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Idiopathic orbital inflammation (IOI), or orbital pseudotumor, is a benign, non-infectious condition representing 8–10% of orbital mass lesions. This article presents a rare case of idiopathic orbital myositis (IOM) in a 45-year-old diabetic woman, who presented with acute right eye pain, diplopia, and motility deficits. Magnetic Resonance Imaging (MRI) revealed typical signs of inflammation, including hyperintense signals in T2-weighted Turbo Spin Echo (TSE) and Short Tau Inversion Recovery (STIR) sequences, along with post-contrast enhancement. Notably, there was no muscle belly enlargement, and the patient did not respond to corticosteroid therapy. Strict glycemic control, however, led to clinical improvement, suggesting a potential link between diabetes and IOM. Additionally, a comprehensive literature review on imaging in IOM was conducted, covering articles published from 2000 to 2024. The review highlights MRI as the primary diagnostic tool for IOM, offering a high sensitivity and specificity in differentiating it from other orbital conditions. This case underscores the importance of modern imaging techniques in diagnosis and emphasizes the need for continued research in evidence-based medicine, especially in complex cases where disease boundaries are not clearly defined. [ABSTRACT FROM AUTHOR]

Background: Calcific myonecrosis (CMN) is a rare condition, often considered to be a late sequela of antecedent trauma. Case Report: We describe here our experience in managing a 56-year-old male referred with a painless swelling on the lateral aspect of the left lower leg with a suspicion of a tumour. Results: Clinical and imaging features were classic of CMN. Conclusion: Clinical assessment, role of ultrasound scan in reaching a diagnosis and the management are highlighted. [ABSTRACT FROM AUTHOR]

Abstract Background: Fish venoms have been poorly characterized and the available information about their composition suggests they are uncomplicated secretions that, combined with epidermal mucus, could induce an inflammatory reaction, excruciating pain, and, in some cases, local tissue injuries. Methods: In this study, we characterized the 24-hour histopathological effects of lionfish venom in a mouse experimental model by testing the main fractions obtained by size exclusion-HPLC. By partial proteomics analysis, we also correlated these in vivo effects with the presence of some potentially toxic venom components. Results: We observed a strong lesion on the skin and evident necrosis in the skeletal muscle. None of the tissue-damaging effects were induced by the fraction containing cytolysins, membrane pore-forming toxins ubiquitously present in species of scorpionfish, stonefish, and lionfish, among others. On the contrary, injuries were associated with the presence of other components, which have remained practically ignored so far. This is the case of an abundant protein, present in venom, with homology to a Golgi-associated plant pathogenic protein 1-like (GAPR1), which belongs to the same protein superfamily as venom CRISPs and insect allergens. Conclusion: This GAPR1-like protein and the hyaluronidase are probably responsible for the hemostasis impairment and hemorrhagic lesions observed in mouse skin, whereas muscle injuries can be indirectly caused by a combination of inflammatory and hemorrhagic events. More information is required to establish the components accountable for the myonecrotic effect.

Stereotactic body radiotherapy is a highly effective form of radiation therapy for palliation of bone metastases, but it can also lead to rare but severe side effects, such as myonecrosis. According to the literature, the incidence of myonecrosis after stereotactic body radiotherapy is low and mostly dose dependent. It is crucial to consider the potential impact of immunotherapy and other systemic therapies in the assessment. The course of radiation myonecrosis can vary, and corticosteroids or vascular endothelial growth factor inhibitors may potentially play a role in its treatment. Herein, we report two patients presenting with myonecrosis after stereotactic body radiotherapy for bone metastasis. [ABSTRACT FROM AUTHOR]

Skeletal muscle necrosis is a common clinical manifestation of snakebite envenoming. The predominant myotoxic components in snake venoms are catalytically-active phospholipases A2 (PLA2) and PLA2 homologs devoid of enzymatic activity, which have been used as models to investigate various aspects of muscle degeneration. This review addresses the changes in the contractile apparatus of skeletal muscle induced by these toxins. Myotoxic components initially disrupt the integrity of sarcolemma, generating a calcium influx that causes various degenerative events, including hypercontraction of myofilaments. There is removal of specific sarcomeric proteins, owing to the hydrolytic action of muscle calpains and proteinases from invading inflammatory cells, causing an initial redistribution followed by widespread degradation of myofibrillar material. Experiments using skinned cardiomyocytes and skeletal muscle fibers show that these myotoxins do not directly affect the contractile apparatus, implying that hypercontraction is due to cytosolic calcium increase secondary to sarcolemmal damage. Such drastic hypercontraction may contribute to muscle damage by generating mechanical stress and further sarcolemmal damage. [ABSTRACT FROM AUTHOR]

