Strongylus vulgaris
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 teh 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.
