JPC SYSTEMIC PATHOLOGY
DIGESTIVE SYSTEM
September 2021
D-P13

 

Signalment (JPC #2317370):  Cow

 

History:  None

 

HISTOPATHOLOGIC DESCRIPTION:  Abomasum, fundus:  Diffusely the mucosa is thickened up to 2mm by elongated and occasionally tortuous, hyperplastic abomasal glands. Multifocally the lamina propria is moderately expanded by lymphocytes, plasma cells, and eosinophils, and there are occasional dense aggregates of lymphocytes within the mucosa (lymphoid nodules). Focally within the deep mucosa are tangential sections of adult trichostrongyle nematodes that are 60µm in diameter and have a 3µm-thick eosinophilic cuticle, multiple longitudinal cuticular ridges, platymyarian-meromyarian musculature, a pseudocoelom, a large digestive tract composed of few multinucleated cells, and reproductive tract containing eosinophilic globular material. Hyperplastic abomasal glands are lined by numerous mucous neck cells (mucous neck cell hyperplasia) that often replace abomasal gland parietal cells (mucous neck cell metaplasia). Abomasal glands are multifocally dilated, lined by attenuated epithelium, and contain cellular and karyorrhectic debris admixed with eosinophils.

 

MORPHOLOGIC DIAGNOSIS:  Abomasum:  Abomasitis, proliferative and eosinophilic, chronic, multifocal, moderate, with parietal cell loss, mucous neck cell hyperplasia and metaplasia, and adult trichostrongyle nematodes, etiology consistent with Ostertagia ostertagi, breed unspecified, bovine.

ETIOLOGIC DIAGNOSIS:  Abomasal ostertagiasis

 

CAUSE:  Ostertagia ostertagi

 

GENERAL DISCUSSION:

• Ostertagiasis is considered the most important parasitic disease of grazing cattle and sheep in temperate climates throughout the world and results in subclinical production loss and clinical disease (diarrhea, wasting, and death in severe cases)
• Common name: Brown stomach worm (difficult to see grossly); microscopically, has prominent longitudinal cuticular ridges (synlophe) that project from the worm when cut transversely
• Family Trichostrongylidae
  • Ostertagia ostertagi and lyrata: Most common in cattle and less common in sheep and goats; rare in horses
  • Teladorsagia (Ostertagia) circumcincta: Most common in sheep and goats

 

LIFE CYCLE: 

• Direct: Eggs in feces develop to infective L-3 larva -> ingested by host -> L-3 exsheaths in rumen; penetrates abomasal glands; undergoes 2 molts to L-5 larva
• Two clinical syndromes: Type I (“summer”) ostertagiasis and Type II (“winter”) ostertagiasis
  • Type I ostertagiasis: Early L-5 larva emerge and mature on the mucosal surface about 3 weeks post infection
    • Seen in lambs and calves at pasture or shortly after a period of high availability of infective larvae; disease is due to the direct development of ingested larvae to adult worms within a relatively short time frame; characterized by chronic gastritis
  • Type II ostertagiasis: Some larvae persist in glands in arrested development (hypobiosis) for up to 4 months before emerging in large numbers and molting to L-5 when environmental conditions improve
    • Usually occurs in yearlings; disease is due to the synchronous maturation and emergence of large numbers of hypobiotic larvae from the mucosa; it occurs when larval intake is low or non-existent; characterized by an acute abomasitis
• Hypobiosis seen at early 4^th stage:
• Northern US: Hypobiosis in fall and winter, emerge in the spring
• Southern US: Hypobiosis in summer, emerge in the fall

 

PATHOGENESIS:

• Larvae damage mucosa > interstitial inflammation and mucous neck cell hyperplasia and metaplasia
• Parietal cells replaced by mucous neck cells (mucous cell metaplasia) > decreased HCl secretion (achlorhydria) > increased abomasal pH (up to 7 or more)
  • Pepsinogen not converted to pepsin > decreased protein digestion (hypoproteinemia); increased plasma pepsinogen levels; bacterial overgrowth in intestines > diarrhea
  • Blood gastrin increases as body tries to stimulate acid secretion (hypergastrinemia) > central effect on satiety center and decreased GI motility > decreased appetite
• Inflammation > increased vascular permeability > leaky junctions between hyperplastic mucous cells > protein loss into abomasum

