Sandbox:Leptospirosis

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Overview

Leptospirosis is a bacterial zoonotic disorder with ubiquitous distribution,common worldwide, especially in developing countries caused by Leptospira species.

Historical Perspective

Association of renal failure with icteric leptospirosis, was first reported over 100 years ago and described by Adolf Weil.

Pathophysiology

The disease leptospirosis involves a spectrum of symptoms ranging from subclinical infection to a severe syndrome of multiorgan infection with high mortality and Weil’s disease represents only the most severe presentation. Severe leptospirosis is frequently caused by serovars of the icterohaemorrhagiae serogroup. The presentation of leptospirosis is biphasic, with the acute or septicemic phase lasting about a week, followed by the immune phase, characterized by antibody production and excretion of leptospires in the urine.[1]

Bacteria shed from the infected animals such as rodents and domesticat animals through urine. These animals may not show signs of disease, but humans shows signs of illness after contact with infected urine, or through contact with water, soil or food that has been contaminated and the outbreaks are associates with floodwaters.

[2][3][4][5]

Pathophysiology

Toxin Production
Immunological Mechanism
Humoral Immunity Innate Immunity
Acute phase Immune phase
  • Also known as Septicemic phase
  • Begins abruptly
  • Characterized by nonspecific signs such as fever, chills, headache and conjunctival suffusion
  • Associate with severe myalgia
  • Other less common findings include: Photophobia, lymphadenopathy, abdominal pain, nausea, vomiting, a transient rash, sore throat, coughing or chest pain
  • Characterestic of this phase also includes: symptoms lasts several days to a week, which is followed by a brief remission, during which the temperature drops and the symptoms disappear
 Anicteric leptospirosis Icteric 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
  • Other symptoms include chills, headache (severe with retro-orbital pain and photophobia), myalgia, abdominal pain, conjunctival suffusion, and skin rash (transient and last <24 hours)
  • 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
  • Rapidly progressive and severe form of leptospirosis
  • Less common form of leptospirosis with incidence of 5%-10%
  • Jaundice is not associate with hepatocellular injury, eventually LFT returns to normal after recovery
  • High mortality rate with a range of 5%-15%

Pathology

Pathology
Pathological findings of leptospirosis are due to the development of the following:
  • Vasculitis
  • Endothelial damage
  • Inflammatory infiltrates composed of moncytic cells, plasma cells, histiocytes, and neutrophils
Gross Findings
Gross findings of various organ systems are present as:[6]
  • Extensive petechial hemorrhages are common
  • Discoloration of organs is seen in severe cases of icteric leptospirosis
Histopathological Findings
Liver:
  • No significant structural destruction is seen[6][7]
  • Intrahepatic cholestasis is seen in few cases
  • Hypertrophy and hyperplasia of Kupffer cells
  • Erythrophagocytosis

Kidney:

  • Common histopathological presentation in kidney includes interstitial nephrits with infiltration of neutrophils and moncytes[6]
  • Leptospires are seen in renal tubules
  • Electron microscopy findings include:[8][9]
    • Thickened tubular basement membrane
    • Denuded tubular brush borders
    • Mitochondrial depletion in tubular cells
  • Glomerular destruction associate with proteinuria is seen in few cases

Heart:

Leptospirosis is associate with interstitial myocarditis.[10][11][12][13]

  • Cellular infiltration predominantly with lymphocytes and plasma cells
  • Petechial hemorrhages (epicardial hemorrhages are common)
  • Epicardial infilteration of mononuclear cells
  • Pericardial effusion
  • coronary arteritis

Lungs:

Common pulmonary presentation in leptospirosis are pulmonary congestion and hemorrhage.[6][13][14][15]

  • Alveolar infiltration by monocytes and neutrophils
  • Hyaline membrane formation
  • Leptospires are seen within the endothelial cells in interalveolar septa, and also attached to capillary endothelial cells

Skeletal muscle:

  • Focal necrosis of muscle fibers with infiltration of histiocytes, neutrophils, and plasma cells

Brain:

  • Perivascular cuffing is seen

Causes

Leptospirosis is caused by various species of Leptospira.

