JPC SYSTEMIC PATHOLOGY
HISTORY: This horse had a large thrombosed mesenteric artery
HISTOPATHOLOGIC DESCRIPTION: Artery, mesenteric: The endothelium and tunica intima are diffusely effaced and replaced by fibrin, hemorrhage, necrotic debris, fibrous connective tissue and many enmeshed eosinophils, plasma cells and macrophages; the internal elastic lamina is effaced and the tunica media is multifocally expanded by abundant fibrous connective tissue, proliferative smooth muscle and fibrin admixed with eosinophils, lymphocytes, plasma cells, hemosiderin-laden macrophages, hemorrhage, small caliber blood vessels and necrotic cellular debris (proliferative and necrotizing endarteritis). Abundant polymerized fibrin is forming a large intraluminal thrombus composed of an eosinophilic, fibrillar mesh that entraps erythrocytes, inflammatory cells and multiple cross and tangential sections of larval nematodes up to 220 um in diameter with a smooth 6 um thick cuticle, platymyarian-meromyarian musculature, prominent lateral cords, a pseudocoelom, and a large, central intestine lined by few multinucleated cells with a prominent brush border (true strongyle larvae). The adventitia is infiltrated by low numbers of lymphocytes and eosinophils surrounding vessels.
MORPHOLOGIC DIAGNOSIS: Artery, mesenteric: Endarteritis, proliferative and necrotizing, eosinophilic and lymphoplasmacytic, diffuse, severe, with focal thrombus, and subendothelial larval strongyles, breed not specified, equine.
ETIOLOGIC DIAGNOSIS: Strongylid arteritis
CAUSE: Strongylus vulgaris
SYNONYMS: Large strongyles, aberrant larval migrans, verminous arteritis
- Common pathogen of horses, donkeys, and zebras, but less prevalent due to anthelminitic use
- Generally asymptomatic unless thrombosis or vascular damage compromises bowel perfusion
- Vascular larval migration causes damage, especially in foals
- Acute infections: vegetative valvular endocarditis
- Chronic infection: caseous and calcareous nodules adhered to the endocardium to include, but not limited to the left ventricular apex
- Horses ingest L3 larvae from contaminated grass, hay or water
- Peak pasture egg counts from July through September
- Worms have predilection for cranial mesenteric artery and its extensions due to the random-walk theory, follow vessel curvature; most larvae won’t enter the aorta due to the perpendicular connection with the aorta
- Larvae cannot cross the internal elastic lamina of blood vessels; larvae enter the vasculature in small arterioles which lack an internal elastic lamina, once they migrate to the larger arteries with internal elastic lamina they are confined to these vessels until the later stages of the lifecycle
- Eggs excreted in feces > hatch in 24-48 hours > L1 larvae serially molt to ensheathed L3 larvae > L3 larvae ingested and exsheath in small intestine > penetrate mucosa/submucosa of ventral colon or cecum > molt to L4 larvae > penetrate submucosal arterioles > migrate in or along the intima to the cranial mesenteric artery (CMA) > after 2-4 months, L4 larvae carried by blood to intestinal subserosal arteries > molt to L5 larvae > L5 exsheath > enter intestinal lumen as immature adults > reach sexual maturity by 6-7 months post-infection
TYPICAL CLINICAL FINDINGS
- Usually no clinical signs; debilitating disease more common in foals
- Large parasite burdens: Weakness, emaciation, anemia, diarrhea
- Possible etiologies for resultant colic:
- Thromboembolic infarction of a section of bowel
- Thickened mesenteric vessels causing increased pressure on abdominal autonomic plexi and interfering with gut innervation
- Response to toxic products from degenerating larvae
- Aberrant migration: Possibly CNS signs and hind limb lameness, renal infarction
TYPICAL GROSS FINDINGS
- Usually in cranial mesenteric artery and extension to the ileo-cecocolic artery; may also be found in the aorta or in the renal, spermatic and celiac arteries
- Varies from barely perceptible tortuous intimal tracks to thickened vessel walls with rough intimal surfaces and layered thrombi; may have verminous aneurysm (vessel wall is thickened and sacculated or rarely ruptures)
- L4/L5 larvae attach to the arterial intima; adults attach to mucosa of the cecum and large intestine
- Subserosal hemorrhage (hemomelasma ilei) may be caused by larval penetration of the gut
- Heart: coronary arterial thrombosis (rare); vegetative valvular endocarditis acutely and endocardial caesous and calcareous nodules on the endocardium chronically; lesions may also be present in the aorta
- Kidney: renal arterial verminous arteritis (rare)
- CNS: embolism of the brachiocephalic trunk
TYPICAL LIGHT MICROSCOPIC FINDINGS
- Acute: focal vasculitis with fibromuscular, elastic repair
- Chronic: marked increase in connective tissue with vascular smooth muscle hyperplasia
- Verminous arteritis: L4 larvae in the intima of arteries with lymphocytes, neutrophils and eosinophils; proliferation of the intima, adventitia, and endothelium; occasional hemorrhage and necrosis; associated fibrin, cellular debris and lymphocytes; L5 larvae in nodules in the intestinal arteries, surrounded by necrotic debris, neutrophils and fewer eosinophils and macrophages
- Intimal, nodular mineralization in the aorta
- Narrowing of vessel lumina
- Sites of larval translocation from intestine to vessels: Multifocal mucosal and submucosal hemorrhage with lymphocytes, neutrophils and eosinophils
- Submucosal arteries may contain larvae and thrombi
ADDITIONAL DIAGNOSTIC TESTS
- Fecal exam
- Small strongyles (cyathostomes): Synchronous emergence may cause hemorrhagic enteritis, hypoalbuminemia and weight loss; they are generally nonpathogenic
- edentatus: The larvae migrate via the portal system to the liver and eventually return to the cecum where they mature into adults. Migrating larvae may cause hemomelasma ilei and fibrin tags on the liver capsule
- equinus: Migrate through peritoneal cavity to liver, then pancreas; re-enter the cecum/right ventral colon by direct penetration
- Arterial migration of strongyles is unique to horses
- Other large strongyles and their hosts:
- Equids - Strongylus, Triodontophorus, Oesophagosdontus, Craterostomum
- Elephants - Decrusia, Equinurbia, Choniangium
- Macropod marsupials - Macropicola, Hypodontus
- Ostriches - Codiostomum
- Ruminants: “Onchocerciasis”; Onchocerca armillata; parasitizes the wall of the aorta of cattle, water buffalos, goats, and camels
- Preferentially infects the aortic arch
- Dogs: Dirofilaria immitis (family: Onchocercidae); American heartworm
- Angiostrongylus vasorum (family: Metastrongyloidae); most pathogenic lung worm of dogs; also infects wild canids
- Spirocera lupi (family: Spiruridae); lesions include esophagus, cardia of the stomach, aorta
- Dipetalonema reconditum (family: Onchocercidae); non-pathogenic
- Elaephoriasis (family: Ochocercidae)
- Cattle: Elaeophora poeli often infects hosts tropical climates; inhabits the aorta
- Mule deer and black tailed deer: Elaeophora schneideri; found in the arteries
- Horses: Elaeophora bohmi; low numbers of Austria horses affected with arteries and veins of the metacarpus, metatarsus, and distal extremities mostly affected
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