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Background: Canine degenerative myelopathy represents a progressive neurodegenerative disorder impacting the spinal cord. Initial clinical signs of canine degenerative myelopathy are typically observed in animals around 8 years of age. The clinical signs are characterized by general proprioceptive ataxia and spastic paresis of the pelvic limbs, with an irrepressible progression to flaccid paraplegia after 1 year of the appearance of the signs. Therefore, canine degenerative myelopathy is considered a differential diagnosis for medullary neoplasms, disc protrusion, and hip dysplasia, and since the clinical signs presented by the animals are similar in all these diseases, genetic testing plays an important role in diagnosis. In several dog breeds degenerative myelopathy was linked to the c.118G>A autosomal recessive variant in exon 2 of the superoxide dismutase 1 (SOD1) gene (SOD1:c.118G>A). In addition, the SOD1:c.118G>A variant in more than 124 breed dogs, suggests that this variant is widely spread and fixed in the species before the breeds' origin. However, there are few studies evaluating this variant in brazilian dogs, and none of them have evaluated it in the Brazilian Golden Retriever dogs. Therefore, this study aimed to evaluate the allele frequency of the SOD1:c.118G>A variant in Golden Retriever dogs from Brazilian kennels. Materials, Methods & Results: A total of 122 Brazilian Golden Retriever DNA samples were used in a PCR procedures with specific primers, previously described, to amplify a 779 base pairs amplicon containing the SOD1:c.118G>A variant in this study, and a non-template control reaction was performed to check possible contamination in the PCR preparation. The genotyping of the animals was performed by direct Sanger sequencing of PCR products that amplified a fragment containing the variant. Considering the 95% confidence interval, the sample size used in the present study was slightly larger than the minimum required to assess the allele frequency of SOD1:c.118G>A variant (122 versus 113 samples). All animals assessed in this study were clinically normal at the time of sampling and were identified as wild-type for the SOD1:c.118G>A variant. Therefore, no alleles of the pathogenic variant (A) were found in the studied population. Discussion: Although all animals assessed in this study were classified as wild-type, this study is the 1st report in Brazil to evaluate the prevalence of this variant in Golden Retriever dogs. The poor prognosis and inexorable progression of canine degenerative myelopathy force most owners to opt for early euthanasia of affected animals. Knowledge of the disease by owners and breeders, as well as the genotyping of their animals, may prevent the spread of the variant among lineages and also assist veterinarians in differential diagnosis and management of cases of canine degenerative myelopathy. The genetics of Brazilian Golden Retriever were mainly derived from USA bloodlines. With this in mind, we may speculate that the results observed in this study may be influenced by the lower prevalence of the SOD1:c.118G>A variant previously found in American Golden Retrievers. The results obtained in the present study, combined with previous studies that described the occurrence of this variant as rare in Golden Retrievers, lead us to speculate that this variant does not impact the Brazilian Golden Retriever dogs. [ABSTRACT FROM AUTHOR]

