Leptospirosis

From Wikipedia, the free encyclopedia
  (Redirected from Weil's disease)
Jump to: navigation, search
Leptospirosis
Classification and external resources
Leptospirosis darkfield.jpg
Leptospira magnified 200 times with dark-field microscope
ICD-10 A27
ICD-9 100
OMIM 607948
DiseasesDB 7403
MedlinePlus 001376
eMedicine article/220563 article/96569 article/788751
MeSH C01.252.400.511

Leptospirosis (also known as field fever,[1] rat catcher's yellows,[2] and pretibial fever[3] among others names) is an infection caused by bacteria of the Leptospira type. Symptoms can range from none to mild such as headaches, muscle pains, and fevers to severe with bleeding from the lungs or meningitis.[4][5] If the infection causes the person to turn yellow, have kidney failure and bleeding it is then known as Weil's disease.[5] If it causes lots of bleeding from the lungs it is known as severe pulmonary haemorrhage syndrome.[5]

There are ten different types of Leptospira that cause disease in humans.[6] It is transmitted by both wild and domestic animals.[5] The most common animals that spread the disease are rodents.[7] It is often transmitted by animal urine or water containing animal urine coming into contact with breaks in the skin, the eyes, mouth, nose or vagina.[4][7] In the developing world the disease most commonly occurs in farmers and poor people who live in cities.[5] In the developed world it most commonly occurs in those involved in outdoor activities in warm and wet areas of the world.[4] Diagnosis is by growing the bacteria from a blood sample, finding its DNA in the blood, or looking for antibodies against the infection.[4]

Efforts to prevent the disease include protective equipment to prevent contact when working with potentially infected animals, washing after this contact, and reducing rodents in areas people live and work.[4] The antibiotic doxycycline, when used in an effort to prevent infection among travellers, is of unclear benefit.[4] Vaccines for animals exist for certain type of Leptospira which may decrease the risk of spread to humans.[4] Treatment if infected is with antibiotics such as: doxycycline, penicillin, or ceftriaxone.[4] Weil's disease and severe pulmonary haemorrhage syndrome result in death rates greater than 10% and 50%, respectively, even with treatment.[5]

It is estimated that seven to ten million people are infected by leptospirosis a year.[8] The number of deaths this causes is not clear.[8] The disease is most common in tropical areas of the world but may occur anywhere.[4] Outbreaks may occur in slums of the developing world.[5] The disease was first described by Weil in 1886 in Germany.[4] Animals who are infected may have no symptoms, mild symptoms, or severe symptoms.[6] Symptoms may vary by the type of animal.[6]

Signs and symptoms[edit]

Leptospiral infection in humans causes a range of symptoms, and some infected persons may have no symptoms at all. Leptospirosis is a biphasic disease that begins with flu-like symptoms (fever, chills, myalgias, intense headache). The first phase (mild leptospirosis) resolves, and the patient is briefly asymptomatic until the second phase (severe leptospirosis) begins. 90 percent of cases of the disease are mild leptospirosis and without any specific treatment and the rest develop to severe leptospirosis. This is characterized by liver damage (causing jaundice), renal failure with same signs and symptoms; the heart and brain can be affected, meningitis of the outer layer of the brain, encephalitis of brain tissue with same signs and symptoms; and lung affected as the most serious and life-threatening of all leptospirosis complications. The infection is often incorrectly diagnosed due to the nonspecific symptoms.

Signs and symptoms of leptospirosis include high fever, severe headache, chills, muscle aches, and vomiting, and may include jaundice, red eyes, abdominal pain, diarrhea, and rash. Initial presentation may resemble pneumonia. The symptoms in humans appear after a 4–14 day incubation period. More severe manifestations include meningitis, extreme fatigue, hearing loss, respiratory distress, azotemia, and renal interstitial tubular necrosis, which results in renal failure and occasionally liver failure (the severe form of this disease is known as Weil's disease, though it is sometimes named Weil Syndrome).[9] Cardiovascular problems are also possible.

