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The epidemiology of tropical myositis in the Mengo Districts of Uganda.

In the five-year period 1964-68 1,335 patients were admitted to Mulago Hospital, Kampala, with tropical myositis. The marked increase in the number of admissions during the study period is attributed to a change in the utilization of the hospital rather than to a true increase in the incidence of the disease. There was found to be only slight variation in incidence between different age and sex groups and there was no convincing evidence that immigrants from high altitude areas, where the disease is rare, were at different risk. There was statistically significant month-to-month variation in admission rates but there was no apparent correlation with rainfall, and no marked seasonal variation. During the quinquennium there was a changing pattern of admission rates for patients from different counties, and some evidence of 'space-time' clustering. These findings are compatible with the primary muscle damage being induced by a virus or the presence of aberrant hookworm larvae, but an ingested toxin cannot be excluded. Trauma may also play a role in determining localization of the disease in some cases.

Age Factors↗

Flow cytometric study of nodular fasciitis, proliferative fasciitis, and proliferative myositis.

DNA ploidy was assessed retrospectively, using flow cytometry, in 13 nodular fasciitis (NF) lesions, three proliferative myositis (PM) lesions, one proliferative fasciitis lesion, and 12 other benign fibrous lesions (BFLs). All were diploid. In view of the large amounts of cellular debris, cell cycle analysis was possible in only seven NF lesions, three PM lesions, and six BFLs. The mean percentage of S phase did not differ markedly between the combination of NF and PM lesions (6.6%) and BFLs (7.1%); the mean percentage of G2 + M phase (5.4%) of the NF/PM lesion combination was twice as large as that of the BFLs (2.5%). No correlation was detected between the cell cycle analysis and the mitotic count, the predominant histologic type in NF lesions, or the predominant stroma in PM lesions.

DNA↗

HLA-D related (DR) antigens in various kinds of myositis.

Forty-eight patients with various kinds of myositis were studied for HLA-A, B, C, and DR antigens and compared to both local and 7th International Workshop controls. No A, B, or C antigens were increased except for B8 in white patients (7/13 or 54%) (p = 0.005, pc = NS) and for B7 in black patients (6/9 or 67%) (p = 0.02, pc = NS). HLA-DR3 occurred in 8/12, or 67% of whites with polymyositis (PM) as compared to 23% of white controls (p = 0.003, pc = 0.02). HLA-DRw6 was found in 7/9, or 78%, of blacks with PM compared to 26% of black local controls (p = 0.005, pc = 0.04) and 38% of black Workshop controls (p-0.05, pc = NS). Dermatomyositis (DM) patients, however, showed no increased frequencies of any HLA antigens. HLA-DR4 was decreased overall (p = 0.005, pc = 0.04). These immunogenetic differences between PM and DM suggest that they are pathogenetically different disorders.

Dermatomyositis↗

Localized eosinophilic myositis of the masseter muscle associated with actinomycosis.

A case of eosinophilic myositis of the masseter associated with pseudotumor and trismus is presented. Extensive eosinophilic infiltrates of the masseter are rarely observed in the absence of parasitic infection or the hypereosinophilic syndrome. This case is reported because of the rarity of the phenomenon and its importance to the surgeon from the standpoint of differential diagnosis and treatment. The pathogenesis of the condition and its relation to other lesions of muscle associated with eosinophilic infiltration are discussed.

Actinomycosis↗

Inclusion body myositis: its relative frequency in elderly people.

Inclusion body myositis (IBM) is a distinct, steroid resistant, form of inflammatory myopathy. Its recognition is the more important because of the preponderant occurrence in the elderly, in whom steroid treatment is hazardous. Since the relative frequency of IBM among inflammatory myopathies in the elderly is undetermined, we retrospectively studied its frequency among all our patients over 50 years, diagnosed between 1980 and 1991 with inflammatory myopathy. Nine of 15 patients with inflammatory myopathy appeared to suffer from IBM. In a further 2 patients this diagnosis was strongly suspected. We conclude that IBM is the most frequent inflammatory myopathy in the elderly. This observation warrants restraint with steroids in the management of inflammatory myopathy in the elderly.

Aged↗

Immunolocalization of ubiquitin in muscle biopsies of patients with inclusion body myositis and oculopharyngeal muscular dystrophy.

In 10/10 inclusion body myositis (IBM) patients and 2/2 oculopharyngeal muscular dystrophy (OPMD) patients, vacuolated muscle fibers contained darkly stained ubiquitin (Ub)-immunoreactive cytoplasmic inclusions. By electronmicroscopy, Ub-immunoreactive material was strictly localized to the 15-21 nm pathologic cytoplasmic tubulofilaments (CTFs). None of 18 control muscle biopsies contained the Ub-immunoreactive inclusions that are typical for IBM and OPMD. Thus, (a) finding that CTFs are ubiquitinated places their protein in the Ub-mediated turnover pathway and provides their first molecular marker; (b) easy accessibility, as compared to the central nervous system, of muscle tissue containing ubiquitinated inclusions should be advantageous for biochemical and molecular studies and may provide information important to both systems.

