Olesya Petrukhina

Climate change and global warming are concerning issues impacting various industries. In the aquaculture industry, these issues are more important in coldwater species, like rainbow trout Oncorhynchus mykiss. Hence, strategies to control these negative effects are worthy of study. Herbal feed additives are reliable tools to increase fish growth and health, thereby mitigating the drawbacks of climate change on fish. In this study, three diets containing 100 (100EO), 200 (200EO), and 400 (400EO) mg/kg essential oil of Abies sibirica (SBF) along with a control diet (CTL; unsupplemented) were fed to triplicate groups of fish for 60 days. Then the fish were exposed to a 96 h heat stress (25 °C) to monitor their survival and biochemical responses. The results showed that growth performance, feed efficiency, heat stress resistance, intestinal activity of digestive enzymes, and skin mucus immunological parameters significantly (p < 0.05) increased in the SBF essential oil treatments, and the highest increases were observed in the 100EO treatment, followed by the 200EO group. Dietary supplementation with SBF essential oil significantly (p < 0.05) mitigated heat stress-induced increases in plasma cortisol and glucose. Moreover, dietary SBF essential oil significantly (p < 0.05) enhanced immunological parameters such as plasma and intestinal lysozyme and immunoglobulin levels, and improved hepatic antioxidant defenses (including catalase, glutathione peroxidase, total antioxidant capacity, and reduced glutathione), while reducing lipid peroxidation. These effects were most pronounced in the 100EO and 200EO treatments, with the highest performance being observed in the former group. In conclusion, dietary SBF essential oil at 100 mg/kg is capable of augmenting growth performance, immunity, and antioxidant capacity, and suppressing physiological stress, thereby augmenting fish resilience against heat stress.

This article examines the issues of studying pathogenetic correlative links between various clinical and laboratory parameters in cats with cardiorenal syndrome. A significant correlation was found between the level of creatininemia and the pulse rate (r = 0.4), respiratory rate (r = 0.7), sleep breathing rate (r = 0.6), systolic (r = 0.3), diastolic (r = 0.3), mean arterial pressure (r = 0.3), QRS complex duration (r = 0.5), QT interval (r = 0.3), P wave voltage (r = 0.3) and R in the second standard lead (r = 0.4), left atrium size (r = 0.7), interventricular septum thickness in diastole (r = 0.7), left ventricular free wall thickness in diastole (r = 0.6), end-diastolic size (r = -0.6; p ≤ 0.05), end-systolic size of the left ventricular chamber (r = -0.5), serum alanine aminotransferase (r = 0.5), lactate dehydrogenase (r = 0.6), aspartic aminotransferase (r = 0.7), creatinine phosphokinase (r = 0.7), cardiac troponin (r = 0.5), serum concentration of urea (r = 0.7), ketone bodies (r = 0.7), malondialdehyde (r = 0.7), diene conjugates (r = 0.7), ceruloplasmin (r = 0.6), superoxide dismutase activity (r = -0.5), catalase (r = -0.7), glutathione peroxidase (r = -0.6). In the body of cats with cardiorenal syndrome, there is an activation of the sympathoadrenal system, myocardial remodeling processes in the form of concentric hypertrophy, oxidative stress and damage to the cell membranes of cardiomyocytes and other cells of the body, while there is an increase in the mass and number of cardiomyocytes, a violation of the diastolic function of the myocardium, a syndrome of damage to the cell membranes of cardiac cells occurs, progressive prerenal azotemia develops against the background of chronic decompensation of the circulatory organs. Changes in the correlative pathogenetic relationships between clinical and laboratory parameters in cats with cardiorenal syndrome can be considered as predictors of a more malignant course of the pathological process.

The aim of the study is to investigate clinical and echocardiographic parameters in dogs with the development of cardiorenal syndrome as a complication of bicuspid valve endocardiosis. The study was conducted on 22 healthy dogs and 55 dogs with bicuspid valve endocardiosis complicated by cardiorenal syndrome. The sick dogs were divided into two groups: the first group was free from cardiorenal complications (n = 24), the second group was with cardiorenal syndrome (n = 31). It was shown that cardiorenal syndrome in dogs can develop as a complication of congestive left ventricular heart failure in left atrioventricular valve endocardiosis. In this case, cardiorenal syndrome is a marker of a more severe course of congestive left ventricular heart failure in dogs, which, in turn, initiates a decrease in renal function. Clinically, cardiorenal syndrome in dogs with endocardiosis is manifested by dyspnea, tachypnea during rest and sleep, tachycardia, systemic arterial hypertension and hypothermia. Echocardiographic studies in dogs with cardiorenal syndrome revealed signs of dilation of the pulmonary vein by 2.25 times (p < 0.001) and the left atrium by 1.66 times (p < 0.001), a decrease in longitudinal contractility of the left myocardium by 1.5 times (p < 0.05) and the right ventricle by 1.25 times (p < 0.05) compared to healthy dogs. In addition, in dogs with cardiorenal syndrome, a restrictive type of diastolic dysfunction of the heart was verified (an increase in peak E by 1.85 times (p < 0.001) and a decrease in peak A of transmitral blood flow by 1.5 times (p < 0.001), a decrease in the time of isovolumic relaxation by 1.74 times (p < 0.001) compared with healthy animals), as well as pronounced eccentric hypertrophy of the left ventricle (an increase in the end-diastolic size of the left ventricle by 1.38 times (p < 0.001) compared with healthy animals).

