In 1940, when I graduated from Harvard Medical School, Dr Kenneth Blackfan was head of pediatrics at the Children's Hospital in Boston. In addition to me, he selected four house officers from my class, the other members being Ed Pratt, Larry Kingsland, and Fred Robbins. We were his last appointees as he died in 1941. Life as a house officer was very different in those days. Our first year was spent in the laboratory in preparation for work on the wards the next year. If unmarried, we lived in the hospital and usually worked 7 days a week. I spent 6 months in bacteriology and 6 months in pathology. On Pearl Harbor day in 1941, I was on a post in pathology when the news came over the radio.
By 1940 we had developed cultural techniques for most of the major pathogenic bacteria. However, our therapeutic and prophylactic resources were meager. Sulfonamide derivatives were becoming available, but penicillin did not become available until about 1944. Few immunizations were available. Only smallpox and pertussis vaccines and diphtheria and tetanus toxoids were given routinely.
In contrast to our knowledge of the bacterial pathogens our knowledge of the so-called viral diseases was very limited at that time. Although poliomyelitis virus had been isolated and studied in monkeys, the etiologic viruses of such common entities as varicella, measles, rubella, and mumps had not been isolated. However, Larry Kingsland and I both had experience with tissue cultures and thought that cultures of human cells might provide the essential living cell medium for the growth of viruses. Dr Farber provided us with the equipment needed for a simple tissue culture system in the department of pathology, but bacterial contaminants ruined our experiments. Further work was impossible as we moved to the wards and then both went off for military service.
In 1947, I was able to return to the problem of growing viruses in cultures of human tissues as Dr Enders and I developed a laboratory at Children's Hospital for virus research. In 1949 we reported the isolation and growth of the poliomyelitis viruses in tissue cultures.1 I was successful in growing in cell cultures mumps, Coxsackie, varicella, cytomegalovirus, and rubella viruses. These findings popularized the use of tissue cultures for the study of viruses and the field of virology underwent a scientific explosion. When the American Public Health Association published a guide on the laboratory diagnosis of viral diseases in 1948, 16 different viruses were described in 345 pages. Thirty-one years later, the same guide had grown to 1138 pages with chapters devoted to groups of viruses.2 The chapter on enteric viruses, for example, described 70 different viruses.
The period after World War II witnessed the development of generations of antibiotic drugs and the extensive use of old and of new vaccines. In the area of disease prevention two magnificent achievements materialized. First was the deployment of smallpox vaccine, leading to the global eradication of that disease. Few of you will remember that as recently as the 1950s, 8 million people died each year from smallpox. If you have not seen a case of smallpox, you never will.
The second magnificent achievement is the ongoing effort to eradicate poliomyelitis by the mass use of vaccine. This effort stems directly from our studies that led to the Salk and Sabin vaccines. It is now difficult to appreciate that in 1955 the year the Salk vaccine was licensed we treated 1035 cases of poliomyelitis at Children's Hospital in Boston. Amazingly, the mass use of polio vaccine has resulted in the eradication of the disease in the Americas; the last case occurred in Peru in 1991. Currently, polio persists in parts of Asia and Africa. The global campaign that is awesome in magnitude continues. In December 1995, India held a mass immunization day when 87.8 million children were given polio vaccine. It is difficult to visualize the logistics of vaccinating 87 million children. In January 1996, another national immunization day was held and 93.6 million children were vaccinated in India. Currently we have vaccines for entities such as measles, rubella, varicella, and hepatitis A and B, developments stemming from the isolation of the responsible viruses during the contemporary explosion of research in the field of virology.
In conclusion, it is appropriate to comment on a topic that has been featured in the media for the last 3 or 4 years—the so-called emerging infectious diseases. The coverage in the media has disturbing connotations. There is the implication that we will soon have drastic Ebola-like virus epidemics sweeping the United States. The Institute of Medicine's definition of emerging infections, a definition now generally adopted, is realistic and not so threatening,3namely, “new, re-emerging, or drug-resistant infections whose incidence in humans has increased within the past two decades or whose incidence threatens to increase in the near future.”
The pediatrician knowledgeable in the field of infectious diseases recognizes and expects that such entities will vary in incidence as the three elements of the classical epidemiologic triad, namely the agent, the human host, and the environment undergo change. The discovery of previously unrecognized agents continues at a rapid pace. The illnesses they cause are not new. They emerge as the etiology of each is identified. The agents themselves can mutate or change in virulence. The emergence of the human immunodeficiency virus probably represents the combination of a change in virulence and in human host habits. It is important to appreciate that RNA viruses do mutate frequently and that changes in influenza virus could at any time produce an epidemic comparable to the ones that we experienced in 1918 and 1919.
The human host is changing in numbers and its immune state may be altered by nature or iatrogenically. Biological immunosuppression as by a human immunodeficiency virus or cytomegalovirus infection may subject us to opportunistic pathogens. For example, five new genera of protozoa belonging to the group Microsporidia have been identified as parasites in acquired immunodeficiency syndrome cases.
In the developing areas of the world the rapid increase in the size of the human population is a major factor in producing morbidity and mortality attributable to infectious agents. About 88 million new people were born last year. In tropical cities the population increase per se, and the migration from rural to urban areas, produces huge slums without proper sanitation or a water supply. It is not generally appreciated that shortly Mexico City, with its 20 million inhabitants, will be one of the largest cities in the world. In such cities the stage is set for the explosive spread of enteric pathogens as happened when cholera appeared in South America in 1991.
As the three major elements of the epidemiologic triad continue to change we can expect the continued emergence of infectious diseases. Fortunately, the complacency regarding infectious agents has disappeared. However, it is not generally appreciated that actually infectious disease mortality in the United States is now increasing.4 Pediatricians will be faced with a continuum of challenges posed by infectious agents.
- Enders JF,
- Weller TH,
- Robbins FC
- ↵Schmidt NJ, Emmons RW, eds. Diagnostic Procedures for Viral, Rickettsial, and Chlamydial Infections. 6th ed. Washington, DC: American Public Health Association; 1989:1–1225
- ↵Lederberg J, Shope RE, Oaks SC Jr, eds. Institute of Medicine Report. Emerging Infections: Microbial Threats to Health in the United States. Washington, DC: National Academy Press; 1992:1–294
- Copyright © 1998 American Academy of Pediatrics