Viperid snake venoms induce severe tissue damage, characterized by the direct toxic action of venom components, i.e., phospholipases A2 (PLA2s) and metalloproteinases (SVMPs), concomitantly with the onset of endogenous inflammatory processes, in an intricate scenario of tissue alterations. Understanding the expression of relevant genes in muscle tissue will provide valuable insights into the undergoing pathological and inflammatory processes. In this study, we have used the Nanostring technology to evaluate the patterns of gene expression in mouse skeletal muscle 1 h, 6 h, and 24 h after injection of the venoms of Bothrops asper and Daboia russelii, two medically relevant species in Latin America and Asia, respectively, with somewhat different clinical manifestations. The dose of venoms injected (30 µg) induced local pathological effects and inflammation in muscle tissue. We focused our analysis on genes related to extracellular matrix (ECM) metabolism, immune system, programmed cell death, and autophagy. The results revealed a complex pattern of expression of genes. Regarding ECM metabolism and regulation, up-regulated genes included proteinase inhibitor Serpine 1, thrombospondin 1, collagens 1A1 and 4A1 (at 1 h in the case of B. asper), TIMP1, MMP-3 (at 24 h), and lysil oxidase (LOX). In contrast, collagen chains 5A3 and 5A1 were down-regulated, especially at 6 h. Transforming growth factor β (TGF-β) and several genes related to myofibroblast regulation were also up-regulated, which might be related to the development of fibrosis. Several genes related to cytokine and chemokine synthesis and regulation and NFκB signaling were also up-regulated. Our observations show a variable expression of genes associated with programmed cell death and autophagy, thus revealing a hitherto unknown role of autophagy in tissue affected by snake venoms. These results provide clues to understanding the complex pattern of gene expression in tissue affected by viperid snake venoms, which likely impacts the final pathophysiology of damaged tissue in envenomings. [ABSTRACT FROM AUTHOR]

Abstract Background Duchenne muscular dystrophy (DMD) is a progressive muscle degenerative disorder, culminating in a complete loss of ambulation, hypertrophic cardiomyopathy and a fatal cardiorespiratory failure. Necroptosis is the form of necrosis that is dependent upon the receptor‐interacting protein kinase (RIPK) 3; it is involved in several inflammatory and neurodegenerative conditions. We previously identified RIPK3 as a key player in the acute myonecrosis affecting the hindlimb muscles of the mdx dystrophic mouse model. Whether necroptosis also mediates respiratory and heart disorders in DMD is currently unknown. Methods Evidence of activation of the necroptotic axis was examined in dystrophic tissues from Golden retriever muscular dystrophy (GRMD) dogs and R‐DMDdel52 rats. A functional assessment of the involvement of necroptosis in dystrophic animals was performed on mdx mice that were genetically depleted for RIPK3. Dystrophic mice aged from 12 to 18 months were analysed by histology and molecular biology to compare the phenotype of muscles from mdxRipk3+/+and mdxRipk3−/− mice. Heart function was also examined by echocardiography in 40‐week‐old mice. Results RIPK3 expression in sartorius and biceps femoris muscles from GRMD dogs positively correlated to myonecrosis levels (r = 0.81; P = 0.0076). RIPK3 was also found elevated in the diaphragm (P ≤ 0.05). In the slow‐progressing heart phenotype of GRMD dogs, the phosphorylated form of RIPK1 at the Serine 161 site was dramatically increased in cardiomyocytes. A similar p‐RIPK1 upregulation characterized the cardiomyocytes of the severe DMDdel52 rat model, associated with a marked overexpression of Ripk1 (P = 0.007) and Ripk3 (P = 0.008), indicating primed activation of the necroptotic pathway in the dystrophic heart. MdxRipk3−/− mice displayed decreased compensatory hypertrophy of the heart (P = 0.014), and echocardiography showed a 19% increase in the relative wall thickness (P

Simple Summary: Blackleg is a bacterial disease that primarily affects cattle but can also affect other cloven-hoofed animals such as sheep and goats. It is caused by the spore-forming bacterium Clostridium chauvoei and is prevalent in many parts of the world, including Brazil. Vaccination is one of the most effective ways to prevent blackleg. In Brazil, various types of vaccine are available, and they are typically administered to young animals. Brazil is a vast country with diverse climates and ecosystems. This can present challenges in terms of disease management strategies that are effective across all regions. In more remote areas, access to veterinary care and supplies may be limited, which can hinder timely diagnosis and treatment. The genus Clostridium is an important group of pathogenic and nonpathogenic Gram-positive anaerobic bacteria with a sporulation capacity and wide distribution in different environments, including the gastrointestinal tracts of healthy and diseased animals and humans. Among the pathogenic species of the genus, Clostridium chauvoei stands out as a histotoxic agent. It causes significant myonecrosis such as blackleg, a disease with high lethality, especially in young cattle, and is responsible for significant livestock losses worldwide. The pathogenicity of the disease is complex and has not yet been fully elucidated. Current hypotheses cover processes from the initial absorption to the transport and deposition of the agent in the affected tissues. The virulence factors of C. chauvoei have been divided into somatic and flagellar antigens and soluble antigens/toxins, which are the main antigens used in vaccines against blackleg in Brazil and worldwide. This review provides important information on the first and current approaches to the agent C. chauvoei and its virulence factors as well as a compilation of data on Brazilian studies related to blackleg. [ABSTRACT FROM AUTHOR]

