Strongylus Vulgaris

~Because we needed to be informed that Strongy is a vulgar bugger. In the meantime, I will keep very tight reigns on my mucous membranes.

~Content Source – Strongylus Vulgaris. Following the fibrin tracks

Pathogenesis due to larval migrations

Strongylus vulgaris is the most pathogenic of the large strongyles because of the prolonged (at least 4 months) and extensive migrations through the mesenteric arterial system and its branches before returning to mature in the cecum and colon.   Larval migrations cause damage to the smooth endothelial surfaces of arteries, providing a focus for clot formation. These clots (thrombi) are accompanied by inflammation and a progressive thickening of the arterial walls.

The time sequence of lesions caused by migrating larvae following experimental infections are summarized in the table below and have been gleaned from many reports in the literature. A summary of these reports has been given by Ogbourne and Duncan in a 1985 publication from the Commonwealth Institute of Parasitology entitled “Strongylus vulgaris in the horse: its biology and importance.

Time sequence of lesions caused by infections with Strongylus vulgaris

  • 0-48 hours after infection – Mucosal hemorrhages in the ileum, cecum and colon.
  • 0-7 days after infection – Inflammation of small intestinal arteries in the submucosa and formation of thrombi along the tracks of migrating larvae. Significant infiltration of neutrophils in the submucosa.
  • 8-10 days after infection – Arteritis extends through the muscularis mucosa to the serosa.
  • 11-21 days after infection – Arteritis extends along all the branches of the ileo-cecal colic artery (supplying the ileum, the dorsal and ventral colon and the cecum) to the cranial mesenteric artery. Arterial walls become thickened and histological sections show a marked cellular infiltration including  neutrophils, macrophages, lymphocytes and plasma cells.
  • 3 weeks-4 months after infection – The wall of the cranial mesenteric artery is thickened and fibrous and thrombi are associated with the presence of 4th stage larvae and immature adults. Fibrin tracks in the aorta associated with some larvae migrating beyond the cranial mesenteric artery.
  • 4-9 months after infection – In the absence of reinfection, arterial lesions  heal. By 9 months after infection, the endothelial lining of affected arteries is smooth again and there are few indications of damage other than histological evidence of fibrosis in arterial walls and the presence of macrophages.

In naturally infected animals, arterial lesions are most commonly seen in the cranial mesenteric artery and its branches. However, lesions have also been found less commonly in other arteries including the abdominal aorta, the renal arteries and the celiac axis.

The walls of the cranial mesenteric and the ileo-ceco-colic arteries are invariably thickened and contain large amounts of thrombus material in which are found S. vulgaris larvae. This lesion is properly called verminous arteritis. The lumen of the cranial mesenteric artery is usually constricted in its diameter due to the thickening of the wall and the presence of thrombi. The lumen of smaller arteries may be entirely occluded.

Some reports in the literature describe aneurysms of the cranial mesenteric artery and its branches. True aneurysms with dilation and thinning of the arterial wall due to a loss of elastic fibres are unusual and  may result from penetration  of the elastic layer of the arterial wall by larvae.

In horses that have died of an acute clinical syndrome, infarction and necrosis of areas of the intestine are usually found at necropsy. These areas of infarction invariably coincide with occlusions (due to thrombi and emboli) in arteries supplying blood to the affected region(s) of the intestine.