Acute Viral Myositis Research Articles

Myositis as a complication of dengue viral infection

Dengue fever is a febrile illness caused by an arbovirus transmitted by the Aedes aegypti mosquito. It occurs as aseasonal epidemic every year in Pakistan. Apart from febrile illness and its associated hemorrhagic complication,dengue fever is associated with multi-system involvement and their respective complications, including myriadneurological complications. In this case report we describe two patients who developed acute viral myositis.

Evaluation of the prevalence and clinical and laboratory features of acute viral myositis in children with influenza referred to the emergency department of Ali Asghar Tehran Hospital in 2019 and 2020.

ABSTRACTIntroduction:Influenza-related viral myositis is observed mostly in children with influenza, and the disease is more common in influenza type B. The aim of the present study was to evaluate the prevalence, and clinical and laboratory features of acute viral myositis in children with influenza in 2019 and 2020.Methods:This retrospective cross-sectional study was performed in Ali Asghar Hospital, from December 2019 to February 2020. Children aged 2–14 years with symptoms of acute onset of fever, along with the symptoms of influenza with or without muscle pain who referred to the emergency department of Hazrat Ali Asghar Children’s Hospital, were included in the study. The data were collected and analyzed by Statistical Package for the Social Sciences (SPSS) version 22.Results:Out of the 105 participants in this study, 62 (59%) were male and the rest were female. The average age of the patients was 5.34 years (SD = 2.63). Clinical signs of lower limb pain, myalgia, lameness, weakness, and lethargy were significantly more common in patients with myositis (P-value < 0.05). In-vitro examination demonstrated that creatine phosphokinase (CPK), aspartate aminotransferase (AST), and aAlanine aminotransferease (ALT) levels were significantly higher in patients with myositis.Conclusion:Based on the present results, the clinical symptoms in patients are quite clear, and based on the symptoms, it is possible to diagnose and treat myositis without relying on laboratory findings; due to the self-limitation of this complication and lack of the need for complex treatments in case of early diagnosis, physicians can diagnose and treat many cases, depending on the clinical symptoms and the accuracy of the examination.

Acute viral myositis: profound rhabdomyolysis without acute kidney injury.

BackgroundAcute viral myositis (AVM) may be triggered by influenza A/B, enteroviruses and other viruses. Severe complications including rhabdomyolysis regularly lead to acute kidney injury (AKI). The aim of this short report was to discuss management and differential diagnosis of massive creatine kinase (CK) elevation.Patient, material and methodsHerein, we report on a 19-year-old Austrian male of African descent with a history of respiratory tract infections and whole-body pain. He further developed acute viral myositis and massive CK elevation up to 440,000 IU/L but without any signs of AKI. A literature search relating AVM, management and differential diagnosis of rhabdomyolysis was conducted in PubMed and UptoDate.ResultsA full panel of serological and autoimmune blood work-up including testing for human immunodeficiency virus (HIV), hepatitis, influenza A/B, Epstein-Barr virus (EBV), antinuclear antibodies (ANA) and autoantibodies against various extractable nuclear antigens (ENA) did not reveal evidence for viral originators or autoimmune diseases. This case indicates that in acute viral myositis associated with extreme CK elevation (>400,000 IU/L) AKI might be completely absent. Potential causes for this clinical phenotype, differential diagnosis and management are discussed.

A Rare Complication of Seasonal Influenza: Case Report and a Brief Review of the Literature

Acute viral myositis is a rare condition that is commonly defined with influenza A, B, and enterovirus in the United States of America. Viral myositis complicated by rhabdomyolysis is even less common but requires prompt attention and diagnosis to prevent complications. We describe the occurrence of acute viral myositis complicated by rhabdomyolysis in a young 43-year-old man that lead to acute renal failure. It also highlights that clinicians should keep in mind that viral upper respiratory infections can be complicated with various clinical manifestations that could extend beyond respiratory symptoms.

Benign acute viral myositis in African migrants: A clinical, serological, and pathological study.

Several viruses have been described as causes of acquired inflammatory myopathies; however, the mechanisms by which they cause muscle disease are still unclear. The aim of this study was to describe the laboratory features of benign acute myositis in a small case series. A detailed pathological and serological analysis was performed in five African migrants who developed an acute viral myositis complicated by rhabdomyolysis. Muscle biopsies clearly documented an inflammatory myopathy with histological features similar to polymyositis including CD8+ T cells surrounding and invading nonnecrotic muscle fibers, CD68+ macrophages and major histocompatibility complex class I antigen upregulation. In addition, positivity for myositis-specific antibodies (MSA), in particular anti-aminoacyl tRNA synthetases, was found in the serum of two patients. Our study demonstrated that T-cell mediated injury occurs in muscle of patients with acute viral myositis, and that MSA may be present in the serum of these patients.