This review illustrates the imaging features of rhabdomyolysis across multiple modalities and in a variety of clinical scenarios. Rhabdomyolysis is the rapid breakdown of striated muscle following severe or prolonged insult resulting in the release of myocyte constituents into circulation. In turn, patients develop characteristically elevated serum creatine kinase, positive urine myoglobin, and other serum and urine laboratory derangements. While there is a spectrum of clinical symptoms, the classic presentation has been described as muscular pain, weakness, and dark urine. This triad, however, is only seen in about 10% of patients. Thus, when there is a high clinical suspicion, imaging can be valuable in evaluating the extent of muscular involvement, subsequent complications such as myonecrosis and muscular atrophy, and other etiologies or concurrent injuries causing musculoskeletal swelling and pain, especially in the setting of trauma. Sequela of rhabdomyolysis can be limb or life-threatening including compartment syndrome, renal failure, and disseminated intravascular coagulation. MRI, CT, ultrasound, and 18-FDG PET/CT are useful modalities in the evaluation of rhabdomyolysis. [ABSTRACT FROM AUTHOR]

Background: Statin-induced necrotizing autoimmune myopathy is an exceptionally rare yet severe complication of statin therapy that may develop in individuals at any time during their exposure to statins. The development of proximal muscle weakness, muscle pain, and elevated creatine kinase (CK) levels in patients while taking statins should prompt clinical consideration of statin-induced myopathy. The pathophysiology arises from the production of auto-antibodies, which target the 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) enzyme, leading to the aggressive breakdown of myofibrils. Case Report: Here, we present a case of a 59-year-old woman with a medical history of dyslipidemia who developed anti-HMGCoA reductase antibodies after taking atorvastatin. She came to the emergency department with complaints of severe proximal muscle weakness. The laboratory workup showed an elevated CK level up to 12 000 IU/L. Despite discontinuing atorvastatin, the patient's elevated CK levels persisted. The patient underwent a muscle biopsy, demonstrating myofibril necrosis. Serological analysis showed anti-HMG-CoA reductase antibodies in the patient's serum, which led to the diagnosis of immune-mediated necrotizing myopathy due to statins. The patient's statin therapy was promptly discontinued, and she was treated with a high dose of IV corticosteroids. After the patient's discharge, brief discontinuation of the corticosteroids resulted in CK elevation and a return of symptoms. This led to the second re-admission and restarting of corticosteroids until stabilization and discharge. Conclusions: This case represents an important reminder for clinicians to recognize the possibility of statin-induced immunemediated necrotizing myopathy in patients presenting with proximal muscle weakness while taking a statin, notwithstanding the rarity of this condition. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the protective effect of the nature product osthole (OST) against Clostridium perfringens type A infection-caused myonecrosis in a mouse model. Male mice were divided into (1) control, (2) infected, (3) OST50 and (4) OST100 treatment groups. In the infected groups, mice were intramuscularly injected with 1 × 108 CFU of C. perfringens per day for 6 days. Mice in the OST50 and OST100 groups were administrated intraperitoneally with OST at the doses of 50 or 100 mg/kg per day post C. perfringens infection. Our results showed that C. perfringens infection caused marked necrosis and inflammatory cell infiltration in the muscle tissues of mice. Mice in the OST50 and OST100 treatment groups displayed significantly attenuated C. perfringens infection-induced lipid peroxidation, oxidative stress, and apoptosis in their muscle tissue. Furthermore, OST treatment significantly downregulated the expressions of NF-κB, IL-1β, and TNF-α mRNA and protein levels, while concomitantly upregulating the expressions of Nrf2 and HO-1 mRNA and protein. OST treatments also inhibited the expression of phosphorylation (p)-p38, p-mTOR, and p-Erk1/2 proteins, and upregulated LC3II and Beclin1 proteins. In summary, our results reveal that OST therapy confers a protective effect against C. perfringens infection-induced oxidative stress and inflammation in muscle tissue, via activation of Nrf2/HO-1 and autophagy pathways and inhibition of p38, Erk1/2 and NF-κB pathways. [ABSTRACT FROM AUTHOR]

Inflammatory myopathies are a rare group of disorders that can cause significant disruption in the ability of an individual to adequately perform activities of daily living. In this case report, we present a case of a girl presenting with a substantial compromise of her ambulation with a muscle biopsy consistent with myonecrosis. She was subsequently diagnosed with an inflammatory myopathy and started on glucocorticoid and methotrexate therapy with minimal symptomatic improvement. Further in her clinical course, hypocalcemia and an undetectable 25-hydroxyvitamin D level were detected. Prompt institution of calcium and vitamin D supplementation significantly improved her myopathic condition. While there is evidence in the literature linking vitamin D deficiency with myopathy, there is a lack of data on the association between hypocalcemia and vitamin D deficiency with myonecrosis, which could represent comorbid states in myonecrosis. Therefore, vitamin D status should be established in all patients with myonecrosis, as vitamin D deficiency is easy to diagnose and treat, as exemplified in our patient’s case, which shows that such treatment could lead to significant clinical improvement.

