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Richard M Krause

Publications and source records attributed to Richard M Krause.

3 recordsLinked to original sources

Evolving microbes and re-emerging streptococcal disease.

Microbes will evolve and the epidemics they cause will continue to occur in the future as they have in the past. Microbes emerge from the evolutionary stream as a result of genetic events and selective pressures that favor new over old. It is nature's way. Microbes and vectors swim in the evolutionary stream, and they swim much faster than humans. Bacteria reproduce every 30 minutes and, for them, a millennium is compressed into a fortnight. They are "fleet afoot," and the pace of research must keep up with them or they will overtake. Microbes were here on Earth 2 billion years before humans arrived, learning every trick of the trade for survival, and they are likely to be here 2 billion years after we depart. Current research on the rise and decline of epidemics is broadly based and includes evolutionary and population genetics of host-microbe relationships. Within this context, the 19th century pandemic of scarlet fever has been described. The possibility is raised that the GAS, which currently cause STSS, possess some of the virulence factors that caused pandemic scarlet fever. Furthermore, the GAS isolated during the recent outbreaks of ARF in certain locales in the United States have the virulence properties of the GAS frequently isolated in the first half of the 20th century. Finally, it is suggested that the strategy to confront emerging infectious diseases should be the study of infectious diseases from all points of view. They remain the greatest threats to our society.

Acute Disease↗

A half-century of streptococcal research: then & now.

Research on Group A streptococci (GAS) before 1950 paved the way for successful clinical trials to prevent acute rheumatic fever (ARF) by treating the prior streptococcal infection with penicillin. Prevention of ARF has led to almost complete disappearance of rheumatic heart disease in the industrialized world, but has yet to be accomplished in developing countries, where most of the world's populations reside. Twenty years of research beginning in 1918 by Lancefield and others delineated the modern classification of haemolytic streptococci and led to the recognition that only Group A is responsible for the pharyngitis that causes ARF. M-protein, identified as a major virulence factor, is a powerful inhibitor of phagocytosis, and antibodies to it promote type-specific phagocytosis and therefore type-specific immunity. Other virulent properties of GAS include a bulky capsule, as well as extracellular toxins such as streptolysins S and O and streptococcal proteinase. McCarty and others pursued the cell biology of GAS and identified the cellular localization of various antigenic components. The discovery of purified M-protein as a helical coiled-coiled fibrillar protein has sparked development of M-protein vaccine. US, UK, and Trinidad scientists described differences between streptococcal infections of the throat and skin and noted particularly that many of the GAS M-types that cause impetigo are less likely to cause pharyngitis. GAS impetigo may cause acute glomerulonephritis, but such infections do not result in ARF. The changing manifestations of disease over time and the evolution of microbes are common themes in medicine today. These themes are relevant to GAS pharyngitis and ARF, especially the decline in the incidence of severe ARF and the decrease in severity of GAS pharyngitis. Research on GAS bacteriophages led to the discovery of a relationship between lysogenic GAS and production of erythrogenic toxin and has broadened approaches to the molecular epidemiology of GAS virulence. The 21st century begins with determination of the complete genome sequence of M-1, M-18, and M-3 strains of GAS. These studies provide evidence for phage-encoded toxins, high-virulence phenotypes, and clone emergence. This research will reveal genetic processes at the molecular level that control the emergence and decline of streptococcal diseases in different places and times and the shifting patterns in clinical manifestations.

Animals↗