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The clinical, roentgenologic, physiologic, and pathologic features of interstitial pulmonary fibrosis in association with polymyositis and dermatomyositis have been described from a retrospective analysis. Presenting complaints ranged from acute febrile pneumonitis without specific muscular symptoms to muscular symptoms with no clinical respiratory symptoms. All patients had diffuse abnormalities on thoracic roentgenograms. High-dosage corticosteroid therapy in those patients with acute febrile pneumonitis resulted in clinical, roentgenographic, and some physiologic improvement. Pulmonary involvement did not appear to progress in most patients with chronic disease who were receiving longterm corticosteroid therapy.

Ten patients with polymyositis were studied with repeated EMG investigations over several years. In the chronic phase of the disease the following neuropathic EMG changes were found; large muscle action potentials with increased duration, grouped polyphasic potentials, loss of motor units and increased motor unit territory. The importance of collateral sprouting of terminal nerve fibres and of reinnervation of muscle is emphasized. Possible explanations for these changes have been considered.

A biometric study was made on 810 muscle spindles in 214 muscles. The absence of atrophy of the intra-fusal muscle fibres and the frequency of spindles with focal dilatation of the periaxial space were the prominent features in denervated muscles. Thickening of the spindle capsule without atrophy of the intra-fusal muscle fibres was often seen in dystrophic muscles. The frequency of changes was greatest in cases of myositis. Eleven spindles were studied by histochemical techniques. In one case of denervation atrophy, all the intrafusal muscle fibres had an enzyme pattern similar to the grouping that occurs in extra-fusal fibres during reinnervation. The outer membranes of the thickened spindle capsule, frequent in dystrophic muscles, were 5-Nucleotidase rich an ATPase poor. The inner membrane was ATPase rich and 5-Nucleotidase poor.

The fine structure of muscle capillaries was analyzed morphometrically in 5 normal controls (41 capillaries), 5 cases of scleroderma (23 capillaries), 4 cases of polymyositis (30 capillaries), 6 cases of dermatomyositis (40 capillaries) and 5 cases of systemic lupus erythematosus (SLE) (50 capillaries). In all 4 connective tissue disorders there was hypertrophy of the endothelial cells and the pericytes. The mean capillary area was also significantly increased in scleroderma, dermatomyositis and SLE but not in polymyositis. In all 4 diseases the number of pinocytotic vesicles per unit endothelial cell area was significantly reduced while the mitochondrial and endoplasmic reticulum fractions of the endothelial area were significantly increased. Replication of the basal lamina around muscle capillaries was observed in 24–74% of the capillaries in inflammatory muscle diseases and in none of the control capillaries. Similar abnormalities of the basement membrane can also occur in other myopathies and in neurogenic atrophies. It is postulated that in the inflammatory myopathies the change is indicative of repeated cycles of capillary degeneration and regeneration and is a primary event rather than being the consequence of muscle fiber necrosis. Endothelial microtubular inclusions were observed in 2 of 6 cases of dermatomyositis and in 2 of 5 cases of SLE. While the inclusions appear to be highly specific for these diseases, their nature and pathogenetic significance remains undetermined.

Adenyl cyclase activity in normal human muscle is stimulated four to seven times by epinephrine and about 18 times by sodium fluoride. The enzyme is present in all particulate fractions of muscle (myofibrils, mitochondria, sarcoplasmic reticulum) but not in the soluble phase. The highest specific activity is found in isolated plasma membrane. Basal enzyme activity was normal in muscle from patients with Duchenne or facioscapulohumeral dystrophy but the response to epinephrine was about 30% of normal and the response to sodium fluoride about half normal. In polymyositis, responses were normal, and intermediate values were found in myotonic dystrophy. In denervated muscle, responses were enhanced. In fetal muscle there was no response to epinephrine but sodium fluoride stimulated, suggesting that the mechanisms of these agents differ.

