Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the ancient Greeks, we have learned that the pathophysiology of the human diseases relies on blood-borne humoral factors. This was the case with the sepsis myocardial depression, whose associated morbidity and mortality remained untouched during the last decades. Despite the growing knowledge of the possible involved mechanisms, our understanding of this serious condition is still in its infancy. Controversies have surrounded the real origin of septic-induced myocardial dysfunction, and it has been ascribed to inflammatory mediators, NO generation, interstitial myocarditis, coronary ischemia, calcium trafficking, endothelin receptor antagonist, and apoptosis. Although not fully understood, myocardial injury/depression remains a challenge for critical care practitioners.
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PMID:Myocardial depression in sepsis. 1870 15

A 50-year-old male patient treated with mesalazine for Crohn's disease was admitted in our unit for a chest pain, associated with nonspecific ST depression or ECG and troponin elevation. Coronarography showed minimal changes while SPECT imagery suggested a posterobasal subendocardial infarction, so that the diagnosis was unclear between ischemic disease and mesalazine-induced myocarditis. Eventually, MRI demonstrated clearly a subendocardial posterior infarction eliciting the diagnosis of mesalazine-induced myocarditis. This case report illustrates, in our opinion, that MRI is of invaluable interest in evaluating the characteristics of myocardium, and must be the cornerstone in the diagnosis of myocardial diseases.
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PMID:[Myocarditis or subendocardial myocardial infarction: role of MRI illustrated by a case report]. 1893 Jan 79

The main purpose of this study was to describe electrocardiographic (ECG) changes in canine babesiosis, and to relate these to clinical severity, outcome and cardiac pathology. Four groups of dogs with babesiosis were studied: mild to moderate anemia, severe anemia, concurrent autoagglutination and concurrent complications. Lead II ECG was recorded at admission for 1 minute in all dogs (121). A six lead ECG was recorded in 88 dogs. Full necropsy was performed on 16 dogs (5 died on arrival, 11 had ECG recording). The following ECG changes were recorded in relatively high prevalence: sinoatrial blocks or sinus arrest (7%), ventricular premature complexes (7%), low R-amplitude (23%), prominent Q (13%), axis deviations (40%), prolonged QRS (32%), ST depression and coving (28%), large T (42%), and notched R (28%). Differences between groups were minor. There was a significantly higher prevalence of sinus bradycardia and irregular rhythm in the non-survivors. Gross pathological changes were pericardial effusion and hemorrhages. Histological changes were hemorrhages, necrosis, inflammation and fibrin microthrombi. The only correlation between pathology and ECG was low R-amplitude and pericardial effusion. The ECG changes were similar to the pattern described for myocarditis and myocardial ischemia, and together with the histopathological findings indicated that the heart suffers from the same pathological processes described in other organs in canine babesiosis, namely inflammation and hypoxia. As the clinical application of the ECG changes found in this study was limited, cardiovascular assessment should be based on functional monitoring rather than ECG.
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PMID:Electrocardiographic changes and cardiac pathology in canine babesiosis. 1908

Chronic graft versus host disease (GVHD) is a common late complication of hematopoietic stem cell transplantation. Polymyositis is a rare manifestation of chronic GVHD after donor lymphocyte infusion (DLI). Patients with both polymyositis and myocarditis have not been reported to date. Here, we report an 18-year-old female patient who developed polymyositis and myocarditis after a DLI. The patient developed the symptoms of fever, generalized myalgia, dysarthria, and asymptomatic sinus tachycardia at DLI day +102, and 17 days after the discontinuation of immunosuppressants. The laboratory testing showed elevated muscle enzymes, and the electromyographic examination revealed myopathic abnormalities compatible with the diagnosis of myositis. The muscle biopsy showed CD8+ T cell infiltration of the muscle fibers. The electrocardiogram (ECG) showed sinus tachycardia with an incomplete right bundle branch block, anteroseptal ST elevation and lateral ST depression. Echocardiography showed mild hypokinesia of the left interventricular septal wall without evidence of infection or leukemic relapse. The patient was immediately treated with 60 mg/day of prednisone and tacrolimus after the diagnosis of polymyositis and myocarditis, apparently associated with chronic GVHD. The cardiac and muscle enzymes decreased and the ECG normalized after immunosuppressant treatment. The follow-up ECG 2 weeks after initiation of therapy was normal.
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PMID:Polymyositis and myocarditis after donor lymphocyte infusion. 1947 35

