Ostertagia ostertagi (Brown Stomach Worm)

TABLE OF CONTENTS

Ostertagia ostertagi (Brown Stomach Worm): Morphology, Life Cycle, Pathogenesis, Clinical Signs, Diagnosis & Treatment

Ostertagia ostertagi, commonly known as the brown stomach worm, is one of the most important gastrointestinal nematodes affecting cattle worldwide. It primarily inhabits the abomasum, where it damages the gastric glands, leading to impaired digestion, reduced productivity, diarrhea, weight loss, and significant economic losses in the cattle industry.

This article provides a comprehensive overview of Ostertagia ostertagi, including its taxonomy, morphology, life cycle, pathogenesis, clinical signs, diagnosis, and treatment. The content is designed for veterinary students, veterinarians, and competitive examination preparation.

Parasite Overview

Common Name: Brown stomach worm
Host: Sheep, goats, and cattle
Predilection Site: Abomasum; rarely the small intestine
Life Cycle: Direct life cycle (no intermediate host)

Taxonomical Classification

Kingdom: Animalia
Phylum: Nematoda
Class: Chromadorea
Order: Strongylida
Superfamily: Trichostrongyloidea
Family: Trichostrongylidae
Subfamily: Ostertagiinae
Genus: Ostertagia
Species: Ostertagia ostertagi
Common Name: Brown stomach worm of cattle

Morphology

Worms are slender.
The cuticle at the anterior end is slightly inflated and transversely striated.
In females, the vulval flap is absent.
Spicules are short, pigmented, with brown ends and 2/3 processes.

Life Cycle

Adult worms inhabit the abomasum of ruminants and produce eggs that are passed in the feces.
Under favorable environmental conditions, eggs hatch into first-stage larvae (L1), which develop into second-stage larvae (L2) and then into the infective third-stage larvae (L3) on pasture.
Animals become infected by ingesting infective L3 larvae while grazing.
After ingestion, L3 larvae exsheath in the rumen and migrate to the abomasum, where they penetrate the gastric glands.
Within the gastric glands, larvae develop into fourth-stage larvae (L4) and then immature adults (L5).
Immature adults emerge from the gastric glands into the lumen of the abomasum, where they mature into adult worms and begin egg production.
Some L4 larvae may undergo hypobiosis (arrested development) within the gastric glands during unfavorable environmental conditions and resume development when conditions become favorable.

Pathogenesis

Reduces the functional gastric gland mass and damages the gastric mucosa.
Causes hyperplasia and thickening of the mucosa.
Produces circular nodules measuring 2–3 mm in diameter, with a central orifice, due to extensive cell division and mucosal hyperplasia.
In heavy infections, the mucosa becomes hyperplastic, giving a “Morocco leather” appearance. Oedema, necrosis, and sloughing of the abomasal mucosa occur, along with hypoalbuminemia due to increased permeability of the abomasal epithelium to pepsin and plasma proteins.

Clinical Signs

Abomasitis, oedema, necrosis, decreased albumin levels, anorexia, and profuse watery diarrhoea (bright green in color) due to the failure of the abomasum to denature chlorophyll. Morbidity is high.

The abomasal mucosa is thickened and oedematous, with oedema of the abomasum, decreased serum protein and albumin levels, and elevated plasma pepsinogen levels. Soiled hindquarters, anaemia, submandibular oedema, and loss of body weight are also observed.

Diagnosis

Clinical signs, fecal examination, and fecal culture.
Estimation of plasma pepsinogen levels.