Pathogenesis
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PATHOGENESIS. The mechanisms of leptospiral pathogenesis are poorly understood; however

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PATHOGENESIS

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Pathogenesis

PATHOGENESIS


Pathogenesis

  • The mechanisms of leptospiral pathogenesis are poorly understood; however

  • Several candidate virulence factors have been identified that might contribute to the pathogenesis of Leptospira infection and disease, including LPS (which is thought of as a general virulence factor of Gram-negative bacteria),

  • hemolysins,

  • outer membrane proteins (OMPs) and other surface proteins, as well as adhesion molecules


Pathophysiology

PATHOPHYSIOLOGY

  • Infection - leptospires appear in the blood - invade all tissues and organs particularly affecting the liver and kidney -cleared from the body by the host's immune response

  • May also settle in the convoluted tubules of the kidneys -shed in the urine for a few weeks to several months or longer

  • Subsequently cleared from the kidneys and other organs (may persist in the eyes for much longer)


Pathophysiology1

PATHOPHYSIOLOGY

  • Produces endotoxin -attach onto the endothelial

    cells - capillary vasculitis (endothelial necrosis and lymphocytic infiltration)

  • Vasculitis and leakage -petechiae, intraparenchymal bleeding and bleeding along serosa and mucosa

  • Lost of fluids into the third space -hypovolaemic shock and vascular collapse


Pathogenesis

  • The most consistent pathologic finding in leptospirosis is vasculitis of capillaries, manifested by

  • endothelial edema,

  • necrosis, and

  • lymphocytic infiltration


Pathogenesis of severe disease

Pathogenesis of Severe Disease

Vasculitis

Damage to small

blood vessels

Leptospira

Massive migration of fluid from

Intravascular to interstitial compartment

Direct cytotoxic injury

Immunological injury

Renal dysfunction, vascular

Injury to internal organs


Pathogenesis

  • Capillary vasculitis is found in every affected organ system.

  • The resulting loss of red blood cells and fluid through enlarged junctions and fenestrae, which cause secondary tissue injury, probably accounts for many of the clinical findings.


Pathogenesis

  • In the kidneys, leptospires migrate to the interstitium, renal tubules, and tubular lumen, causing 

  • interstitial nephritis and

  •  Acute tubular necrosis.


Pathogenesis

  • Capillary vasculitis is readily identified. Although the glomeruli are spared, the progression from normal renal function to decreased glomerular filtration rate to renal failure requiring dialysis can be rapid


Pathogenesis

  • Renal failure is usually due to tubular damage, but hypovolemia from dehydration and from altered capillary permeability can also contribute to renal failure.


Pathogenesis

  • Liver involvement is marked by centrilobular necrosis and Kupffer cell proliferation. Jaundice may occur as a result of hepatocellular dysfunction


Pathogenesis

  • Pulmonary involvement is secondary to alveolar and interstitial vascular damage resulting in hemorrhage.

  • This complication is considered to be the major cause of leptospirosis-associated death.


Cardiac lesions

Cardiac lesions

  • Interstitial myocarditis was the predominant feature on histopathological examination. These authors suggested that leptospirosis be viewed as an infective systemic vasculitis


Pathogenesis

  • Hemorrhage, focal necrosis, and inflammatory infiltration have been documented within the adrenal gland.


Pathogenesis

  • The skin is affected by epithelial vascular insult.

  • Skeletal muscle involvement is secondary to edema, myofibril vacuolization, and vessel damage.

  • Muscular microcirculation is impaired and capillary permeability is increased, with resultant fluid leakage and circulatory hypovolemia.


Pathogenesis

  • The damage to the vascular system as a whole can result in capillary leakage, hypovolemia, and shock.

  • Patients with leptospirosis may develop disseminated intravascular coagulation (DIC), hemolytic uremic syndrome (HUS), or thrombotic thrombocytopenic purpura (TTP).


Pathogenesis1

Pathogenesis

  • Leptospiraare present in the water bodies

  • Enter through breaks in the skin ( cuts and abrasions ) and mucous membranes

  • Enters through Mouth – Nose – Conjunctive

  • Rarely enters though ingestion.

  • Incubation period 1 – 2 weeks

  • When multiples blood stream produces fever.

  • May establish organ involvement in Kidney and Liver,

  • May produce hemorrhage and necrosis in the tissues and initiates dysfunction of these organs


Pathogenesis

  • PATHOGENESIS

  • Leptospira-skin,mucosa

  • Initial stage leptospiremia toxic symptoms (1~3days)

  • three symptoms: fever, myalgia, fatigue;

  • three signs: conjunctivalsuffussion; muscle tenderness; enlargement of lymphonodes


Multiorgan involvement

Multiorgan involvement

  • • Ocular

  • – Suffusion – dilation of the conjunctival vasculature,

  • subconjuctivalhaemorrhage, uveitis

  • – Icterusscleral with conjunctival suffusion-pathognomic of Weil’s disease


Multiorgan involvement1

Multiorgan involvement

  • GI

  • – Jaundice not associated with hepatocellular necrosis.

  • Bilirubin, ALT, AST will normalise


Pathogenesis

  • Cardiac

  • – Myocarditis, 1st degree heart block, coronary arteritis


Pathogenesis

  • Hepatitis – Leptospirosis

  • Hepatitis is the frequent complication

  • Elevation of serum creatinephospholipase enzyme raise differentiates from Viral hepatitis where the enzyme is not raised 


Pathogenesis

  • Pulmonary

  • – Spectrum ranging from cough, dyspnoea, haemoptysis to ARDS

  • – Pulmonary haemorrhage may cause death

  • – Radiology reveals diffuse small opacities which may disseminate or coalesce – a sign of intra-alveolar and interstitial haemorrhage


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