Incubation (time of exposure to first symptoms) in animals is anywhere from 2 to 20 days. In dogs, leptospirosis most often damages the liver and kidney. In addition, recent reports describe a pulmonary form of canine leptospirosis associated with severe hemorrhage in the lungs—similar to human pulmonary hemorrhagic syndrome.[10][11] Vasculitis may occur, causing edema and potentially disseminated intravascular coagulation (DIC). Myocarditis, pericarditis, meningitis, and uveitis are also possible sequelae.[12]

Eye finding may include conjunctival suffusion

Cause[edit]

Scanning electron micrograph of a number of Leptospira sp. bacteria atop a 0.1 µm polycarbonate filter
The Native American lifestyle exposed them to the leptospiral life cycle

Leptospirosis is caused by a spirochaete bacterium called Leptospira spp. At least five important serotypes exist in the United States and Canada, all of which cause disease in dogs:[12][13][14]

  • Icterohaemorrhagiae
  • Canicola
  • Pomona
  • Grippotyphosa
  • Bratislava

Other (more common) lethal infectious strains exist. Genetically different leptospira organisms may be identical serologically and vice versa. Hence, some argue about strain identification. The traditional serologic system currently seems more useful from a diagnostic and epidemiologic standpoint—but this may change with further development and spread of technologies like polymerase chain reaction (PCR).

Leptospirosis is transmitted by the urine of an infected animal, and is contagious as long as the urine is still moist. Rats, mice, and moles are important primary hosts—but a wide range of other mammals including dogs, deer, rabbits, hedgehogs, cows, sheep, raccoons, opossums, skunks, and certain marine mammals carry and transmit the disease as secondary hosts. In Africa, the banded mongoose has been identified as a carrier of the pathogen, likely in addition to other African wildlife hosts.[15] Dogs may lick the urine of an infected animal off the grass or soil, or drink from an infected puddle.

House-bound domestic dogs have contracted leptospirosis, apparently from licking the urine of infected mice in the house. The type of habitats most likely to carry infective bacteria are muddy riverbanks, ditches, gullies, and muddy livestock rearing areas where there is regular passage of wild or farm mammals. The incidence of leptospirosis correlates directly with the amount of rainfall, making it seasonal in temperate climates and year-round in tropical climates. Leptospirosis also transmits via the semen of infected animals.[16]

Humans become infected through contact with water, food, or soil that contains urine from these infected animals. This may happen by swallowing contaminated food or water or through skin contact. The disease is not known to spread between humans, and bacterial dissemination in convalescence is extremely rare in humans. Leptospirosis is common among water-sport enthusiasts in specific areas, as prolonged immersion in water promotes the entry of the bacteria. Surfers and whitewater paddlers[17] are at especially high risk in areas that have been shown to contain the bacteria, and can contract the disease by swallowing contaminated water, splashing contaminated water into their eyes or nose, or exposing open wounds to infected water.[18]

At risk occupations[edit]

Occupations at risk include veterinarians, slaughterhouse workers, farmers, sewer maintenance workers, waste disposal facility workers, land surveyors, and people who work on derelict buildings.[19] Slaughterhouse workers can contract the disease through contact with infected blood or body fluids. Rowers, kayakers and canoeists also sometimes contract the disease.[12]

Diagnosis[edit]

Kidney tissue, using a silver staining technique, revealing the presence of Leptospira bacteria

On infection the microorganism can be found in blood and Cerebrospinal fluid (CSF) for the first 7 to 10 days (invoking serologically identifiable reactions) and then moving to the kidneys. After 7 to 10 days the microorganism can be found in fresh urine. Hence, early diagnostic efforts include testing a serum or blood sample serologically with a panel of different strains.

Kidney function tests (blood urea nitrogen and creatinine) as well as blood tests for liver functions are performed. The latter reveal a moderate elevation of transaminases. Brief elevations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltransferase (GGT) levels are relatively mild. These levels may be normal, even in children with jaundice.

Diagnosis of leptospirosis is confirmed with tests such as enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR). The MAT (microscopic agglutination test), a serological test, is considered the gold standard in diagnosing leptospirosis. As a large panel of different leptospira must be subcultured frequently, which is both laborious and expensive, it is underused, especially in developing countries.

Differential diagnosis list for leptospirosis is very large due to diverse symptomatics. For forms with middle to high severity, the list includes dengue fever and other hemorrhagic fevers, hepatitis of various etiologies, viral meningitis, malaria, and typhoid fever. Light forms should be distinguished from influenza and other related viral diseases. Specific tests are a must for proper diagnosis of leptospirosis.

