JPC SYSTEMIC PATHOLOGY
CARDIOVASCULAR SYSTEM
April 2022
C-P02

Signalment (JPC #CG-10):  Horse

 

HISTORY:  This horse had a large thrombosed mesenteric artery

 

HISTOPATHOLOGIC DESCRIPTION:  Artery, mesenteric: The tunica intima, including the endothelium, is diffusely effaced and replaced by fibrin, hemorrhage, edema, 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). There is a large, intraluminal thrombus adherent to the exposed subendothelial connective tissue composed of a abundant polymerized eosinophilic fibrin with entrapped erythrocytes, previously described 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 vasa vasorum vessels. 

 

MORPHOLOGIC DIAGNOSIS:  Artery, mesenteric:  Endarteritis, proliferative and necrotizing, eosinophilic and lymphoplasmacytic, diffuse, severe, with focal thrombus, and intimal larval strongyles, breed not specified, equine.

 

ETIOLOGIC DIAGNOSIS:  Strongylid arteritis

 

CAUSE:  Strongylus vulgaris

 

SYNONYMS:  Large strongyles, aberrant larval migrans, verminous arteritis

 

GENERAL DISCUSSION

• Common pathogen of horses, donkeys, and zebras, but currently less prevalent due to anthelminitic use
• Generally asymptomatic unless thrombosis or vascular damage compromises bowel perfusion; vascular damage due to larval migration is more common 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

 

PATHOGENESIS

• 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

 

LIFE CYCLE

• 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, or 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, D-P24) may be caused by larval penetration of the gut
• Heart: coronary arterial thrombosis (rare); vegetative valvular endocarditis acutely and endocardial caseous and calcareous nodules 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

 

DIFFERENTIAL DIAGNOSIS

• 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

 

COMPARATIVE PATHOLOGY:

• 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

 

Other vascular nematode parasites:

• Ruminants, camelids: “Onchocerciasis”; Onchocerca armillata; parasitizes the wall of the aorta of cattle, water buffalos, goats, and camels
  • Preferentially infects the aortic arch
• Dogs:
  • Dirofilaria immitis (filarid nematode, C-P03, P-P02); American heartworm
  • Angiostrongylus vasorum (family: Metastrongyloidae, P-P02); most pathogenic lung worm of dogs; also infects wild canids
  • Spirocera lupi (family: Spiruridae, C-P01); lesions include esophagus, cardia of the stomach, aorta
  • Dipetalonema reconditum (filarid nematode); non-pathogenic
• Cattle, deer, horses: 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

 

REFERENCES:

1. Bowman DD. Georgis’ Parasitology for Veterinarians. 10th ed. St. Louis, MO: Saunders Elsevier; 2013:419-420.
2. DeLay J, Peregrine AS, Parsons DA. Verminous arteritis in a 3-month-old thoroughbred foal. Can Vet J. 2001;42:289-291.
3. Gardiner CH, Poynton SL. Strongyles. In: An Atlas of Metazoan Parasites in Animal Tissues. Washington, DC; Armed Forces Institute of Pathology:2006; 22-24.
4. Gelberg, HB. Alimentary system and the peritoneum, omentum, mesentery, and peritoneal cavity. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:464.
5. Miller LM, Gal A. Cardiovascular system and lymphatic vessels. In: Zachary JF, ed. Pathologic Basis for Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:685-687.
6. Robinson WF, Robinson NA. Cardiovascular system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 3. 6th ed. St. Louis, MO: Elsevier; 2016:32,61,85-87.
7. Uzal FA, Plattner BL, Hostetter JM. Alimentary system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 3. 6th ed. St. Louis, MO: Elsevier; 2016:216-217.

 

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