Ultrastructural and molecular changes in the left and right ventricular myocardium associated with ascites syndrome in broiler chickens raised at low altitude

The present study examines ultrastructural and molecular changes in ventricular myocardium associated with ascites cases in fast-growing broilers raised at low altitude. Extensive ultrastructural lesions were seen in the left and right ventricular myocardium of broilers with fulminant heart failure and ascites. Significant changes included lesions in the myofibril contractile apparatus, altered mitochondria, marked reduction in the myofibril component, and changes in the extracellular matrix (ECM) architecture. No lesions were observed in hearts of slow growing broilers, but mild to moderate changes (predominantly in the left ventriculum) were apparent in the hearts from some clinically normal, fast-growing broilers. SDS-PAGE profiles of washed myofibrils showed several distinctly different bands in preparations from left ventricular myocardium of ascitic birds. Western blot analysis of these samples revealed several fragments of myosin heavy chain, M-protein, and titin. Based on gelatinolytic activity, matrix metalloproteinases (MMP) in the cytosolic fraction of ventricular myocardium homogenates were identified as MMP-2. The relative activity of this enzyme appears to be considerably higher in preparations from broilers, particularly in the preparations from the left ventriculum of fast-growing broilers, in comparison to leghorns or slow growing broilers. The nature and distribution of the changes in the heart indicate that chronic cardiomyopathic process in the left ventricular myocardium occurs during the development of ascites. It is postulated that progressive deterioration of the left heart pump function caused by initial lesions in the left ventricular myocardium is a significant factor in the development of pulmonary hypertension and the pathogenesis of ascites in broilers raised at low altitude.     

Familial dilated cardiomyopathy of young Portuguese water dogs

A novel dilated cardiomyopathy (DCM) in 12 related Portuguese Water Dogs was identified by retrospective analysis of postmortem and biopsy case records. Male and female puppies born to clinically healthy parents typically died at 13 (+/- 7.3) weeks of age (range, 2-32 weeks) because of congestive heart failure. Puppies died suddenly without previous signs or with mild depression followed by clinical signs of congestive heart failure 1-5 days before death. There was no sex predilection. The hearts were enlarged and rounded, with marked left ventricular and atrial dilation. No other significant structural cardiac defects were noted. The histologic changes in the myocardium were diffuse and characterized by myofibers of irregular sizes separated by an edematous interstitium. The myofibers had multifocal swollen, cleared segments often involving perinuclear areas that contained granular, phosphotungstic-acid-hematoxylin-positive material consistent with mitochondria. There was loss of the cross-striation pattern, and intercalated discs were difficult to identify. There was no evidence of concurrent myocardial fibrosis; rare chronic inflammatory infiltrates were noted in one dog. Noncardiac skeletal muscles were not affected. The underlying cause is unknown. From the pedigree analysis, an autosomal recessive pattern of inheritance is suspected. Based on the histologic findings, this DCM is most likely due to an underlying molecular (biochemical or structural) defect. The early onset and rapid progression of the disease makes this a clinically distinctive form of canine DCM.     

Cardiomyopathy in Dystrophin-Deficient Hypertrophic Feline Muscular Dystrophy

A colony of cats affected with hypertrophic feline muscular dystrophy was used to study the occurrence of cardiomyopathy associated with dystrophin deficiency. Affected male and female cats, obligate carrier females, and unaffected healthy littermates were followed from 12 weeks of age into adulthood. Thoracic radiography, 2-D echocardiography, and 2-D-derived M-mode echocardiography were performed at 3-month intervals until 12 months of age and regularly thereafter. From 9 months of age, all affected cats had larger hearts than normal and carrier animals. Left ventricular wall thickness in systole and in diastole and interventricular septal thickness in systole were greater in affected cats 12 months and older when compared with normal or heterozygous animals (P < .05). The myocardium of affected cats was diffusely hypoechoic and thickened. Multiple hyperechoic foci were in the myocardium and papillary musculature. Shortening fraction was normal in all cats. Changes seen in carrier females included enlargement and hyperechogenicity of the papillary musculature after the age of 2 years. Gross and light microscopic examination revealed left ventricular wall thickening with multiple foci of mineralization in 2 of 5 hearts from dystrophin-deficient cats. Although approximately 10% of the normal dystrophin amount was present in the skeletal muscle, dystrophin could not be detected in the myocardium. Early onset concentric myocardial hypertrophy was present in all adult cats. Lesions were mainly localized in the myocardium of the left ventricular free wall and interventricular septum, papillary musculature, and the endocardium. Clinical signs of heart failure developed only infrequently in cats with hypertrophic feline muscular dystrophy.     