Background: Congenital myotonia is a genetic neuromuscular disorder characterized by delayed relaxation of the musculature following a strong contraction. Variants in the skeletal muscle chloride channel 1 gene (CLCN1) have been linked to this disorder across several species. The CLCN1_c.1775A>C, an autosomal recessive variant, was identified as a potential causative factor for congenital myotonia in New Forest Pony. While the CLCN1_c.1775A>C variant has been studied in different breeds of horses, it remains unexplored in Brazilian Quarter Horses. Therefore, this study aimed to assess the prevalence of the CLCN1_c.1775A>C variant among Brazilian Quarter Horses across various disciplines. Materials, Methods & Results: In this study, 96 DNA samples were obtained from athletic Brazilian Quarter Horses representing various disciplines, 24 each from cutting, reining, barrel racing, and bull-cacthing ("vaquejada"). DNA viability was assessed via PCR targeting the ß-actin gene. Subsequently, a previously described set of specific primers was employed to amplify the region encompassing the CLCN1_c.1775A>C variant. The resulting purified PCR products underwent Sanger direct sequencing, and their electropherograms were analyzed. Notably, none of the horses in this cohort were found to carry the CLCN1_c.1775A>C variant. The inbreeding coefficient (F) was calculated using pedigree data sourced from the 96 Quarter Horses according to Brazilian Quarter Horse Breeders Association records encompassing 4 generations. The average F value for the entire cohort was found to be 0.2%. However, when assessed across disciplines, the average F values varied, with cutting at 0.002 (0.2%), reining at 0.003 (0.3%), barrel racing at 0.0008 (0.08%), and bull-cacthing at 0.001 (0.1%), respectively. Notably, within this cohort, 48 horses were identified as inbred, exhibiting an average F of 1.5%. Discussion: Genetic variants associated with conditions such as hyperkalemic periodic paralysis, myosin heavy chain myopathy, and polysaccharide storage myopathy type 1 have been previously documented in Quarter Horses globally, including Brazil. However, as in the present study, the CLCN1 c.1775A>C variant was also not detected in American Quarter Horses affected by muscular disorders. Although this variant has been implicated as the cause of congenital myotonia in a New Forest pony, its correlation with cases of congenital myotonia in Quarter Horses has not been established yet. Although the inbreeding coefficient and the prevalence of endogamous horses observed in this study were lower compared to findings in other studies, the presence of inbreeding and shared ancestors within Quarter Horses lineages was evident. High rates of inbreeding may disseminate undesirable genetic variants, since popular stallions may improve the athletic performance of its progenies but also may transmit alleles with pathogenic variants, as seen in other genetic disorders in horses. Differently, since it was not observed in this group of evaluated Quarter Horses nor in other previous studies, it may be that the CLCN1 c.1775A>C is a 'de novo' variant related strictly to congenital myotonia in the New Forest pony. Nevertheless, it is imperative to highlight the potential for congenital myotonia to inflict significant harm upon horses. Investigations into new cases are essential to establish both clinical and etiological diagnoses, thereby enabling the assessment of the requisite preventive measures against this disorder. [ABSTRACT FROM AUTHOR]

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Background: Polioencephalomalacia (PEM) is a neurological disease in ruminants, which is characterized by malacia of brain gray matter. Thiamine deficiency and sulfur intoxication are the most common causes of PEM in sheep. Affected animals present signs of cerebrocortical syndrome, including amaurosis, ataxia, head pressing, mental depression, seizures, and opisthotonus. The neurological examination aims to determine the neurolocalization of the lesions and advanced imaging techniques are useful for confirming the affected area(s) in the central nervous system. The aim of this study is to describe clinical features and ante-mortem diagnosis using magnetic resonance imaging (MRI) in a sheep with PEM. Case: A 18-month-old male Dorper sheep from a flock started receiving concentrate 7 days before. According to the owner, no clinical signs of abnormality were observed on the previous morning. However, in the afternoon, the animal became selfisolated and did not follow the flock to the sheepfold. The following day, he was found in recumbency. Physical examination revealed lateral recumbency, rectal temperature 39.5ºC, 52 bpm, 120 bpm, congested mucous membranes, capillary refill time 1 s, ruminal (4/5 min) and intestinal hypomotility. The assessment of the central nervous system revealed a decreased level of consciousness, focal seizures, opisthotonus, and absence of menace response. The following differential diagnoses were listed: PEM, head trauma, focal symmetrical encephalomalacia, bacterial encephalitis, and rabies. Treatment was composed of dexamethasone [0.2 mg/kg - i.v., SID (1st-3rd day), 0.1 mg/kg, i.v., SID (4th-6th day), and 0.05 mg/kg, i.v., SID (7th-9th day)]; mannitol [1 g/kg - i.v. and diazepam 0.4 mg/kg, i.v. single dose at admission]; vitamin B1 [10 mg/kg - i.m., SID], furosemide [1 mg/kg - i.v., SID for 3 days] and sulfadoxine/trimethoprim [30 mg/kg - i.m., SID for 10 days]. After the initial treatment, the patient showed mild clinical improvement; however, the amaurosis was still present. Magnetic resonance imaging of the brain was performed on the 2nd day of hospitalization, showing a symmetrical hypersignal in the parietal and occipital cortices, in the axial and sagittal sequences weighted in T2 and FLAIR. Discussion: This study aimed to describe the clinical signs and MRI findings in a sheep with PEM. In this case, the sudden change to the feed composition probably led to ruminal dysbiosis, inhibition of thiamine-producing microorganisms and proliferation of bacteria that synthesize thiaminase. Thiamine therapy proved to be effective and capable of reverting the clinical signs. The decrease in the level of consciousness, cortical blindness, and opisthotonus are due to alterations in the parietal cortex, in the occipital cortex, and in the cerebellum, respectively, which were demonstrated by hypersignal areas in the MRI. Therefore, the neurolocalization of the lesion based on neurologic examination and the MRI findings were related. The physicochemical and cytological evaluations of the cerebrospinal fluid, and dosage of thiamine and the concentration of hydrogen sulphide in the rumen were not performed. However, the response to thiamine treatment associated with the neurologic examination and MRI findings helped in determining the diagnosis. Additionally, MRI can be used as a useful tool for the ante mortem diagnosis of PEM. [ABSTRACT FROM AUTHOR]

