Leptospirosis is a disease caused by bacteria in the genus Leptospira; there are roughly 17 species. Because the organisms survive in surface waters (such as swamps, streams, and rivers) for extended periods, the disease is often waterborne.
Dogs contract leptospirosis by direct contact with infected urine or contaminated water sources, through bite wounds, by eating infected tissue, or exposure during birth. Once in the body, leptospires spread rapidly via the lymph system to the bloodstream and then to all tissues. If the animal mounts an immune response and survives, leptospires will be cleared from most organs and the bloodstream. However, the infection persists in sites hidden from the immune system; the most common hidden site is the kidneys. Persistence in the kidneys results in a carrier state; the infected animal may shed leptospires in the urine for at least a year.
Infections may be without signs or cause various early signs, including fever, jaundice, joint or muscle pain, loss of appetite, weakness, and discharge from the nose or eyes. This may progress within a few days to a kidney crisis characterized by loss of appetite, vomiting, dehydration, and lumbar pain from inflammation of the kidneys. Sudden kidney failure occurs in 80 to 90% of dogs that are severely affected. In dogs that develop milder forms of kidney failure, excessive intake of water followed by excessive urination may be the primary sign.
Kidney failure and liver disease are treated with fluid treatment and other supportive measures to maintain normal fluid, electrolyte, and acid-base balance. Your veterinarian will likely recommend antibiotics to treat the cause of disease.
Commercial vaccines for dogs are available for 4 of the subtypes of leptospirosis. Vaccinated dogs may still be susceptible to infections with other subtypes. Vaccination is recommended at yearly intervals. Dogs that have recently been exposed to leptospirosis may be treated with anti-biotics given by mouth for 7 to 10 days to prevent infection.
Last full review/revision July 2011 by Otto M. Radostits, CM, DVM, MSc, DACVIM (Deceased); David A. Ashford, DVM, MPH, DS; Craig E. Greene, DVM, MS; Eugene D. Janzen, DVM, MVS; Bert E. Stromberg, PhD; Max J. Appel, DMV, PhD; Stephen C. Barr, BVSc, MVS, PhD, DACVIM; J. P. Dubey, MVSc, PhD; Paul Ettestad, DVM, MS; Kenneth R. Harkin, DVM, DACVIM; Delores E. Hill, PhD; Johnny D. Hoskins, DVM, PhD; Jodie Low Choy, BVMS; Barton W. Rohrbach, VMD, MPH, DACVPM; J. Glenn Songer, PhD; Joseph Taboada, DVM, DACVIM; Charles O. Thoen, DVM, PhD; John F. Timoney, MVB, PhD, Dsc, MRCVS; Ian Tizard, BVMS, PhD, DACVM