Under circumstances of limited access (e.g., developing countries) to specific diagnostic means, close attention must be paid to the medical history of the patient. Factors such as certain dwelling areas, seasonality, contact with stagnant contaminated water (bathing, swimming, working on flooded meadows, etc.) or rodents in the medical history support the leptospirosis hypothesis and serve as indications for specific tests (if available).

Leptospira can be cultured in Ellinghausen-McCullough-Johnson-Harris medium (EMJH), which is incubated at 28 to 30 °C.[20] The median time to positivity is three weeks with a maximum of three months. This makes culture techniques useless for diagnostic purposes, but is commonly used in research.

Prevention[edit]

Doxycycline may be used as a prophylaxis once a week, to prevent infection in high risk areas.[21] Effective rat control and avoidance of urine contaminated water sources are essential preventive measures.Human vaccines are available in a few countries, including Cuba and China.[5] Currently, no human vaccine is available in the US. Animal vaccines only cover a few strains of the bacteria. Dog vaccines are effective for at least one year.[22]

Treatment[edit]

Effective antibiotics include penicillin G, ampicillin, amoxicillin and Doxycycline. In more severe cases cefotaxime or ceftriaxone should be preferred.

Glucose and salt solution infusions may be administered; dialysis is used in serious cases. Elevations of serum potassium are common and if the potassium level gets too high special measures must be taken. Serum phosphorus levels may likewise increase to unacceptable levels due to renal failure.

Treatment for hyperphosphatemia consists of treating the underlying disease, dialysis where appropriate, or oral administration of calcium carbonate, but not without first checking the serum calcium levels (these two levels are related). Corticosteroids administration in gradually reduced doses (e.g., prednisolone) during 7–10 days is recommended by some[citation needed] specialists in cases of severe haemorrhagic effects. Organ specific care and treatment are essential in cases of renal, liver, or heart involvement.

Epidemiology[edit]

It is estimated that seven to ten million peoples are infected by leptospirosis annually.[8] Annual rates of infection vary from 0.02 per 100,000 in temperate climates to 10 to 100 per 100,000 in tropical climates.[21] This leads to a lower number of registered cases than likely exists.

History[edit]

The disease was first described by Adolf Weil in 1886 when he reported an "acute infectious disease with enlargement of spleen, jaundice, and nephritis." Leptospira was first observed in 1907 from a post mortem renal tissue slice.[23] In 1908, Inada and Ito first identified it as the causative organism[24] and in 1916 noted its presence in rats.[25]

Leptospirosis was postulated as the cause of an epidemic among Native Americans along the coast of present-day Massachusetts that occurred immediately before the arrival of the Pilgrims in 1620 and killed most of the native population.[26] Earlier proposals included plague, yellow fever, smallpox, influenza, chickenpox, typhus, typhoid fever, trichinellosis, meningitis, and syndemic infection of hepatitis B virus with the delta agent.[27][28][29][30] The disease may have been brought to the New World by Europeans and spread by the high-risk daily activities of the Native Americans[citation needed].

Before Weil's characterization in 1886, the disease known as infectious jaundice was very likely the same as Weil's disease, or severe icteric leptospirosis. During the Egyptian campaign, Napoleon's army suffered from what was probably infectious jaundice.[31] Infectious jaundice occurred among troops during the American Civil War.[32]

It was also reported among troops at Gallipoli and other battles of World War I, where the sodden conditions of trench warfare favored infection. Terms used in early 20th century descriptions of leptospirosis include the pseudo-dengue of Java, seven-day fever, autumn fever, Akiyama disease, and marsh or swamp fever. L icterohaemorrhagiae was identified as the causative agent in pre-World War II outbreaks in Japan, which were characterized by jaundice and a high mortality rate.

In October 2010 British rower Andy Holmes died after contracting Weil's Disease.[33] His death has raised awareness of the disease among the public and medical professionals.[34]

Names[edit]

Leptospirosis has many different names including: "7-day fever",[1] "harvest fever",[1] "field fever",[1] "canefield fever",[1] "mild fever",[1] "rat catcher's yellows",[2] "Fort Bragg fever",[3] and "pretibial fever".[3]

It has historically been known as "black jaundice"[35] and in Japan it is called "nanukayami fever".[36]

Other animals[edit]

In dogs when leptospirosis is caused by L. interrogans it may be referred to as "canicola fever".[36] Leptospirosis should be strongly suspected and included as part of a differential diagnosis if the sclerae of a dog's eyes appear jaundiced (even slightly yellow). The absence of jaundice does not eliminate the possibility of leptospirosis, and its presence could indicate hepatitis or other liver pathology rather than leptospirosis. Vomiting, fever, failure to eat, reduced urine output, unusually dark or brown urine, and lethargy are also indications of the disease.