Objectives TNF-like weak inducer of apoptosis (TWEAK) and its sole receptor fibroblast growth factor-inducible 14 (Fn14) are involved in various inflammatory conditions. This study was performed to investigate the potential role of TWEAK/Fn14 in immune-mediated necrotizing myopathy (IMNM). Methods Muscle biopsies from patients with IMNM (n  = 37) and controls (n  = 11) were collected. Human muscle cells were treated with TWEAK in vitro. Muscle biopsies and cultured muscle cells were analysed by immunostaining and quantitative PCR. Serum levels of TWEAK and Fn14 were detected by ELISA. Results TWEAK and Fn14 were overexpressed in IMNM muscle biopsies. The percentage of Fn14-positive myofibers correlated with disease severity, myonecrosis, regeneration and inflammation infiltrates. Fn14-positive myofibers tended to be surrounded or invaded by CD68 + macrophages. TWEAK treatment had a harmful effect on cultured muscle cells by inducing the production of multiple chemokines and pro-inflammatory cytokines. Serum Fn14 levels were increased in patients with IMNM and correlated with muscle weakness. Conclusions TWEAK/Fn14 signalling was activated in IMNM, most likely aggravating muscle damage via amplifying inflammatory response and macrophages chemotaxis. Fn14 seems to be a biomarker for assessing disease severity in IMNM. In addition, Fn14 may also contribute to muscle injury repair. [ABSTRACT FROM AUTHOR]

Diabetic myonecrosis is a rare complication of poorly controlled diabetes mellitus which commonly affects the thigh and is managed conservatively. Spontaneous ischemic necrosis of muscle is noted without a reduction in vascular supply. Pyomyositis caused by Staphylococcus aureus infection is another rare complication. Atypical presentation of myonecrosis and pyomyositis can occur in the form of simultaneous or sequential involvement of multiple muscle groups. We present a rare case of myonecrosis with pyomyositis in a 39-year-old male patient with a background of type 2 diabetes mellitus who presented with a 5-day history of worsening pain of the right thigh radiating to the right ankle, associated with groin swelling and fever. It is important for clinicians to have a low threshold of suspicion of this rare condition due to the other diverse and similar diagnoses, as well as to prevent further complications and morbidity.

Duchenne muscular dystrophy (DMD) is one of the most devastating myopathies, where severe inflammation exacerbates disease progression. Previously, we demonstrated that adiponectin (ApN), a hormone with powerful pleiotropic effects, can efficiently improve the dystrophic phenotype. However, its practical therapeutic application is limited. In this study, we investigated ALY688, a small peptide ApN receptor agonist, as a potential novel treatment for DMD. Four-week-old mdx mice were subcutaneously treated for two months with ALY688 and then compared to untreated mdx and wild-type mice. In vivo and ex vivo tests were performed to assess muscle function and pathophysiology. Additionally, in vitro tests were conducted on human DMD myotubes. Our results showed that ALY688 significantly improved the physical performance of mice and exerted potent anti-inflammatory, anti-oxidative and anti-fibrotic actions on the dystrophic muscle. Additionally, ALY688 hampered myonecrosis, partly mediated by necroptosis, and enhanced the myogenic program. Some of these effects were also recapitulated in human DMD myotubes. ALY688's protective and beneficial properties were mainly mediated by the AMPK-PGC-1α axis, which led to suppression of NF-κβ and TGF-β. Our results demonstrate that an ApN mimic may be a promising and effective therapeutic prospect for a better management of DMD. [ABSTRACT FROM AUTHOR]

Many neuromuscular disorders can have a differential impact on a specific myofibre type, forming the central premise of this review. The many different skeletal muscles in mammals contain a spectrum of slow‐ to fast‐twitch myofibres with varying levels of protein isoforms that determine their distinctive contractile, metabolic, and other properties. The variations in functional properties across the range of classic 'slow' to 'fast' myofibres are outlined, combined with exemplars of the predominantly slow‐twitch soleus and fast‐twitch extensor digitorum longus muscles, species comparisons, and techniques used to study these properties. Other intrinsic and extrinsic differences are discussed in the context of slow and fast myofibres. These include inherent susceptibility to damage, myonecrosis, and regeneration, plus extrinsic nerves, extracellular matrix, and vasculature, examined in the context of growth, ageing, metabolic syndrome, and sexual dimorphism. These many differences emphasise the importance of carefully considering the influence of myofibre‐type composition on manifestation of various neuromuscular disorders across the lifespan for both sexes. Equally, understanding the different responses of slow and fast myofibres due to intrinsic and extrinsic factors can provide deep insight into the precise molecular mechanisms that initiate and exacerbate various neuromuscular disorders. This focus on the influence of different myofibre types is of fundamental importance to enhance translation for clinical management and therapies for many skeletal muscle disorders. [ABSTRACT FROM AUTHOR]

Myositis and myonecrosis are rare sequela of coronavirus disease 2019 (COVID-19). Until now, it has not been seen in muscles of the head and neck. We present a 22-year-old male with 4 months of retroauricular headaches following COVID-19 infection. Magnetic resonance imaging revealed rim-enhancing fluid collections in the bilateral masticator spaces which were sampled by fine-needle aspiration. We also discuss this case in the context of the current understanding of COVID-19-related myositis.