Veterinary specialists have lately observed comorbidity of heart and kidney diseases known as cardiorenal syndrome. Cardiorenal syndrome is typically defined as dysfunction of a primarily intact kidney under the influence of a complex of pathogenetic damaging factors that arise against the background of an underlying cardiac disease. The purpose of the work is to study the biochemical profile of blood serum in cats with cardiorenal syndrome arising against the background of hypertrophic cardiomyopathy. The studies were carried out on 24 physiologically healthy (control) cats, 24 diseased cats with uncomplicated forms of pathology (first group) and 25 cats with hypertrophic cardiomyopathy complicated by cardiorenal syndrome (second group). It was shown that cardiorenal syndrome may occur as a complication of hypertrophic cardiomyopathy in animals. Biochemical tests in animals with feline cardiorenal syndrome verified cytolysis of cardiomyocytes (increased serum activity of lactate dehydrogenase by 2.69 times, creatine phosphokinase by 2.02 times, increased serum concentration of cardiac troponin by 5.20 times as compared to healthy animals), azotemia (increased concentration in serum creatinine by 2.72 times, urea by 2.94 times, symmetric dimethylarginine by 2.60 times and cystatin C by 1.90 times as compared to healthy animals), enhanced ketogenesis, systemic inflammatory process (increased serum concentration of C-reactive protein by 1.55 times as compared to healthy animals), hypercholesterolemia, oxidative stress (decrease in serum activity of superoxide dismutase by 1.63 times, catalase by 4.67 times and glutathione peroxidase by 1.71 times, increase in the concentration of malondialdehyde by 1.79 times, ceruloplasmin by 2.50 times and diene conjugates by 1.85 times as compared to healthy animals), electrolyte imbalance in the form of hyperkalemia, hyponatremia, hyperphosphatemia and hypomagnesemia. Biochemical indicators such as serum concentrations of creatinine, troponin I, cystatin C, symmetric dimethylarginine and C-reactive protein can be considered reliable diagnostic markers for the presence of cardiorenal syndrome.

This research presents novel insights into the temporal dynamics of clinical and instrumental parameters pertaining to the emergence of cardiorenal syndrome in feline patients afflicted with hypertrophic cardiomyopathy. It elucidates that within pedigreed felines, the progression of congestive heart failure syndrome may precipitate the subsequent evolution and exacerbation of secondary renal damage, thus significantly complicating the trajectory of the primary pathological process. This study establishes, for the first time, theprevalence of cardiorenal syndrome, affecting 51.0% of the population within the broader cohort of cats afflicted with hypertrophic cardiomyopathy (n= 49). Moreover, it substantiates the role of the cardiorenal continuum in felines as apredictor of amore severe course of hypertrophic cardiomyopathy. Manifesting as concentric myocardial hypertrophy in domestic felines, cardiorenal syndrome is characterized by dyspnea, hypothermia, and circulatory insufficiency. Statistically significant findings include an elevated median nocturnal respiratory rate of 34.0 breaths/min (p0.001) compared to clinically healthy counterparts (18.0 breaths/min) in affected felines. Additionally, felines afflicted with hypertrophic cardiomyopathy and cardiorenal syndrome exhibit astatistically significant (p 0.001) elevation in median mean arterial blood pressure to 140.0 mmHg compared to clinically healthy counterparts (104.0 mmHg), sinus tachycardia at 199.0 beats/min (171.5 beats/min in healthy felines), resulting in astatistically significant (p 0.001) reduction in PQ intervals by 67.0 ms (75.5 ms in healthy felines), and an increase in QT interval by 204.0 ms (165.5 ms in healthy felines). Electrocardiographic assessments reveal indications of compromised intra-atrial and intraventricular conduction in hypertrophic cardiomyopathy-afflicted felines with cardiorenal syndrome, along with an augmented amplitude of the ventricular complex. Echocardiographic evaluations confirm alterations such as pulmonary vein dilation, pronounced left atrial anteroposterior enlargement, interventricular septal and left ventricular free wall hypertrophy, decreased longitudinal contractility of the left and right ventricles, and clinically significant diastolic dysfunction.

