A Case Report on Parvovirus B19 Associated Myositis

Introduction: Whilst there are reports of viral myopathies affecting children and the immunocompromised, infective myositis is a relatively rare inflammatory myopathy in adults. The clinical spectrum can range from benign myalgias to more serious complications in certain risk groups. Case Presentation: We present two cases of myositis as a result of parvovirus B19 infection.
Conclusion: Viral myositis and parvovirus B19 associated myositis should be considered in adults presenting with significant myalgia.

Role of spinal microglia in myositis-induced central sensitisation: An immunohistochemical and behavioural study in rats

There is increasing evidence that spinal glial cells play an important role in chronic pain states. However, so far no data on the role of microglia in muscle pain are available. The aim of the present study was to investigate the involvement of spinal microglial cells in chronic muscle pain. In a rat model of chronic muscle inflammation (injection of complete Freunds adjuvant into the gastrocnemius-soleus muscle) alterations of microglia were visualized with quantitative OX-42 immunohistochemistry in the dorsal horn of the segments L4 and L5 12 days after induction of inflammation. In behavioural experiments the influence of chronic intrathecally applied minocycline - a specific microglia inhibitor - or an antibody against tumour necrosis factor-alpha (TNF-alpha: a cytokine released from microglia) on pain-related behaviour was investigated after 1, 3, 6, and 12 days. The immunhistochemical data show that in the deep laminae of the spinal dorsal horn microglial cells reacted with morphological changes to the muscle inflammation. Following inflammation, the mean boundary length surrounding the OX-42 immunostained area was significantly shorter. This indicates that microglial cells were activated by the myositis and withdrew their processes. Chronic intrathecal administration of minocycline or anti TNF-alpha with an osmotic mini-pump largely normalised the inflammation-induced changes in spontaneous exploratory behaviour and attenuated the hypersensitivity to mechanical stimulation. Both the immunohistochemical and behavioural data show that spinal microglial cells are involved in nociceptive processes in the cause of a chronic muscle inflammation. (C) 2008 European Federation of International Association for the Study of Pain Chapters. Published by Elsevier Ltd. All rights reserved.

Myositis ossificans traumatica of the medial pterygoid muscle: a case report.

In this report, we present a case of myositis ossificans traumatica (MOT) of the medial pterygoid muscle that had developed after mandibular block anesthesia administered for endodontic treatment of the lower right second molar, demonstrating typical features of this condition. MOT should be considered as a differential diagnosis when there is severe limitation of jaw opening and an associated trauma. Panoramic radiographs and axial and coronal computed tomography (CT) scans can effectively delineate the calcified mass. Other imaging studies that may be helpful include magnetic resonance imaging (MRI), bone scans, and ultrasound. As shown in our case, calcified masses were found in the right mandibular angle, which severely limited jaw opening. Some earlier reported cases of MOT were treated by extraoral surgical approaches with complete removal of the evolving muscle. The aim of this case report is to present only the diagnostic imaging aspects of myositis ossificans traumatica.

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

Describe the clinical and laboratory profile, follow-up, and outcome of a series of cases of acute viral myositis. A 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. Between 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/mm(3). 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. Typical 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.

Influenza-associated myositis in children

BACKGROUND: Influenza-associated myositis (IAM) is an infrequent and poorly known complication of influenza virus infection in children. The aim of this study was to describe five cases of IAM and to review the literature on IAM in children. PATIENTS AND METHODS: We conducted a retrospective analysis of cases of IAM diagnosed at two university children's hospitals in Switzerland during two consecutive influenza seasons. Findings were compared with 39 individual case reports and five publications summarizing an additional 272 cases identified by a medical online library (MEDLINE) search. RESULTS: Overall, 316 cases were analyzed. IAM typically occurred in school-aged children with a 2:1 male predominance. Influenza B and A viruses were identified in 76% and 24% of cases, respectively. The median interval between onset of influenza and onset of IAM was 3 days (range 0-18). The calf muscles were involved alone or together with other muscle groups in 69% and 31% of cases, respectively. Blood creatine phosphokinase (CPK) concentration was invariably elevated. Median duration to clinical recovery was 3 days (range 1-30). Rhabdomyolysis occurred in ten of 316 patients (3%), was more common in girls (80%), more often associated with influenza A (86%), and led to renal failure in eight patients (80%). CONCLUSION: Clinical and laboratory findings of IAM are highly characteristic and allow a rapid diagnosis during the influenza season.

