Leptospirosis natural history, complications and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]


Leptospirosis is transported by the natural carriers such as feral, semi-domestic, farm and pet animals.[1] Incubation period for leptospirosis varies between 3-20 days. The disease can cause wide range of symptoms from mild flu-like symptoms to severe disease with multi organ failure causing death. The first phase resolves and the patient is asymptomatic briefly before the second phase begins that is characterized by meningitis, liver damage (causing jaundice), and renal failure.[2] The disease leptospirosis is poorly known and unaware of its natural history is mainly due to the wide range of non specific symptoms, subclinical nature of the disease in animals and non specific laboratory tests making the disease difficult to diagnose.[3] Outcome of the patient depends upon the pathogenic serovar and immunological status.

Natural History

Natural history of leptospirosis varies with each patient. It might be mild or asymptomatic, and go unrecognized or in some patients the illness may progress to kidney or liver failure, aseptic meningitis, life-threatening pulmonary hemorrhage and other syndromes.

Acute Phase

Immune phase

  • It is also known as leptospiruric phase.
  • Circulating (IgM) antibodies are produced and leptospires are present in the urine.
  • Characterestic findings that differentiate from other febrile illnesses are myalgia and conjunctival suffusion.[5]
  • Myalgia often involves in calf muscles, less commonly involves abdominal and para-spinal muscles.

Anicteric leptospirosis

  • More common but serious illness is uncommon.
  • Most of cases present either subclinical or of very mild severity.
  • Few cases present with a febrile illness of sudden onset.
  • May progress to aseptic meningitis in ≤25% of patients and more common in younger age group than the patients with icteric leptospirosis.
  • Mortality is very less when compared to icteric leptospirosis.

Icteric leptospirosis

Severe leptospirosis

Sever form of leptospirosis with organ failure including liver and kidney involvement is known as Weil's disease.


Complications of leptospirosis are associated with localization of pathogen (leptospires) within the tissues during the immune phase, eventually present during the second week of the illness.

Life threatening complications

Common Complications

Less Common Complications


The prognosis of leptospirosis depends upon several known and unknown factors, among which the type of pathogenic serovar and the host’s immune status are the important factors which determines the outcome.[1] Most patients recover completely from leptospirosis but the duration of recovery varies from months to years with or without late sequelae. The late sequelae may include neuropsychiatric problems such as paresis, paralysis, mood swings and depression. The major causes of death include renal failure, cardiopulmonary failure and hemorrhage. Patients with risk factors such as old age and multiple underlying co-morbid conditions are often associated with more severe leptospirosis and increased mortality.


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  2. Heuter, Kerry J.,Langston, Cathy E. (2003). "Leptospirosis: A re-emerging zoonotic disease". The Veterinary Clinics of North America. 33: 791–807.
  3. Vieira ML, Gama-Simões MJ, Collares-Pereira M (2006). "Human leptospirosis in Portugal: A retrospective study of eighteen years". Int J Infect Dis. 10 (5): 378–86. doi:10.1016/j.ijid.2005.07.006. PMID 16600656.
  4. 4.0 4.1 Bal AM (2005). "Unusual clinical manifestations of leptospirosis". J Postgrad Med. 51 (3): 179–83. PMID 16333189.
  5. Forbes AE, Zochowski WJ, Dubrey SW, Sivaprakasam V (2012). "Leptospirosis and Weil's disease in the UK". QJM. 105 (12): 1151–62. doi:10.1093/qjmed/hcs145. PMID 22843698.
  6. Katz AR, Ansdell VE, Effler PV, Middleton CR, Sasaki DM (2001). "Assessment of the clinical presentation and treatment of 353 cases of laboratory-confirmed leptospirosis in Hawaii, 1974-1998". Clin Infect Dis. 33 (11): 1834–41. doi:10.1086/324084. PMID 11692294.
  7. Salkade HP, Divate S, Deshpande JR, Kawishwar V, Chaturvedi R, Kandalkar BM; et al. (2005). "A study of sutopsy findings in 62 cases of leptospirosis in a metropolitan city in India". J Postgrad Med. 51 (3): 169–73. PMID 16333187.
  8. Watt G, Padre LP, Tuazon M, Calubaquib C (1990). "Skeletal and cardiac muscle involvement in severe, late leptospirosis". J Infect Dis. 162 (1): 266–9. PMID 2355200.
  9. 9.0 9.1 Chakurkar G, Vaideeswar P, Pandit SP, Divate SA (2008). "Cardiovascular lesions in leptospirosis: an autopsy study". J Infect. 56 (3): 197–203. doi:10.1016/j.jinf.2007.12.007. PMID 18262280.
  10. Parsons M (1965). "Electrocardiographic Changes in Leptospirosis". Br Med J. 2 (5455): 201–3. PMC 1846500. PMID 20790602.
  11. Shaked Y, Shpilberg O, Samra D, Samra Y (1993). "Leptospirosis in pregnancy and its effect on the fetus: case report and review". Clin Infect Dis. 17 (2): 241–3. PMID 8399874.
  12. Carles G, Montoya E, Joly F, Peneau C (1995). "[Leptospirosis and pregnancy. Eleven cases in French Guyana]". J Gynecol Obstet Biol Reprod (Paris). 24 (4): 418–21. PMID 7650320.