Ultrastructural observations on autolytic changes of atrial specific granules in pig heart.

The progressive autolytic changes of atrial specific granules (ASGS) up to 24 hours after death were studied electron microscopically. Tissue samples taken from the left auricular myocardium of four pig hearts at 0, 0.5, 1.5, 3.5, 6, 12 and 24 hours post mortem were fixed for 24 hours by immersion in 2.5 per cent cacodylate buffered glutaraldehyde (pH 7.4). Two pig hearts were kept at 20 degrees C and two at 4 degrees C. Although typical autolytic changes were seen in many organelles, no remarkable modifications in aspect, distribution, content and diameter of ASGS were observed in all samples. The results of this study indicate that ASGS are not morphologically affected by the autolytic processes, at least during the first 24 hours. Hence, the electron microscopic evaluation of ASGS does not need a particular fixation method such as perfusion. This may eliminate technical problems when slaughterhouse material is used.     

Abnormalities of the volar and plantar sesamoid bones in Rottweilers

The fore and hind feet of 50 unselected Rottweilers were examined clinically and radiographically for abnormalities of their volar and plantar sesamoid bones. Lesions were found in 22 (44 per cent), invariably affecting the No. 2 and/or No. 7 sesamoids. The majority occurred in the forelimb. Clinical signs were detected in only five dogs and local analgesia in these cases indicated that the sesamoid changes were not the cause of the presenting lameness. Radiographically the defect varied from small radiodense foci separated from an otherwise normal sesamoid, to gross distortion of the bone into a number of calcified bodies. In none of these dogs was the sesamoid abnormality demonstrated to cause lameness and it was not necessary, therefore, to treat the condition surgically. It is postulated that these lesions result from disordered ossification with subsequent degenerative changes.     

High mortality with severe dystrophic cardiac calcinosis in C3H/OUJ mice fed high fat purified diets

Severe degenerative myocardial disease occurred in female C3H/OUJ mice fed purified diets for 36 weeks; the diet contained 5% or 20% fat as non-hydrogenated soybean oil. Deaths of lactating females of this group (17/35 high fat diet and 7/35 low fat diet animals) were due to sudden cardiovascular collapse. Cardiomegaly with marked atrial and ventricular myocardial mineralization was seen at necropsy. Histologically, the random, myopathic foci were characterized by severe myocardial degeneration, mineralization, and fibrosis. Mural thrombosis, pulmonary arteriosclerosis, and mild myocardial inflammatory cell infiltrates were also present. Pathological changes were similar to those of dystrophic cardiac calcinosis, an incidental necropsy finding in certain mouse strains.     