B-mode ultrasonography of one or both orbits was performed in 47 patients with Graves's disease to determine whether a single mechanism is responsible for the different degrees of eye changes. According to clinical criteria, 30 patients had no or nonthreatening eye changes (Class 0 to 1), and 17 had more severe changes (Class 2 to 4). Ultrasonic changes, primarily in extraocular muscles, were minimal to moderate in 44 patients, equivocal in two and absent in only one patient. This uniform orbital involvement, even in the absence of clinical signs, favors the theory of a single and common pathologic mechanism in the thyroidal and ocular derangement in Graves's disease. Ultrasonic patterns resembling those in pseudotumor or tumor of the eye were found in eight patients with Graves's disease. In such cases misinterpretation was avoided by ultrasonography of the other eye. (N Engl J Med 290:1447–1450, 1974)

A muscle selected for biopsy must be actively, but not terminally, involved by the disease, and the specimen must be obtained atraumatically with the fibers oriented longitudinally in its long axis. Formalin-fixed paraffin-embedded sections are inadequate for interpretation of muscle diseases. Artifacts are avoided by flash-freezing specimens in isopentane cooled to –170 C. in liquid nitrogen. Minimal lesions, which might otherwise be missed, then become evident. Histochemical typing of muscle fibers using the myosin ATPase reaction is essential for complete histopathologic interpretation of diseases of muscle. Simple methods applicable in any laboratory are described for flash-freezing and for recommended stains. The appearance of normal muscle is described and the variations to be expected in denervation and disuse atrophy, muscular dystrophy, and polymyositis, as well as selected other diseases, are outlined.

Plasma levels of 11-hydroxycorticosteroids (11-OHCS), deoxycorticosterone (DOC), aldosterone, Δ4-androstenedione, testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured following the intramuscular administration of αl-24 ACTH Zn and substituted αl-18 ACTH 1 mg in 5 dexamethasone-suppressed healthy male volunteers. There was a marked rise in the plasma concentration of 11-OHCS, DOC and aldosterone following the injection of each preparation, αl-24 ACTH Zn having the more prolonged duration of action of at least 24 hr. In contrast, in 2 patients with collagenoses treated with αl-24 ACTH Zn 0.5 mg im twice weekly for 27 and 48 months respectively, there was no rise in the plasma level of aldosterone following αl-24 ACTH Zn 1 mg im, whereas plasma deoxycorticosterone reached higher levels than those observed in the normal subjects in the 1 patient in whom it was estimated. The plasma level of the adrenocortical androgen, Δ4-androstenedione, increased, whereas the ...

Connective tissue disorders may present with various otolaryngologic symptoms. The manifestations may represent vasculopathy, arthopathy, neuropathy or a combination of pathological processes. Rheumatoid arthritis may involve the middle ear, temporomandibular joints and larynx with mild symptoms or may be life-threatening in instances of cricoarytenoid arthritis. Dermatomyositis with its cutaneous and muscular symptoms prevalent in the head and neck is frequently associated with malignancy in patients over 40. Scleroderma not only affects the gastrointestinal tract but can also produce significant limitations of respiratory function. Systemic lupus erythematosus, polyarteritis modosa, Wegener's granulomatosis and giant cell arteritis produce numerous vascular changes in structures of otolaryngologic significance. In this puzzling group of disorders, protean symptoms may precede the development of a fulminant, widespread and fatal disease.

Muscle blood flow (MBF) was measured using the local (133)Xenon injection method in patients with Duchenne type muscular dystrophy (six), limb-girdle dystrophy (four), polymyositis (seven), and in normal controls (11). Measurements were made at rest and during hyperaemia induced by ischaemic exercise and by histamine injection. Capillary diffusion capacity was measured with the (51)Cr-EDTA method in three patients with Duchenne dystrophy and in six normal controls. Patients with Duchenne dystrophy had normal MBF during rest and during hyperaemia after exercise and significantly increased MBF after histamine injection. The capillary diffusion capacity was higher than normal, but not significantly. In limb-girdle dystrophy MBF was normal, while in polymyositis it was significantly decreased in all three circulatory states. The relevance of the findings to the proposed ischaemic aetiology of Duchenne dystrophy is considered.