Adolescent↗

Ubiquitinated inclusions in inclusion-body myositis patients are immunoreactive for cathepsin D but not beta-amyloid.

The nature of the inclusions in the human muscle disease inclusion-body myositis (IBM) has been the subject of debate. Parallels with Alzheimer's disease have been drawn after these inclusions were found to be ubiquitinated, and immunoreactive with antibodies to beta-amyloid (A beta) and certain amyloid-associated proteins. We have used a battery of antibodies against A beta and associated proteins to immunostain muscle biopsies from patients with IBM. Although the inclusions are ubiquitinated, we could not show immunoreactivity for A beta or the associated proteins investigated. We did, however, find that the ubiquitinated inclusions colocalised with the lysosomal marker, cathepsin D.

Alzheimer Disease↗

Encephalomyelitis and myositis in a boxer puppy due to a Neospora-like infection.

A 10-week-old Boxer dog from Uppsala, Sweden, was killed because of hind limb paralysis. The hind limb muscles were grossly atrophied and encephalomyelitis and myositis were the predominant microscopic lesions. Neospora caninum-like tachyzoites were found in the brain and skeletal muscles, and tissue cysts were found in the brain. The organism was not Toxoplasma gondii, as T. gondii antibody was not found in the indirect fluorescent antibody test in serum samples from the puppy and the dam, and the organism in the dog's brain did not react with T. gondii antibody in the immunoperoxidase test.

Animals↗

Ubiquitin and beta-amyloid-protein in inclusion body myositis (IBM), familial IBM-like disorder and oculopharyngeal muscular dystrophy: an immunocytochemical study.

We used immunocytochemistry to identify ubiquitin and beta-amyloid-protein in muscle biopsies from patients with three neuromuscular disorders characterized by the presence of rimmed vacuoles in muscle fibres: inclusion body myositis (IBM), familial IBM-like disorder and oculopharyngeal muscular dystrophy (OPMD). Labelling with anti-ubiquitin antibodies was observed in all three diseases, but it was frequent in IBM, less common in familial IBM-like disorder and rare in OPMD. This labelling is thought to correspond to the presence of IBM-type filaments (16-18 nm in external diameter) which are characteristic but not specific for IBM or familial IBM-like disorder, as they may also occur in other diseases including OPMD. Labelling with anti-beta-amyloid-protein antibody was seen in a few fibres in IBM but not in the other two conditions. The structures labelled with this antibody have yet to be determined. Labelling with anti-ubiquitin or anti-beta-amyloid-protein antibodies was not correlated with the presence of acid phosphatase activity.

Adult↗

Focal myositis: a clinicopathological study.

Focal myositis is a rare, benign inflammatory condition that may clinically simulate a soft tissue sarcoma. It was first described in 1977 and around 30 cases have been reported to date. We report two further cases on which we have performed immunocytochemistry and electron microscopy. Histology of both lesions was identical, showing a destructive inflammatory myopathy with evidence of regeneration. Stains for micro-organisms were negative and no viral particles were seen on electron microscopy. The immunocytochemical profile of our two cases differed from that of polymyositis: with a panel of T- and B-cell markers the cellular infiltrate was found to be composed of T-lymphocytes and variable numbers of macrophages: sub-typing in one case revealed the T-cells to be predominantly CD4+ cells. Use of antibodies to MHC class 1 and 2 antigens showed occasional positive inflammatory cells only. Clinicopathological correlations and the differential diagnosis are discussed.

Aged↗

Bilateral and recurrent myositis ossificans in an athlete: a case report and review of treatment options.

An unusual case of recurrent myositis ossificans (MO) bilaterally in the hamstring muscles of a 47-year-old athlete secondary to trauma is presented with a review of the literature of current treatment options. MO is a common condition that occurs among athletes in association with muscle and/or tendon strain or contusion. After an extensive literature review, we believe this to be the first case reported of recurrent and bilateral MO in a nonsurgical setting from recurrent hamstring strains. Plain radiographs and physical examination revealed the appearance and chronology of this pathology. Treatment options to improve flexibility and decrease morbidity are discussed along with prophylaxis for future injury. Treatment of mobility and flexibility, rehabilitation goals and treatment with nonsteroidal anti-inflammatory drugs, bisphosphonates, and magnesium are discussed along with prophylaxis.

Baseball↗

Surgical and traumatic wound infections, cellulitis, and myositis in horses.

Surgical site infections (SSIs) and traumatic wound management remain challenging clinical scenarios. The prevention of SSIs involves meticulous surgical technique and aftercare. Traumatic wounds require thorough evaluation to assess the involvement of synovial structures and radiographs to check for fractures. Chronic wounds can require a biopsy and histologic evaluation to obtain a diagnosis, because many underlying pathologic processes grossly appear similar but different treatment regimens are required. Early recognition and diagnosis of cellulitis and myositis enable the rapid aggressive intervention necessary for a positive outcome. Any delay in diagnosis and treatment increases the complication and mortality rates and makes these conditions difficult to treat successfully.