Soft tissue necrosis can occur at different tissue levels, with numerous underlying causes. In this pictorial review, we highlight myonecrosis, and its accompanying stages, fat necrosis, devitalized soft tissue seen with infection, and necrotizing soft tissue infections. Imaging examples are provided with each entity. [ABSTRACT FROM AUTHOR]

Abdominal wall and spinal soft tissue findings are frequently encountered on CT or MR imaging of the abdomen and pelvis. Many of these entities have specific imaging findings, for which a definitive diagnosis can be made without the need for further work up. These abdominal wall and spinal findings may be diagnostically challenging for sub-specialized abdominal radiologists who are unfamiliar with their appearance and appropriate management. This review article describes and illustrates pathognomonic or characteristic abdominal wall and spinal pathologies, which reside outside the abdominopelvic cavity. The cases selected all have findings that allow a confident diagnosis without further imaging or intervention. The cases presented include myonecrosis, intramuscular abscess, myositis, iliopsoas bursitis, Morel-Lavallée lesion, hydrocele of canal of Nuck, Klippel Trenaunay Weber syndrome, neurofibroma with target sign, perineural cysts, filum terminale lipoma, calvarial bone flap, transverse rectus abdominis muscle (TRAM) flap, liposuction, and hidradenitis suppurativa, among others. Although not all-encompassing, this paper will help abdominal radiologists to accurately diagnose a variety of abdominal and pelvic extra-cavitary soft tissue pathologies by identifying key radiologic findings. [ABSTRACT FROM AUTHOR]

Pathological and inflammatory events in muscle after the injection of snake venoms vary in different regions of the affected tissue and at different time intervals. In order to study such heterogeneity in the immune cell microenvironment, a murine model of muscle necrosis based on the injection of the venom of Daboia russelii was used. Histological and immunohistochemical methods were utilized to identify areas in muscle tissue with a different extent of muscle cell damage, based on the presence of hypercontracted muscle cells, a landmark of necrosis, and on the immunostaining for desmin. A gradient of inflammatory cells (neutrophils and macrophages) was observed from heavily necrotic areas to less damaged and non-necrotic areas. GeoMx® Digital Spatial Profiler (NanoString, Seattle, WA, USA) was used for assessing the presence of markers of various immune cells by comparing high-desmin (nondamaged) and low-desmin (damaged) regions of muscle. Markers of monocytes, macrophages, M2 macrophages, dendritic cells, neutrophils, leukocyte adhesion and migration markers, and hematopoietic precursor cells showed higher levels in low-desmin regions, especially in samples collected 24 hr after venom injection, whereas several markers of lymphocytes did not. Moreover, apoptosis (BAD) and extracellular matrix (fibronectin) markers were also increased in low-desmin regions. Our findings reveal a hitherto-unknown picture of immune cell microheterogeneity in venom-injected muscle which greatly depends on the extent of muscle cell damage and the time lapse after venom injection. [ABSTRACT FROM AUTHOR]

Clostridium septicum is a very rare cause of severe spontaneous pediatric enterocolitis and is often associated with underlying malignancy or immunocompromise. Likewise, cyclic neutropenia is a rare congenital immunodeficiency that is characterized by cyclical periods of neutropenia, often with more severe symptoms in the pediatric population. Here, we present a unique case of spontaneous C. septicum enterocolitis, sepsis, and myonecrosis in a child with undiagnosed cyclic neutropenia. Early recognition of pediatric sepsis, frequent reevaluation and identification of rapidly progressive infection, and early surgical intervention are critical for the effective management of a rare and severe infection. [ABSTRACT FROM AUTHOR]

Diabetic myonecrosis is an uncommonly encountered and underdiagnosed complication of diabetes mellitus. It could be a manifestation of poor glycemic control, and hence, progressive microvascular disease; however, it is usually self-limiting. A known but poorly controlled type 2 diabetes mellitus patient presented with sudden onset and worsening right thigh pain and swelling. Magnetic resonance imaging showed hypertrophy and hyperintensity of the adductor muscles with non-enhanced regions denoting areas of necrosis. Conservative management of bed rest, analgesics, and controlled blood glucose yielded a positive response. Diagnosis of diabetic myonecrosis can be challenging as many diseases mimic this condition, resulting in delayed recognition, diagnosis, and initiation of prompt treatment. Magnetic resonance imaging findings rather than laboratory markers are the mainstay of diagnosis as it localizes the affected muscles and excludes other mimics. [ABSTRACT FROM AUTHOR]