Background and Aim: The pathogenesis of staphylococcal infections is mediated by virulence factors, such as enzymes, toxins, and biofilms, which increase the resistance of microorganisms to host immune system evasion. Testing and searching for standardized multi-level algorithms for the indication and differentiation of biofilms at the early stages of diagnosis will contribute to the development of preventive measures to control the critical points of technology and manage dangerous risk factors for the spread of infectious diseases. This research aimed to study the main stages of Staphylococcus aureus biofilm formation in in vitro experiments and to analyze the dynamics of respiratory syndrome development in chickens infected with these bacteria. Materials and Methods: Experimental reproduction of the infectious process was performed using laboratory models: 10-day-old White Leghorn chickens (n = 20). Before the experiments, the birds were divided into two groups according to the principle of analogs: Group I (control, n = 10): the birds were intranasally inoculated with 0.5 cm3 of 0.9% NaCl solution; Group II (experiment, n = 10): the birds were intranasally inoculated with a suspension of S. aureus bacteria, 0.5 cm3, concentration 1 billion/cm3. Results: Colonization of individual areas of the substrate under study in vitro occurred gradually from the sedimentation and adhesion of single motile planktonic cells to the attachment stage of microcolony development. Staining preparations with gentian violet due to the “metachromosia” property of this dye are a quick and fairly simple way to differentiate cells and the intercellular matrix of biofilms. Fixation with vapors of glutaraldehyde and osmium tetroxide preserves the natural architecture of biofilms under optical and scanning electron microscopy. Pure cultures of S. aureus microorganisms were isolated from the blood, lungs, small intestine, liver, kidneys, and spleen after 5–10 days during experimental infection of chickens. Clinical signs of respiratory syndrome developed within 5–6 days after infection. Acute and subacute serousfibrinous airsacculitis, characterized by edema and thickening of the membranes of the air sacs and the presence of turbid, watery, foamy contents in the cavity, was the most characteristic pathomorphological sign. The signs of acute congestive hyperemia and one-sided serous-fibrinous pneumonia developed with significant thickening of fibrinous deposits. In Garder’s gland, there was an increase in the number of secretory sections, indicating hypersecretion of the glands. In the lymphoid follicles of Meckel’s diverticulum, leukocytes, usually lymphocytes, and pseudoeosinophils were detected. Conclusion: Hydration and heteromorphism of the internal environment of biofilms determine the localization of differentiated cells in a three-dimensional matrix for protection against adverse factors. The most characteristic pathomorphological sign was the development of acute and subacute serous-fibrinous airsacculitis when reproducing the infectious process in susceptible models. There was a significant thickening of fibrinous deposits and signs of acute congestive hyperemia and one or two serous-fibrinous pneumonia developed. Keywords: airsacculitis, avian, biofilm, pathogenesis, respiratory syndrome pneumonia, Staphylococcus aureus.

Urinary tract infections occupy a special niche among diseases of infectious etiology. Many microorganisms associated with urinary tract infections, such as Klebsiella oxytoca, Enterococcus spp., Morganella morganii, Moraxella catarrhalis, Pseudomonas aeruginosa, Proteus mirabilis, Staphylococcus aureus, Staphylococcus spp., and Candida spp., can form biofilms. The aim of this research was to study the effect of the enzyme L-lysine-Alpha-oxidase (LO) produced by the fungus Trichoderma harzianum Rifai on the biofilm formation process of microorganisms associated with urinary tract infections. Homogeneous LO showed a more pronounced effect than the culture liquid concentrate (cCL). When adding samples at the beginning of incubation, the maximum inhibition was observed in relation to Enterococcus faecalis 5960—cCL 86%, LO 95%; Enterococcus avium 1669—cCL 85%, LO 94%; Enterococcus cloacae 6392—cCL 83%, LO—98%; and Pseudomonas aeruginosa 3057—cCL 70%, LO—82%. The minimum inhibition was found in Candida spp. Scanning electron microscopy was carried out, and numerous morphological and structural changes were observed in the cells after culturing the bacterial cultures in a medium supplemented with homogeneous LO. For example, abnormal division was detected, manifesting as the appearance of joints in places where the bacteria diverge. Based on the results of this work, we can draw conclusions about the possibility of inhibiting microbial biofilm formation with the use of LO; especially significant inhibition was achieved when the enzyme was added at the beginning of incubation. Thus, LO can be a promising drug candidate for the treatment or prevention of infections associated with biofilm formation.