An outbreak of acute viral myositis with different outcomes: A case series

Viral myositis is induced by direct muscle invasion, molecular mimicry, production of immune complexes, immune dysregulation, and various other mechanisms. The pathogenesis of this entity is still unclear. Here, we report a case series of viral myositis with varied clinical presentations who had different outcomes ranging from complete recovery to death. To report a variety of clinical and laboratory presentation of an outbreak of viral myositis. This was a case series of seven patients, describing clinical, electrophysiological, and laboratory tests and histopathology and treatment results. The study showed a benign course in 2, recurrence in 1, fulminant necrotizing myositis in 4, and coexisting Guillain–Barre syndrome in 2 with 1 patient culminating to death in the latter group. The variability in outcome of viral myositis suggests that there are some genetic factors which lead to fulminant necrotizing myositis in contrast to the patients experiencing a benign course of myositis.

Clinical and laboratory description of a series of cases of acute viral myositis

ObjectiveDescribe the clinical and laboratory profile, follow‐up, and outcome of a series of cases of acute viral myositis. MethodA retrospective analysis of suspected cases under observation in the emergency department was performed, including outpatient follow‐up with the recording of respiratory infection and musculoskeletal symptoms, measurement of muscle enzymes, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), transaminases (AST and ALT), blood count, C‐reactive protein, and erythrocyte sedimentation rate in the acute phase and during follow‐up until normalization. ResultsBetween 2000 and 2009, 42 suspected cases were identified and 35 (27 boys) were included. The median age was 7 years and the diagnosis was reported in 89% in the first emergency visit. The observed respiratory symptoms were cough (31%), rhinorrhea (23%), and fever (63%), with a mean duration of 4.3 days. Musculoskeletal symptoms were localized pain in the calves (80%), limited ambulation (57%), gait abnormality (40%), and muscle weakness in the lower limbs (71%), with a mean duration of 3.6 days. There was significant increase in CPK enzymes (5,507 ± 9,180 U/L), LDH (827 ± 598 U/L), and AST (199 ± 245 U/L), with a tendency to leukopenia, (4,590 ± 1,420) leukocytes/mm3. The complete recovery of laboratory parameters was observed in 30 days (median), and laboratory and clinical recurrence was documented in one case after ten months. ConclusionTypical symptoms with increased muscle enzymes after diagnosis of influenza and self‐limited course of the disease were the clues to the diagnosis. The increase in muscle enzymes indicate transient myotropic activity related to seasonal influenza, which should be considered, regardless of the viral identification, possibly associated with influenza virus or other respiratory viruses.

Clinical and laboratory description of a series of cases of acute viral myositis

ObjectiveDescribe the clinical and laboratory profile, follow-up, and outcome of a series of cases of acute viral myositis. MethodA retrospective analysis of suspected cases under observation in the emergency department was performed, including outpatient follow-up with the recording of respiratory infection and musculoskeletal symptoms, measurement of muscle enzymes, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), transaminases (AST and ALT), blood count, C-reactive protein, and erythrocyte sedimentation rate in the acute phase and during follow-up until normalization. ResultsBetween 2000 and 2009, 42 suspected cases were identified and 35 (27 boys) were included. The median age was 7 years and the diagnosis was reported in 89% in the first emergency visit. The observed respiratory symptoms were cough (31%), rhinorrhea (23%), and fever (63%), with a mean duration of 4.3 days. Musculoskeletal symptoms were localized pain in the calves (80%), limited ambulation (57%), gait abnormality (40%), and muscle weakness in the lower limbs (71%), with a mean duration of 3.6 days. There was significant increase in CPK enzymes (5507±9180U/L), LDH (827±598U/L), and AST (199±245U/L), with a tendency to leukopenia (4590±1420) leukocytes/mm3. The complete recovery of laboratory parameters was observed in 30 days (median), and laboratory and clinical recurrence was documented in one case after 10 months. ConclusionTypical symptoms with increased muscle enzymes after diagnosis of influenza and self-limited course of the disease were the clues to the diagnosis. The increase in muscle enzymes indicate transient myotropic activity related to seasonal influenza, which should be considered, regardless of the viral identification, possibly associated with influenza virus or other respiratory viruses.

Acute viral myositis – particular aspects in the epidemiology of respiratory virus diseases in 2013

Results There were 578 clinically diagnosed cases of respiratory virus spread by age: 0-3 years: 40 cases (6.92%); 4-7 years: 81 cases (14.01%); 8-14 years old: 107 cases (18.51%); 15-20 years 38 patients (6.57%); over 20 years in 312 cases (53.97%); acute viral myositis was observed in a total of 22 patients (3.80%). Calendar distribution was as follows: in March, 14 cases (63.63%) compared to 6 cases (27.27%) in February, 1 case (4.54%) in January and 1 case (4.54%) in April 2013. The area of origin was urban in 18 cases (81.81%) and rural in 4 cases (18.19%). Mild clinical forms were common in 20 cases (90.9%), severe forms were determined by the prolonged evolution of the disease and association of neurological complications (polyradiculoneuritis) in 2 cases (9.1%). Positive diagnosis was clinical (myalgia, functional impotence of the lower limb) and laboratory confirmed (muscle enzymes). Evolution was favorable in all cases under treatment: corticosteroids (hydrocortisone hemisuccinate, dexamethasone medrol) and neurotrophic. Two patients received virological diagnosis, but in one of them we isolated influenza type B; this viral strain was isolated in most cases investigated virologically and confirmed with influenza viruses in patients with respiratory virus.