Epizootic myocarditis associated with encephalomyocarditis virus in a group of rhesus macaques (Macaca mulatta)

Six cases of fatal myocarditis associated with encephalomyocarditis virus occurred over a 14-month period in a group of outdoor-housed juvenile rhesus macaques. All animals were younger than 3 years of age and died or were euthanized following acute onset of dyspnea or pulmonary effusion (3 of 6) or were found dead without premonitory signs (3 of 6). Gross findings included pulmonary congestion (6 of 6), variable degrees of pleural effusion (4 of 6), multifocal pale tan foci throughout the myocardium (3 of 6), hepatomegaly and hepatic congestion (3 of 6), and pericardial effusion (1 of 6). Histologically, affected myocardium was infiltrated multifocally by lymphoplasmacytic and histiocytic inflammation admixed with necrotic and degenerate myofibers and infrequent mineralization (6 of 6). Pulmonary edema was present in all animals. Encephalomyocarditis virus was confirmed in 6 of 6 hearts by immunohistochemistry, and virus was isolated from one case by polymerase chain reaction. Sequencing of virus isolated from 1 affected animal indicated infection with a novel encephalomyocarditis virus. Encephalomyocarditis virus should be considered as a differential etiology in outbreaks of myocarditis and pulmonary edema in juvenile primates.     

The pathomorphology and pathogenesis of acute cardiovascular failure in swine. 2. Histopathologic findings in the myocardium of swine of different populations

Histopathological alterations of the myocardium (inflammatory processes, fibrolysis, fibronecrosis, dystrophic calcification, fatty degeneration of fibres, sarcosporidia) were recorded for quantitative evaluation from 200 hearts which had been collected from clinically intact pigs for slaughter of different populations (Leicoma, land race, Schwerfurt breed, Belgian land race). Both incidence and severity of myocardial damage in pigs of stress-sensitive populations were higher with significance than those in the less stress-sensitive Leicoma population oriented to breeding. The highest rate of pathological processes was recorded from hearts of the Schwerfurt breed. These alterations were interpreted as objectively measurable expressions of breed-dependent differences in cardiovascular stability. In this context, rates of damage were higher in hearts of low absolute mass.     

Concurrent clinical intraocular findings in horses with depigmented punctate chorioretinal foci

Objective To report concurrent clinical intraocular findings in horses with depigmented punctate chorioretinal foci and to document any correlation with equine recurrent uveitis (ERU). Procedure Records of 131 horses (241 eyes) examined at the University of Georgia Veterinary Teaching hospital from 2001 to 2010 were reviewed with either clinically normal fundi or depigmented punctate chorioretinal foci in the absence of other fundic pathology. Data collected included patient signalment, concurrent clinical ocular findings and follow‐up information. Sex, presence of no other intraocular findings, presence of ERU, presence of cataracts, and presence of vitreal disease were compared between normal and foci groups using chi‐squared analysis. Age and length of follow‐up time were compared using a student’s t‐test. Results Ninety‐one horses (167 eyes) with chorioretinal foci and forty horses (74 eyes) with clinically normal ocular fundi were examined. Fifty‐eight (64%) horses with chorioretinal foci and 20 (50%) horses with clinically normal fundi had a normal intraocular examination. There was no significant difference in any of the criteria examined between groups. Conclusions Horses with depigmented punctate chorioretinal foci, in the absence of other fundic pathology, are not more likely to have intraocular disease or ERU than horses with clinically normal ocular fundi. These findings suggest that depigmented punctate fundic foci in horses are not indicative of or associated with ERU.     

The pathomorphology and pathogenesis of acute cardiovascular failure in swine. 1. Histopathologic findings in the myocardium of swine of different age groups

Myocardia were histologically examined for the presence of pathomorphological processes in 143 pigs of varying age groups (one, three, seven to nine, and 24 months). Some of them had been slaughtered in clinically intact condition. Others had died of non-cardial diseases. Numerous alterations were recorded, with the following among them being more suitable than others for quantitative assessment and thus objective appraisal of the myocardium: inflammatory infiltrations, granular or hyaline disintegration of fibres, fibre necrosis, dystrophic calcification of fibres, degenerative fat infiltration, and sarcosporidiosis. These parameters were increasingly detectable along with growing age of animals. Inflammatory infiltrations were among the most common findings from pigs for slaughter, aged seven to nine months (40.4 percent of myocardial samples or 58 percent of hearts), followed by muscle fibre necroses (26.4 or 42.0 percent). Most of these disorders were but slightly manifest and were considered to be indicators of catabolic or reparative processes in the myocardium. Attention should be given to them, whenever it comes to pigs with cardiac or circulatory disturbances.     

