by an extraordinarily wide range of symptoms, many of which mimic other disease syndromes. The disease was initially named erythema migrans for the distinctive skin lesion that results from the bite of the spirochete-carrying ticks. Diagnosis of the condition, especially during its early stages, is difficult. Treatment relies on antibiotics, but this approach becomes less effective as the disease progresses. The disease is caused by infection with Borrelia burgdorferi, a spirochete, and it is transmitted by certain ticks in a complex cycle that also involves mice and deer.
The emergence of Lyme disease is directly linked to changes in land use patterns. In the eastern United States (and in Europe) during the seventeenth, eighteenth, and much of the nineteenth centuries, vast expanses of land were cleared for farming. In the United States during the 1900s, however, much of the East Coast underwent reforestation, in large part owing to the decline of the small farm and the shift of agriculture to the Midwest. New-growth forest now provides an ideal habitat for deer.
Reforestation was accompanied by increased residential development in wooded, suburban areas. The resulting proximity of people, mice, deer, and ticks has created nearly perfect conditions for the transmission of the Lyme disease spirochete to human hosts. Although people are becoming aware of the risk of contracting Lyme disease, ecological trends that favor the survival of reservoir and vector hosts continue. There is little reason to think that the upward climb in incidence will level off or decline soon.
Few, if any, infectious disease specialists 10 years ago would have predicted an infectious etiology for gastritis, peptic ulcer, or duodenal ulcer disease. Yet there is now considerable evidence that a bacterium, Helicobacter pylori, infects gastric-type epithelium in virtually all patients with these conditions.
H. pylori was identified initially as an unknown bacillus in biopsies of involved areas of active chronic gastritis (Warren and Marshall, 1983). Evidence that H. pylori infection is the cause, and not the consequence, of gastritis and ulcers is of several types. First, acute infection with H. pylori in humans results in chronic superficial, or type B, gastritis (Dooley et al., 1989). Second, H. pylori infection is not associated with other types of gastritis, which would be expected if it were merely infecting already damaged epithelium (O'Connor et al., 1984). Third, antimicrobial therapy directed against H. pylori has been shown to heal gastritis and duodenal ulcers in infected patients at least as effectively as acid-suppressive therapy (Glupczynski et al., 1988; Morgan et al., 1988; Rauws et al., 1988). Fourth, gastritis developed following experimental ingestion of H. pylori by human volunteers (Morris and Nicholson, 1989). Finally, recurrence of duodenal