Introduction/aims: Duchenne muscular dystrophy (DMD) is caused by pathogenic variants in the DMD gene, making muscle fibers susceptible to contraction-induced membrane damage. Given the potential beneficial action of cannabidiol (CBD), we evaluated the in vitro effect of full-spectrum CBD oil on the viability of dystrophic muscle fibers and the in vivo effect on myopathy of the mdx mouse, a DMD model., Methods: In vitro, dystrophic cells from the mdx mouse were treated with full-spectrum CBD oil and assessed with cell viability and cytotoxic analyses. In vivo, fourteen-day-old mdx mice received 10 mg/kg/day of the full-spectrum CBD oil for 14 days. We analyzed creatine kinase (CK) levels, liver damage markers, and histopathology of the diaphragm (DIA) and quadriceps (QUA [myonecrotic fibers with positive IgG staining, regenerated fibers/central nuclei, the minimum Feret's diameter, the fibrosis area, the inflammatory area, the presence of macrophages, and NF-kappa B content])., Results: In vitro treatment with full-spectrum CBD oil showed a dose-dependent cytotoxic effect; however, in vivo 10 mg/kg treatment was safe and effectively improved DMD histopathological assessment parameters in DIA and QUA: reduction of central nuclei: 1.7% ± 2.0% versus 22.4% ± 5.3% and 11.1% ± 10.7% versus 32.3% ± 4.6%; reduction of IgG+ myofibers: 0.6% ± 0.7% versus 8.4% ± 1.6% and 0.9% ± 0.3% versus 7.5% ± 1.0%; increase in myofiber size: 85.2 ± 3.2 versus 64.3 ± 4.0 μm and 106.5 ± 8.6 versus 81.2 ± 4.8 μm; decrease in inflammatory area: 6.2% ± 2.7% versus 15.1% ± 2.6% and 5.3 ± 4.1 versus 17.3% ± 2.8%; reduced macrophage area: 0.05% ± 0.1% versus 10.8% ± 4.3% and 1.0% ± 0.7% versus 10.3% ± 4.9%; NF-κB levels: 0.6% ± 0.1% versus 1.7% ± 0.2% and 1.7% ± 0.1% versus 5.2% ± 2.1%; and fibrosis: 5.6% ± 1.8% versus 12.0% ± 3.7% and 1.3% ± 0.5% versus 4.7% ± 1.5%. It also reduced serum CK., Discussion: Full-spectrum CBD oil may represent a promising new approach to treating DMD, but its potential toxicity must be considered., (© 2025 Wiley Periodicals LLC.)

Background: Fish venoms have been poorly characterized and the available information about their composition suggests they are uncomplicated secretions that, combined with epidermal mucus, could induce an inflammatory reaction, excruciating pain, and, in some cases, local tissue injuries., Methods: In this study, we characterized the 24-hour histopathological effects of lionfish venom in a mouse experimental model by testing the main fractions obtained by size exclusion-HPLC. By partial proteomics analysis, we also correlated these in vivo effects with the presence of some potentially toxic venom components., Results: We observed a strong lesion on the skin and evident necrosis in the skeletal muscle. None of the tissue-damaging effects were induced by the fraction containing cytolysins, membrane pore-forming toxins ubiquitously present in species of scorpionfish, stonefish, and lionfish, among others. On the contrary, injuries were associated with the presence of other components, which have remained practically ignored so far. This is the case of an abundant protein, present in venom, with homology to a Golgi-associated plant pathogenic protein 1-like (GAPR1), which belongs to the same protein superfamily as venom CRISPs and insect allergens., Conclusion: This GAPR1-like protein and the hyaluronidase are probably responsible for the hemostasis impairment and hemorrhagic lesions observed in mouse skin, whereas muscle injuries can be indirectly caused by a combination of inflammatory and hemorrhagic events. More information is required to establish the components accountable for the myonecrotic effect., Competing Interests: Competing interests: The authors declare that they have no competing interests.

Introduction: Gas gangrene, is an aggressive and life-threatening necrotizing infection of soft tissues. We report a case of upper-limb trauma resulting in clostridial gas gangrene., Case Report: A 36-year-old healthy male presented to our department with a left humeral shaft fracture and an open elbow fracture. During surgery wound discharge, and diffuse crepitations due to gaseous accumulation were noted around the medial elbow and forearm. Debridement and fasciotomy were performed, and IV penicillin and clindamycin were administrated. The infection spread into adjacent soft tissues, requiring repeated surgical interventions and long-term IV antibiotics till resolution., Conclusion: Early and repeated debridements are imperative in traumatic gas gangrene, to preserve limb and function., Competing Interests: Conflict of Interest: Nil, (Copyright: © Indian Orthopaedic Research Group.)

Clostridial myonecrosis is a highly fatal infectious disease of the muscle that is caused by pathogenic clostridia. When it occurs in equine muscle, the infection can cause a variety of clinical signs. The present report described a case of acute myonecrosis caused by Clostridium septicum in a horse, which had a favorable clinical evolution. A 6-year-old mare was admitted to a veterinary hospital due to increased volume and lameness in the left pelvic limb after an intramuscular injection of an anti-inflammatory drug. The diagnosis of myonecrosis caused by C. septicum was based on clinical and laboratory findings. The animal showed significant improvement after 5 months of treatment and was discharged from the hospital. There is very limited information regarding myonecrosis caused by C. septicum in horses in Brazil; our study showed that early diagnosis and prompt appropriate treatment can ensure significant improvement and recovery of affected animals. [ABSTRACT FROM AUTHOR]