The present study was performed in the Department of Medicine and in Veterinary clinic of Bangladesh Agricultural University (BAU), Mymensingh from January to June 2002. Myositis was produced experimentally by injecting oil of turpentine in the gluteal muscles of 4 goats of which 2 goats were given treatment with Diclofenac sodium @1mg/kg body weight (treatment group) for consecutive 3 days and remaining 2 goats were reared as control without giving treatment (control group). All the goats were observed for 7 days. Myositis was characterized by reduced appetite, increased body temperature (1-2°F), lameness, local swelling and cellular changes in blood level. The appetite in both groups reduced sharply from 1st day of myositis and improved from day 2 and became normal on 3rd day after treatment. Body temperature reduced to normal level from 2nd day after administration of diclofenac sodium but in control group, it came down in the same condition from 4th day onward. Moderate lameness was observed in all the goats of both groups. In treatment group lameness reduced completely in 100% goats after 2 consecutive days of treatment but in control group similar result was observed on day 6. Moderate local swelling was reduced to normal level in treatment group 2 days post treatment remain moderate in control group. Total leukocyte count (TLC) was increased significantly (p < 0.05) in both groups in myositic condition than in healthy condition and it came down to normal level in treatment group 3 days post treatment and in control group it remained higher. Similar changes were observed in Neutrophil count. The number of lymphocyte was reduced significantly (p < 0.05) in myositic condition than in healthy ones which again reached to normal level within 3 days of treatment. Key words: Myositis, goat, Non-steroidal anti-inflammatory drug (NSAID) DOI = 10.3329/bjvm.v6i1.1345 Bangl.  J. Vet. Med. (2008). 6 (1): 99-102

1. 1) Eleven young males of the Kikuyu tribe in Kenya were found by muscle biopsy to be heavily infected with T. spiralis. It is probable that they contracted the infection from a wild pig. 2. 2) No previous record of the occurrence of trichinosis in either man or animal has been traced from any African country south of the Sahara. 3. 3) In eight of 10 survivors, muscle biopsies showed larval densities ranging from 420 to 2,800 per g. with an average of 1,849. A description is given of the clinical and laboratory findings in these patients. 4. 4) Specimens from 15 muscle groups in an untreated fatal infection showed an average larval density of 3,249 per g., ranging from 5,190 in the tongue to 1,850 in the sacrospinalis. There were 2,095 larvae per g. in the diaphragm. Very few previous observations on the distribution of larvae in the muscles of man have been traced; the widely held view that the diaphragm is the most heavily infected muscle in man is probably incorrect. A description is given of clinical, laboratory and autopsy findings in this case. 5. 5) Histological examination of postmortem material revealed universal myositis with muscle necrosis; in many sections a large proportion of the muscle fibres were replaced by larvae and cellular infiltration. The heart showed a moderately severe myocarditis. Muscle biopsies from the survivors showed heavy infections, but there was much less infiltration and less damage to the muscles. 6. 6) Treatment with prednisone was given alone or in combination with dithiazinine or diethylcarbamazine. Prednisone was rapidly effective in relieving symptoms, but neither of the other drugs appeared to have any effect on the course of the disease. 7. 7) Six patients were seen 15 months later; biopsies showed high densities of living encysted larvae with no sign of calcification. All the patients were well with no residual symptoms. 8. 8) The Kenya and a London strain of T. spiralis were compared. Morphologically the adult worms and larvae appeared to be identical. The Kenya strain differed markedly in its infectivity to rats; it produced very few adults and very few larvae with infecting doses which would have been expected to produce very heavy infections. 9. 9) The recent appearance of trichinosis in Kenya can probably be explained by previous failures in diagnosis, or to a relaxation of native taboos which prevented the people in the affected area from eating the meat of wild pigs. It is unlikely that the parasite has been recently introduced. Investigations have been started to discover the extent of trichinosis in man and animals in Kenya.

Case History The following case history from an article by Dr. E. C. Rosenow, “Experimental and Clinical Studies on Focal Infection and Elective Localization: Newer Findings and Their Significance,”1 is of particular interest from the roentgenologic standpoint. The apparently negative X-ray pulpless tooth is an important factor in the systemic condition of the patient. Such data will tend to emphasize the importance of extracting all pulpless teeth when systemic conditions warrant such elimination, regardless of the evidence disclosed by the roentgen ray. In other words, the positive and negative roentgenograms of pulpless teeth fall into the same group. “Case 2.—A middle-aged physician who had had repeated attacks of acute tonsillitis for many years, after two such attacks and while in medical school, developed hydrops of the left knee. He had had repeated attacks of lumbago, usually with mild myositis, involving chiefly the flat muscles around the back, neck and thorax. As foul-smelling, cheesy plugs ke...

