Leptospirosis Clinical Presentation

  • Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Apr 17, 2012
 

History

A good clinical history is often the key to accurate diagnosis in leptospirosis. Important features include a plausible exposure history and a clinical picture consistent with the disease.

Leptospirosis occurs worldwide wherever risk of contact with the urine, kidneys, or conception products of infected animals exists. Typically, rodents, dogs, cattle, and pigs are considered reservoirs for this organism; however, increasing diversity of travel and exotic-pet trade are expanding the list. The leptospires may live for years in the renal tubules of animals and are excreted in the urine into standing water or soil. This explains sources of both direct infection (eg, body fluids or organs of infected animals) and indirect infection (eg, inoculated soil or water). In 2004, cases were linked to flood water in urban endemic regions of Hawaii. In tropical settings, leptospirosis is becoming more prevalent among travelers and residents. For example, recreational activities in rivers (eg, white-water rafting) may be a significant risk factor for infection with leptospires.

Leptospires can live outside the body for several weeks. They enter the body through disrupted skin or mucosal barriers, such as abrasions or waterlogged skin. Other means of infection have been documented, including inhalation of aerosolized leptospires and direct infection across intact mucus membranes or conjunctivae. After an incubation period of 2-30 days (typically 5-14 d), clinical symptoms ensue. A plausible history of possible exposure must precede clinical symptoms in order to consider the diagnosis of leptospirosis.

Expert consensus is that leptospirosis occurs as two recognizable clinical syndromes. A third syndrome of asymptomatic infection is more controversial. Anicteric leptospirosis is a self-limited disease similar to a mild flulike illness. Icteric leptospirosis, also known as Weil disease, is a severe illness characterized by multiorgan involvement or even failure. Two distinct phases of illness are observed in the mild form—the septicemic (acute) phase and the immune (delayed) phase. In icteric leptospirosis, the 2 phases of illness are often continuous and indistinguishable. At disease onset, clinically predicting the severity of disease is not possible. Subsequent sequelae depend on the serovar involved and the health, nutritional status, and age of the patient, as well as the rapidity of definitive and supportive treatment.

An acute illness follows any infection with any serovar of leptospirosis. Most of the following symptoms develop in varying degrees: high temperature (38-40°C), rigors, sudden headache, nausea and vomiting, anorexia, diarrhea, cough, pharyngitis, nonpruritic skin rash, and muscle pain. Muscle pains are typically localized to the calf and lumbar areas. This phase of illness lasts 5-7 days and either regresses to a relatively asymptomatic period or progresses to a more severe illness. In anicteric leptospirosis, the acute illness is followed by 1-3 days without fever and then progresses to 4-30 days of the immune (delayed) phase of the illness.

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Physical

The physical examination findings differ depending on the severity of disease and the time from onset of symptoms. Patients may appear mildly ill or toxic. Early in the disease, temperatures as high as 40°C and tachycardia are common. Hypotension, oliguria, and abnormal chest auscultation at presentation may portend severe illness. When fever is severe and prolonged, hypotension and shock due to volume depletion may also occur. The fever typically subsides within 7 days.

Early in the disease, the skin is warm and flushed. Additional skin findings include a transient petechial eruption that can involve the palate. Later in severe disease, jaundice and purpura can develop. The classic ocular finding of conjunctival suffusion occurs early irrespective of disease severity. Conjunctival suffusion is characterized by redness of the conjunctiva that resembles conjunctivitis but that does not involve inflammatory exudates.

Uveitis is a common feature following acute leptospirosis; however, patients who receive antibiotics during the acute phase of illness may develop only mild uveitis.[7]

Muscle tenderness can occur with the myositis of early infection. This can be particularly prominent in the paraspinal and calf muscles but can involve any muscle. Neurologic examination can reveal signs of meningitis, including neck stiffness and rigidity and photophobia. Early in the disease, the stiffness on neck examination can be confused as muscular in origin; however, this symptom may actually represent early meningismus.

Lung examination results may be normal in early or mild illness. In severe illness, signs of consolidation due to alveolar hemorrhage may be found. In patients with cardiac-related pulmonary edema, rales and wheezes can be heard.

The incidence of pulmonary involvement has increased over the past few years, affecting up to 70% patients. Alveolar hemorrhage that manifests as dyspnea and hemoptysis is the main pulmonary manifestation. This clinical manifestation may be severe and can occur in the absence of typical presentations of Weil disease.