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Background: Post-anesthetic myopathy is the most common complication associated with general anesthesia in horses. Polysaccharide storage myopathy (PSSM) is characterized by an abnormal accumulation of glycogen and glycogen-related polysaccharides in the skeletal muscle, which is categorized in type 1 (PSSM1) and type 2 (PSSM2). The purpose of this study is to report the clinical, pathological and molecular findings in a Percheron mare with post-anesthetic myopathy associated with a PSSM1. Case: A 9-year-old Percheron mare was submitted to a caesarean section due to clinical dystocia during labor. Xylazine was employed during pre-anesthesia, followed by induction with ketamine and diazepam, while anesthetic maintenance was obtained with isoflurane. The mare showed good recovery, however 24 h later, sternal recumbency and hyperthermia (41° C) were observed. The mare was euthanized, and a necropsy was performed. Samples of multiple tissues were collected and routinely processed for histology. At necropsy, segments of skeletal muscles had bilateral pale areas. The kidneys had old and recent infarcts. The heart had whitish areas in the myocardium. The brain showed focally extensive reddish areas, with flattening of gyri. Histologically, skeletal muscle fibers had in the sarcoplasm multiple homogeneous globular clear eosinophilic formations, in addition to mild hyaline necrosis. In the heart and in the kidney, there were extensive areas of acute coagulative necrosis. The brain showed marked multifocal fibrinoid degeneration of vessels and hemorrhage. Refrigerated liver samples were submitted to DNA extraction to detect mutations in the GYS1 (type 1 PSSM) and RyR1 genes (malignant hyperthermia). A positive result for a homozygous dominant mutation in GYS1 (type 1 PSSM) was observed, while the mutation responsible for malignant hyperthermia was not identified. Discussion: The diagnosis of post-anesthetic myopathy associated with PSSM was obtained by the presence of amylase resistant polysaccharide complex inclusions, glycogen subsarcolemmal aggregates, and central cytoplasmic corpuscles containing glycogen through PAS-amylase resistant histochemical technique, associated to the myopathy microscopical features. Microscopic findings were related to clinical history, and the diagnosis of PSSM underlying post-anesthetic myopathy was determined. The predisposition of the Percheron horse has been described as an inherited predisposition leading to PSSM susceptibility, as was observed in the present case. We speculated that the anesthetic procedure resulted in the precipitation of the drug and a presentation of an acute anesthetic myopathy, while the muscle damage most likely occurred due to the ischemia caused by systemic hypotension. In addition to these lesions, other lesions were considered related to the use of the anesthetics, which may predispose to vasculogenic injuries. This horse was diagnosed as being homozygous dominant for the GYS1 gene, which causes a gain-offunction and results in glycogenolysis with glycogen accumulation in myofibers. Horses that are homozygous for the GYS1 gene may exhibit more severe histological changes in the skeletal muscle fibers, such as necrosis, anisocytosis, endomysial fibrosis, and fatty infiltration. In PSSM, there is a bilateral involvement of the skeletal muscles with areas of degeneration of whitish or greyish coloration, as well as pale muscle with whitish streaks due to coagulative necrosis and edema. In our study, we observed bilateral skeletal muscle lesions and cardiomyocyte necrosis. Post-anesthetic myopathy, along with skeletal muscle lesions, may predispose to vasculogenic injuries, with kidney and brain lesions in horses. Dominant homozygosis for the GYS1 gene with consequent PSSM1 disease probably aggravated the condition in this Percheron, with more severe histological muscular lesions. Our study should bring attention to the use of anesthetics in horses with PSSM1, especially in the Percheron breed. [ABSTRACT FROM AUTHOR]