The results of the experimental analysis reported in this and the two preceding papers (10, 11) indicate that in murine pneumococcal infections penicillin per se destroys the invading organisms only in those parts of the lesions where the bacteria are multiplying rapidly and are thus maximally susceptible to the bactericidal action of the drug. In areas where the bacterial growth rate is slowed, either because the pneumococci have reached a maximum population density, or because the accumulated exudate affords a relatively poor medium for rapid growth, the destructive effect of the antibiotic is greatly diminished. In such portions of the lessions the cellular defenses of the host are observed to play a major role in eliminating the bacteria. In sites where frank suppuration has developed, however, even the combined actions of the penicillin and the cellular defenses of the host are relatively ineffective in ridding the tissues of bacteria. Here, because of the poor medium provided by the pus, the pneumococci remain metabolically sluggish and therefore are not killed rapidly by the penicillin. At the same time the leucocytes in the necrotic exudate have deteriorated to the point where they cannot effectively perform their phagocytic functions. As a result, bacteria persist in such lesions for many days in spite of the most intensive penicillin treatment administered both locally and systemically. A strict analogy cannot be drawn between the action of penicillin upon specific pneumococcal lesions produced in the laboratory and its effect upon acute bacterial infections in man. Host-parasite relationships in acute bacterial infections are determined not only by the strain of parasite and the specific host involved, but also by the site in the body at which the infection occurs (16). Nevertheless, in spite of the number of variables involved, it may be possible, by means of selected laboratory models, to illustrate general principles of infection which in all probability apply to human disease. Bearing in mind the limitations of the methods employed in the present experiments, it would appear justifiable to draw the following conclusions concerning the clinical use of penicillin in acute infections caused by penicillin-sensitive bacteria. The earlier that treatment is begun the more likely is penicillin to effectuate a rapid cure. When therapy is started before the bacteria have reached a maximum population density in any part of the lesion, and before a cellular exudate is formed, the great majority of the infecting organisms will be in a state of active multiplication and thus will be killed promptiy by the bactericidal action of the drug. If, on the other hand, treatment is delayed until the bacterial growth has attained its maximum in older parts of the lesion, and the inflammatory reaction has become well advanced, the resultant slowing of bacterial metabolism will so interfere with the bactericidal action of the penicillin that ultimate destruction of many of the bacteria will have to depend upon the slower clearing effect of the phagocytic cells. In such instances of delayed therapy specific antibody, which is formed relatively slowly, may play an important role in recovery (6). If relapse is to be avoided, however, penicillin therapy must often be continued longer in well established infections than in those treated at a very early stage. Still further delay in treating infections which are prone to cause tissue destruction and suppuration, may lead to the establishment of abscesses. Fully developed abscesses often will not respond to chemotherapy alone; they will ultimately require drainage. As shown by the present murine experiments, the relative ineffectiveness of penicillin under these circumstances is due not only to the failure of the drug to kill the metabolically sluggish bacteria surviving in the pus, but also to the ineffectiveness of the phagocytic cells, most of which are non-motile or dead. Even if specific antibody gains access to such purulent foci, many of the bacteria will continue to survive because of the degenerated state of the leucocytes. It is evident, therefore, that the stage of the infection at which penicillin treatment is begun is often crucial. Equally critical may be the location of the infection. Bacterial lesions in different sites of the body vary greatly in their responses to penicillin therapy. This inconstancy of therapeutic effectiveness is due primarily to the participation of host factors of defense which differ widely in various tissues and at the same time play a major role in the curative action of the antibiotic. In cases of pneumococcal pneumonia, for example, in which each milliliter of the patient's blood contains more than 1000 pneumococci, blood cultures may become negative in a matter of minutes after the start of intensive treatment (17). The remarkable promptness with which penicillin therapy controls such acute bacteriemia is due, first, to its suppressive effect upon the primary infection in the lungs and regional lymph nodes from which the bacteria are being poured into the blood stream (16) and, secondly, to its synergistic action with the cellular defenses of the circulation. The latter are known to be extraordinarily efficient, perhaps more so than in any other tissue of the body (18). Assisting them in destroying the circulating bacteria is the penicillin's own bactericidal effect, which operates rapidly upon the metabolically active organisms in the plasma. Rarely, if ever, as they often do in other tissues of the body (10), do bacteria in the bloodstream reach such numbers, or do inflammatory cells accumulate intravascularly to such an extent, as to create metabolic conditions which depress the bactericidal actions of the antibiotic. In contrast, more prolonged and extensive penicillin therapy is needed to cure pneumococcal endocarditis (19), meningitis (19, 20), or infections of the serous cavities (3, 4). The cellular defenses of the heart valves and of the "open" fluid-containing cavities of the body are relatively inefficient as compared to those that operate in the bloodstream and in tissues with tightiy knit architectures such as the lungs and lymph nodes (16). In endocarditis relatively few phagocytic cells ever reach the site of the offending bacteria (21), and in infections of fluid-containing cavities, the phagocytic efficiency of the mobilized leucocytes is seriously interfered with by the "dilution effect" of the fluid (22, 23). Accordingly, final destruction of the bacteria must depend primarily upon the bactericidal effect of the antibiotic itself, since little assistance is provided by phagocytosis. It is no wonder, therefore, that such infections, as compared to bacteriemia, are relatively refractory to penicillin therapy. Certainly penicillin, in spite of its remarkable therapeutic properties, falls far short of being a therapia sterilans magna (24). Its effectiveness does not depend solely upon the inherent susceptibility of the infecting agent to its antimicrobial action. How readily it will cure a given infection is determined also by the state of growth of the bacteria in the various zones of the lesions, the influence of the purulent exudate upon the bactericidal action of the drug, and the destructive effect of the inflammatory phagocytes upon the invading bacteria. Optimal use of penicillin as a therapeutic agent requires due consideration of all of these factors. Finally, it should be emphasized that the conclusions drawn from this experimental analysis cannot be applied to antibiotic therapy in general. They pertain only to the action of penicillin in acute infections caused by penicillin-sensitive bacteria which act in the host as extracellular parasites (16). The most common human infections included in this category are those caused by pneumococci and Group A beta hemolytic streptococci.7 Whether they apply also to infections due to penicillin-sensitive staphylococci may be questioned because of recent evidence that certain pathogenic strains will survive phagocytosis (27). In diseases such as tuberculosis, brucellosis, and typhoid fever, which are treated with antibiotics having properties different from those of penicillin (28) and which are caused by bacteria capable of intracellular parasitism (28), factors other than those considered in the present analysis must certainly be involved in the curative effect of antimicrobial therapy.