We present a notable case of a 15-year-old male infected with influenza B virus who showed the clinical manifestations of myocardial ischemia. He was admitted to our hospital with sudden chest pain. He had febrile illness for the past 2 days. Rapid antigen test for influenza revealed positive influenza B virus antigen. The initial electrocardiogram showed elevation of the ST-segments in leads II, II, aVF and reciprocal depression in leads V1 and V2. Serum test showed elevation of creatine kinase and troponin T. Gadlinium-enchanced magnetic resonance imaging, Tl-201 and I-123 beta-methyl-p-iodephenyl-pentadecanoic acid scintigram, coronary angiography revealed no abnormality. Follow-up electrocardiogram showed ST-segment change improvement over the course. Myocarditis associated with influenza B virus seemed to be caused by endothelial impairment and disturbance of microcirculation rather than direct injury to cardiac myocytes.
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PMID:Myocarditis mimicking acute coronary syndrome following influenza B virus infection: a case report. 1982 64

Pekin ducks were infected by the mucosal route (oral, nasal, ocular) with one of two strains of Eurasian lineage H5N1 highly pathogenic avian influenza virus: A/Muscovy duck/Vietnam/453/2004 and A/duck/Indramayu/BBVW/109/2006 (from Indonesia). Ducks were killed humanely on days 1, 2, 3, 5 and 7 after challenge, or whenever morbidity was severe enough to justify euthanasia. Morbidity was recorded by observation of clinical signs and cloacal temperatures; the disease was characterized by histopathology; tissue tropism was studied by immunohistochemistry and virus titration on tissue samples; and viral shedding patterns were determined by virus isolation and titration of oral and cloacal swabs. The Vietnamese strain caused severe morbidity with fever and depression; the Indonesian strain caused only transient fever. Both viruses had a predilection for a similar range of tissue types, but the quantity of tissue antigen and tissue virus titres were considerably higher with the Vietnamese strain. The Vietnamese strain caused severe myocarditis and skeletal myositis; both strains caused non-suppurative encephalitis and a range of other inflammatory reactions of varying severity. The principal epithelial tissue infected was that of the air sacs, but antigen was not abundant. Epithelium of the turbinates, trachea and bronchi had only rare infection with virus. Virus was shed from both the oral and cloacal routes; it was first detected 24 h after challenge and persisted until day 5 after challenge. The higher prevalence of virus from swabs from ducks infected with the Vietnamese strain indicates that this strain may be more adapted to ducks than the Indonesia strain.
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PMID:Infection studies with two highly pathogenic avian influenza strains (Vietnamese and Indonesian) in Pekin ducks (Anas platyrhynchos), with particular reference to clinical disease, tissue tropism and viral shedding. 1993 11

Toxoplasma gondii infection is frequently asymptomatic; however, it can be severe or even fatal to some hosts. In this study, diagnosis of disseminated toxoplasmosis in one red kangaroo (Macropus rufus) and one great grey kangaroo (Macropus giganteus) from the La Plata Zoo, Argentina and the isolation and molecular characterization of T. gondii are reported. Both male kangaroos showed depression and sudden death. Toxoplasma gondii infection was diagnosed by fresh examination, histopathology, immunohistochemistry, PCR and bioassay in mice. During fresh examination many protozoan cysts were observed in diaphragm, heart and hind limb muscles of M. rufus. Cysts were also observed in samples from M. giganteus, although in lower number. Cysts from both kangaroos stained strongly with T. gondii anti-serum by immunohistochemistry. The M. rufus showed more considerable histopathological lesions like non-suppurative meningoencephalitis, myositis and myocarditis. All mice inoculated with tissues from both kangaroos developed IFAT titers to T. gondii (titer >or=800) and brain cysts at necropsy. Both T. gondii isolates were maintained by mice passages and the M. rufus isolate was also maintained in cell culture. Toxoplasma gondii DNA from tissue samples was analyzed by PCR-RFLP analysis using the markers 5'SAG2, 3'SAG2, BTUB, GRA6, SAG3, c22-8, L358, PK1, c29-2 and Apico. Genotyping revealed that the T. gondii isolate from M. rufus was clonal type III and the isolate from M. giganteus was clonal type II. This is the first report of disseminated toxoplasmosis in M. rufus and M. giganteus in Argentina caused by genotypes of T. gondii considered non-virulent in a mouse model.
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PMID:Toxoplasmosis and genotyping of Toxoplasma gondii in Macropus rufus and Macropus giganteus in Argentina. 2004 55

