Leptospirosis pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
No edit summary
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Leptospirosis}}
{{CMG}}; {{AE}}{{VSKP}}
{{CMG}}; {{AE}}{{VSKP}}
==Pathophysiology==
==Pathophysiology==

Revision as of 19:59, 28 February 2017

Leptospirosis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Leptospirosis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Imaging Findings

Treatment

Medical Therapy

Surgery

Primary Prevention

Future or Investigational Therapies

Case Studies

Case #1

Leptospirosis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Leptospirosis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Leptospirosis pathophysiology

CDC on Leptospirosis pathophysiology

Leptospirosis pathophysiology in the news

Blogs on Leptospirosis pathophysiology

Directions to Hospitals Treating Leptospirosis

Risk calculators and risk factors for Leptospirosis pathophysiology

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]

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]

Reservoirs

The major reservoir for leptospirosis is rat.[2]

Transmission

Pathogenic leptospires live in the renal system and the genital tracts of domestic animals which act as sites of persistence.[3][4] 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. The major route of infection by leptospires is probably by transmission through indirect contact with leptospires secreted into the environment. Humans are considered dead end hosts, but sometimes they also act as carriers. Mammalian species (e.g. rodents, insectivores, dogs, pigs and cattle) act as the main carriers of the disease.[5] Leptospires are excreted in urine into the environment, where they can survive for several months, depending on favourable environmental conditions such as humid and temperate areas. Infection can occurs either by direct contact with the carrier’s urine or through indirect transmission via urine-contaminated environment. The pathogen may also be excreted in the products of abortion in mammalian animal species.[3]

[6][7][8][9]

Pathophysiology

Toxin Production
Type of toxin production depends on the serovar

Hemolytic toxins:

Hemolysins are produced from several serovars such as serovars ballum, hardjo, pomona, and tarassovi which are sphingomyelinases

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:[10]
  • 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[10][11]
  • 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[10]
  • Leptospires are seen in renal tubules
  • Electron microscopy findings include:[12][13]
    • 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.[14][15][16][17]

  • 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.[10][17][18][19]

  • 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

References

  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. ↑ Picardeau, M. (2013). "Diagnosis and epidemiology of leptospirosis". Médecine et Maladies Infectieuses. 43 (1): 1–9. doi:10.1016/j.medmal.2012.11.005. ISSN 0399-077X.
  3. ↑ 3.0 3.1 Ellis WA, O'Brien JJ, Cassells JA, Neill SD, Hanna J (1985). "Excretion of Leptospira interrogans serovar hardjo following calving or abortion". Res Vet Sci. 39 (3): 296–8. PMID 4081333.
  4. ↑ Ellis WA, McParland PJ, Bryson DG, Thiermann AB, Montgomery J (1986). "Isolation of leptospires from the genital tract and kidneys of aborted sows". Vet Rec. 118 (11): 294–5. PMID 3705357.
  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. ↑ 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.
  7. ↑ BEESON PB, HANKEY DD (1952). "Leptospiral meningitis". AMA Arch Intern Med. 89 (4): 575–83. PMID 14902167.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 10.0 10.1 10.2 10.3 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ AREAN VM (1957). "Leptospiral myocarditis". Lab Invest. 6 (5): 462–71. PMID 13464040.
  17. ↑ 17.0 17.1 Ramachandran S, Perera MV (1977). "Cardiac and pulmonary involvement in leptospirosis". Trans R Soc Trop Med Hyg. 71 (1): 56–9. PMID 871034.
  18. ↑ 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.
  19. ↑ 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.
Retrieved from "https://www.wikidoc.org/index.php?title=Leptospirosis_pathophysiology&oldid=1296562"