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

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Presentation Transcript
slide3

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
slide6

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

slide8

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.
slide9

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

  • interstitial nephritis and
  •  Acute tubular necrosis.
slide10

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

slide11

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

slide12

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

slide13

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
slide15

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

slide16

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.
slide17

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
slide19

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
slide22

Cardiac

  • – Myocarditis, 1st degree heart block, coronary arteritis
slide23

Hepatitis – Leptospirosis

  • Hepatitis is the frequent complication
  • Elevation of serum creatinephospholipase enzyme raise differentiates from Viral hepatitis where the enzyme is not raised 
slide24

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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