Neurological complications of dengue fever: Experience from a tertiary center of north India

Introduction:Dengue, an acute viral disease transmitted by Aedes mosquitoes, is highly endemic in many tropical and subtropical areas of the world. Neurological complications of dengue infection have been observed more frequently in the recent past and some studies highlighted varied neurological complications arising in the course of dengue illness. In this retrospective study, we report various neurological complications observed during the last 2 years in patients of dengue fever.Materials and Methods:The patients presenting with neurological complications with positive serology (IgM antibody) for dengue infection were consecutively recruited from the Department of Neurology/Medicine from a tertiary center of Lucknow, India. These patients were subjected to a detailed clinical evaluation, laboratory assessment including blood count, hematocrit, coagulation parameters, biochemical assays, serology for dengue fever, enzyme-linked immunosorbent assay for human immunodeficiency virus and other relevant investigations.Results:Twenty-six patients with neurological complications associated with confirmed dengue infection were observed during the last 2 years. Eighteen of these patients were male. Of the 26 patients, 10 patients were suffering from brachial neuritis, four patients had encephalopathy, three patients were consistent with the diagnosis of Guillain Barre syndrome, three patients had hypokalemic paralysis associated with dengue fever and two patients had acute viral myositis. Opsoclonus-myoclonus syndrome was diagnosed in two patients, myelitis in one patient and acute disseminated encephalo-myelitis also in one patient.Conclusion:Dengue fever was associated with widespread neurological complications. Brachial neuritis and opsoclonus-myoclonus syndrome were observed for the first time in this study.

Herpes Zoster Meningitis Confirmed by Detection of Varicella-Zoster Virus DNA Using the Polymerase Chain Reaction -A case report-

Acute viral meningitis and myositis are rare complications of varicella-zoster virus (VZV) reactivation. A 71-years-old immunocompetent man, who presented with lower back pain radiating to the left lower extremities, developed vesicles on the L5 dermatomal area. The next day, he had complained of aberrant vesicles on the trunk, face and scalp, with generalized myalgia, headache and dizziness. He was confirmed with VZV meningitis and myositis, as demonstrated by the presence of VZV DNA in the blood and cerebral spinal fluid using a polymerase chain reaction (PCR) amplification. PCR has been used in patients with a VZV infection associated neurological symptoms, and provides a useful tool for the early diagnosis of VZV-associated neurological disease. The patient was treated with bed rest, with intravenous acyclovir for the VZV infection, and intravenous Patient-controlled Analgesia for pain management and the prevention of postherpetic neuralgia. When he visited the outpatient department 3 months later, the skin lesion, leg pain, headache and myalgia had all improved, without sequelae. Here, this case is reported, with a discussion of the relevant literature on its diagnosis and management.

Predominant right leg dysfunction without asymmetric muscle inflammation in CD1 Swiss mice with coxsackievirus B1-induced myositis

To establish the existence of predominant right leg involvement in Coxsackievirus B1-induced myositis (CB1 myositis) 189 neonatal CD1 Swiss mice were inoculated with 300 pfu CB1, and regularly observed for posture, mobility, and gait. After 2 and 4 weeks, quantitative comparison of motor dysfunction of right and left leg yielded an asymmetry score; on light microscopy mononuclear cell infiltration and muscle fiber necrosis were quantified in bilateral hamstring muscles, using a five-grade scale (0–4). Motor asymmetries were seen during acute viral myositis as soon as hind leg dysfunction appeared, and animals with a predominant dysfunction of one leg preserved that preference throughout the observation period. At 2 weeks, mice with predominant right leg dysfunction ( n = 34) significantly outnumbered those with predominant left leg dysfunction ( n = 11) ( p = 0.01). At 2 and 4 weeks, infiltration and necrosis in hamstrings from legs with predominant dysfunction were not higher than in those from contralateral legs, and infiltration in right-sided hamstrings was not higher than in left-sided ones, nor was infiltration at 4 weeks. At 4 weeks right-sided muscles were more necrotic (mean ± SD, 1.8 ± 1.5) than left-sided muscles (1.1 ± 1.2; p = 0.03). In the absence of predominant inflammatory disease of the right leg, we interpret the hind leg asymmetry as a preferential use of the left leg, due to left-leggedness, and suggest that in CD1 Swiss mice left-leggedness is associated with increased susceptibility to CB1 myositis.