Clostridial infections, particularly clostridial myonecrosis, can be fulminant and fatal; they often arise without an obvious history of trauma. The majority of equine clostridial myonecrosis cases are associated with intramuscular injection. This paper presents the first report of clostridial myositis by C. perfringens in a donkey after an injection of flunixin meglumine on the neck, describing the clinical, necroscopic, and histopathological events. Bacterial isolation and biochemical tests confirmed the definitive diagnosis of C. perfringens. [ABSTRACT FROM AUTHOR]

Literature shows that phospholipases A 2 isolated from snake venoms of the genus Bothrops are involved in the local inflammatory response. However, the mechanisms by which these enzymes trigger this process have not yet been clarified. Toll-Like receptors (TLRs) are transmembrane proteins that recognize pathogens associated molecular patterns (PAMPs), or even damage associated molecular patterns (DAMPs). After this recognition, an innate immune response is activated resulting in cytokines liberation contributing to inflammation. Thus, the purpose of this work was to study the participation of different TLRs during the local inflammatory process induced by B. jararacussu snake venom and by two isolated phospholipases A 2 , BthTX-I or BthTX-II, from this venom in a model of experimental envenoming. For this, sub-lethal doses of B. jararacussu venom (BjussuV), BthTX-I or BthTX-II were injected in the gastrocnemius muscle. Myotoxic activity was evaluated by histological analysis and by quantification of plasma levels of total-creatine kinase (CK). The pro-inflammatory cytokines TNF-α and IL-1β was measured in both muscle tissue homogenate and plasma. A quantification of the gene expression of TLRs 2, 4, 5 and 9 in muscle tissue homogenate was performed by the real-time polymerase chain reaction (RTq-PCR). According to the results, it can be observed that, when compared to the control, there was a significant increase of CK and TNF-α in the bloodstream of the animals injected with both BjussuV, BthTX-I and BthTX-II. In muscle tissue homogenate, it was observed a significant increase in both cytokines, TNF-α and IL-1β, levels compared to the control animals. The results point to an important increase in the gene expression of TLR2 and TLR4, suggesting that these TLRs can be important targets for the development of future therapies for local treatment for victims of snakebites. [Display omitted] • Bothrops jararacussu venom, BthTX-I and BthTX-II induces myotoxicity and CK liberation. • Bothrops jararacussu venom and myotoxins induces TLR2 and TLR4 gene expression. • Bothrops jararacussu venom and myotoxins induces muscle TNF-α and IL-β liberation. [ABSTRACT FROM AUTHOR]

Clostridial myonecrosis or gas gangrene (myonecrosis) and tetanus are relatively rare nowadays, but they are still considered serious conditions associated with poor prognosis and high mortality. Life-threatening infections caused by Clostridium species have been known and studied for centuries, as they differed from other infections in terms of typical clinical manifestations, challenges of therapy and prevention. The aim of the study was to analyse the global incidence of gas gangrene and tetanus and challenges of prevention and treatment of these diseases. The review of up-to-date scientific literature demonstrated that gas gangrene continues to be a problem due to its rapid progression and challenging treatment. There are two main forms of the disease—traumatic and spontaneous. Traumatic gas gangrene is usually caused by C. perfringens, C. septicum, C. novyi (oedematiens), or C. histolyticum. Its incidence increases dramatically during wars, natural disasters, and other calamities. The literature review demonstrated that over the past 40 years there has been a rise in the frequency of spontaneous gas gangrene caused by C. septicum in people with compromised immune systems, in injecting drug users, and in women during various gynecological procedures and during normal delivery. Despite the effectiveness of the tetanus immunisation programme, the infection remains widespread in countries with insufficient vaccination coverage. The risk of tetanus in developed countries is high among elderly unvaccinated or partially vaccinated people, among injecting drug users, and vaccine refusers. The paper describes some clinical cases of gas gangrene and tetanus which demonstrate problems associated with challenging diagnosis and treatment, low awareness among primary healthcare personnel about mechanisms of anaerobic infection development, and anti-vaccination movement.

BackgroundImmune-mediated myositis (IMM) is a cause of rhabdomyolysis, stiffness, and muscle atrophy predominantly affecting Quarter horses. Limited information is available with regard to outcome, prognostic indicators, and associations with concurrent diseases.Hypothesis/objectivesTo report outcomes and associations between outcome and clinical and laboratory parameters, and presence of concurrent illness.AnimalsSixty-eight horses; 52 Quarter horses and related breeds and 16 other breeds.MethodsRetrospective cohort study (1991-2014). Medical records of horses with histological diagnosis of IMM were reviewed. Data recovery included signalment, laboratory variables, therapy, and outcome. Logistic regression was used to quantify the association between potential prognostic factors and survival to discharge.ResultsQuarter horses were younger (mean < 4 years, range 3 months-21 years) than other breeds (mean < 10 years, range 1-23 years). Pathogens causing concurrent or recent infection included S. equi equi, S. equi zooepidemicus, C. pseudotuberculosis, Anaplasma phagocytophilum, herpes virus-1, and influenza. The most common clinical signs consisted of rapidly progressive diffuse symmetrical muscle atrophy (80%), stiff gait (74%), and fever (44%). All horses that received medical therapy immediately upon admission survived to discharge (survival proportion = 87%). Leucocytosis was a common finding (60%). Horses with concurrent fever and other illness had a poor prognosis for hospital discharge.Conclusions and clinical importanceHorses with IMM can have a favorable outcome. Horses with concurrent fever and another illness had decreased probability of survival to discharge.

