Coxsackie B virus infections in new zealand patients with cardiac and non‐cardiac diseases

Abstract

From 1979 to 1981, a total of 910 cardiac patients and 776 noncardiac patients were studied and compared for evidence of coxsackie B virus infections. Of 78 cardiac patients with coxsackie B infection, 30 had pleurodynia, 18 myocarditis, and 20 pericarditis. The age-adjusted rates of infection per 100 cases of defined category were 7.2, 13.3, and 7.0, respectively. Of 69 noncardiac patients with coxsackie B infection, 27 presented with pyrexia of unknown origin, 14 with upper respiratory tract infection, and 9 with meningitis. The age-adjusted rates of infection per 100 population were 10.6, 11.0, and 8.4, respectively. The sex-specific, age-adjusted rates for both cardiac and noncardiac patients were generally higher in male than female. For cardiac patients, the highest percentage with coxsackie B virus infection occurred in the 20-39-year age group, while in the noncardiac group, it was the 0-19-year age group. Coxsackie B2 and B4 were the two most prevalent serotypes found in both cardiac and noncardiac patients. Coxsackie B infections occurred mainly during summer and autumn. The level of coxsackie B immunity in 1,020 normal persons aged 1-60 years and from all 18 health districts of New Zealand was studied. The geometric mean titre of antibody from these normal persons was highest for serotypes B2 and B4. The least prevalent type antibody was B6 where 970(95.1%) of normal persons tested had no antibody to this serotype. The percentage of normal persons with antibody-type present were 30.4, 63.4, 54.1, 71.3, and 51.8 for B1-5, respectively.

The group B coxsackieviruses and myocarditis

“…Coxsackievirus involvement in paediatric myocarditis is clear (see references above as well as [27][28][29]). It has been assumed the CVB also cause the majority of enterovirus-related adult myocarditis, although the data for this rest primarily upon serological studies showing a correlation between higher than expected antibodies against CVB and the presence of heart disease [11,25,26,[30][31][32][33][34][35][36]. While isolation of infectious virus from adult heart tissue has been rare [37][38][39][40], enteroviral involvement in myocarditis has been made clear by the direct detection of enterovirus RNA in heart muscle by nucleic acid hybridisation and RT-PCR [41][42][43]; reviewed in [25,26].…”

Host Factors Regulating Viral Clearance

“…Viruses, bacteria, fungi and parasites are known to induce inflammatory heart disease in humans, although most clinical cases of myocarditis are suspected to be of viral ori gin [1], Among the 20 or more common viruses associated with myocarditis in hu mans [2], indirect serological evidence sug gests the coxsackieviruses group B, serotypes B1-B5, are the major cause of this disease [2][3][4][5][6], These viruses are ubiquitious, by age 30, 18-94% of humans have serologic evi dence of infection to at least one of the CVB serotypes [6][7][8][9], This group of viruses is clas sified within the enterovirus genus of the Picornaviridae family, i.e., they are small nonenveloped RNA genome viruses sur rounded by a protein capsid which does not contain essential glycoproteins or lipids [10], A 'hallmark feature' generally ascribed to the coxsackieviruses group B is that they pro duce lytic infections [10,11], a description which likely originated from studies of the mechanics of virus replication in selected cell lines which yielded high titers of virus while undergoing lysis during the process. However, several reports of nonlytic replica tion of these viruses and long-term persis tence under certain conditions suggest addi tional mechanisms for viral pathology in dis eases with inflammatory cell involvement.…”

Life‐threatening human parvovirus B19 infection transmitted by intravenous immune globulin

“…In this case, fulminant hepatitis seems to have been caused by B19 infection following pre‐existing coxsackie B4 infection. Coxsackie B4 virus infection usually causes asymptomatic or self‐limiting febrile illness but occasionally causes myocarditis, meningitis, hepatitis and fever of unknown origin (Lau, 1983). Experimental intranasal B19 infection in adult volunteers has confirmed that viraemia appears from 7 to 10 d after infection and continues for another 7 d (Anderson et al , 1985), indicating that the B19 infection in this case may have occurred during the last 10 d of January.…”