  • Family = Leptospiraceae
  • Order = Spirochaetales

Not all species of Leptospira are pathogenic, some species are harmless and saprophytes that reside in the environment. Until now there are 50 nonpathogenic serovers and 250 pathogenic serovers are identified. Serovar is the basic unit of Leptospira taxonomy and each serovar consist of closely related isolates based on serological reactions to the bacterial lipopolysaccharide Severe leptospirosis is frequently caused by serovars of the icterohaemorrhagiae serogroup.

Epidemiology and Demographics

Overview

Leptospirosis caused by pathogenic Leptospira species have been found worldwide, except in Antarctica. It is most common in warm, humid environments and in the areas with a high disease incidence in humans include the Caribbean and Latin America, Oceania and parts of Asia. During the past few decades, leptospirosis has become seriously neglected, especially in countries of temperate regions. The main reasons for this situation are probably: 1) a relatively less number of cases noted in the temperate climate zone 2) well established, quite effective methods of therapy and prevention of the disease 3) seemingly well-determined epidemiologic situation concerning the disease.[16]

Prevalence

Leptospirosis, is a zoonotic emerging infectious disease with a worldwide distribution.[17] Tropical climatic conditions are most favourable for survival of leptospires and the morbidity is high due to extreme weather events such as cyclones and floods occurring in recent years.[18][19]

Incidence

Leptospirosis is an increasing public health problem worldwide, evidenced by markedly increasing incidence rates and multiple outbreaks allover the world.

Case Fatality Rate

Higher morbidity due to leptospirosis is observed in regions with higher proportion of surface fresh waters such as lakes, rivers, developed canal systems.[20][21] Case fatality rate due to leptospirosis is > 10%, and > 500,000 cases of severe leptospirosis are reported each year.

Age

Gender

Developed Countries

Developing Countries

Leptospirosis is a neglected disease with a greatest burden on impoverished populations from developing countries and tropical regions.[22]

Natural History, Complications & Prognosis

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.

Complications

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.

  • Aseptic meningitis

Daignosis

History & Symptoms

The clinical presentation of leptospirosis is biphasic, with the acute or septicemic phase lasting about a week, followed by the immune phase, characterized by antibody production and excretion of leptospires in the urine.[1] Leptospirosis can occur in several forms, which include mild, flu-like symptoms that may not be recognized as leptospirosis, as well as unusual syndrome or fulminant illness without two distinct phases.

The incubation period of leptospirosis in humans is usually 7 to 12 days, with a range of 2 to 29 days.

Treatment

Primary Prevention

Secondary Prevention

For leptospirosis there is no specific vaccines for prevention, but it can be prevented by proper disinfection such as 1% sodium hypochlorite, 70% ethanol, iodine-based disinfectants, quaternary ammonium disinfectants, accelerated hydrogen peroxide, glutaraldehyde, formaldehyde, detergents and acid or by pasturization. These organisms are also sensitive to moist heat (121°C [249.8°F] for a minimum of 15 min).

