Clostridial myonecrosis, haemolytic anaemia, hepatopathy, osteitis and transient hypertrophic cardiomyopathy after intramuscular injection in a Thoroughbred gelding.

A 9-year-old Thoroughbred gelding was presented for swelling over the left neck and inappetence. There was recent history of intramuscular administration of flunixin meglumine into the left neck. On examination, there was evidence of focal myositis, anaemia, haemolysis and pigmenturia. Culture of aspirated fluid from the left side of the neck produced a heavy growth of a Clostridium species. Complications of infection included haemolytic anaemia, hepatopathy, osteitis and transient hypertrophic cardiomyopathy. Treatment included intravenous fluid therapy, antibiotics, anti-inflammatory drugs, blood transfusion and surgical debridement. There was complete resolution of clinical, haematological, biochemical and echocardiographic abnormalities, and the horse returned to ridden work. This report highlights the complications that can arise from clostridial myonecrosis, including the effect on the myocardium.

[Infective endocarditis in patients with hypertrophic obstructive cardiomyopathy: five cases report].

OBJECTIVE: To analyze the clinical characteristics of infective endocarditis in patients with hypertrophic obstructive cardiomyopathy. METHODS: Clinical characteristics from 5 patients with infective endocarditis and hypertrophic obstructive cardiomyopathy hospitalized from January 2000 to December 2010 in our hospital were analyzed. RESULTS: Four patients were diagnosed with left ventricular outflow tract obstructive cardiomyopathy with outflow pressure gradient from 36 to 140 mm Hg (1 mm Hg = 0.133 kPa) and left atrial size 44 - 68 mm. Another patient was diagnosed as ventricular hypertrophic cardiomyopathy with significant right-ventricular outflow tract hypertrophy (30 mm), high pressure gradient (164 mm Hg) and enlarged right atrial (56 mm × 53 mm), there was a 17 mm × 8 mm vegetation on right-ventricular outflow tract in this patient. Blood cultures were positive for streptococcus viridans in all five patients, and enterococcus faecium was revealed in one aortic valve vegetation culture. Transthoracic echocardiogram was performed 2 - 4 times for each patient, the vegetations of two patients was detected only by transesophageal echocardiography. The mitral valve vegetation was detected in two patients, the aortic and mitral valve vegetations were detected in one patients, mitral and tricuspid vegetations in one patient and right ventricular outflow tract vegetation in one patient. The four hemodynamically stable patients were successfully treated with antibiotic therapy, one patient received urgent surgery (replacement of the aortic and mitral valve as well as septal myectomy). All patients recovered and follow-up (1 - 6 years) was available in 4 patients and no complication was observed. CONCLUSION: The risk of infective endocarditis complicating hypertrophic obstructive cardiomyopathy is the highest in patients with both outflow obstruction and marked valve insufficiency, these patients should receive prophylactic antibiotic therapy during procedures that predispose to infective endocarditis.

Porphyromonas gingivalis-induced cellular hypertrophy and MMP-9 activity via different signaling pathways in H9c2 cardiomyoblast cells.

BACKGROUND: Little is known about the pathogenesis of cardiomyocyte hypertrophy caused by periodontitis pathogens. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis on cardiomyocyte hypertrophy. METHODS: Matrix metalloproteinase (MMP)-2 and MMP-9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P. gingivalis-medium treatment with or without SB203580 (p38 mitogen-activated protein kinase cascade [p38] inhibitor), U0126 (mitogen-activated protein kinase kinase [MAPKK] inhibitor), LY294002 (phosphoinositide 3-kinase [PI3K] inhibitor), cyclosporin A (CsA; calcineurin inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor), proinflammatory interleukin (IL)-1, or anti-inflammatory IL-10 in cultured cardiomyoblast H9c2 cells. RESULTS: P. gingivalis medium increased MMP-9 activities and cellular sizes (+87%) of H9c2 cells, whereas Actinobacillus actinomycetemcomitans medium and Prevotella intermedia medium had no effects. The increased activity of MMP-9 treated with P. gingivalis medium was not mediated through p38, extracellular-regulated kinase (ERK), PI3K, calcineurin, and JNK signaling pathways and was not inhibited by IL-10. However, the hypertrophy of H9c2 cells induced with P. gingivalis medium was reduced by administration of SB203580 (-37%), U0126 (-35%), LY294002 (-49%), CsA (-49%), and SP600125 (-24%). CONCLUSIONS: Our findings suggest that P. gingivalis medium elevated MMP-9 activity and induced cardiomyoblast hypertrophy. However, P. gingivalis-induced H9c2 cell hypertrophy was mediated through p38, ERK, PI3K, calcineurin, and JNK signaling pathways, which are in a totally different regulatory pathway from P. gingivalis-elevated MMP-9 activity. These findings provide evidence that P. gingivalis infection activated multiple factors via different pathways to induce the development of hypertrophy of H9c2 cardiomyoblast cells.

Septicaemia with Neisseria elongata ssp. nitroreducens in a patient with hypertrophic obstructive cardiomyopathia.

Neisseria elongata ssp. nitroreducens, a commensal of the human upper respiratory tract, is a newly recognized cause of endocarditis. We report the isolation of the organism from blood cultures of a 30-y-old man with hypertrophic obstructive cardiomyopathy. The patient was successfully treated with benzylpenicillin and netilmicin in combination, followed by ceftriaxone and amoxicillin.

[Virus and dilated cardiomyopathies]. / Virus et cardiomyopathies dilatées.

