THIS paper presents a case of acute benign pericarditis associated with Coxsackie virus Group B, Type 5, infection. The clinical history, along with the laboratory findings, is noted, and the etiologic relation of the virus to acute benign pericarditis is discussed. Case Report A 25-year-old man was in good health until 6 weeks before admission, when pain in the anterior aspect of the chest, aggravated by respiration, fever and shortness of breath intensified in the reclining position, suddenly developed. The maximum temperature was 103°F. He was hospitalized elsewhere for 4 days with a diagnosis of pleurisy. Upon discharge he was . . .

Acute Benign Pericarditis Associated with Coxsackie Virus Group B, Type 5

SINCE the recognition of the Coxsackie viruses in 19481 a number of diverse human illnesses have been associated with these viruses. The gamut of clinical manifestations attributed to the Coxsackie viruses include herpangina,2 3 4 "three-day fever,"4 aseptic meningitis,5 6 7 8 9 10 11 epidemic pleurodynia,12 13 14 pericarditis,15 16 17 18 myocarditis in infants,19 20 21 22 23 orchitis24 and a syndrome of lymphadenopathy and splenomegaly.25 During the spring and summer of 1957 an epidemic of infections due to Coxsackie virus Group B, Type 5, occurred in Salt Lake City, Utah. Laboratory evidence was obtained in 17 cases to incriminate this virus as the etiologic agent in the acute illnesses.§ The clinical manifestations varied strikingly . . .

Adult pericarditis and myocarditis due to Coxsackie virus group B, type 5.

The events leading to the isolation of varicella-zoster virus (VZV) are described beginning with the pioneering contributions of Ernest Tyzzer and Ernest Goodpasture and the early epidemiologic observations that indicated a relationship between varicella and zoster. Isolation, propagation, and immunologic proof of the coidentity of the viruses from the two clinical entities evolved from the introduction of human cell culture systems, a development that revolutionized virus research. Now the social significance of VZV is increasing. This reflects an aging population, increasing use of immunosuppressive therapeutic procedures, and the advent of a biologic immunosuppressive agent, the virus that causes AIDS. Currently there are unsolved problems: For unknown reasons varicella is often an adult disease in the tropics, and cell cultures fail to demonstrate VZV in throat washings from cases. These peculiarities warrant elucidation.

Varicella and Herpes Zoster: A Perspective and Overview

Introduction Exposure to cold was postulated as the cause of acute benign pericarditis by Hodges,*who described the syndrome in 1854.1Nearly a century later Christian, reviewing the still obscure cause of this disease, suggested it was of viral etiology.2Subsequent studies have tended to support this thesis by implicating many different viruses, but only infectious mononucleosis and Coxsackie virus infections have been repeatedly associated with the syndrome. Acute benign pericarditis is often observed during epidemics of pleurodynia, and its association with Coxsackie virus infections in this specific circumstance is well recognized.3-6However, the relative importance of these and other viruses in the etiology of pericarditis at other times remains uncertain. It is the purpose of this report to describe the virologic investigation of 34 patients with sporadic acute benign pericarditis and to provide the clinician with a contemporary perspective into the etiology of this syndrome. Materials

Acute benign pericarditis. Virologic study of 34 patients.

Since the discovery of the prototype Coxsackie viruses by Dalldorf and Sickles, in 1948, 1 the existence of a number of additional immunologically different types has been uncovered. The known Coxsackie viruses have been placed in two different groups on the basis of histopathological changes produced in the mouse. At the present time, there are at least 19 immunologically different viruses within Group A and 5 immunologically different types within Group B. The viruses of the Coxsackie family have a ubiquitous distribution, and their recovery from the stools of normal persons, or at least from persons with no objective or subjective evidence of illness, is by no means unusual. However, the accumulating evidence over the past few years has served to establish the causal relationship of the Coxsackie viruses to certain diseases. Thus, it is now generally accepted that viruses in the Coxsackie A group are the etiologic agents of

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The varied clinical manifestations of Coxsackie virus infections: observations and comments on an outbreak in California.

DURING the late summer and early fall of 1947, an epidemic acute febrile illness characterized by headache, pyrexia and paroxysmal pain in the region of the diaphragm occurred in Massachusetts. Clinically it closely resembled a malady first described in Iceland by Finsen1in 1856, who called it "pleurodynia." The same syndrome has since been variously designated as "Bornholm disease," "epidemic muscular rheumatism," "acute benign dry pleurisy," "epidemic pleuritic pain," "Bamle disease" and "devil's grip." The last name was based on the description of the pain in the chest experienced by one of Dabney's2patients in the first outbreak reported from the United States. The literature on the disease was reviewed by Sylvest3in 1934 and has been brought up to date by Scadding.4 The etiology remains obscure. Small5found inclusion bodies in the erythrocytes in 2 cases, which induced him and Torrey6to believe that the disease was caused by a

Herbert R. Morgan

Papers

Epidemic pleurodynia: clinical and etiologic studies based on one hundred and fourteen cases