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12.1.1 Equine Mouth
*(of primary importance in USA) First instars in mucosa of oral cavity nearly one month (21-28 days) before molting and development to 2nd instar which passes on to stomach where they are more pathogenic.
12.1.2 OVINE
1. Elaeophora schneideri - Skinworm - 6.12cm - Nematode Microfilariae in mucosae of mouth and nasal cavity where lesions are observed - see blood vascular system.
12.1.3 Canine
1. Trichomonas canistomae- trichomonad - 7-12 microns - protozoa
12.1.4 Feline
1. Trichomona felistomae - trichomonad - 6-11 microns Protozoa. The above two protozoa are nonpathogenic.
12.1.5 Poultry
1.Trichomonas gallinae trichomonad6-19 microns - Protozoa.
(See crop esophagus proventriculus) Lesions seen in mouth of pigeon in addition to the above locations.
1. Gongylonema pulchrum
Esophageal or gulletworm -145mm - nematode. Hosts are sheep, cattle, pigs, goat, zebra, buffalo, less common in horse and camels the, donkey and boar and rarely in man. May occur also in tongue and on the lips.
The adult worm lies in a zigzag fashion embedded in the mucosa or submucosa. The cuticle of the anterior end possesses a large number of round or oval thickenings (blebs). Cervical alae are well developed. Tail end of the male is alate and asymetrical with a number of papillae.
Life Cycle
Indirect: Larvated eggs pass in feces, hatch after being ingested by coprophagous beetle and develop to the infective stage. Infection of definative host occurs with the ingestion of infected beetles. Larvae probably excysts in stomach and migrate to the oral cavity and esophageal mucosa. The primary lesion is a mild catarrhal inflammatory reaction.
Diagnosis
Is rarely made clinically except on necropsy examination - such findings on meat inspection renders this organ as unfit for human consumption. This genus belongs to a group of nematodes commonly referred to as spiurids described below under the super family Spiuroides.
2. Hypoderma bovis larvae "oxwarbles"
Dipterous - arthropod
3. Hypoderma lineatum larvae
"Oxwarbles" Dipterous-arthropod (see subcutis and skin parasites)
1. Life Cycle:
(Where known) involve an arthropod intermediate host. Transfer hosts are often important in epidemiology.
2.Eggs are usually thick shelled:
Contain a larva (ovoviviparous) and do not hatch until ingested by the arthropod.
3. A pharnx or cyclindrial buccal capsule is usually present.
Two lips (or divisions there of)are present.
4. Hind end of males
Is usually spirally coiled and bears lateral caudal alae papillae, and spicules. There is no copulatory bursa. Most of the genera inhabit the upper digestive tract.
Genera of importance: Gongylonema, Spirocerca, Physaloptera, Draschia, Tetrameres Acuria.
Spirocerca lupi - "Esophageal worm 80mm - nematodes"
- a. Hosts - Spirocerca lupi is found in the esophagus the stomach, and the aorta of the dog and wild canidae such as the coyote, the fox and the wolf.
- b.Incidence - Common in most warm countries of the world. In the U.S.it occurs primarily in the Southeast. The worms are fairly large and relatively thick and are blood red in color.
1. Arthropod intermediate hosts:
Dung beetles: Eggs in the feces of infected dogs do not hatch until they are ingested by one of several species of adult coprophageous beetles (especially Geotrupes blackburnii). In which the infective third stage larvae develop and encyst in the insects trachea tubes. Infected dung beetles are then ingested by the definitive host (dog) or any of a large number of transport (paratenic) hosts.
2. Transfer hosts:
Various birds small mammals, amphibians and reptiles.
An exceptionally wide variety of animals can serve as transfer hosts. Transfer hosts are basically unsuitable hosts and the larvae do not develop to maturity but again encyst as third stage infective larvae. Encystment usually is in the walls of the intestinal tract or in the mesentery. Encystment in other organs occurs occasionally.
3. Definitive host:
The dog as the definitive host is infected by eating the beetles directly or by ingestion of transfer host tissues. In eithercase, the larvae excyst in the stomach and being a complex migration pattern.