Pulmonary involvement has emerged as a serious cause of mortality, becoming the main cause of leptospirosis-associated death in some countries.[8, 9]

Myocarditis may occur in severe disease. All of the physical findings of biventricular heart failure can be found, including elevated jugular venous pulsations; a new S3 gallop; and dysrhythmias, including atrial fibrillation, heart blocks of varying severity, and ventricular ectopy.

Abdominal examination may reveal liver enlargement and tenderness due to hepatitis. Acalculous cholecystitis, which may be suggested by a positive Murphy sign, is a finding of profound systemic illness. Pancreatitis has also been described in severe cases.[10]

Heme-positive stool and even gross blood can be found on rectal examination in patients with DIC and bleeding.

In severe disease, delirium may develop either as a consequence of shock or independent of it. Delirium may be an early finding in severe disease. Late in disease and into convalescence, prolonged mental symptoms may persist, including depression, anxiety, irritability, psychosis, and even dementia.

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Contributor Information and Disclosures
Author

Sandra G Gompf, MD, FACP, FIDSA  Associate Professor of Infectious Diseases and International Medicine, University of South Florida College of Medicine; Chief, Infectious Diseases Section, Director, Occupational Health and Infection Control Programs, James A Haley Veterans Hospital

Sandra G Gompf, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Ana Paula Velez  MD, Assistant Professor of Medicine, Division of Infectious Disease and International Medicine, University of South Florida College of Medicine and James A Haley Veterans Affairs Medical Center; Attending Physician, Moffitt Cancer Center

Ana Paula Velez is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Maria D Mileno, MD  Associate Professor of Medicine, Division of Infectious Diseases, The Warren Alpert Medical School of Brown University

Maria D Mileno, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Charles V Sanders, MD  Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, American Geriatrics Society, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, Infectious Diseases Society of America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors Juan D Diaz, DO; Matthew R Jezior, MD; Cecily K Peterson, MD; and Joseph T Morris, MD, to the development and writing of this article.

References
  1. Yang CW. Leptospirosis in Taiwan--an underestimated infectious disease. Chang Gung Med J. Mar-Apr 2007;30(2):109-15. [Medline].

  2. Chierakul W, Tientadakul P, Suputtamongkol Y, et al. Activation of the coagulation cascade in patients with leptospirosis. Clin Infect Dis. Jan 15 2008;46(2):254-60. [Medline].

  3. Wagenaar JF, Goris MG, Sakundarno MS, et al. What role do coagulation disorders play in the pathogenesis of leptospirosis?. Trop Med Int Health. Jan 2007;12(1):111-22. [Medline].

  4. Katz AR, Buchholz AE, Hinson K, Park SY, Effler PV. Leptospirosis in hawaii, USA, 1999-2008. Emerg Infect Dis. Feb 2011;17(2):221-6. [Medline].

  5. Gaspari R, Annetta MG, Cavaliere F, et al. Unusual presentation of leptospirosis in the late stage of pregnancy. Minerva Anestesiol. Jul-Aug 2007;73(7-8):429-32. [Medline].

  6. Khosravi M, Bastani B. Acute renal failure due to leptospirosis in a renal transplant recipient: a brief review of the literature. Transplant Proc. May 2007;39(4):1263-6. [Medline].

  7. Pappachan JM, Mathew S, Thomas B, et al. The incidence and clinical characteristics of the immune phase eye disease in treated cases of human leptospirosis. Indian J Med Sci. Aug 2007;61(8):441-7. [Medline].

  8. Dolhnikoff M, Mauad T, Bethlem EP, et al. Pathology and pathophysiology of pulmonary manifestations in leptospirosis. Braz J Infect Dis. Feb 2007;11(1):142-8. [Medline].

  9. Dall'Antonia M, Sluga G, Whitfield S, et al. Leptospirosis pulmonary haemorrhage: a diagnostic challenge. Emerg Med J. Jan 2008;25(1):51-2. [Medline].

  10. Spichler A, Spichler E, Moock M, et al. Acute pancreatitis in fatal anicteric leptospirosis. Am J Trop Med Hyg. May 2007;76(5):886-7. [Medline].

  11. Khositseth S, Sudjaritjan N, Tananchai P, et al. Renal magnesium wasting and tubular dysfunction in leptospirosis. Nephrol Dial Transplant. Mar 2008;23(3):952-8. [Medline].

  12. Chakurkar G, Vaideeswar P, Pandit SP, et al. Cardiovascular lesions in leptospirosis: an autopsy study. J Infect. Mar 2008;56(3):197-203. [Medline].

  13. Brett-Major DM, Coldren R. Antibiotics for leptospirosis. Cochrane Database Syst Rev. Feb 15 2012;2:CD008264. [Medline].