In dogs, penicillin is most commonly used to end the leptospiremic phase (infection of the blood), and doxycycline is used to eliminate the carrier state.

References[edit]

  1. ^ a b c d e f Mosby's Medical Dictionary (9 ed.). Elsevier Health Sciences. 2013. p. 697. ISBN 9780323112581. 
  2. ^ a b McKay, James E. (2001). Comprehensive health care for dogs. Minnetonka, MN.: Creative Pub. International. p. 97. ISBN 9781559717830. 
  3. ^ a b c James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0. :290
  4. ^ a b c d e f g h i j Slack, A (Jul 2010). "Leptospirosis.". Australian family physician 39 (7): 495–8. PMID 20628664. 
  5. ^ a b c d e f g h McBride, AJ; Athanazio, DA; Reis, MG; Ko, AI (Oct 2005). "Leptospirosis.". Current opinion in infectious diseases 18 (5): 376–86. PMID 16148523. 
  6. ^ a b c "Leptospirosis". The Center for Food Security and Public Health. May 2005. Retrieved 15 March 2014. 
  7. ^ a b Wasiński, B; Dutkiewicz, J (2013). "Leptospirosis--current risk factors connected with human activity and the environment.". Annals of agricultural and environmental medicine : AAEM 20 (2): 239–44. PMID 23772568. 
  8. ^ a b c "Leptospirosis". NHS. 07/11/2012. Retrieved 14 March 2014. 
  9. ^ "Weil syndrome definition – Medical Dictionary definitions of popular medical terms easily defined on MedTerms". Medterms.com. 2012-10-09. Retrieved 2013-07-19. 
  10. ^ Klopfleisch R, Kohn B, Plog S, Weingart C, Nöckler K, Mayer-Scholl A, Gruber AD. (2011). "An Emerging Pulmonary Haemorrhagic Syndrome in Dogs: Similar to the Human Leptospiral Pulmonary Haemorrhagic Syndrome?". Vet Med Int. 33: 928541. doi:10.4061/2010/928541. PMC 3025382. PMID 21274452. 
  11. ^ Kohn B, Steinicke K, Arndt G, Gruber AD, Guerra B, Jansen A, Kaser-Hotz B, Klopfleisch R, Lotz F, Luge E, Nöckler K. (2010). "Pulmonary abnormalities in dogs with leptospirosis". J Vet Intern Med. 24 (6): 791–807. doi:10.1111/j.1939-1676.2010.0585.x. PMID 20738768. 
  12. ^ a b c Langston CE, Heuter KJ (July 2003). "Leptospirosis. A re-emerging zoonotic disease". Veterinary Clinics of North America, Small Animal Practice 33 (4): 791–807. doi:10.1016/S0195-5616(03)00026-3. PMID 12910744. 
  13. ^ Kohn B, Steinicke K, Arndt G, Gruber AD, Guerra B, Jansen A, Kaser-Hotz B, Klopfleisch R, Lotz F, Luge E, Nöckler K. (2010). "Pulmonary abnormalities in dogs with leptospirosis". J Vet Intern Med. 24 (6): 1277–82. doi:10.1111/j.1939-1676.2010.0585.x. PMID 20738768. 
  14. ^ Klopfleisch R, Plog S, Kohn B, Weingart, Gruber AD. (2011). "An emerging pulmonary haemorrhagic syndrome in dogs—similar to the human leptospiral pulmonary haemorrhagic syndrome?". Veterinar Medicine International. 
  15. ^ "Human disease leptospirosis identified in new species, the banded mongoose, in Africa". Sciencedaily.com. 2013-05-14. Retrieved 2013-07-19. 
  16. ^ Kiktenko VS; Balashov, NG; Rodina, VN (1976). "Leptospirosis infection through insemination of animals". J Hyg Epidemiol Microbiol Immunol. 21 (2): 207–213. PMID 987112. 
  17. ^ Shaw RD (June 1992). "Kayaking as a risk factor for leptospirosis". Mo Med 89 (6): 354–7. PMID 1620089. 
