The kind of leptospirosis manifested by severe jaundice was first described as a human disease in 1886 by A. Weil. Named Weil’s disease the following year, the term was meant to designate a distinctive infectious jaundice, and it would not be known until much later that leptospirosis was caused by numerous leptospires that triggered various clinical syndromes. The first of the causative pathogens were independently discovered in 1915 by R. Inada among Japanese mine workers and by P. Uhlenhut and W. Fromme among German soldiers. Leptospira, a genus of the family Treponemataceae, order Spirochaetales, is a fine threadlike organism with hooked ends (see Figure VIII.81.1) that is pathogenic for humans and other mammals, producing meningitis, hepatitis, and nephritis both separately and together. In the past, the disease killed between 15 and 40 percent of those infected. Modern treatment has reduced mortality to about 5 percent. As a zoonosis, the disease is generally maintained in rodent reservoirs.

Etiology and Epidemiology

Leptospires are obligate aerobes and classified serologically as a bacterium, subdivided into two species. One is Leptospira biflexa, which includes the various water spirochetes, whereas the other, Leptospira interrogans, embraces the parasitic strains. The species interrogans (so named because of an appearance like a question mark) is now subdivided by the main antigen into 187 serotypes or serovars. Human leptospirosis generally results from direct or indirect exposure to the urine of infected animals, although it can also be transmitted by handling infected animal tissue, by animal bites, and by the ingestion of contaminated food and water.