Abstract

The concept that infectious (and other) diseases emerge and reemerge is not new, and neither is the search for causes of disease emergence. However, societies frequently overlook or forget that microbes evolve, adapt, and emerge in response to nonmicrobial and even nonbiologic changes in the physical and social environment. Sometimes we need to be rudely reminded of this lesson. Two scientists who have delivered such reminders, both in the form of landmark reports, are Rudolf Virchow, a 19th century German pathologist, statesman, and anthropologist, and Joshua Lederberg, the American microbiologist who coined the phrase “emerging infectious diseases” within the last decade (Photo). We owe much to the pioneering vision of these scientists. Infectious diseases have been emerging for at least as long as humans have inhabited the earth. Every student of microbiology, medicine, and public health learns about the triangle of host, environment, and agent; what is not clear is how the three change over time, often in response to changes in another side of the triangle. Factors that influence such changes do evolve, but many are surprisingly constant. How easily and often some of these factors are overlooked is often both consequential and tragic; a historical example illustrates this point. Rudolf Virchow, the founder of cellular pathology, wrote the first textbook in that field and established the principle that disease results from disturbed cellular function. As a young physician and anatomic pathologist in Berlin, he was assigned by the central government to investigate an epidemic in Upper Silesia, a sector of the Prussian Empire populated by a Polishspeaking minority. He completed the field portion of his investigation on March 10, 1848 (exactly 150 years before the International Conference on Emerging Infectious Diseases). The report he wrote was remarkable. Even though Virchow was working before the germ theory of disease was accepted, at a time when disease causation was highly debated and microbes were not well described, he seems to have correctly diagnosed typhus (or possibly relapsing fever) as the cause of the Silesian epidemic (1). Even though Virchow’s diagnosis cannot be confirmed, it is consistent with clinical descriptions and epidemiologic inference. He clearly demonstrated that the conditions and vectors for typhus and relapsing fever (famine and malnutrition, humid climate, poor housing, poverty) were present in Upper Silesia in 1847 to 1848. The agents that cause epidemic louse-borne typhus fever (Rickettsia prowazekii) and relapsing fever (Borrelia recurrentis) were not described until many years later. Virchow’s report was a scathing criticism of the Prussian government, which he squarely blamed for the epidemic. Virchow considered the Silesian outbreak investigation a defining Emerging Infectious Diseases: A Brief Biographical Heritage

Highlights

  • Despite our increasing knowledge of the role of patient race/ethnicity in drug prescribing practice for specific conditions, how or whether these specific effects translate into overall antimicrobial drug use by race/ethnicity remains unclear. We address this gap in knowledge by describing the extent of racial/ethnic disparities in overall antimicrobial drug prescription fill rates in the United States

  • We found a large disparity in antimicrobial drug fill rates by race/ethnicity: white persons reported making twice as many antimicrobial drug prescription fills as persons who were not white

  • The survey measures reported antimicrobial drug fills and not actual use [8]; the fill rates we report are substantially lower than those measured by others using sales data [1] or other national surveys [9]

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Summary

Objectives

We aimed to accurately map current and new BU-endemic areas and compare and contrast the changing incidence in these locations, to document disease severity and associate this with diagnostic delay, and to identify times of increased transmission risk. We aimed to clarify year-to-year changes in capsular serotypes, genotypes of penicillin and macrolide resistance, and diversity of sequence types (STs) in all pneumococcal isolates collected throughout Japan during April 2010–March 2017. We aimed to explore the genetic relationships of the 2015 and 2016 isolates from CAR with this reported population structure of NmW/cc. We aimed to estimate the influenza-associated severe acute respiratory infection (SARI) hospitalization using the methods recommended by the World Health Organization (5)

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