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Written by Administrator-GL
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Thursday, 17 July 2008 |
BROWN STOMACH WORM
Ostertagia circumcincta
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Up to 12mm in length- males smaller
Most commonly occurs in areas of rainy winters.
Infective larvae that are picked up in March and April in southern climates will remain in "arrested development" or as "inhibited" larvae for four to five months.
Commonly brought on by stress such as moving.
Larvae in the glands of the abomasum wall cause irritation and erosion of cells. Continual, rapid replacement of damaged cells prevents cellular maturation. Consequently, the abomasum develops a lining of immature cells that are not joined together well and that do not secrete hydrochloric acid and the enzyme pepsinogen, two important elements of digestion. As a result, fluid leaks between cells into the gut. The pH of the gut contents rises from pH2 to pH7, resulting in poor digestion and increased growth of bacteria. The gut becomes more inflamed. Fluid absorption, a major function of the intestine, is blocked, causing profuse, watery diarrhea. Albumin is an important blood protein, of which large amounts may be lost in fluid leaked into the gut. Lost albumin must be replaced from the diet. This is difficult to achieve since improper digestion prevents adequate absorption of nutrients in the intestine.
Ostertagiasis is worsened by the fact that infected animals lose their appetite and do not feed. Weight loss occurs: animals may lose up to 20 percent of their body weight in 7 to 10 days. Death may follow.
Anterior Brown Stomach Worm
Posterior Male Brown Stomach Worm
Hypobiotic larvae – in the abomasum
Images from University of Pennsylvania 2003
Life Cycle
Stage 1: Eggs are deposited in feces.
Stage 2: Approximately 1-2 weeks after leaving the body, eggs produced by adult parasites become infective L3 larvae.
If the eggs dry out before they hatch, they become dormant and can survivie for up to 4 months even in harsh dry hot summer of the south and cold winters of the north.
Stage 3: Molt into L3, which is the infective stage.
After the ruminant ingests the L3 larvae, the parasites invade abomasal glands, develop to adulthood and emerge from the glands in 3 weeks. During emergence, HCL-producing cells (parietal cells) and cells that secrete pepsinogen (chief cells) are damaged. The resulting elevation in abomasal pH prevents conversion of pepsinogen to pepsin thereby disrupting protein digestion. The parasites also destroy epithelium and intercellular junctions, allowing serum proteins and red blood cells to leak into the abomasal lumen, and pepsinogen into the circulation.
Stage 4: Adult worms graze the lining or mucosa and cause irritation and fluid loss, interfering with the digestive function of the stomach. Dyspepsia or "heartburn" results so that feed, especially hot rations such as grain, is not tolerated well. Feed conversion for weight gain, body maintenance, reproductive fitness and milk production is then compromised. Larvae or immature worms invade the gastric glands, which are pits in the lining of the stomach, disrupting normal structure and function of these glands.
Infectious stage: 6 to 7 days
(Minimum number of days for parasite to reach infectious larval stage)
Prepatent period about 17 days.
Prepatent - Period of time between introduction into the body and apparent symptoms
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Site of Infection: Abomasum |
Symptoms of Infection:
- Profuse watery green diarrhea
- Rapid weight loss
- Mild to moderate anemia
- Hypoproteinemia
- Rough haircoat
- Anorexia
- Submandibular edema-bottlejaw.
- Subclinical disease reduces weight gain and productivity.
EGG:
Ostertagia circumcincta eggs appear in fecal exam.
Post Mortem (Necropsy) Findings:
- If the animals have been diarrheal for a few days, worms may have been shed, and the type and severity of gross lesions may also be of considerable diagnostic value.
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Additional Information:
The Parasite
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Last Updated ( Thursday, 17 July 2008 )
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