Cardiomyopathy in stranded pygmy and dwarf sperm whales

Necropsy and histologic examinations were performed in 23 pygmy sperm whales (Kogia breviceps) and 6 dwarf sperm whales (Kogia simus) that had been stranded singly or in cow-calf pairs along the southeastern coastline of the United States. At necropsy, the gross findings in the adult whales included pale, flabby right ventricles. Microscopically, lesions in the hearts of the whales were characterized by moderate to extensive myocellular degeneration, atrophy, and fibrosis. Similar changes were not seen in 5 of 6 sexually immature whales or in the whale calves. Hepatic changes were consistent with heart failure. The cause of the myocardial lesions was not determined. The systemic effects of failing myocardium probably were a major reason for the stranding of the adult whales.     

Myocardial and pancreatic lesions induced by T-2 toxin, a trichothecene mycotoxin, in swine

Myocardial and pancreatic lesions induced by sublethal doses of T-2 toxin in swine were characterized by light and electron microscopy. Toxin was given intravenously to six 17- to 18-week-old pigs. Pigs were killed 24 or 48 hours after treatment. Grossly, subendocardial hemorrhages, multifocal pinpoint white foci in myocardium, and pancreatic edema occurred in one treated pig. Histologic changes in myocardium of treated pigs consisted of multifocal edema, mononuclear cell infiltration, myofiber hyalinization, vacuolation, and contraction bands with nuclear pyknosis. Ultrastructurally, there were areas of edema, myofibrillar disorganization, dilation of sarcoplasmic reticulum, and formation of hypercontraction bands. Myocardial mineralization was seen in the pig with gross lesions. Pancreatic changes in treated pigs consisted of multifocal acinar degeneration and necrosis. Ultrastructural changes included irregular dilation of rough endoplasmic reticulum and abnormal zymogen granules. Thus, in addition to radiomimetic lesions of the gastrointestinal tract and lymphoid organs, heart and pancreas are target organs of T-2 toxin in swine.     

Systemic Proteoglycan Deposition Is Not a Characteristic of Equine Degenerative Suspensory Ligament Desmitis (DSLD)

Recently Degenerative Suspensory Ligament Desmitis (DSLD) has been proposed to be a disease characterized by systemic deposition of proteoglycan (PG) in connective tissues. To investigate this hypothesis, 6 clinically affected Peruvian Paso horses were compared to 2 unaffected quarterhorses and one unaffected standardbred. Histological sections of limb ligaments and tendons, nuchal ligaments, aortas, hearts, eyes, visceral organs and brains from both groups were stained with H&E as well as special stains for PG. Safranin-O stained sections were found to be optimal for elucidating the presence of PG. Although lesions characteristic of DSLD were present in suspensory ligaments of each clinically affected horse, including foci of chondroid metaplasia with abundant PG, a similar but less pronounced pattern of PG deposition was present in control horses. In contrast to findings of the previous study, PG deposition was not unique to DSLD horses, and PG deposition in aortas and nuchal ligaments of some control horses exceeded levels of PG present in similar tissue of DSLD horses. Furthermore, the “vascular lesion” described in the media of arteries as cellular separation and intercellular amorphous matrix deposition was within the spectrum of changes recognized in both affected and unaffected horses. We found no evidence that DSLD is a systemic PG deposition disease.     

Studies Into Equine Electrocardiography and Vectorcardiography: IV. Vector Distributions in some Arrhythmias

The paper describes the changes in P, QRS and T vector orientations in the H plane in the aberrant beats in cases of partial atrioventricular block and premature atrial and ventricular systoles.

The sites of possible atrial ectopic foci are discussed in relation to the anatomy of the atrial chambers and the orientation of the P vectors associated with atrial ectopic beats.