Background and Aim: Fungal infections are a growing problem for both humans and animals due to the emergence of pathogenic strains resistant to modern antifungal treatments. To evaluate the efficacy of new antifungal drugs, it is essential to develop animal models that demonstrate typical responses to both the infection (pathogenesis and clinical course) and to the treatment, including adverse effects. In this study, we established a rabbit otitis model by infection of an aggressive multidrug-resistant strain from dogs, Malassezia pachydermatis C23, with no need for concomitant immunosuppression. Materials and Methods: Twenty healthy adult male gray giant rabbits (1 year old, 5.5 kg) were inoculated once with M. pachydermatis C23 at 108 colony-forming units/mL. We observed the clinical signs of the disease and collected ear smears and blood samples every 5 days. Results: The infection progressed rapidly and exhibited characteristic clinical signs without spontaneous recovery for at least 1 month. In fact, substantial deterioration was observed as evidenced by blood parameters. Conclusion: This rabbit otitis model established using an aggressive drug-resistant fungus strain without immunosuppression could prove valuable for testing novel antifungal agents. Keywords: in vivo model, Malassezia pachydermatis, otitis media, rabbit.

The issues of changes in clinical, laboratory and instrumental parameters in cats with hepatocardial syndrome formed against the background of hypertrophic cardiomyopathy were studied. It is known that in high-bred cats with congestive heart failure, secondary hepatopathy can develop and progress. It was shown that hepatocardial syndrome occurs in 33.7 % of cats, out of the total number of patients with hypertrophic cardiomyopathy (n = 83). It has been established that hepatocardial complications in cats are a risk factor for a more severe course of hypertrophic cardiomyopathy. Hepatocardial syndrome in cats with hypertrophic cardiomyopathy is characterized by severe hypothermia, circulatory and respiratory failure. In sick animals, an increase in frequency of breathing during sleep was recorded (33.39.3 versus 17.91.8 times/min; p 0.001). Domestic cats with hepatocardial syndrome had a decrease in mean arterial blood pressure (100.219.3 versus 107.219.1 mm Hg; p 0.05), sinus tachycardia (200.319.6 17.8 times/min; p 0.001), which leads to a significant decrease in PQ intervals (57.99.9 versus 64.99.9 ms; p 0.001) and QT intervals (168.917, 2 vs 157.518.6 ms; p 0.001). Sick cats had a significant increase in the time of refilling of capillaries with blood, slowdown in intraventricular conduction, increase in voltage of ventricular and atrial complex on electrocardiograms, expansion of pulmonary vein, significant dilatation of left atrium, extreme concentric hypertrophy of left ventricle, increase in transverse contractility of myocardium of left ventricle and decrease in longitudinal contractility myocardium of left and right ventricles, cardiomyocyte cytolysis syndrome, cholestasis, and hypoalbuminemia

Background and Aim: It is known that during the early postpartum and lactation periods in dairy cows, metabolic disorders develop, that is, ketosis, which can lead to secondary damage to internal organs. Therefore, it is important to address the issues of changing the lactating cows' clinical, laboratory, and physiological parameters regarding the development of hepatocardial syndrome. This study aimed to provide clinical and diagnostic justification for developing hepatocardial syndrome in highly productive dairy cows. Materials and Methods: The study was conducted on 20 black and white cows in the early postpartum period (7–10 days after birth), with a milk production level of >4500 kg of milk during the previous lactation period, a positive result in the formol colloid sedimentary test, the presence of deafness and splitting of heart sounds, changes in the size, or increased pain sensitivity of the percussion field of the liver. Clinically healthy dairy cows in the early postpartum period were used as controls (n = 24). Clinical, electrocardiographic, echocardiographic, and biochemical parameters were also evaluated. Results: Dairy cows with hepatocardial syndrome developed arterial hypertension and sinus tachycardia, which led to a significant decrease in PQ and QT intervals at ECG. A significant increase in the diastolic size of the interventricular septum, systolic size of the free wall of the left ventricle, and diastolic and systolic sizes of the left ventricle and a significant decrease in the shortening fraction of the left ventricular myocardium were observed in the cows due to the development of hepatocardial syndrome. The affected cows demonstrated a significant increase in serum activity of gamma-glutamyl transferase, alanine aminotransferase, lactate dehydrogenase, creatine phosphokinase, alkaline phosphatase, troponin, malondialdehyde, diene conjugates, and ceruloplasmin and a decrease in glucose concentration. In addition, they demonstrated decreased activity of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. Conclusion: Hepatocardial syndrome in dairy cows occurs due to ketosis, characterized by arterial hypertension, sinus tachycardia, a moderate decrease in myocardial contractility, oxidative stress, and cytolysis of cardiomyocytes and hepatocytes. Therefore, the control and prevention of the development of hepatocardial syndrome will make it possible to maintain the productive health and longevity of dairy cows.