References

  1. ↑ 1.0 1.1 Levett, P. N. (2001). "Leptospirosis". Clinical Microbiology Reviews. 14 (2): 296–326. doi:10.1128/CMR.14.2.296-326.2001. ISSN 0893-8512.
  2. ↑ Budihal, Suman Veerappa (2014). "Leptospirosis Diagnosis: Competancy of Various Laboratory Tests". JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH. doi:10.7860/JCDR/2014/6593.3950. ISSN 2249-782X.
  3. ↑ BEESON PB, HANKEY DD (1952). "Leptospiral meningitis". AMA Arch Intern Med. 89 (4): 575–83. PMID 14902167.
  4. ↑ King SD, Urquhart AE (1975). "Laboratory investigations on four cases of leptospiral meningitis in Jamaica". West Indian Med J. 24 (4): 196–201. PMID 1224630.
  5. ↑ Silva MV, Camargo ED, Batista L, Vaz AJ, Ferreira AW, Barbosa PR (1996). "Application of anti-leptospira ELISA-IgM for the etiologic elucidation of meningitis". Rev Inst Med Trop Sao Paulo. 38 (2): 153–6. PMID 9071036.
  6. ↑ 6.0 6.1 6.2 6.3 AREAN VM (1962). "The pathologic anatomy and pathogenesis of fatal human leptospirosis (Weil's disease)". Am J Pathol. 40: 393–423. PMC 1949541. PMID 13862141.
  7. ↑ De Brito T, Machado MM, Montans SD, Hoshino S, Freymüller E (1967). "Liver biopsy in human leptospirosis: a light and electron microscopy study". Virchows Arch Pathol Anat Physiol Klin Med. 342 (1): 61–9. PMID 4298629.
  8. ↑ PENNA D, DE BRITO T, PUPO AA, MACHADO MM, AYROZA PA, DE ALMEIDA SS (1963). "KIDNEY BIOPSY IN HUMAN LEPTOSPIROSIS". Am J Trop Med Hyg. 12: 896–901. PMID 14072448.
  9. ↑ Sitprija, Visith; Evans, Hilary (1970). "The kidney in human leptospirosis". The American Journal of Medicine. 49 (6): 780–788. doi:10.1016/S0002-9343(70)80059-6. ISSN 0002-9343.
  10. ↑ De Biase L, De Curtis G, Paparoni S, Sciarra D, Campa PP (1987). "Fatal leptospiral myocarditis". G Ital Cardiol. 17 (11): 992–4. PMID 3446572.
  11. ↑ Brito, T. De; Morais, C. F.; Yasuda, P. H.; Lancellotti, Carmen P.; Hoshino-Shimizu, Sumie; Yamashiro, E.; Alves, V. A. Ferreira (2016). "Cardiovascular involvement in human and experimental leptospirosis: Pathologic findings and immunohistochemical detection of leptospiral antigen". Annals of Tropical Medicine & Parasitology. 81 (3): 207–214. doi:10.1080/00034983.1987.11812114. ISSN 0003-4983.
  12. ↑ AREAN VM (1957). "Leptospiral myocarditis". Lab Invest. 6 (5): 462–71. PMID 13464040.
  13. ↑ 13.0 13.1 Ramachandran S, Perera MV (1977). "Cardiac and pulmonary involvement in leptospirosis". Trans R Soc Trop Med Hyg. 71 (1): 56–9. PMID 871034.
  14. ↑ Nicodemo AC, Duarte MI, Alves VA, Takakura CF, Santos RT, Nicodemo EL (1997). "Lung lesions in human leptospirosis: microscopic, immunohistochemical, and ultrastructural features related to thrombocytopenia". Am J Trop Med Hyg. 56 (2): 181–7. PMID 9080878.
  15. ↑ Zaltzman M, Kallenbach JM, Goss GD, Lewis M, Zwi S, Gear JH (1981). "Adult respiratory distress syndrome in Leptospira canicola infection". Br Med J (Clin Res Ed). 283 (6290): 519–20. PMC 1507945. PMID 6790049.
  16. ↑ Hartskeerl RA, Collares-Pereira M, Ellis WA (2011). "Emergence, control and re-emerging leptospirosis: dynamics of infection in the changing world". Clin Microbiol Infect. 17 (4): 494–501. doi:10.1111/j.1469-0691.2011.03474.x. PMID 21414083.
  17. ↑ Levett PN (2001). "Leptospirosis". Clin Microbiol Rev. 14 (2): 296–326. doi:10.1128/CMR.14.2.296-326.2001. PMC 88975. PMID 11292640.
  18. ↑ Lau CL, Smythe LD, Craig SB, Weinstein P (2010). "Climate change, flooding, urbanisation and leptospirosis: fuelling the fire?". Trans R Soc Trop Med Hyg. 104 (10): 631–8. doi:10.1016/j.trstmh.2010.07.002. PMID 20813388.
  19. ↑ Vijayachari P, Sugunan AP, Shriram AN (2008). "Leptospirosis: an emerging global public health problem". J Biosci. 33 (4): 557–69. PMID 19208981.
  20. ↑ Jansen A, Schöneberg I, Frank C, Alpers K, Schneider T, Stark K (2005). "Leptospirosis in Germany, 1962-2003". Emerg Infect Dis. 11 (7): 1048–54. doi:10.3201/eid1107.041172. PMC 3371786. PMID 16022779.
  21. ↑ Baranton G, Postic D (2006). "Trends in leptospirosis epidemiology in France. Sixty-six years of passive serological surveillance from 1920 to 2003". Int J Infect Dis. 10 (2): 162–70. doi:10.1016/j.ijid.2005.02.010. PMID 16298537.
  22. ↑ McBride AJ, Athanazio DA, Reis MG, Ko AI (2005). "Leptospirosis". Curr Opin Infect Dis. 18 (5): 376–86. PMID 16148523.
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