Leptospirosis overview

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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 a zoonotic disease caused by Leptospira sps. that affects humans and a wide range of animals, including mammals, birds, amphibians, and reptiles.[1] Even though leptospirosis is relatively rare in human, it is one of the world's most common zoonotic disease. The infection is commonly transmitted to humans by carriers such as rodents and other mammals through contaminated water sources by animal urine to come in contact with unhealed breaks in the skin, eyes or with the mucous membranes. Due to the ability of leptospire, they can survive for a prolonged period outside the animal host, especially in the environment favored by warm moist conditions with a neutral pH, which makes the disease more prevalent in tropical and sub-tropical regions. Outside of tropical areas, leptospirosis cases have a relatively distinct seasonality with most of them occurring August-September/February-March.[2] Recently, with the improved health and safety methods in the work place, more infections are occurring due to recreational activities rather than occupational exposure.[3][4] Animal body fluids such as urine, semen and products of conception with pathogenic leptospires, pose a potential risk to humans through prolonged excretion of bacteria. Other less common mechanisms of transmission include direct infection from animal urine, human to human spread, sexual transmission and via breast milk.[5][6][7]

Historical Perspective

Adof Weil is the first physician described about the severe form of leptospirosis and the name Weil's disease is named after him in the year 1886. He also described the jaundice with splenomegaly, renal failure, skin rash and conjunctival suffusion.[8] Japanees scientists Kitamura and Hara named this disease as autumn fever and seven day disease in 1918.[9]


Leptospirosis is classified into an anicteric and icteric form of leptospirosis based on the clinical presentation.


Pathological findings of leptospirosis are due to the development of the following:[12][13][14][15]


Leptospirosis is caused by an infection with Leptospira. Several species of Leptospira have identified and have been classified, genotypically, which include both pathogenic and saprophytic species. Among the pathogenic species, over 300 serovars have been identified by serotyping methods.[10]

Differential Diagnosis

Leptospirosis must be differentiated from other diseases that cause fever, diarrheanandausea and vomiting such as ebola, typhoid fever, malaria, yellow fever and other enteric bacterial infections. Moderate to severe leptospirosis must be differentiated from dengue fever.

Epidemiology and Demographics

Leptospirosis occurs worldwide but is most common in temperate or tropical climates. It is an occupational hazard for many people who work outdoors or with animals, for example: farmers, sewer workers, veterinarians, fish workers, dairy farmers or military personnel. It is a recreational hazard for campers or those who participate in outdoor sports in contaminated areas and has been associated with swimming, wading and whitewater rafting in contaminated lakes and rivers. The incidence is also increasing among urban children. Epidemiology of human leptospirosis is complex and dynamic, due to the interaction of pathogen, host, animal reservoir and environment. With the increase in urban population, occupational and recreational exposure to surface water and climatic changes results in the increase in the prevalence of leptospirosis recently.

Risk Factors

The risk of acquiring leptospirosis is associated with contact with animals, which made leptospirosis as an important occupational disease, especially affecting farmers, slaughterhouse workers, pet traders, veterinarians, rodent catchers and sewer workers who are in contact with mammalian species which acts as a natural carriers of leptospires.[11] According to World health organization survey highest risk groups are subsistence farmers and people living in urban slums.[12] Common risk factors in the development of leptospirosis include occupational exposure to animals, tropical or temperate climates and water sports in contaminated lakes and rivers.

Natural History, Complications & Prognosis

Leptospirosis is transported by the natural carriers such as feral, semi-domestic and farm and pet animals.[11] 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.[13] 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.[14] Outcome of the patient depends upon the pathogenic serovar and immunological status.


Clinical symptoms of leptospirosis are very wide, with mild anicteric presentation at one end to severe leptospirosis with severe jaundice and multiple organ involvement. Classic presentation of leptospirosis is a biphasic illness, and the onset of Symptoms within 2–30 days (incubation period) of exposure to the bacteria. Serious symptoms may manifest earlier on days 4–6 of the illness depending on the type of pathogen and host immunological status.[15] As the clinical manifestations of the disease are non specific, the clinical diagnosis is difficult. The laboratory investigations for leptospirosis should be considered in patient with an abrupt onset of fever, chills, conjunctival suffusion, headache, myalgia and jaundice with history of occupational exposure to infected animals or contaminated with animal urine.[16] The diagnosis of leptospirosis is based upon clinical suspicion and lab findings so, lab tests should be considered in a patient with a history of contact with potentially infected animals, soil or surface waters contaminated by animal urine.[10] Leptospires can be found in blood and CSF for the first 7 to 10 days and then in the urine. Hence, in the early diagnosis, specimen of choice should be, blood or CSF for culture. From the second week onwards serological tests are useful in the diagnosis.