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The article discusses the evaluation of Boxer dogs in Brazil for inherited deafness and presbycusis using brainstem auditory-evoked potential (BAEP) techniques. Veterinary practice with BAEP for identifying congenital sensorineural hearing loss is noted to establish mean inter-peak latencies in waveforms. Normative data is presented supporting prior findings on the prevalence of unilateral deafness in breeds with white coat pigmentation and periocular patches.

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Copyright of Revista Academica Ciencia Animal is the property of Revista Academica Ciencia Animal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Academica Ciencia Animal is the property of Revista Academica Ciencia Animal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Academica Ciencia Animal is the property of Revista Academica Ciencia Animal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Tendon injury is a major cause of lameness and decreased performance in athletic equines. Various therapies for tendonitis have been described; however, none of these therapies results in complete tissue regeneration, and the injury recurrence rate is high even after long recovery periods involving rest and physiotherapy. Methods: A lesion was induced with collagenase gel in the superficial digital flexor tendon in the center portion of the metacarpal region of eight equines of mixed breed. After two weeks, the lesions of the animals in the treated and control groups were treated through the intralesional administration of mesenchymal stem cells derived from adipose tissue (adMSCs) suspended in platelet concentrate (PC) and with phosphate buffered saline (PBS), respectively. Serial ultrasound analyses were performed every two weeks. After 16 weeks of therapy, a biopsy was performed for histopathological, immunohistochemical and gene expression (type I collagen (COL1A1), type III collagen (COL3A1), tenascin-C (TNC), tenomodulin (TNMD), and scleraxis (SCX)) analyses. Results: Differences in the ultrasound and histopathological analyses were observed between the groups. Improved results were reported in the group treated with adMSCs suspended in PC. There was no difference in the gene expression levels observed after the different treatments. The main results observed from the histopathological evaluation of the treated group were as follows: a prevention of the progression of the lesion, a greater organization of collagen fibers, and a decreased inflammatory infiltrate. A lack of progression of the lesion area and its percentage was observed in the ultrasound image, and increased blood flow was measured by Power Doppler. Conclusions: The use of adMSCs combined with PC for the therapy of experimentally induced tendonitis prevented the progression of the tendon lesion, as observed in the ultrasound examination, and resulted in a greater organization and decreased inflammation, as observed in the histopathological evaluation. These data demonstrate the therapeutic potential of this therapy for the treatment of equine tendonitis [ABSTRACT FROM AUTHOR]

Background: Oculocutaneous albinism (OCA) is an autosomal recessive hereditary pigmentation disorder affecting humans and several other animal species. Oculocutaneous albinism was studied in a herd of Murrah buffalo to determine the clinical presentation and genetic basis of albinism in this species. Results: Clinical examinations and pedigree analysis were performed in an affected herd, and wild-type and OCA tyrosinase mRNA sequences were obtained. The main clinical findings were photophobia and a lack of pigmentation of the hair, skin, horns, hooves, mucosa, and iris. The results of segregation analysis suggest that this disease is acquired through recessive inheritance. In the OCA buffalo, a single-base substitution was detected at nucleotide 1,431 (G to A), which leads to the conversion of tryptophan into a stop codon at residue 477. Conclusion: This premature stop codon produces an inactive protein, which is responsible for the OCA buffalo phenotype. These findings will be useful for future studies of albinism in buffalo and as a possible model to study diseases caused by a premature stop codon. [ABSTRACT FROM AUTHOR]

