The pathogenic bacterial spirochetes of the Leptospiragenus are responsible for the infectious disease called leptospirosis. Both humans and animals can be infected and it is one of the most common infectious diseases of animals that can be transmitted naturally to humans. About 9 in every 10 people affected will experience mild flu-like symptoms. These include myalgia (muscle pain), chills, and headaches in the early stages. More severe presentations of the disease include internal hemorrhaging and multiple organ failure, which is life-threatening and is referred to as Weil’s disease.

Historical Significance

Leptospirosis was long recognized in several parts of the world. In ancient China, it was observed as an occupational disease of those who harvested rice, whereas in Japan it was given the name akiyami, also known as autumn fever, which is still used today. In Europe, in the 19th century, it was believed to be a relative of the plague, but it was evidently not as contagious and was called bilious typhoid. In the late 1800s, it was recognized as an occupation hazard of sewer workers.

Adolph Weil in 1886 made a publication that documented the most severe presentation of leptospirosis, hence the designation Weil’s disease. It was not until 1907 that special staining methods were employed to identify the microbial culprit of Weil’s disease. It was noted as having hooked ends and looked very much like a question mark, which lead to it being called Spirochaeta interrogans. In 1917, rats were implicated as sources of infection to humans, while infections in dogs and livestock were recognized many years later.

Pathophysiology

Leptospires are gram-negative, coiled, aerobic bacteria that are motile with paired flagella and hooked ends, which allows them to burrow into cells. The pathogenic Leptospira interrogans has many serovars associated with different animals, such as goats, sheep, pigs, dogs, cats, and wild animals. However, the most common source globally are rats and the urine or urine contaminated media (e.g., water, food, and soil) of infected animals is the most important source of the pathogen.

The pathogenesis of leptospirosis is not entirely clear. However, a number of suggestions have been put forward to elucidate the virulent factors involved. The production of endotoxins has been observed in many serotypes. Virulent leptospires have been demonstrated to attach to epithelial cells in in vitro studies. They have also been shown to cause LPS-mediated adherence of neutrophils to platelets and endothelial cells. This leads to aggregation and suggests a possible link to the development of thrombocytopenia in affected patients. LPS and other outer membrane proteins are very immunogenic and determine the specificity of the serotype.

The disappearance of the causative organism from the bloodstream and the appearance of antibodies is known as the second stage or immune phase of acute leptospirosis. Studies propose the severity of the symptoms may be immune-mediated, because the levels of circulating immune complexes correlate with symptom-related disease severity. Leptospirosis immunity is for the most part humoral (i.e., antibody-mediated). There are some reports of cell-mediated immune responses to the disease, but this is not a significant component. Anecdotal evidence of this was observed by the clinical course of the disease in patients who had acquired immune deficiency syndrome.