The purpose of this study was to quantify the effect of difenoconazole (DFC) on the activity of a few enzymes commonly found on soil: dehydrogenase, urease, phosphatase and protease. Three experimental variants were established: in field conditions with variable temperature (10-21 ?C, variants A1-A3), under laboratory conditions with constant temperature (30 ?C, variants B1-B3) and untreated soil (C variant). The commercial product "Score 250EC" with 250 g DFC L-1 was used at the following concentrations: 0.037 mg DFC g-1 soil (variants A1 and B1), 0.075 mg DFC g-1 soil (variants A2 and B2) and 0.150 mg DFC g-1 soil (variants A3 and B3). The dehydrogenase, phosphatase and urease activities decreased significantly (p<0.05) both under filed (variants A1-A3) and laboratory (variants B1-B3) conditions compared to untreated soil (variant C). The protease activity was reduced in variants A1-A3 compared to variant C and increased at the dose of 0.150 mg DFC g-1 soil in the variant B3.

Knowledge and management of aquatic ecosystems (formerly Bulletin Français de la Pèche et de la Pisciculture), an international journal on freshwater ecosystem

Serotonin is considered to be the neurotransmitter that controls several types of behavior: aggressiveness, impulsivity, food selection, stimulation, sexual behavior, reaction to pain, and emotional manifestations. The aim of this study was to determine the serotonin values in 43 dogs, divided into three different experimental variants: (1) between two groups of medium (n = 6) and small (n = 4) breed shelter dogs; (2) in dogs with (n = 15) and without (n = 10) owners after administration of pre-spaying/neutering anesthesia; (3) in different behavioral states (n = 8) classified as follows: M1—happy, M2—aggressive, M3—calmed status, post-exposure to a stressful situation, compared to the reference time referred to as M0. There were no significant differences (p ≥ 0.05) regarding the serotonin values between the two groups of medium and small breed shelter dogs. Following anesthesia, the average mean serotonin values were significantly lower (p ≤ 0.003), by 63.85 ng/mL, in stray dogs compared to dogs with owners. No significant differences (p ≥ 0.05) were found when comparing the reference time M0 to M1, M2, and M3. The differences decreased significantly (p ≤ 0.05), by 89.61 ng/mL, between M1 and M2 and increased significantly (p ≤ 0.008), by 112.78 ng/mL, between M2 and M3.

Canine morbillivirus, also known as canine distemper virus (CDV), is the causative agent of canine distemper (CD), which is a serious contagious disease of canines, large felids, and, occasionally, raccoons. This study included seven raccoons from the Timisoara Zoological Garden, Romania. CDV was detected using RT-qPCR on blood samples, but several other exams were also performed—clinical, bacteriological, immunohistochemistry (IHC) and histopathology, toxicological screening, and necropsy—which confirmed CDV infection. Severe digestive disorders (diarrhea and frequent hematemesis) were observed. The necropsy findings included pseudo membranous gastroenteritis, congestion, and pulmonary edema in two raccoons. Immunohistochemistry showed immunolabeled CDV antigenantibodies on the viral nucleocapsid. Histopathology revealed lymphocyte depletion in mesenteric lymphnodes and intranuclear and intracytoplasmic inclusions in the enterocytes of the small intestine. Based on the RT-qPCR assay, laboratory tests, and the lesions observed, it was established that the raccoons were infected with CDV, which was the cause of death in two cases. The results from the necropsy, histology, and immunohistochemistry in the raccoons are comparable with reported CDV lesions in dogs. In conclusion, several exams may be performed to establish the etiology of possible interspecific viral infection, but only very specific exams can identify aCDV infection. Laboratory analyses must be completed by RT-qPCR assay or IHC to establish infection with uncommon viruses in raccoons with high accuracy.

Perinatal parvoviral infection in puppies leads to necrotizing myocarditis, resulting in either high mortality or gradual heart damage. We believe that canine parvovirus 2 (CPV-2) myocardial infection is not being fully recognized as a cause of myocarditis, cardiac injury, and fibrosis repair in young dogs, despite the significant reduction in the epidemic of canine parvoviral myocarditis due to extensive vaccination. This study analyzed formalin-fixed, paraffin-embedded tissues obtained from 40 canine cases aged less than two years, spanning the period from 2019 to 2021. The objective was to test for the presence of CPV 2. Cardiac necrosis, inflammation, or fibrosis were observed in the diagnosed cases, but the age-matched controls did not have any cardiac abnormalities and tested positive for CPV. The presence of myocardial CPV-2 was detected in young dogs with mild myocarditis, suggesting that the period of vulnerability to myocarditis in the heart may be greater than what has been previously documented. CPV-2 was found in dogs who had extensive myocardial fibrosis, indicating that CPV-2 had caused previous injury to the heart muscle. Although vaccinations are common, these findings indicate that CPV-2 continues to be a major contributor to cardiac injury in dogs.

Canine parvovirus type 2 (CPV-2) remains an important cause of morbidity and mortality in young dogs worldwide. Although the enteric form of the disease is well characterized, myocardial involvement associated with CPV-2 infection remains incompletely understood. The present retrospective study aimed to investigate myocardial lesions in young dogs and to evaluate their association with CPV-2 DNA detection using histopathological examination and PCR-based molecular analysis of formalin-fixed paraffin-embedded (FFPE) cardiac tissue. A total of 27 dogs aged between 3 and 11 months, submitted for diagnostic necropsy between 2019 and 2021, were included in the study. Histopathological evaluation was performed on myocardial tissue sections stained with hematoxylin and eosin, while conventional PCR targeting the VP1/VP2 region was used for the detection of CPV-2 DNA. Associations between PCR positivity and histopathological findings were assessed using Fisher’s exact test. Myocardial abnormalities were identified in all examined cases (27/27, 100%), with myocarditis consistently observed throughout the study population. Cardiomyocyte necrosis and myocardial fibrosis were identified in 9/27 (33.3%) and 14/27 (51.9%) cases, respectively. CPV-2 DNA was detected in 9/27 myocardial tissue samples (33.3%). Cardiomyocyte necrosis was significantly more frequent in CPV-2-positive dogs than in PCR-negative animals (77.8% vs. 11.1%; p ≈ 0.001). Similarly, myocardial fibrosis was identified more frequently in CPV-2-positive cases (100.0% vs. 27.8%; p ≈ 0.001). Myocarditis was present in all examined animals and therefore could not be evaluated statistically according to PCR status. The detection of CPV-2 DNA in myocardial tissues exhibiting histopathological lesions supports a possible association between CPV-2 infection and myocardial injury in young dogs. However, the retrospective design, limited sample size, and the use of conventional PCR do not allow conclusions regarding causality or direct viral involvement in lesion development. Further studies incorporating larger case series and complementary diagnostic techniques are needed to clarify the pathogenesis and clinical significance of CPV-2-associated myocardial lesions.