Research in bacterial population genetics has increased in the last 10 years. Population genetic theory and tools and related strategies have been used to investigate bacterial pathogens that have contributed to recent episodes of temporal variation in disease frequency and severity. A common theme demonstrated by these analyses is that distinct bacterial clones are responsible for disease outbreaks and increases in infection frequency. Many of these clones are characterized by unique combinations of virulence genes or alleles of virulence genes. Because substantial interclonal variance exists in relative virulence, molecular population genetic studies have led to the concept that the unit of bacterial pathogenicity is the clone or cell line. Continued new insights into host-parasite interactions at the molecular level will be achieved by combining clonal analysis of bacterial pathogens with large-scale comparative sequencing of virulence genes.

Ehrlichiae are small, gram-negative, obligately intracellular bacteria that reside within a phagosome. The first human ehrlichial infection was recognized in the United States in 1987. It was later shown to be caused by a new species, Ehrlichia chaffeensis. In 1994, an ehrlichial pathogen within neutrophils that is closely related to the known veterinary pathogens E. equi and E. phagocytophila was found to infect humans. Molecular methods were required to detect, characterize, and identify these fastidious and uncultivated bacteria. Subsequently, E. chaffeensis infection was documented in more than 400 patients in 30 states, Europe, and Africa. Likewise, approximately 170 cases of human granulocytic ehrlichiosis have been diagnosed, most since 1994, predominantly in the upper midwestern and northeastern states, but also in northern California. The disease caused by ehrlichiae is generally undifferentiated but is often associated with leukopenia, thrombocytopenia, and elevated serum hepatic transaminase levels in tick-exposed patients. Infection ranges from subclinical to fatal; tetracycline appears to be an effective therapy. The emergence of these two newly recognized tickborne infections as threats to human health is probably due to increased clinical cognizance, but as in other emerging tickborne infections, it is likely that the rapid increase in identified cases signals a true emergence of disease associated with a changing vector-host ecology.

In September 1994, in response to a reported epidemic of plague in India, the Centers for Disease Control and Prevention (CDC) enhanced surveillance in the United States for imported pneumonic plague. Plague information materials were rapidly developed and distributed to U.S. public health officials by electronic mail, facsimile, and expedited publication. Information was also provided to medical practitioners and the public by recorded telephone messages and facsimile transmission. Existing quarantine protocols were modified to effect active surveillance for imported plague cases at U.S. airports. Private physicians and state and local health departments were relied on in a passive surveillance system to identify travelers with suspected plague not detected at airports. From September 27 to October 27, the surveillance system identified 13 persons with suspected plague; no case was confirmed. This coordinated response to an international health emergency may serve as a model for detecting other emerging diseases and preventing their importation.

Three recent outbreaks of locally acquired malaria in densely populated areas of the United States demonstrate the continued risk for mosquitoborne transmission of this disease. Increased global travel, immigration, and the presence of competent anopheline vectors throughout the continental United States contribute to the ongoing threat of malaria transmission. The likelihood of mosquitoborne transmission in the United States is dependent on the interactions between the human host, anopheline vector, malaria parasite, and environmental conditions. Recent changes in the epidemiology of locally acquired malaria and possible factors contributing to these changes are discussed.