Electron microscopic examination of Coxsackie A4 virus-infected hind limb muscles of suckling mice showed generalized myositis with almost total loss of normal muscle cell architecture. Degenerative changes included dilatation of sarcoplasmic reticulum with concurrent disruption of myofibrils, presenting the appearance of dense amorphous masses in some areas; large accumulations of membrane-bound vesicles; swelling, distortion, and mineralization of mitochondria; increase in lipid deposits; pyknosis of the nuclei; edema and inflammatory infiltration. Virus particles were present in a number of different configurations in muscle fibers: individual particles or small accumulations within vacuoles, two-dimensional linear arrays between membranes, and three-dimensional crystalline arrays, usually in close apposition to sarcoplasmic reticulum or sarcolemma.

Summary This is a case report of a 28-year-old white woman who died from inanition as a result of a marked motor disturbance of the gastrointestinal tract. This disturbance was apparently due to primary atrophy of the musculature of the intestine and was associated with a generalized skeletal muscular disorder: polymyositis or a muscular dystrophy.

A clinical finding is presented which is of interest in disease states with asymmetric lid positioning. It is suggested that Hering's law applies to the levator palpebrae superioris as well as the extraocular muscles concerned with motion of the globe. Two cases of myasthenia gravis are presented; one case of orbital myositis, and one case of asymmetric lid positioning of undetermined etiology, all of which seem to indicate that the levator palpebrae superioris obeys the same law of equal innervation as previously ascribed only to the extraocular muscles involved in ocular motility.

Es wird uber eine Art der Auswertung elektromyographischer Potentiale berichtet, bei der sowohl die Aktionspotentialdauer als auch die Phasenzahl erfast wird. Durch Division der letzteren durch die erstere ergibt sich der „Phasenquotient“, dessen Verhalten im Normalfall, bei „Myositis“, Progressiver Muskeldystrophie, leichten und schweren neurogenen Erkrankungen untersucht wird. Es ergibt sich, das der Phasenquotient bei der „Myositis“ geringgradig, bei Progressiver Muskeldystrophie deutlicher erniedrigt ist und dadurch eine elektromyographische Unterscheidung dieser beiden Krankheitsbuder moglich wird. Bei neurogenen Erkrankungen ist er regelmasig erhoht und kann in leichten Fallen oft der einzige elektromyographische Hinweis sein, der die Diagnose einer neurogenen Storung erlaubt.