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.

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.

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.

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.

Objective-To compare pathological changes and viral antigen distribution in tissues of calves with and without preexisting subclinical bovine viral diarrhea virus (BVDV) infection following challenge with bovine herpesvirus-1 (BHV-1). Animals-24 Friesian calves. Procedures-12 calves were inoculated intranasally with noncytopathic BVDV-1a; 12 days later, 10 of these calves were challenged intranasally with BHV-1 subtype 1. Two calves were euthanized before and 1, 2, 4, 7, or 14 days after BHV-1 inoculation. Another 10 calves were inoculated intranasally with BHV-1 only and euthanized 1, 2, 4, 7, or 14 days later. Two calves were inoculated intranasally with virus-free tissue culture fluid and euthanized as negative controls. Pathological changes and viral antigen distribution in various tissue samples from calves with and without BVDV infection (all of which had been experimentally inoculated with BHV-1) were compared. Results-Following BHV-1 challenge, calves with preexisting subclinical BVDV infection had earlier development of more severe inflammatory processes and, consequently, more severe tissue lesions (limited to lymphoid tissues and respiratory and digestive tracts) and greater dissemination of BHV-1, compared with calves without preexisting BVDV infection. Moreover, coinfected calves had an intense lymphoid depletion in the Peyer patches of the ileum as well as the persistence of BVDV in target organs and the reappearance of digestive tract changes during disease progression. Conclusions and Clinical Relevance-In calves, preexisting infection with BVDV facilitated the establishment of BHV-1 infection, just as the presence of BHV-1 favors BVDV persistence, thereby synergistically potentiating effects of both viruses and increasing the severity of the resultant clinical signs.

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.

Effects of low-flow ischemia and reperfusion of the large colon on mucosal architecture were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline values. Systemic hemodynamic and metabolic variables were maintained constant and in a normal physiologic range. Full-thickness biopsy specimens were obtained from the left ventral colon for histomorphologic and morphometric examination at baseline and at 30-minute intervals for 6 hours; additional biopsy specimens were collected at 185, 190, and 195 minutes (corresponding to 5-, 10-, and 15-minute periods of reperfusion in group-3 horses). There were no differences among groups at baseline or across time in group-1 horses for any of the histopathologic variables. There were significant (P < 0.05) increases in percentage of surface mucosal disruption, estimated and measured percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, and cellular debris index during 0 hour to 3 hours, compared with baseline, and from 3 hours to 6 hours, compared with 3 hours in horses of groups 2 and 3. Estimated percentage depth of mucosal loss and cellular debris index were significantly (P < 0.05) greater in group-3 horses, compared with group-2 horses during the interval from 3 to 6 hours. There were trends toward greater percentage of surface mucosal disruption and mucosal edema during the early phase of reperfusion (3 to 4 hours) and greater mucosal hemorrhage, measured percentage depth of mucosal loss, and mucosal interstitial-to-crypt ratio during the late phase (4 to 6 hours) of reperfusion in group-3 horses vs group-2 horses. Reestablishment of colonic arterial blood flow after low-flow ischemia caused greater mucosal injury than did a comparable period of continued ischemia. Thus, reperfusion injury was detected in the large colon of horses after low-flow arterial ischemia. The serial mucosal alterations that developed in the colon were comparable in horses of groups 2 and 3; however, reperfusion exacerbated colonic mucosal injury.

Ibuprofen treatment was compared with saline solution treatment in an endotoxin-induced experimental model of bovine mastitis. Acute mastitis was induced in healthy lactating Holstein cows (n = 12) by intrammamary inoculation of 1 mg of Escbericbia coli 026:B6 lipopolysaccharide in a single quarter per cow. Cows were assigned at random to ibuprofen (25 mg/kg of body weight, IV, n = 6) or 0.9% sodium chloride solution control (1.25 ml/kg, IV, n = 6) treatment groups. Ibuprofen or saline solution was administered once, 2 hours after endotoxin administration. The clinical course of endotoxin-induced mastitis and hematologic, clinical biochemical, and plasma mineral changes were monitored and compared between ibuprofen-treated and control cows. Clinical monitoring and blood sample collection were performed at 0, 2, 4, 6, 8, 12, 24, 48, 96, and 192 hours after endotoxin challenge. Rectal temperature and heart and respiratory rates were significantly (P < 0.05) increased in saline treated cows, compared with cows treated with ibuprofen, Blood eosinophil count and serum phosphorus, sodium, and total carbon dioxide concentrations were significantly (P < 0.05) decreased in saline-treated cows, compared with cows treated with ibuprofen. Ibuprofen treatment did not significantly change ruminations per minute, electrical conductivity of milk, quarter size, or quarter inflammation. The remaining hematologic, serum biochemical, plasma mineral, and coagulation values also were not changed significantly in response to ibuprofen treatment. Untoward effects attributed to ibuprofen administration were not observed. These results indicate that ibuprofen may provide empiric relief of clinical signs of coliform-induced mastitis.