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Copyright of Revista Acadêmica: Ciência Animal is the property of Revista Academica: Ciencia Animal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Acadêmica: Ciência Animal is the property of Revista Academica: Ciencia Animal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The Ehlers-Danlos syndrome (EDS) consists of a group of diseases characterized by defective collagen production or failure in its organization, resulting in changes in the strength and extensibility of connective tissue. This report describes the dermatological and histological findings observed in a 3-month-old crossbreed cat with rupture and detachment of skin in the thoracic limb and rupture of the skin in the cervical region. Upon dermatological examination, the cat presented fragile and hyperextensible skin in the cervical region and a skin extensibility index of 21%. Histopathological evaluation of the skin specimens revealed evident disorganization of collagen bundles in dermis and in the Masson's trichrome staining, follicular dysplasia was found. The presumptive diagnosis of EDS was made based on the clinical and histopathological findings. Sanger sequencing did not detect any mutated alleles for the c.3420delG mutation in COL5A1 gene, which was an autosomal dominant mutation previously been associated with Ehlers-Danlos syndrome in cats. The absence of this mutation in the reported cat suggests that other mutation may also be responsible for the development of cutaneous asthenia in this or maybe other genes related to collagen metabolism. [ABSTRACT FROM AUTHOR]

The brainstem auditory evoked potential (BAEP) evaluates the integrity of the auditory pathways to the brainstem. The aim of this study was to evoke BAEPs in 21 clinically normal horses. The animals were sedated with detomidine hydrochloride (0.013mg.kg-1 BW). Earphones were inserted and rarefaction clicks at 90 dB and noise masking at 40 dB were used. After performing the test, the latencies of waves (I, II, III, IV, and V) and interpeaks(I-III, III-V, andI-V) were identified. The mean latencies of the waves were as follows: wave I, 2.4 ms; wave II, 2.24 ms; wave III, 3.61 ms; wave IV, 4.61ms; and wave V, 5.49ms. The mean latencies of the interpeaks were as follows: I-III, 1.37ms; III-V, 1.88ms; and I-V, 3.26ms. This is the first study using BAEPs in horses in Brazil, and the observed latencies will be used as normative data for the interpretation of tests performed on horses with changes related to auditory system or neurologic abnormalities. [ABSTRACT FROM AUTHOR]

The exercise-induced collapse (EIC) is a hereditary disease characterized by muscle weakness, impaired locomotion and collapse after intense exercise. This autossomic recessive disorder affects mainly Labrador Retriever presenting the mutation c. 767G>T in the dynamin 1 (DNM1) gene. The objective of this study is to report the first case of exercise-induced collapse in Labrador Retriever in Brazil. The molecular test detected the specific genetic mutation and confirmed the clinical diagnosis in a Labrador Retriever with clinical history of weakness and collapse after exercise. It is important to include this disease as part of the differential diagnosis of neuromuscular diseases in Labrador Retriever and use the molecular test to guide matings. [ABSTRACT FROM AUTHOR]

Background: In horses, systemic calcinosis is a rare syndrome characterised by muscle lesion associated with the mineralisation of large muscle groups or other organs, in the absence of an alternative cause for the calcification, such as toxic, enzootic or metabolic. Molecular and histopathological aspects of the disease are still poorly elucidated., Objectives: To describe the epidemiological, pathological and molecular aspects of systemic calcinosis in a convenience sample of six horses submitted to necropsy in the Southern and Midwestern regions of Brazil., Study Design: Retrospective exploratory study., Methods: Post-mortem necropsy records of six horses with a cause of death compatible with systemic calcinosis, were reviewed followed by histopathology, immunohistochemistry, microbiology and molecular investigation., Results: The affected horses were all Quarter Horses with a mean age of 16.8 months, and an average disease course of 15.5 days. Muscle necrosis and mononuclear infiltration were observed in all animals in association with mineral deposition variably affecting the muscle tissue and/or other organs such as heart, lung and kidney. All tested animals (5/6) showed positive PCR results for the E321G MYH1 gene variant, which encodes the heavy chain of fast-contracting skeletal muscle myosin and is associated with myopathy. Three horses demonstrated positive immunostaining for Streptococcus equi, which is a known trigger for immune responses., Main Limitations: The study was limited by the small sample size, molecular evaluation was not completed in one animal due to technical limitations, lack of pre-mortem evaluation of calcium metabolism and lack of accurate descriptions in the necropsy reports of involvement of each muscle individually., Conclusions: In horses, systemic calcinosis syndrome causes immune-mediated muscle lesions in association with calcification of organs and tissues, varying greatly among animals. The E321G MYH1 variant was present in all horses tested for the variant and could be involved in the pathophysiology of systemic calcinosis., (© 2025 EVJ Ltd.)