  18. ^ transworld.net: Seven Surfing Sicknesses.
  19. ^ "Weils Disease at Work". 
  20. ^ Rule PL, Alexander AD (1986). "Gellan gum as a substitute for agar in leptospiral media". J Clin Microbiol 23 (3): 500–504. PMC 268682. PMID 3754265. 
  21. ^ a b Pavli A, Maltezou HC (2008). "Travel-acquired leptospirosis". J Travel Med 15 (6): 447–53. doi:10.1111/j.1708-8305.2008.00257.x. PMID 19090801. 
  22. ^ Goldstein RE (November 2010). "Canine leptospirosis". The Veterinary Clinics of North America. Small Animal Practice 40 (6): 1091–101. doi:10.1016/j.cvsm.2010.07.008. PMID 20933138. 
  23. ^ Stimson, AM (1907). "Note on an organism found in yellow-fever tissue". Public Health Reports 22 (18): 541. doi:10.2307/4559008. 
  24. ^ Inada R, Ito Y (1908). "A report of the discovery of the causal organism (a new species of spirocheta) of Weil's disease". Tokyo Ijishinshi 1915: 351–60. 
  25. ^ Inanda R, Ido Y, Hoke R, Kaneko R, Ito H (1916). "The Etiology, Mode of Infection and Specific Therapy of Weil's Disease". J Exper Med 23 (3): 377. doi:10.1084/jem.23.3.377. 
  26. ^ Marr JS, Cathey JT (February 2010). "New hypothesis for cause of an epidemic among Native Americans, New England, 1616–1619". Emerg Infect Dis 16 (2): 281–6. doi:10.3201/eid1602.090276. PMC 2957993. PMID 20113559. 
  27. ^ Webster N (1799). A brief history of epidemic and pestilential diseases. Hartford CT: Hudson and Goodwin. 
  28. ^ Williams H (1909). "The epidemic of the Indians of New England, 1616–1620, with remarks on Native American infections". Johns Hopkins Hospital Bulletin 20: 340–9. 
  29. ^ Bratton TL (1988). "The identity of the New England Indian epidemic of 1616–19". Bull Hist Med 62 (3): 351–83. PMID 3067787. 
  30. ^ Speiss A, Speiss BD (1987). "New England pandemic of 1616–1622. cause and archeological implication". Man in the Northeast 34: 71–83. 
  31. ^ Edward Rhodes Stitt; Richard Pearson Strong (1944). Stitt's Diagnosis, prevention and treatment of tropical diseases (7th ed.). York, PA: Blakiston. 
  32. ^ Neill M (1918). "The problem of acute infectious jaundice in the United States". Public Health Rep 33 (19): 717–26. doi:10.2307/4574792. 
  33. ^ Leggat, David (27 October 2010). "Rowing: Rare disease kills rowing great". The New Zealand Herald. Retrieved 14 October 2011. 
  34. ^ Forbes AE, Zochowski WJ, Dubrey SW, Sivaprakasam V (July 2012). "Leptospirosis and Weil's disease in the UK". QJM : Monthly Journal of the Association of Physicians 105 (12): 1151–62. doi:10.1093/qjmed/hcs145. PMID 22843698. 
  35. ^ David Clapham (2004). Small Water Supplies: A Practical Guide. Routledge. p. 125. ISBN 9781134457496. 
  36. ^ a b Dorland's illustrated medical dictionary (32nd ed. ed.). Philadelphia: Elsevier/Saunders. 2012. p. 1231. ISBN 9781455709854. 

Further reading[edit]

  • Bharti, A. R.; Nally, JE; Ricaldi, JN; Matthias, MA; Diaz, MM; Lovett, MA; Levett, PN; Gilman, RH; Willig, MR; Gotuzzo, Eduardo; Vinetz, Joseph M; Peru-United States Leptospirosis Consortium (2003). "Leptospirosis: a zoonotic disease of global importance". Lancet Infect. Dis. 3 (12): 757–71. doi:10.1016/S1473-3099(03)00830-2. PMID 14652202. 

External links[edit]