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Cardiovascular: parasitic arteritis

ISSN 2398-2977


Synonym(s): verminous arteritis

Introduction

  • Cause: lesions in wall of major arteries attributable to migratingStrongylus vulgarislarvae   Strongylus spp  .
  • Signs: lesions in cranial mesenteric artery implicated in some cases of colic   Abdomen: pain - adult  .
  • Diagnosis: history and clinical signs.
  • Treatment: depends upon presentation.
  • Prognosis: depends upon severity of condition. Severity of colic induced ranges from mild, recurrent, to severe, rapidly fatal. Aneurysms may rupture and lead to sudden death.

Presenting signs

  • A localized inflammatory response in the artery is the most common presentation   →   embolic occlusion of larger or smaller mesenteric arteries   →   focal ischemia of jejunum, colon or cecum   →   colic.

Acute presentation

  • Occasionally see ruptured aneurysms of cranial mesenteric artery with catastrophic blood loss into the abdomen and profound anemia.
  • Or bleeding may be limited after rupture (eg hematoma confined within mesentery) and no effect on mucous membranes.
  • Aortic rupture due to aneurysm occurs most commonly between right coronary artery and brachiocephalic trunk where parasitic arteritis involved and leads to sudden death   Aorta: rupture  .
  • Pulmonary artery/renal artery rupture occasionally.

Age predisposition

  • More commonly seen in horses <6 years old.

Cost considerations

  • May be fatal, or require abdominal surgery.

Special risks

  • Care must be taken with anesthesia as horse compromised due to blood loss/shock.

Pathogenesis

Etiology

Predisposing factors

General
  • Poor management - failure to implement adequate deworming program.

Pathophysiology

  • Larval migration   →   arteries   →   localized inflammation   →   embolic occlusion   →   infarction   →   areas of devitalized intestine and subsequent colic.
  • May   →   ballooning of artery (aneurysm)   →   rupture.
Thromboembolic colic
  • Arteritis most commonly occurs at root of cranial mesenteric arteries, or occasionally the renal arteries.
  • MigratingStrongylus vulgarislarve   →   damage to tunica intima of cranial mesenteric arteries/aorta   →   narrowing of lumen, or localized (often severe) arteritis with variable numbers of larvae.
  • Changes in the vessel wall (especially exposure of collagen) encourage platelet adhesion   →   release reaction   →   platelet aggregation which along with fibrin   →   thrombus formation.
  • Sites of arterial damage   →   turbulent blood flow   →   eddy currents   →   allow platelets to settle on endothelial surface.
  • Colic commonly results due to embolic occluson of mesenteric arteries   →   focal ischemia of jejunum, colon or cecum.

Aneurysm formation

  • Destruction/disruption to muscular layer   →   localized enlargement/ballooning (aneurysm) of arterial wall.
  • Aneurysms may rupture   →   catastrophic blood loss and possibly sudden death, especially if aorta involved.

Timecourse

  • Colic may be mild, intermittent and recurrent, or may be of rapid onset and progression.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Poole A W (1993)Thrombosis in the horse - the role of platelets in its pathogenesis and therapy. Equine Vet Educ (2), 99-102 (A comparison between platelet function in the horse and other species related to anti-thrombotic therapy both present and future) VetMedResource.
  • Drudge J H (1979) Clinical aspects of Strongylus vulgaris infection in the horse. Vet Clin North Am Pract (2), 251-265 PubMed.