 

TYPICAL CLINICAL FINDINGS:

• Cardinal signs in sheep and cattle: Loss of appetite, diarrhea, and wasting
• Clinical pathology:
  • Hypoproteinemia  
  • Achlorhydria
  • Elevated plasma pepsinogen
  • Hypergastrinemia
  • Abnormally elevated abomasal pH (>4.5)

 

TYPICAL GROSS FINDINGS: 

• Widespread areas of irregularly thickened mucosa with a convoluted surface pattern (“Morocco leather”)
• Worms are brown and threadlike, but difficult to see on mucosa unaided
• Submandibular edema due to hypoproteinemia (bottle jaw) is most commonly associated with Haemonchus contortus

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Thickened abomasal mucosa; mucus neck cell hyperplasia/metaplasia; decreased parietal cells; mucosal lymphoid nodules
• Lamina propria infiltrated by eosinophils, lymphocytes, plasma cells, globule leukocytes; few neutrophils
• Trichostrongyles
  • Cuticle with external longitudinal cuticular ridges (synlophe)
  • Platymyarian-meromyarian musculature
  • Large intestine composed of a few multinucleated cells
  • Lateral chords
  • Eggs are thin-shelled and contain a morula

 

ADDITIONAL DIAGNOSTIC TESTS: 

• Fecal flotation
• Elevated plasma pepsinogen
• Hypergastrinemia
• Serum antibodies

 

DIFFERENTIAL DIAGNOSIS: 

For gross lesions:

• Ruminant abomasal nematodes: Hemonchus , Ostertagia sp. and Trichostrongylus axei. (HOT); all trichostrongyles with similar morphology
  • Hemonchus contortus (sheep and goats) and placei (cattle): “Barber pole worm”; 2cm long, red and white females, red males; adults and L-4 attach to mucosa and suck blood; anemia; hypoproteinemia/edema; edematous and hemorrhagic abomasal rugae; reddish brown/bloody abomasal contents
  • Trichostrongylus axei: Cattle, sheep, goats, and horses; similar lesions to Ostertagia sp. (mucous metaplasia/hyperplasia, decreased parietal cells, erosions, eosinophilic and lymphoplasmacytic inflammation), smooth cuticle (lack ridges), intraepithelial tunnels, usually occur with other GI parasites, may also infect small intestine
• Lymphoma: Multiple nodules that are variable in size
• Other causes of mucous neck cell hyperplasia and parietal cell loss (metaplasia)
  • Chronic hypertrophic gastritis: Idiopathic; occurs in dogs (giant hypertrophic pyloric gastropathy of older small dogs; giant hypertrophic gastropathy of Basenjis and humans (Menetrier disease); possibly immune mediated

 

COMPARATIVE PATHOLOGY:

Trichostrongyle stomach nematodes in other species:

• Teladorsagia circumcincta in sheep
• Ollulanus tricuspis in cats
• Trichostrongylus axei in horses
• Hyostrongylus rubidus in swine; causes thin sow syndrome
• Nochtia nochti in nonhuman primates
• Genera Teladorsagia, Marshallagia, Spiculopteragia, and Camelostrongylus in non-domestic ruminants (including farmed deer): Can be primary cause of Ostertagiosis-like syndrome

 

REFERENCES:

1. Gardiner CH, Poynton SL. An Atlas of Metazoan Parasites in Animal Tissues. Washington, DC: Armed Forces Institute of Pathology; 1999:26.
2. Jones MEB, Gasper DJ, Mitchell E. Bovidae, antilocapridae, giraffidae, tragulidae, hippopotamidae In: Terio KA, McAloose D, St. Leger J ed. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier Inc. 2018:138.
3. Gelberg HB. Alimentary system and the peritoneum, omentum, mesentery, and peritoneal cavity. In: Zachary JF, McGavin MD, eds. Pathologic Basis of Veterinary Disease. 6^th St. Louis, MO: Elsevier Mosby; 2017:400.
4. Uzal FA, Plattner BL, Hostetter JM. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. Philadelphia, PA: Elsevier Ltd; 2016:205-207.

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