Animals↗

West Nile virus encephalitis with myositis and orchitis.

This report documents the hospital course and autopsy findings of a 43-year-old man with a renal allograft who died of West Nile virus (WNV) encephalitis. Central nervous system (CNS) findings were those of severe necrotizing and hemorrhagic encephalitis affecting gray matter regions limited to the diencepahlon, rhombencephalon, spinal cord, and limbic system. The bilateral process exhibited preferential involvement of motor neurons. Brain imaging obtained 6 days before death demonstrated an unusual pattern of involvement corresponding with the autopsy findings, confirming that imaging may be a specific diagnostic guide in WNV encephalitis. Extra-CNS findings include myositis with T-lymphocyte infiltration of nerve fibers, suggesting that the virus may reach the CNS via peripheral nerves. Orchitis with dense T-lymphocyte infiltration and syncytial cell formation thought to be due to WNV were also noted.

Adult↗

Zygomatic abscess with temporal myositis - a rare extracranial complication of acute otitis media.

Acute mastoiditis is the most common complication of acute otitis media (AOM) and its early recognition and management still poses a challenge due to potentially serious consequences. The incidences of extracranial and intracranial suppurative complications of AOM in children have decreased significantly, yet they remain a serious clinical problem, especially when caused by bacteria resistant to antibiotics. The authors presented a case of rare AOM complication - zygomatic abscess with temporal myositis. A 6-year-old boy was admitted to the ENT Department with 4 weeks of ear pain, treated for AOM with cefuroxime axetyl and amoxicilline, with acute mastoiditis and subsequent abscess formation in zygomatic and preauricular region. The inflammatory process spread through anterior air cells to the zygomatic cells leading to a fistula formation in the zygomatic bone and breakthrough into the temporal muscle. The surgical procedures applied were: myringotomy with drainage, cortical mastoidectomy and revision of zygomatic area and treatment with antibiotics (ceftriaxon). Enterococcus faecalis and Streptococcus viridans were found in the culture of middle ear and mastoid effusion. After half a year of follow-up the child had a normal hearing. Severe complications of AOM are rare today. An early diagnosis in order to promote adequate management and prevent inherently suppurative complications is essential.

Abscess↗

A rare cause of painful cervical swelling: myositis ossificans progressiva in childhood. Report of a case.

Myositis ossificans progressiva (MOP) is a rare condition of which we report a case in a 13-year-old girl with involvement of the cervical paraspinal and periscapular muscles. No ectopic ossifications were visible on plain radiographs. Computed tomography disclosed diffuse inflammation. Plain radiographs of the toes confirmed the diagnosis by visualizing characteristic bone abnormalities. Knowledge of the digital abnormalities seen in MOP is important to avoid unnecessary diagnostic investigations, most notably a surgical biopsy, which may trigger a flare of the disease. The prognosis is guarded.

Adolescent↗

Eosinophilic myositis due to Sarcocystis hominis in a beef cow.

A case of eosinophilic myositis (EM) in an 8-year-old beef cow was investigated. The animal originated from a herd in which a high incidence of the disease had been observed in slaughtered adult females over a period of 2 years. Histologically, the lesions in the muscles were characterized as granulomas with a central core of degenerate eosinophils and remnants of necrotic muscle fibres, surrounded by a rim of epithelioid cells and fibrous tissue with an infiltrate consisting predominantly of eosinophils radiating outwards. Degenerate sarcocysts with a thick (7-9 microm) wall were present in the suppurative centre of most lesions. Intact sarcocysts with similar morphology were present in adjacent muscle fibres but without an associated inflammatory reaction. By transmission electron microscopy the sarcocysts were identified as Sarcocystis hominis, based on the morphology of villar protrusions of the sarcocyst wall, which were broad-based and cylindrical, with a blunt distal end, and contained numerous long microfilaments. Circumstantial evidence indicated a human source of infection, human faecal material having been spread on the pasture grazed by the cattle. The findings supported a causal relationship between S. hominis infection and EM in cattle.

Animals↗

IL-6-deficient mice show impaired inflammatory response in a model of myosin-induced experimental myositis.

Inflammatory/immune reactions against muscle cells are responsible for the damage in idiopathic inflammatory myopathies. We investigated the role of IL-6, a cytokine known to contribute to local leukocyte accumulation, in a model of myosin-induced experimental myositis. After injection of rabbit myosin in CFA/pertussis toxin, normal mice develop clinically evident muscle deficit and damage, as demonstrated by myofiber necrosis and leukocyte infiltration, while IL-6-deficient mice have no clinical or histological signs of muscle damage. This study evidences that selective deficiency of IL-6 directly or indirectly hinders the local inflammatory response and its harmful effects in this model of muscle damage.

Animals↗