Leptospirosis and weil’s syndrome

Abstract

Leptospirosis remains the most important zoonosis in the world and is caused by the bacterium of the genus Leptospira. Clinical manifestations vary from oligosymptomatic infections to the severe, ictero-hemorrhagic form, called Weil’s syndrome, which include acute kidney injury (AKI). After reaching the bloodstream, the Leptospira can reach all organs, preferentially affecting the liver, kidneys, heart, and skeletal muscle, causing a vasculitis with endothelial damage and inflammatory infiltrate. The pathogenic mechanisms of leptospirosis can be divided into direct effects caused by Leptospira and the effects of the host immune response. Leptospira isolated from the kidneys of chronically infected animals show an increased amount of lipopolysaccharides (LPS), suggesting that LPS expression facilitates the permanence of the bacteria in the renal tissue. The clinical picture in the early phase is often nonspecific, with fever, headache, anorexia, diarrhea, nausea, vomiting, and malaise, as well as myalgia, more pronounced in the calf region, constituting the most common signs and symptoms. Given this presentation, which comprises approximately 85-90% of cases, the disease is often underdiagnosed and misdiagnosed as viral infections, such as dengue. The two main mechanisms that have been associated with kidney injury by Leptospira are direct nephrotoxic action of the microorganism and toxin effect with immune response induction and indirect effects such as dehydration, rhabdomyolysis, and hypoxia due to hemodynamic changes.