Deficient skeletal muscle regeneration, which often leads to permanent sequelae, is a common clinical finding in envenomations caused by snakes of the family Viperidae, such as those of Bothrops alternatus and B. diporus in South America. The causes of such poor muscle regenerative outcome are still incompletely understood. Using a murine experimental model of envenomation by the venoms of these two species, we assessed whether traces of venom components that remain in muscle tissue days after envenomation affect myoblasts and myotube formation in culture. The kinetics of drop in venom concentration in the tissue was assessed by ELISA and Western blot, and by the quantification of venom phospholipase A 2 activity. A rapid drop of venom components was observed in muscle, although a band of 58–63 kDa remained even 168 h after venom injection, and venom phospholipase A 2 activity was detected in muscle tissue days after envenomation. Muscle homogenates from envenomated animals were cytotoxic to myoblasts in culture and inhibited the formation of myotubes even in conditions where homogenates were devoid of cytotoxicity. These deleterious effects were abrogated when homogenates were incubated with antivenom. Our findings agree with previous observations with the venom of Bothrops asper and provide further evidence that one of the causes of the poor skeletal muscle regeneration after Bothrops sp venom-induced myonecrosis is the deleterious action on myogenic cells of traces of venom components remaining in the tissue. [Display omitted] • Traces of Bothrops alternatus and B. diporus venoms preclude in vitro muscle regeneration. • Muscle homogenates obtained from envenomed animals were cytotoxic to myoblasts in culture. • Neutralization of venom components may contribute to an improved regenerative response. [ABSTRACT FROM AUTHOR]

Diabetic myonecrosis is an uncommon complication related to long‐standing poorly controlled diabetes. A 33‐year‐old Sudanese male patient with type one diabetes presented with progressive, severe bilateral thigh pain with low‐grade fever. Laboratory results show hyperglycemia with ketonuria and elevated creatine kinase but normal white cell blood count. The patient was diagnosed initially with diabetic ketoacidosis with pyomyositis and received analgesic and insulin; the patient partially improved. After the second evaluation, bilateral thigh MRI was requested and shows diffuse edema involving the medial muscle group of the upper third of the right side with intramuscular facial edema, appearing as low signal in T1 and high signal in T2 and fat suppression images with no evidence of collection or abscess. Diagnosis of diabetic myonecrosis was made. The patient was managed conservatively and discharge on aspirin with full recovery. [ABSTRACT FROM AUTHOR]

ABSTRACT: Clostridium perfringens is considered one of the main causative agents of superacute enterocolitis, usually fatal in the equine species, due to the action of the β toxin, and is responsible for causing severe myonecrosis, by the action of the α toxin. The great importance of this agent in the equine economy is due to high mortality and lack of vaccines, which are the main form of prevention, which guarantee the immunization of this animal species. The aim of this study was to evaluate three different concentrations (100, 200 and 400μg) of C. perfringens α and β recombinant toxoids in equine immunization and to compare with a group vaccinated with a commercial toxoid. The commercial vaccine was not able to stimulate an immune response and the recombinant vaccine was able to induce satisfactory humoral immune response in vaccinated horses, proving to be an alternative prophylactic for C. perfringens infection.

Objectives: Clindamycin (CLI) and erythromycin (ERY) resistance is increasing among group A streptococci (GAS) causing invasive disease and alternative treatments are urgently required. In this study, the efficacy of the newer oxazolidinone tedizolid (TZD) was compared with the first drug in this class, linezolid (LNZ), in experimental murine myonecrosis caused by ERY-susceptible/CLI-susceptible (ERYS/CLIS) or ERY- resistant/CLI-resistant (ERYR/CLIR) GAS. Methods: Normal adult outbred Swiss Webster female mice (10 per group) were infected intramuscularly with ERYS/CLIS (ATCC 12384) or ERYR/CLIR (15-003) GAS. Treatments began 4 h post-infection and continued for 72 h. TZD and LNZ (10, 20 and 40 mg/kg) were given intraperitoneally every 12 h. Saline, penicillin (PEN), CLI and ERY were given every 6 h. Survival and infection severity signs and symptoms were followed for 12 days. Results: Both GAS strains were susceptible to LNZ, TZD and PEN; strain 15-003 was confirmed as constitutively resistant to ERY and CLI. Blood levels following a 40 mg/kg dose of LZD and TZD were 30.9 ± 4.0 μg/mL and 21.9 ± 5.3 μg/mL, respectively. Both TZD and LNZ were highly efficacious for the treatment of severe experimental myonecrosis caused by ERYS/CLIS and, importantly, ERYR/CLIR GAS. Conclusion: In the current era of emerging macrolide/lincosamide resistance among GAS, these data support the use of TZD and LNZ as first-line antibiotics for the treatment of life-threatening GAS infections in humans.