  14. Dursun B, Bostan F, Artac M, et al. Severe pulmonary haemorrhage accompanying hepatorenal failure in fulminant leptospirosis. Int J Clin Pract. Jan 2007;61(1):164-7. [Medline].

  15. Shenoy VV, Nagar VS, Chowdhury AA, Bhalgat PS, Juvale NI. Pulmonary leptospirosis: an excellent response to bolus methylprednisolone. Postgrad Med J. Sep 2006;82(971):602-6. [Medline]. [Full Text].

  16. Meaudre E, Asencio Y, Montcriol A, et al. [Immunomodulation in severe leptospirosis with multiple organ failure: plasma exchange, intravenous immunoglobulin or corticosteroids?]. Ann Fr Anesth Reanim. Feb 2008;27(2):172-6. [Medline].

  17. Wang Z, Jin L, Wegrzyn A. Leptospirosis vaccines. Microb Cell Fact. Dec 11 2007;6:39. [Medline]. [Full Text].

  18. Boyer AS, Runyan RB. TGFbeta Type III and TGFbeta Type II receptors have distinct activities during epithelial-mesenchymal cell transformation in the embryonic heart. Dev Dyn. Aug 2001;221(4):454-9. [Medline].

  19. Centers for Disease Control and Prevention. Brief report: Leptospirosis after flooding of a university campus--Hawaii, 2004. MMWR Morb Mortal Wkly Rep. Feb 10 2006;55(5):125-7. [Medline]. [Full Text].

  20. Centers for Disease Control and Prevention. Outbreak of leptospirosis among white-water rafters--Costa Rica, 1996. MMWR Morb Mortal Wkly Rep. Jun 27 1997;46(25):577-9. [Medline]. [Full Text].

  21. Cox TE, Smythe LD, Leung LK. Flying foxes as carriers of pathogenic Leptospira species. J Wildl Dis. Oct 2005;41(4):753-7. [Medline].

  22. Dall'Antonia M, Sluga G, Whitfield S, et al. Leptospirosis pulmonary haemorrhage: a diagnostic challenge. Emerg Med J. Jan 2008;25(1):51-2. [Medline].

  23. Doudier B, Garcia S, Quennee V, et al. Prognostic factors associated with severe leptospirosis. Clin Microbiol Infect. Apr 2006;12(4):299-300. [Medline].

  24. Faine S. Leptospira and Leptospirosis. Boca Raton: CRC Press Inc; 1994.

  25. Farr RW. Leptospirosis. Clin Infect Dis. Jul 1995;21(1):1-6; quiz 7-8. [Medline].

  26. Masuzawa T, Okamoto Y, Une Y, et al. Leptospirosis in squirrels imported from United States to Japan. Emerg Infect Dis. Jul 2006;12(7):1153-5. [Medline]. [Full Text].

  27. Moore GE, Guptill LF, Glickman NW, et al. Canine leptospirosis, United States, 2002-2004. Emerg Infect Dis. Mar 2006;12(3):501-3. [Medline].

  28. O'Neil KM, Rickman LS, Lazarus AA. Pulmonary manifestations of leptospirosis. Rev Infect Dis. Jul-Aug 1991;13(4):705-9. [Medline].

  29. Sanford JP. Leptospirosis. In: Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill, Inc; 740-3.

  30. Sejvar J, Bancroft E, Winthrop K, et al. Leptospirosis in "Eco-Challenge" athletes, Malaysian Borneo, 2000. Emerg Infect Dis. Jun 2003;9(6):702-7. [Medline]. [Full Text].

  31. Speelman P. Leptospirosis. In: Harrison's Principle of Internal Medicine. 14th ed. New York, NY: McGraw-Hill, Inc; 1036-38.

  32. Tappero J, Ashford D, Perkins N. Leptospira species (Leptospirosis). In: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. Philadelphia, Pa: Churchill Livingstone; 2000:2495-500.

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Darkfield microscopy of leptospiral microscopic agglutination test. (This image is in the public domain and thus free of any copyright restrictions. Courtesy of the Centers for Disease Control/Mrs. M. Gatton)
A scanning electron micrograph depicting Leptospira atop a 0.1-µm polycarbonate filter. (This image is in the public domain and thus free of any copyright restrictions. Courtesy of the Centers for Disease Control/Rob Weyant)
Silver stain, liver, fatal human leptospirosis. (This image is in the public domain and thus free of any copyright restrictions. Courtesy of the Centers for Disease Control/Dr. Martin Hicklin)
 
 
 
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