Surgical Treatment of Traumatic Myositis Ossificans of the Extensor Carpi Radialis Muscle in a Dog

OBJECTIVES To report clinical signs, diagnostic imaging findings, and outcome in a dog with traumatic myositis ossificans of the origin of the extensor carpi radialis muscle. STUDY DESIGN Clinical report. ANIMALS An 8-month-old intact female Irish Setter Dog. METHODS After radiographic and computed tomographic evaluation of an osseous proliferation arising from the cranial cortex of the right distal humeral diaphysis, the protruding bone was surgically removed and evaluated by histopathology. RESULTS Traumatic myositis ossificans was successfully treated with surgical removal of the osseous proliferation resulting in improved postoperative range of motion of the right elbow joint. There was no evidence of lameness or abnormal bone regrowth associated with the surgical site radiographically at follow up. CONCLUSION Surgical removal of a traumatic myositis ossificans lesion resulted in full return to function in a young, competitive show dog.

Suspected immune-mediated myositis in a pony

Immune-mediated myositis and other forms of inflammatory myopathy are well recognised in dogs and man (Griffiths 1991). In equine medicine, inflammatory muscle disease is less well documented. Only a single report could be found in the literature containing mention of immune-mediated myositis in a horse unassociated with systemic disease, in which case the condition was multifocal (Beech 2000). We report a case of localised muscle atrophy and weakness in a pony. A diagnosis of chronic myositis was made after histological examination of biopsies of affected muscles. The histological appearance, elimination of other causes and response to treatment suggested an immune-mediated aetiology.

Novel mutations in ACVR1 result in atypical features in two fibrodysplasia ossificans progressiva patients

Fibrodysplasia Ossificans Progressiva (FOP) is a rare, heritable condition typified by progression of extensive ossification within skeletal muscle, ligament and tendon together with defects in skeletal development. The condition is easily diagnosed by the presence of shortened great toes and there is severe advancement of disability with age. FOP has been shown to result from a point mutation (c.617G>A) in the ACVR1 gene in almost all patients reported. Very recently two other mutations have been described in three FOP patients. We present here evidence for two further unique mutations (c.605G>T and c.983G>A) in this gene in two FOP patients with some atypical digit abnormalities and other clinical features. The observation of disparate missense mutations mapped to the GS and kinase domains of the protein supports the disease model of mild kinase activation and provides a potential rationale for phenotypic variation. © 2009 Petrie et al.

The IFITM5 mutation c.-14C > T results in an elongated transcript expressed in human bone; And causes varying phenotypic severity of osteogenesis imperfecta type V

Background The genetic mutation resulting in osteogenesis imperfecta (OI) type V was recently characterised as a single point mutation (c.-14C > T) in the 5' untranslated region (UTR) of IFITM5, a gene encoding a transmembrane protein with expression restricted to skeletal tissue. This mutation creates an alternative start codon and has been shown in a eukaryotic cell line to result in a longer variant of IFITM5, but its expression has not previously been demonstrated in bone from a patient with OI type V. Methods Sanger sequencing of the IFITM5 5' UTR was performed in our cohort of subjects with a clinical diagnosis of OI type V. Clinical data was collated from referring clinicians. RNA was extracted from a bone sample from one patient and Sanger sequenced to determine expression of wild-type and mutant IFITM5. Results: All nine subjects with OI type V were heterozygous for the c.-14C > T IFITM5 mutation. Clinically, there was heterogeneity in phenotype, particularly in the manifestation of bone fragility amongst subjects. Both wild-type and mutant IFITM5 mRNA transcripts were present in bone. Conclusions The c.-14C > T IFITM5 mutation does not result in an RNA-null allele but is expressed in bone. Individuals with identical mutations in IFITM5 have highly variable phenotypic expression, even within the same family.

A novel ACVR1 mutation in the glycine/serine-rich domain found in the most benign case of a fibrodysplasia ossificans progressiva variant reported to date

Fibrodysplasia Ossificans Progressiva (FOP) is a rare, autosomal dominant condition, classically characterised by heterotopic ossification beginning in childhood and congenital great toe malformations; occurring in response to a c.617 G>A ACVR1 mutation in the functionally important glycine/serine-rich domain of exon 6. Here we describe a novel c.587 T>C mutation in the glycine/serine-rich domain of ACVR1, associated with delayed onset of heterotopic ossification and an exceptionally mild clinical course. Absence of great toe malformations, the presence of early ossification of the cervical spine facets joints, plus mild bilateral camptodactyly of the 5th fingers, together with a novel ACVR1 mutation, are consistent with the 'FOP-variant' syndrome. The c.587 T>C mutation replaces a conserved leucine with proline at residue 196. Modelling of the mutant protein reveals a steric clash with the kinase domain that will weaken interactions with FKBP12 and induce exposure of the glycine/serine-rich repeat. The mutant receptor is predicted to be hypersensitive to ligand stimulation rather than being constitutively active, consistent with the mild clinical phenotype. This case extends our understanding of the 'FOP-variant' syndrome.