| 1 |
Review Eosinophilic myocarditis temporally associated with conjugate meningococcal C and hepatitis B vaccines in children. 2008
Barton M, Finkelstein Y, Opavsky MA, Ito S, Ho T, Ford-Jones LE, Taylor G, Benson L, Gold R. · Division of Infectious Diseases, the Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada. · Pediatr Infect Dis J. · Pubmed #18664932 No free full text.
Abstract: We report the first cases of tissue-proven eosinophilic myocarditis after single vaccine administration of conjugate meningococcal C and hepatitis B vaccine, respectively. The nature of histopathologic findings strongly supports hypersensitivity reaction and negates viral etiology, which is typically characterized by a lymphocytic infiltrate. Both episodes resolved with corticosteroid therapy.To enhance discussion of our cases, we performed a systematic review of the literature on postimmunization myocarditis or pericarditis, and identified 37 publications, reporting 269 cases during the search period (1966-2007). Time of onset of cardiac symptoms in all patients ranged from 1 to 30 days postimmunization.
|
| 2 |
Article The tyrosine kinase p56lck is essential in coxsackievirus B3-mediated heart disease. 2000
Liu P, Aitken K, Kong YY, Opavsky MA, Martino T, Dawood F, Wen WH, Kozieradzki I, Bachmaier K, Straus D, Mak TW, Penninger JM. · Heart and Stroke/Lewar Centre of Excellence in Cardiovascular Research, University of Toronto, University Health Network, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4. · Nat Med. · Pubmed #10742150 No free full text.
Abstract: Infections are thought to be important in the pathogenesis of many heart diseases. Coxsackievirus B3 (CVB3) has been linked to chronic dilated cardiomyopathy, a common cause of progressive heart disease, heart failure and sudden death. We show here that the sarcoma (Src) family kinase Lck (p56lck) is required for efficient CVB3 replication in T-cell lines and for viral replication and persistence in vivo. Whereas infection of wild-type mice with human pathogenic CVB3 caused acute and very severe myocarditis, meningitis, hepatitis, pancreatitis and dilated cardiomyopathy, mice lacking the p56lck gene were completely protected from CVB3-induced acute pathogenicity and chronic heart disease. These data identify a previously unknown function of Src family kinases and indicate that p56lck is the essential host factor that controls the replication and pathogenicity of CVB3.
|