Vasculitis

VASCULITIS

Arteritis

  • Parasitic arteritis is a very common form of arterial disease in animals .
  • The lesions are characterized by inflammatory reaction and thickening of the arterial wall, often accompanied by endothelial damage and thrombosis.  
  • Thrombi may partially or completely occlude the artery and emboli arising from pieces of thrombi that have broken loose may occlude vessels distal to the site where parasites have lodged.Rupture of arteries as a result of parasitic lesions is rare.

Etiology

  • The two parasite species which cause by far the most severe damage to arteries are strongylus vulgaris in horses and Dirofilaria immitis in dogs.
  • Other species eliciting varying degrees of arteritis are Onchocerca armillata in cattle, Elaeophora schneideri in sheep, Angiostrongylus vasorum and Spirocerca lupi in dogs, and Aelurostrongylus abstrusus in cats.
  • Strongylus vulgaris is often referred to as the most important parasite of horses. It is widely distributed and infects horses of all ages, fatal natural infection having been observed in foals as early as 21 days after birth.

Pathogenesis

  • The pathogenesis of Strongylus vulgaris infection is associated with the larval migration of the parasite through the tissues of the host.
  • Third-stage infective larvae ingested by the grazing animal penetrate the wall of the intestine, molt in the submucosa to become fourth-stage larvae, and invade terminal branches of intestinal arteries to begin their migration.
  • This penetration and early migration of larvae results in inflammatory reactions and small haemorrhages throughout the intestinal wall. This coincides with the rise in body temperature detected 5–7 days after heavy infections.
  • The temperature reaction generally subsides as the fourth-stage larvae migrate in the intima of the mesenteric arteries causing inflammatory reactions and mural thrombi.
  • By 2–3 weeks post-infection the larvae reach the cranial mesenteric artery where they remain for several months. They molt to become fifth-stage larvae and eventually return to the lumen of the large intestine where they complete their maturation and start producing eggs 6–7 months after infection.
  •  During their long stay in the cranial mesenteric artery, the larvae induce a severe fibrinous inflammatory reaction which can involve all layers of the arterial wall (verminous arteritis).
  • In chronic infections, the wall of the artery becomes thickened and the lumen partly occluded by thrombi, cellular debris, and larvae which remain firmly attached to the intima.

Clinical Presentation 

  • Clinical signs in animals include
    • dullness,
    • progressive weight loss and
    • varying degrees of pyrexia,
    • often with intermittent abdominal discomfort.

  • At post mortem, aneurysmal dilatation of the artery may sometimes be observed. Larval migration of Strongylus vulgaris was generally recognized as a major etiological factor of equine colic, although its incidence is decreasing due to the availability of efficient anthelmintics.
  • Acute colic due to thromboembolic infarction of the caecum or large intestine is a well-documented complication of verminous enteritis. Colic signs have also been observed in early massive infections, before verminous lesions develop in the cranial mesenteric artery.
  • Possible mechanisms for colic include damage to and impairment of nervous innervation to the intestine by migrating larvae, release of toxins by degenerating larvae, and hypersensitivity or allergic reactions to Strongylus vulgaris . A diarrhoeic syndrome in field cases of verminous arteritis has also been described.
  • The pathophysiology is poorly understood but it may be a response to altered intestinal circulation, local irritation and/or severe ulceration of the mucosa of the caecum and colon caused by thromboembolism.
  • Clinical signs and lesions have been associated with aberrant larval migration in the aorta, coronary, iliacic, spermatic and renal arteries, and in the heart, kidney, brain and spinal cord.

Spirocerca lupi associated vascular damages

  • The spiruroid worm Spirocerca lupi is primarily a parasite of dogs. The major clinical signs of spirocercosis are associated with the presence of adult worms in the oesophagus.
  • However, significant lesions are also caused by the migrating larvae which spend about 3 months in the adventitia and media of the aorta.
  • Aortic lesions include the formation of small nodules containing larvae, thickening of the intima and media, and deposition of atheromatous plaques.
  • Weakness of the aortic wall and partial rupture of the layers sometimes leads to the development of shallow aneurysmal pouches, with possible rupture and fatal hemorrhage. In most cases, aortic lesions do not produce any clinical signs.
Last modified: Tuesday, 5 June 2012, 1:46 PM