4. Lesions and migration pattern:
First the larvae penetrate the wall of the stomach and migrate into the adventitia of the arteries draining the stomach and concentrate in the wall of the thoracic aorta in about 3 weeks. (Inflammation and scarring occur During this 3 week period a molt takes place to the fourth stage. Then several things can happen.
a. Esophageal granuloma:
Most worms then pass to the wall of the esophagus by tranversing the connective tissue or the walls of small arteries. The worms are usually in the esophageal wall by the end of the third month and cause the formation of a granuloma of variable size. (Sometimes just a swelling, other times a large pedunculated mass). A fistulous communication is established to the esophageal lumen and patency occurs in the fifth or 6th month.
b. Aortic Nodules or Aneurysms:
Some may remain in the wall of the aorta and lead to formation of nodules or aneurysms as the typical lesion.
c. Ectopic sites:
As with most migrating parasites, abnormal sites are sometimes reached. Worms can encyst somewhere along the migration route or they may mirate in the wrong vessels or tissues (even after reaching the thoracic aorta) and reach ectopic sites such as the stomach, trachea, subcutaneous tissues or the urinary bladder.
d. Ossifying spondylitis:
There is sometimes an associated ossifying spondylitis adjacent thoracic vertebra, apparently due to irritaton by migrating larvae.
e. Associated Osteosarcoma and Hypertrophied Pulmonary Osteoarthropathy.
Finally, there seems to be a strong association of Spirocerca with the formation of a highly malignant osteosarcoma. This can occur with any dog, but there is a marked breed predisposition to malignancy formation in hounds, pointers and setters. About 90% of esophageal sarcomas in the dog are associated wiith this parasite. Malignancy is usually seen in 5-7 year old animals. Often a presumptive diagnosis can be made even without finding worms because the lesions are so characteristic. If this happenens, it leads to a very large mass in the whole area and metastasis to the lungs and other tissues. Also, it can lead to hypertropic pulmonary osteoarthropathy. (A thickening of the distal long bones associated with a space occupying lesion in the thorax).
5. Clinical Signs:
Clinical signs associated with Spirocerca vary depending on where the major lesions develop. A large granuloma in the esophagus may interfere with swallowing and those in the stomach may cause persistent vomiting. Aortic aneurysms may
rupture and lead to sudden death by extravasation If malignancy occurs, a wide variety of symptoms may occur.
6. Epidemiology and Importance of Transfer Hosts:
Bailey at Auburn recorded an 8% infecton rate in Alabama in a 1963 survey, but Georgia surveys in the
Southeast show a 36% infecton rate in some areas. Alabama, Mississippi and East Texas appear to be
very high incidence area. It is generally felt that dogs become infected more by eating infected transfer hosts than by ingesting the beetle itself. Even in high incidence areas, few beetles are found with infective larvae. Therefore transport hosts (by eating many beetles) can serve as accumulators of larvae. Bailey considers the feeding on the intestinal tract of chickens as primary source of larvae for dogs. It has been shown that rural dogs allowed to roam are more apt to be infected than confined well fed dogs - probably because roaming dogs tend to supplement their diets on birds, small mammals and other host. Studies have revealed that about 6% of wild birds of 14 different species carried the third stage encysted larvae, especially aggressive type birds such as the Blue Jay, Cardinal, and Blackbird. There has been a decreasing incidence in recent years. Bailey con- siders this to be due to better care of dogs and the shift to confinement poultry operations.
7. Diagnosis:
Diagnosis can be made by:
- a. Clinical signs
- b. Radiography with contrast media
- c. Stool exam NANO3 (1.36 specific gravity) Flotation
- d. Artificial gastric juice and direct counts - Cabrera & Bailey, JAVAM. Vol. 145 No. 6. (1964)
Recovery of eggs is dependent on a patent opening to the lumen of the digestive tract and therefore is not a consistent finding.
Remember ,
That sugar and salt flotation solutions (S. G. = 1.22) will not float the typical embryonated eggs. (NaNO3 S.G. = 1.36 will). Cabrera and Bailey claim higher recovery of ova after artificial gastric juice digestion of feces and direct counts.
