Bornholm disease in Upper Silesia. (1/11)

Bornholm disease is generally attributed to infection with Coxsackie viruses of the B group, but in 1954-56 a number of sporadic cases occurred in Bytom, Upper Silesia, which were shown on virological examination to be caused by Coxsackie A4. In 1957, however, in the same area, an epidemic of Bornholm disease broke out for which Coxsackie B virus was clearly responsible. Re-examination of stocked material from the earlier sporadic cases to make sure that no B-type virus was present confirmed that these cases had been caused by A4. Clinically, the epidemic cases showed a preponderance of abdominal pains and comparatively infrequent chest pain, whereas the reverse was true of the sporadic cases; vomiting was also considerably less frequent in the sporadic than in the epidemic cases.  (+info)

ISOLATION OF ENTERIC VIRUSES IN ONTARIO DURING 1960-1962. (2/11)

During the past three years at the Central Laboratory, Ontario Department of Health, 681 isolations were made in tissue culture from 6822 specimens submitted for virus studies by physicians and hospitals from all over Ontario. Nearly 74% of the isolates were enteroviruses, approximately 5% adenoviruses and about 1% reoviruses. The remaining 20% are still to be identified.Although the bulk of isolations was made during the same three-month period (August, September and October) of each year, the predominant virus types varied from year to year. Poliovirus 1 was most commonly encountered in 1960, Coxsackie B5 in 1961 and Echo 9 in 1962.Among other types isolated in smaller numbers were Coxsackie A1, 9 and 10, Coxsackie B1, 2, 3 and 4, Echo 1, 2, 5, 6, 7, 8, 11, 14, 17, 18 and 19, Reovirus 1, 2 and 3, Adenovirus 1, 2, 3, 4, 5, 7 and 16, as well as Frater-type virus. Most of these types were isolated for the first time in Ontario and represent additions to the existing list of viruses known to occur in this province.  (+info)

Epidemic myalgia in adults associated with human parechovirus type 3 infection, Yamagata, Japan, 2008. (3/11)

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The post-viral syndrome: a review. (4/11)

The post-viral syndrome is described and its aetiology is discussed. Many features of the syndrome point to hysteria and altered medical perception as causes but much evidence for organic disease is also presented. Current interest focuses on recent or persisting infection with Coxsackie viruses. A balanced view of the syndrome as a mixture of organic and psychiatric dysfunction is offered. Widely differing estimates of incidence are quoted, possibly owing to varying medical awareness of the syndrome. Many drug therapies have been tried without success and management of the post-viral syndrome is hampered by the reluctance of patients to accept psychiatric support once the diagnosis is known. Many names have been proposed for the syndrome, some implying a purely physical or purely psychogenic aetiology: post-viral syndrome is suggested as the most appropriate term. Increased awareness of the syndrome will lead to an increase in its diagnosis in general practice: the role of the Myalgic Encephalomyelitis Association in promoting a combined psychiatric and organic view of the disease among sufferers is emphasized.  (+info)

Association of group B coxsackie viruses with cases of pericarditis, myocarditis, or pleurodynia by demonstration of immunoglobulin M antibody. (5/11)

Tests for immunoglobulin M (IgM) antibody to group B coxsackieviruses were performed on sera from 259 patients with a clinical diagnosis of pericarditis, myocarditis, or pleurodynia on whom there were no definitive serological or virus isolation findings to establish a viral etiology, and on 259 "control" patients with clinical diagnoses of viral or mycoplasmal pneumonia or pneumonitis. IgM antibodies to coxsackievirus types B1, B3, B4, B5, and B6 were detected by a micro-immunodiffusion technique, and antibodies to virus type B2 were detected by reduction of neutralizing antibodies with ethanethiol. Of the patients with pericarditis, myocarditis, or pleurodynia, 27% (70) had IgM antibody to group B coxsackieviruses, as compared with 8% in the control group. On retrospective review of the clinical diagnosis, some of the patients in the control group with IgM antibody were found to have had additional clinical findings which could be attributed to a coxsackievirus infection. Coxsackievirus IgM antibody was demonstrable in 30% of 113 patients in the study group for whom virus isolation had been attempted with negative results. The presence of coxsackievirus IgM is discussed in relation to the time of serum collection, age of the patients, and month of onset of illness.  (+info)

A six-year study of coxsackievirus B infections in heart disease. (6/11)

Virological examination of 385 patients with suspected heart disease and 26 with Bornholm disease over a period of 6 years suggested that Coxsackie group B virus infections were associated with at least half the cases of acute myocarditis and one third of the cases of acute non-bacterial pericarditis. Complement-fixation tests revealed only a few cardiac illnesses associated with other infections (influenza and Mycoplasma pneumoniae). No evidence of infection was found in chronic cardiac disease.  (+info)

Concept of benign myalgic encephalomyelitis. (7/11)

The reports of the 15 recorded outbreaks of benign myalgic encephalomyelitis have been reviewed and in one instance the original clinical data studied. We believe that a lot of these epidemics were psychosocial phenomena caused by one of two mechanisms, either mass hysteria on the part of the patients or altered medical perception of the community. We suggest that the name "myalgia nervosa" should be used for any future cases of functional disorder which present the same clinical picture.  (+info)

Viral infections of Toronto children during 1965. I. Enteroviral disease. (8/11)

Enteroviruses were isolated from feces and/or cerebrospinal fluid of 29 of 43 Toronto children who contracted aseptic meningitis, pleurodynia, abdominal pain or febrile upsets between June and October, 1965. Coxsackie A9 virus was the dominant agent in aseptic meningitis and Coxsackie B1 virus in pleurodynia and other syndromes. Sero-logical evidence of recent Coxsackie B1 and Echo 6 infection was obtained in two additional patients with aseptic meningitis who did not yield virus, and elevated Coxsackie B1 antibody titres were found in one patient with pericarditis. A newborn infant died with myocarditis due to Coxsackie B1 virus following infection of the mother during the immediate antenatal period. Paired sera collected only two to four days apart from patients with enteroviral syndromes or mumps meningoencephalitis frequently showed four-fold or greater increases of antibody levels.  (+info)

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