Oesophagostomum (Nodular worm)

Oesophagostomum: (Nodular worm)

Oesophagostomum species are responsible for en­teritis in ruminants and pigs. The more pathogenic species in ruminants occur in the subtropics and trop­ics and are associated with nodule formation in the intestine.

Major Species	Hosts	Location/Site	Distribution
Oesophagostomum columbianum	sheep and goat	Caecum and colon	Worldwide, more important in tropical and subtropical areas
Oesophagostomum venulosum	sheep and goat
Oesophagostomum radiatum	Cattle and Buffalo
Oesophagostomum dentatum	Pig
Oesophagostomum quadrispinulatum

Other species found in the pig are Oe. longicaudatum, Oe. granatensis and Oe. brevicaudum and in sheep and goats Oe. asperum.

Identification                                                                                              

Gross:

• Stout white worm 1.0-2.0 cm long.
• Readily differenti­ated by its tapered head from Chabertia.

Microscope:

• The buccal capsule is small. In many species it is sur­rounded by leaf crowns.
• The external crown, if present, is compressed and so there is only a narrow opening into the buccal capsule.
• Around the anterior oesophagus there is an inflated cuticular cephalic vesi­cle (Fig.). This terminates in a cervical groove which is followed in some species by broad cervical alae.
• The position of cervical papillae and the leaf crown arrangements are used to identify species.

Epidemiology

• In temperate areas, there is evidence that Oe. Venulosum undergoes hypobiosis at the L₄ stage in sheep during autumn and winter.
• In the pig species, Oe. Dentatum and Oe. Quadrispinulatum, survival of both free-living L₃ on the pasture and hypobiotic L₄ in the host occur during autumn and winter; the hypobiotic larvae complete their development in the spring often coincident with farrowing. There is also some evidence that larvae develop in faeces on the skin of pigs and it seems likely that, in housed animals, transmission is by contact between sows and their litters, infection occurring either orally or percutaneously. Pen to pen transmission may also occur via dipteran flies which can carry L₃ on their legs.
• In tropical and subtropical areas, Oe. Columbianum and Oe. Radiatum, in sheep and cattle respectively, are especially important. In Oe. Columbianum infections, the prolonged survival of the L₄ within the nodules in the gut wall and the lack of an effective immunity made control difficult until the advent of effective anthelmintics. In contrast, cattle develop a good im­munity to Oe. Radiatum, partly due to age and partly to previous exposure so that it is primarily a problem in weaned calves.

Life Cycle:

The adult parasites live in the caecum and colon

 

Eggs passed in the feces and development of L₃ occurred in environment

Final host get infected by the ingestion of L₃

L₃ enter the mucosa of any part of the small or large intestine and in some species (Oe. columbianum, Oe. radiatum, Oe. quadrispinulatum) become enclosed in obvious nodules in which to L₄ takes place

These L₄ then emerge on to the mucosal surface, migrate to the co­lon, and develop to the adult stage

PPP: 45days

Note:

• there is limited evidence that skin penetration is possible, at least in pigs
• On reinfection occurred by the larvae which remain arrested as L₄ in nodules for up to one year.
• however, with Oe. Venulosum nodules are absent while in Oe. Dentatum they are barely visible.

Pathogenesis

• All species are capable of causing a severe enteritis including Oe. Venulosum, which does not provoke nodule formation.
• In the intestine Oe. Columbianum L₃ migrate deep into the mucosa, provoking an inflammatory response with the formation of nodules which are visible to the naked eye.
• On reinfection, this response is more marked, the nodules reaching 2.0cm in diameter and containing greenish eosinophilic pus and an L₄. When the L4 emerge there may be ulceration of the mucosa.
• Diarrhoea occurs coincident with emergence about a week after primary infection and from several months to a year after reinfection.
•  In heavy infections, there may be ulcerative colitis and the disease runs a chronic debilitating course with effects on the production of wool and mutton.
• The nodules in the gut wall also render the intestines useless for processing as sausage skins and surgical suture material.
• In Oe. radiatum infections in cattle, the pathogenic effect is also attributed to the nodules (up to 5.0mm in diameter) in the intestine and it appears that as few as 500 larvae are sufficient to produce clinical signs.
•  Necropsy reveals a severely inflamed mucosa studded with yellowish-green purulent nodules.
• In the later stages of the disease, anaemia and hypoalbuminaemia develop due to the combined ef­fects of protein loss and leakage of blood through the damaged mucosa.
• Oesophagostomum infections in the pig are less of­ten associated with clinical disease, but are responsible for poor productivity.

Clinical Signs:

In acute infections in ruminants:

·         Severe dark green diarrhoea (the main clinical sign)

·         rapid loss of weight and sometimes submandibular oedema.

In chronic infections (which occur primarily in sheep):

• inappetence and emaciation with intermit­tent diarrhoea and anaemia are the main signs of oesophagostomosis.
• Pregnant sows show inappetence, become very thin, and following farrowing; milk production is reduced with effects on litter performance.

Diagnosis:

• Clinical History with epidemiology
• Clinical signs
• Coproscopy
• Note: Since the acute disease occurs within the prepatent period, eggs of Oesophagostomum spp. are not usually present in the faeces. In the chronic disease eggs are present and L₃ can be identified following faecal culture.
• PM examination

Treatment and Control

• The treatment and control of ruminant infections with Oesophagostomum spp. is similar to that of the trichostrongyles.
• Anthelmintics therapy