Myocarditis and Croup Caused by Coxsackie Virus

Myocarditis has long been recognized as a complication of rheumatic fever, diphtheria, scarlet fever and whooping cough. It also occurs in association with poliomyelitis and more rarely with other virus infections such as influenza, mumps, psittacosis, infectious mononucleosis, primary atypical pneumonia, varicella, measles, infectious hepatitis and yellow fever (Lyon, 1956; Silber, 1958). Myocarditis has also been described as occurring without evidence of such primary disease and has then been labelled variously as Fiedler's, idiopathic, interstitial, isolated or aseptic myocarditis. The association of myocarditis and pericarditis with epidemic pleurodynia was reported by Bing (1933) and Heckscher (1933). This disease was subsequently shown to be caused by infection with the Coxsackie group B viruses (Curnen, Shaw and Melnick, 1949). More recently these viruses have been incriminated as a cause of aseptic myocarditis in newborn infants and myocarditis and pericarditis in both children and adults. In the newborn infant Coxsackie infections are usually severe and commonly fatal. The disease is generalized and the predominant lesion in most cases is cardiac, although many infants also show lesions in the central nervous system, liver, adrenals and other tissues. Outbreaks of neonatal myocarditis have occurred in maternity homes and nurseries at times of prevalence of Coxsackie infection in the general population. These have been reported from Johannesburg (Gear and Measroch, 1953; Javett, Heymann, Mundel, Pepler, Lurie, Gear, Measroch and Kirsch, 1956; Gear, 1958), Cape Town (Suckling and Vogelpoel, 1958; Simenhoff and Uys, 1958; Naude, Selzer and Kipps, 1958; Kipps, Naude, Don and Cooper, 1958), Southern Rhodesia (Montgomery, Gear, Prinsloo, Kahn and Kirsch, 1955), Amsterdam (Dekking, 1955; van Creveld and de Jager, 1956; Verlinde, van Tongeren and Kret, 1956), Czechoslovakia (Vanek, Lukes, Potuznik, Polodnikova and Vilim, 1959; Lukes, 1959) and Hungary (Domok, Molnar and Rudnai, 1960). A similar outbreak but without virus confirmation occurred in a newborn nursery in Melbourne (French, 1953). Sporadic cases have been reported from the United States (Kibrick and Benirschke, 1956, 1958a; 1958b; Sabin, 1957; Benirschke, Kibrick and Craig, 1958; Benirschke and Pendleton, 1958; Newton and Hosier, 1958; Hosier and Newton, 1958; Sprunt, 1958; Sussman, Strauss and Hodes, 1959; Rapmund, Gauld, Rogers and Holmes, 1959; Moossy and Geer, 1960; Brown, Lenz and Agate, 1960; Woodward, McCrumb, Carey and Togo, 1960), Hawaii (Delaney and Fukunaga, 1958), the Transvaal (Gear, Measroch and Prinsloo, 1956) and Australia (Jack, 1958). There have been fewer reports of myocarditis caused by Coxsackie group B viruses in older children and the disease has usually been less severe than in the newborn infant (McLean, Croft, Prince and Heckmann, 1957; Varcasia and Castelli, 1957; Kagan and Bernkopf, 1957; Hosier and Newton, 1958; McLean, Walker and McNaughton, 1960). Many of the older children present with pericarditis (Kagan and Bernkopf, 1957; McLean, Walker and Bain, 1958; Walker, McNaughton and McLean, 1959; Gordon, Lennette and Sandrock, 1959; Brodie and Marchessault, 1960; Woodward et al., 1960), but this may be associated with clinical evidence of myocardial involvement (Kagan and Bernkopf, 1957). In adults pericarditis has been the usual manifestation (Weinstein, 1957; Fletcher and Brennan, 1957, 1958; Movitt, Lennette, Mangum, Berk and Bowman, 1958; Bell and Meis, 1959; Gillett, 1959; Roberts, Lydon and MacIntosh, 1959; Sode and Baker, 1959; Woodward et al., 1960) and some cases, as in children, have shown clinical evidence of severe myocardial damage (Null and Castle, 1959; Woodward et al., 1960). Coxsackie group A viruses may also be a cause of heart disease. Infection with these has been reported