Dilated cardiomyopathy is so called when an etiological investigation is negative and no cause can be found for ventricular dilatation-hypokinesia. Current research points to genetic, immunological and infectious factors, often associated, and the passage of subclinical viral myocarditis to chronic disease. There is a lot of evidence in favour of this hypothesis. In the experimental model, the relationship between viral myocarditis and dilated cardiomyopathy has been demonstrated with, as cofactors, a genetic predisposition and an immunitary deficiency leading to an auto-immune subacute myocarditis. In the clinical setting, the enterovirus with a high cardiac tropism seems to play an epidemiological role in the genesis of dilated cardiomyopathy. The concentrations of neutralising anti-coxsackie B virus antibodies is higher in subjects with dilated cardiomyopathy than in a control population. The frequency of lymphocytic infiltration, a marker of dysimmunitary myocarditis, is variable from study to study but the presence of sequences of enterovirus genome in the myocardium could explain slow replication of the virus progressively destroying the myocytes. Techniques of molecular hybridization with or without prior genic amplification by the "Polymerase Chain Reaction" have demonstrated such sequences of specific enterovirus genome but discordant results require further studies.

[The management by medical treatment of an intracranial mycotic aneurysm in a patient with infectious endocarditis with negative blood cultures and hypertrophic myocardiopathy]. / Curación con tratamiento médico de un aneurisma micótico intracraneal en un paciente con endocarditis infecciosa con hemocultivos negativos y miocardiopatía hipertrófica.

A case of intracranial mycotic aneurysm due to culture-negative infective endocarditis involving a patient with hypertrophic cardiomyopathy is reported. The patient, a 22-year-old woman with no history of known prior disease, had fever, headache and focal neurologic symptoms 3 days before admission. An echocardiogram performed after admission disclosed an obstructive hypertrophic cardiomyopathy and a gross vegetation on septal leaflet of mitral valve. Cerebral angiography revealed a mycotic aneurysm involving a peripheral branch of the left middle cerebral artery. Causal agent was not identified, and empiric treatment with penicillin G and streptomycin achieved medical cure and disappearance of the aneurysm 2 weeks later. Four months after endocarditis had been cured, the patient was electively operated because of progression of mitral regurgitation. Six months later, she is asymptomatic.

Bizarre nuclei of myocardial fibers in an infant with dilated cardiomyopathy. Light, electron-microscopic, and immunoperoxidase studies of a necropsy case.

The authors present the case of a 9-month-old child with clinical dilated cardiomyopathy that at necropsy showed myocardial cells with volumous, bizarre, and pleomorphic nuclei. These nuclear alterations were also found in other tissues. The myocardial ultrastructural studies revealed degenerative cytoplasmatic changes, nuclear membrane invaginations forming tubules, vesicles, and cytoplasmatic pseudoinclusions, and intranuclear vermicelar bodies, which all suggest virus-induced lesions. Although the ultrastructural studies and immunoperoxidase tests for virus identification were negative, the authors believe that a virus is most probably the agent of these alterations. This case seems to be the first reported on dilated cardiomyopathy with bizarre nuclear alterations in the myocardial fibers having strong evidence pointing to viral etiology.

[Case of infectious endocarditis in hypertrophic cardiomyopathy]. / Sluchai na infektsiozen endokardit pri khipertrofichna kardiomiopatiia.

A patient with hypertrophic cardiomyopathy and infectious endocarditis has been described, confirmed clinically and bacteriologically. L-forms of alpha-streptococcus were isolated from the hemocultures. Aortic valve was affected in the course of the septic process. That morbid state was very favourable influenced by the treatment with high dose penicillin, combined with streptomycin. The control hemocultures 40 days after the discontinuation of the treatment proved to be negative.

Virological study of idiopathic cardiomyopathy: serological study of virus antibodies and immunofluorescent study of myocardial biopsies.

In 113 patients with idiopathic cardiomyopathy paired sera obtained 2--4 weeks apart were examined for neutralizing antibody to coxsackie B 1--6, and echo 4, 6, 7, 9 and 11 viruses. Only eight cases (6.9 per cent) showed a significant change in titer, indicating a virus infection during or shortly before the study. Complement-fixing antibody titers were measured in 126 patients and neutralizing antibodies in 116 patients with idiopathic cardiomyopathy. More patients had complement-fixing antibody titers greater than or equal to 1 : 4 to coxsackie B and herpes simplex virus than did controls (p less than 0.05). Neutralizing antibody titers to coxsackie B 1 and B 3 virus were also higher in patients (p less than 0.01 for titers greater than or equal to 1 : 4 and p less than 0.05 for titers greater than or equal to 1 : 16). Complement-fixing antibody titers greater than or equal to 1 : 4 to herpes simplex virus were more frequent (p less than 0.05) in hypertrophic cardiomyopathy and those to coxsackie B, herpes simplex and influenza A virus were more frequent in congestive cardiomyopathy. Neutralizing antibody titers were more common to coxsackie B 3 (p less than 0.05 for titers of greater than or equal to 1:4) in hypertrophic cardiomyopathy, while in congestive cardiomyopathy they were more common to B 1 (p less than 0.01 for titers greater than or equal to 1 : 4 and p less than 0.05 for titers greater than or equal to 1 : 16), to coxsackie B 3 virus (p less than 0.001 for titers greater than or equal to 1 : 4 and p less than 0.04 for titers greater than or equal to 1 : 16) and to coxsackie B 5 (p less than 0.05 for titers greater than or equal to 1 : 4 or more) and to echo 6 virus (p less than 0.05 for titers greater than or equal to 1 : 4 and greater than or equal to 1 : 128). Immunofluorescent study of 61 cases showed no virus antigens in the biopsied myocardium even in patients who had significant changes in neutralizing antibody titers in paired sera. These results suggest a relationship between virus infection and idiopathic cardiomyopathy not only of the congestive type but also of the hypertrophic type. However, they do not provide definite proof of the virus infection theory of the disease.