease.

Objective: To compare the degree of mRNA expression for matrix metalloproteinases (MMPs), tissue inhibitors (TIMPs), and lysyl oxidase in myocardial samples from dogs with cardiac and systemic diseases and from healthy control dogs. Sample: Myocardial samples from the atria, ventricles, and septum of 8 control dogs, 6 dogs with systemic diseases, 4 dogs with dilated cardiomyopathy (DCM), and 5 dogs with other cardiac diseases. Procedures: Degrees of mRNA expression for MMP-1, -2, -3, -9, and -13; TIMP-1, -2, -3, and -4; and lysyl oxidase were measured via quantitative real-time PCR assay. Histologic examination of the hearts was performed to identify pathological changes. Results: In myocardial samples from control dogs, only TIMP-3 and TIMP-4 mRNA expression was detected, with a significantly higher degree in male versus female dogs. In dogs with systemic and cardiac diseases, all investigated markers were expressed, with a significantly higher degree of mRNA expression than in control dogs. Furthermore, the degree of expression for MMP-2, TIMP-1, and TIMP-2 was significantly higher in dogs with DCM than in dogs with systemic diseases and cardiac diseases other than DCM. Expression was generally greater in atrial than in ventricular tissue for MMP-2, MMP-13, and lysyl oxidase in samples from dogs with atrial fibrillation. Conclusions and Clinical Relevance: Degrees of myocardial MMP, TIMP, and lysyl oxidase mRNA expression were higher in dogs with cardiac and systemic diseases than in healthy dogs, suggesting that expression of these markers is a nonspecific consequence of end-stage diseases. Selective differences in the expression of some markers may reflect specific pathogenic mechanisms and may play a role in disease progression, morbidity and mortality rates, and treatment response.

Colostrum-deprived calves (n = 34) were fed various amounts of colostrum, colostrum substitute, or milk replacer to establish a range in titer of passively acquired viral neutralizing antibody in serum. The calves were then challenge exposed intranasally with a virulent, noncytopathic bovine viral diarrhea virus (BVDV-890). After viral challenge exposure, calves were monitored for fever, leukopenia, thrombocytopenia, and diarrhea. In addition, viral isolation and viral titration were performed on specimens of nasal secretions, buffy coat cells, and serum obtained from the calves. Fever and systemic spread of virus were detected in calves that had viral neutralizing titer of 256 or lower. Calves that had viral neutralizing titer lower than 16 developed severe clinical disease manifested by fever, leukopenia, thrombocytopenia, and diarrhea. Seventy and duration of signs of disease decreased as titers of passively acquired viral neutralizing antibody increased. These results indicate that low to intermediate titers of passively acquired viral neutralizing antibody were not sufficient to fully protect calves from virulent bovine viral diarrhea virus.

Sequential histologic, immunologic, and virologic features of herpesvirus-induced keratitis were studied in 18 experimentally infected cats. Histologic changes were assessed by use of light microscopy, and the presence of viral antigen, B lymphocytes, and T lymphocytes was verified immunohistochemically. Flow cytometry was used to monitor changes in blood T lymphocytes (CD4 and CD8 homologues) and B lymphocytes. Cellular immunity was assessed by use of the lymphocyte proliferation assay. Development of stromal keratitis was preceded by prolonged absence of corneal epithelium, decreased numbers of circulating lymphocyte subsets, decreased mitogen responses, and acquisition of viral antigen by the corneal stroma. Return to normal of circulating lymphocyte numbers and function was temporally associated with the arrival of neutrophils and B and T lymphocytes in the corneal stroma. Sequelae to stromal inflammation were fibrosis and scarring. Findings suggest that suppression of local immune responses allows virus access to the corneal stroma, and that subsequent keratitis is mediated by an immune response to viral antigen.

Static lung compliance, static lung volumes, and transfer factor for carbon monoxide were measured in 12 anesthetized adult Texel ewes seropositive for maedi-visna virus (MVV) and in 11 breed-, sex-, and age-matched seronegative controls. Median static lung compliance in MVV-infected sheep (1.24 L.kPa-1; range, 0.27 to 2,20 L.kPa-1) was not significantly different from that in controls (1.58 L.kPa-1; range, 0.82 to 2.08 L.kPa-1). Median body weight of MVV-infected sheep (56 kg; range, 40 to 75 kg) was significantly (P < 0.05) less than that of controls (65 kg; range, 53 to 87 kg). Median effective alveolar lung volume in MVV-infected sheep (3.36 L; range, 1.44 to 4.52 L) was significantly (P < 0.01) less than that in controls (4.12 L; range, 3.75 to 4.90 L). Median effective end expiratory lung volume in MVV-infected sheep (1.20 L; range, 0.56 to 1.99 L) was significantly (P < 0.001) less than that of controls (1.98 L; range: 1.76 to 2.78 L). Median lung volumes expressed per unit of body weight did not differ significantly between the groups. Median single-breath transfer factor for carbon monoxide in MVV-infected sheep (7.89 mmol-min-1.kPa-1; range, 3.45 to 12.74 mmol.min-1.kPa-1) was significantly (P < 0.001) less than that in controls (14.10 mmol.min-1-kPa-1; range, 10.02 to 18.30 mmol.min-1-kPa-1). Median transfer factor expressed per liter of alveolar volume in MVV-infected sheep (2.44 mmol.min-1-kPa-1.L-1; range, 1.28 to 3.72 mmol.min-1-kPa-1.L-1) gm significantly (P < 0.05) less than that in controls (3.22 mmol.min-1-kPa-1.L-1; range, 2.47 to 3.74 mmol.min-1-kPa-1.L-1). These findings indicate that static lung volumes and transfer factor for carbon monoxide are significantly decreased in adult sheep naturally infected with MVV.