All patients with suspected leptospirosis require antimicrobial therapy. Antimicrobial therapy is the mainstay of therapy for Leptospirosis. Antimicrobial therapies include either penicillin, ampicillin, doxycycline or ceftriaxone. Patients with meningitis often require high-dose penicillin, whereas patients with Weil's disease often require either azithromycin or doxycycline. Supportive measures include detoxification and normalization of electrolyte imbalances. Dialysis is reserved for patients with severe disease who fail antimicrobial therapy.


Leptospirosis can be prevented by avoiding the risk factors by practicing general measures, from contact with infected sources and animals. Also, it can be minimized by taking antibiotic prophylaxis in high-risk group who will have occupational exposure with infected sources.


  1. Leptospirosis. Centers for Disease Control and Prevention (2015). https://www.cdc.gov/leptospirosis/ Accessed on July 28, 2016
  2. Leptospirosis. National Organization for Rare Diseases (2015). http://rarediseases.org/rare-diseases/leptospirosis/ Accessed on July 28, 2016
  3. Philipp R, Waitkins S, Caul O, Roome A, McMahon S, Enticott R (1989). "Leptospiral and hepatitis A antibodies amongst windsurfers and waterskiers in Bristol City Docks". Public Health. 103 (2): 123–9. PMID 2786228.
  4. Philipp R, King C, Hughes A (1992). "Understanding of Weil's disease among canoeists". Br J Sports Med. 26 (4): 223–7. PMC 1479000. PMID 1490212.
  5. Ganoza CA, Matthias MA, Saito M, Cespedes M, Gotuzzo E, Vinetz JM (2010). "Asymptomatic renal colonization of humans in the peruvian Amazon by Leptospira". PLoS Negl Trop Dis. 4 (2): e612. doi:10.1371/journal.pntd.0000612. PMC 2826405. PMID 20186328.
  6. SPINU I, TOPCIU V; et al. (1963). "[MAN AS A VIRAL RESERVOIR IN AN EPIDEMIC OF LEPTOSPIROSIS OCCURRING IN THE JUNGLE]". Arch Roum Pathol Exp Microbiol. 22: 1081–100. PMID 14166972.
  7. Kiktenko VS, Balashov NG, Rodina VN (1976). "Leptospirosis infection through insemination of animals". J Hyg Epidemiol Microbiol Immunol. 21 (2): 207–13. PMID 987112.
  8. Adler B (2015). "History of leptospirosis and leptospira". Curr Top Microbiol Immunol. 387: 1–9. doi:10.1007/978-3-662-45059-8_1. PMID 25388129.
  9. Kobayashi, Yuzuru (2001). "Discovery of the causative organism of Weil's disease: historical view". Journal of Infection and Chemotherapy. 7 (1): 10–15. doi:10.1007/s101560170028. ISSN 1341-321X.
  10. 10.0 10.1 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.
  11. 11.0 11.1 Levett PN (2001). "Leptospirosis". Clin Microbiol Rev. 14 (2): 296–326. doi:10.1128/CMR.14.2.296-326.2001. PMC 88975. PMID 11292640.
  12. McBride AJ, Athanazio DA, Reis MG, Ko AI (2005). "Leptospirosis". Curr Opin Infect Dis. 18 (5): 376–86. PMID 16148523.
  13. Heuter, Kerry J.,Langston, Cathy E. (2003). "Leptospirosis: A re-emerging zoonotic disease". The Veterinary Clinics of North America. 33: 791–807.
  14. 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.
  15. Faine, S (1982). Guidelines for the control of leptospirosis. Geneva Albany, N.Y: World Health Organization Obtainable from WHO Publication Centre USA. ISBN 924170067X.
  16. LastName, FirstName (2003). Human leptospirosis : guidance for diagnosis, surveillance and control. Geneva: World Health Organization. ISBN 9241545895.