Myocarditis associated with reovirus was diagnosed in 17-day-old, male turkey poults, based on virus isolation, reverse transcriptase-polymerase chain reaction (RT-PCR), demonstration of reovirus antigen in the cytoplasm of mononuclear inflammatory cells and myocytes in the heart by immunohistochemistry (IHC), and reovirus particles in the endoplasmic reticulum of myocytes by transmission electron microscopy (TEM). Clinical signs in the poults included anorexia, growth depression, and increased mortality. Gross lesions in the six poults examined were increased pericardial fluid, mild-to-moderate dilation of right ventricles, pale-yellow myocardium, and ascites. Other lesions in a few birds included mild pulmonary edema, congestion, and pale serosa of the small intestine that had watery contents in their lumens. Microscopically, in the heart, there was mild-to-severe necrosis of myocytes and infiltration of primarily lymphocytes mixed with a few heterophils, macrophages, and occasionally, plasma cells and multinucleated giant cells. There was mild-to-moderate lymphoid depletion in the bursa of Fabricius. Reovirus was isolated from the heart of the turkey poults in chicken-embryo liver cells and was confirmed by RT-PCR, IHC, and TEM. A retrospective search of the laboratory database for cases of myocarditis associated with reovirus in turkeys revealed that this condition has occurred sporadically in California turkey flocks since 1991. This is the first documentation of myocarditis in turkey poults associated with reovirus.
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PMID:Myocarditis associated with reovirus in turkey poults. 2009 52

A 15-day-old Brown Swiss calf, whose dam had suffered from foot-and-mouth disease, was presented with a history of depression and failure to suckle. The calf had an irregular cardiac rhythm and increased plasma cardiac troponin I (cTnI) detected with a commercial human immunoassay. The calf died the following day and myocarditis was detected. The cTnI assay may be useful in diagnosis of myocarditis in cattle.
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PMID:High cardiac troponin I plasma concentration in a calf with myocarditis. 2059 29

We compared characteristic lesions occurring in chickens and domestic ducks naturally infected with H5N1 HPAI virus in April and May 2008. Infected chickens generally exhibited pale-green, watery diarrhoea, depression, neurological signs and cyanosis of wattles and combs, and infected ducks generally exhibited neurological signs and watery diarrhoea. Gross petechial or ecchymotic haemorrhage affected the heart, proventriculus, liver, muscle, fat, and pancreas in chickens, and muscle in ducks. Necrotic foci were primarily present in the pancreas of both species and in the heart of domestic ducks. Histopathologically, chickens exhibited multifocal encephalomalacia, multifocal lymphohistiocytic myocarditis, multifocal necrotic pancreatitis and haemorrhage of several organs and tissues; ducks exhibited lymphohistiocytic meningoencephalitis with multifocal haemorrhages, multifocal necrotic pancreatitis, and severe necrotic myocarditis with mineralisation. The characteristic histopathologic findings of 2008 HPAI were multifocal encephalomalacia and necrotic pancreatitis accompanied by lymphohistiocytic myocarditis, and haemorrhage in various organs and tissues in chickens, whereas in ducks, they were severe necrotic myocarditis with mineralisation and necrotic pancreatitis, accompanied with lymphohistiocytic meningoencephalitis. The high mortality of domestic ducks may be intimately associated with heart failure resulting from increased H5N1 HPAI viral cardiotropism.
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PMID:Comparative histopathological characteristics of highly pathogenic avian influenza (HPAI) in chickens and domestic ducks in 2008 Korea. 2115 30


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