Bunostomum

Bunostomum spp.
Kingdom Eukaryota
Phylum Nematoda
Class Secernentea
Sub-class Rhabditia
Order Strongylida
Family Ancylostomatidae
Genus Bunostomum
Species Bunostomum spp.

Also Known As: Hookworm Dermatitis — Bunostomosis

Caused By: Bunostomum phlebotomum — B. trigonocephalum

Introduction

Bunostomum spp. are small intestinal endoparasites of large and small ruminants and camelids. B. phlebotomum is seen primarily in calves and B. trigonocephalum in lambs.

They are greyish-white worms, 1-3cm in length and stout in stature, especially when compared to other nematodes. Their anterior end is bent dorsally giving them a hooked figuration. The buccal capsule is funnel shaped and bordered with a pair of chitinous cutting plates which serve to attach the parasite to the intestinal mucosa. They are usually only found in the proximal few metres of the small intestine.

Eggs of Bunostomum spp. are irregular and ellipsoid, thin shelled and have 4-8 blastomeres.

These parasites can cause both gastrointestinal disease and also integumentary damage during percutaneous invasion.

Signalment

Young animals 5-8 months old are most commonly infected.

100-200 B. phlebotomum and 20-100 B. trigonocephalum is adequate to cause disease in calves and lambs respectively and burdens of 2000 and 300 worms respectively are large enough to cause mortality.

Older animals often carry worms asymptomatically.

Lifecycle

Bunostomum spp. have a direct lifecycle, taking 24-36 hours to hatch and 5-16 days to develop into ensheathed L3 infective larvae.

Hot weather restricts survival on pasture to 6-7 weeks, and the larvae/eggs do not survive the winter on pastures in temperate countries.

The percutaneous route of infection is most important but animals can also acquire infection orally. Larvae then migrate to the lungs and trachea, reaching the intestine after they are coughed up and swallowed. Larvae moult both in the lungs and when they reach the abomasum or intestine.

Eggs are shed into the faeces by infected individuals.

The pre-patent period is 7-9 weeks and maximal parasite longevity is 1-2years.

Clinical Signs

Direct digestive signs of disease include diarrhoea which often contains mucus and/or blood, anorexia, inappetance and weight loss or stunted growth. Hypoproteinaemia due to parasitic consumption may cause peripheral oedema, e.g. bottle-jaw.

Consequent bleeding and fluid loss often causes anaemia and/or dehydration and associated pallor, prostration, emaciation and weakness.

Signs of pain and discomfort will vary with the individual.

Skin disease usually manifests in the feet and limbs as pruritus, erythema, oedema, alopecia, hyperkeratosis and papule/pustule formation. The coat in affected areas is often rough and poor and easily epilated. Claws and hooves also exhibit defective growth, fragility and overgrowth.

Larval migration through the lungs may also cause a cough and other respiratory signs.

Recovery results in partial protection to reinfection but adults may then carry and shed worms.

Diagnosis

At necropsy, adults can be demonstrated in the proximal segments of the small intestine and identified microscopically.

Eggs can also be detected by the floatation technique and morphologically identified. They cannot be differentiated from Trichostrongylid spp. or Oesophagostomum spp. unless faecal samples are fresh.

Treatment

All commercial endoparasiticides are effective and resistance is not currently a significant problem.

Control

Avoidance of marshy and damp areas for grazing stock and prophylactic worming regimes are the usual control measures implemented.


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References


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This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 31 July 2011.