     

Anatomy of the Sinus Node of Camels (Camelus dromedarius)

Anatomy of the sinus node was studied in six camel hearts (Camelus dromedarius) with serial histologic sectioning. The sinus node in this species of animal was located 0.5 mm beneath the epicardium, near the junction between the cranial vena cava and the right atrium at the sulcus terminalis. Its shape was elongated, bent oblong with 28.25 mm length, 5.75 mm width and 5.38 mm thickness. The maximum section area was 101.66 mm². The central artery of the node originated from the circumflexus branch of the left coronary artery and, throughout its length in the substance of the sinus node, had an internai elastic membrane. Histologically, the sinus node of this animal contained a central artery and a framework of collagen fibres, which were distributed around the central artery. The nodal cells were irregularly organized around the central artery and two types, i.e.‘p’ cells and transitional cells were present. The ‘p’ cells had a perinuclear clear zone but the transitional cells contained more myofibrils. The intercalated dises were not present. At the periphery of the sinus node there were many nerve fibres and a ganglion. The purkinje fibres were present within atrial myocardium, as well as within ventricular myocardium. The glycogen content of the sinus nodal cells was higher than that of the atrial myocardial cells.     

A case of juvenile form of dilated cardiomyopathy in a 6-month-old Shiba Inu dog

A 6-month-old Shiba Inu dog was brought to the Veterinary Medical Teaching Hospital because of a cough, exercise intolerance, and pulmonary edema. The dog had a Levine 2/6 systolic murmur. Transthoracic echocardiography revealed left atrial and ventricular dilatation (left atrium to aortic ratio: 2.8), mitral and tricuspid valve regurgitation, and severe left ventricular myocardial hypokinesia (fractional shortening was 11.8%). Bubble contrast echocardiography did not reveal a congenital shunt; therefore, the dog was clinically diagnosed with early onset dilated cardiomyopathy. From the first visit, the dog was treated with pimobendan, taurine, torasemide, and isosorbide dinitrate. After 435 days, echocardiography revealed that systolic function had not improved. On Day 465, atrial fibrillation was confirmed via electrocardiogram, and treatment with diltiazem hydrochloride was initiated. The dog continued to appear clinically stable thereafter, until it died suddenly 1087 days after the initial visit. A postmortem histopathological examination identified severe enlargement of the left atrial and ventricular chambers as well as attenuated wavy fibers in the ventricular myocardium, which confirmed dilated cardiomyopathy in a juvenile. This is the first report of a juvenile form of dilated cardiomyopathy in a Shiba Inu dog. This case report provides evidence that the extended prognosis of this dog differed from that in previously reported cases of dilated cardiomyopathy in young dogs.Key clinical message:This is the first reported case of a juvenile form of dilated cardiomyopathy in a Shiba Inu dog. This report provides evidence that the prognosis of this dog differed from that in previously reported cases of dilated cardiomyopathy in young dogs.     

Prevalence of perioperative arrhythmias in 50 young, healthy dogs

The objective of this study was to assess the type and frequency of cardiac dysrhythmias occurring after routine ovariohysterectomy or orchidectomy in young, healthy dogs by using 2 anesthetic protocols (group I: propofol and isoflurane; group II: thiopental and halothane). Fifty dogs under 2 years of age, judged to be clinically normal by physical examination and standard electrocardiography, were evaluated by using 24-hour ambulatory electrocardiography. The most common dysrhythmias in the postoperative period were 2nd degree atrioventricular block (44%), ventricular premature complexes (44%), and atrial premature complexes (32%). For study purposes, more than 100 ventricular or atrial premature complexes per 24 hours, or any occurrence of R-on-T phenomenon, ventricular or atrial tachycardia were classified as clinically significant arrhythmias. Significant arrhythmias were observed in 9 dogs in the postoperative period, 5 of which were in group I and 4 in group II. All of these dogs were under 1 year of age. The R-on-T phenomenon occurred in 4 dogs in group II and 1 dog in group I. Results from this study show that significant arrhythmias, including R-on-T phenomenon, can occur in the perioperative period in young, healthy dogs undergoing routine surgeries with both protocols used.     

Chronic myocarditis and circulatory syndrome in a White Leghorn strain induced by an avian leukosis virus: light and electron microscopic study

Specific-pathogen-free white leghorn chickens were inoculated at 1 day of age with avian leukosis virus (ALV, RAV-1). All chickens in Expt. 1, killed 33 or 64 days postinoculation, had focal chronic lymphocytic or lymphoplasmacytic myocarditis. Among those held beyond 33 days, eight of 22 developed lesions in the myocardium that resulted in a chronic circulatory syndrome (CCS) typical of right-sided heart failure. Chickens in Expt. 2 were held for 210 days, and 21% of 125 developed CCS. In Expt. 2, ALV particles were found by electron microscopy in myocardium of 100%, 72%, and 89% of inoculated chickens that developed CCS, lymphoid leukosis, or that had no gross lesions, respectively. These findings were in accord with the immunoperoxidase staining of tissue sections for group-specific antigen of ALV. In areas of extensive virus replication, there were often abnormal virus particles and also round bodies, which may have been remnants of host-cell membranes formed in the budding process. In contrast to findings in hearts, the spleens were usually negative for virus and viral antigen.     

Anatomical features of ossa cordis in the Steller sea lion

Irregular triangular cartilage or bone fragments are sometimes found in the fibrous triangle of the heart. Ossa cordis and/or cartilago cordis has been demonstrated in various terrestrial animal species. Regarding marine mammals, sperm whales lack heart bones, and there have been no studies on bones or cartilage in pinniped hearts. Therefore, we examined the ossa cordis and/or cartilago cordis of the Steller sea lion. Eleven Steller sea lion hearts were examined morphologically and histologically. Before dissection, some hearts were imaged by CT to confirm the presence of ossa cordis or cartilago cordis. As a result, ossa cordis-like fragments were confirmed in four adults and one pup. All of the fragments were found at the right fiber triangle, and one adult had ossified tissue, including adipose tissue in the bone marrow cavity. The ossa cordis probably support the aorta because they surround the aorta as in other terrestrial animals. Steller sea lions can dive to a few hundred meters, but they need to rest on land frequently. Hence, their ossa cordis help maintain heart function during the tachycardia that occurs upon repeated surfacing and movements on land after diving in water.     

Pathology of vitamin D deficiency in growing turkeys

Turkey poults were fed a vitamin D-deficient diet and examined for clinical signs and structural changes of bone and parathyroid glands. Vitamin D-deficient poults developed ricketic changes during days 10 to 14. Control poults (deficient diet plus vitamin D) did not develop rickets. In deficient poults, lengths of proliferating-prehypertrophied zones of growth plates increased significantly in the proximal tibiotarsus but were only slightly elongated in the distal tibiotarsus. Unmineralized hypertrophic chondrocyte zones increased in length rapidly in conjunction with a decrease in the length of mineralized hypertrophic degenerative zones; this occurred more rapidly in proximal than in distal tibiotarsus. Other ricketic changes included decreases in bone ash, total femoral bone ash (calcium, phosphorus, magnesium), bone length, and body weight. Plasma alkaline phosphatase was increased, calcium was normal, and phosphorus was normal or elevated. Parathyroids were hyperplastic and had foci of degeneration. Vitamin D3 metabolites 25OHD3, 1,25(OH)2D3, and 24,25(OH)2D3 were rapidly depleted. Increase in bone ash Ca/P ratios in deficient poults suggests that phosphorus may be selectively released from ricketic bone. Low 25OHD3 and 1,25(OH)2D3 of control poults early in the experiment suggests that 1,400 IU of vitamin D3/kg of feed may not be an adequate level of vitamin D3 for growing turkey poults.