JEFFHESTER
UKC Forum Member
Registered: Apr 2008
Location: Athens, Tn.
Posts: 864 |
THAT'S IT!!!!
quote: Originally posted by Lone Pine JB
none of the above.
It's a parasite called Dracunculus insignis.
I see it pretty frequently.
That's it!! Never heard of it, no treatment to remove it, besides surgery. You ever known a dog to get these? According to the article if a dog eats the contaminated meat, he can contract them. I guess a person wouldn't know unless he skinned his dog. Thanks for your help everyone.
Jeff
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Description
The North American guinea worms are nematodes found in numerous furbearing species in the U.S. and Canada. Two species of worms, Dracunculus insignis and D. lutrae, are recognized under this common name. The slender worms reside in the subcutaneous spaces of the legs, resulting in ulcerations in these affected areas.
Distribution
D. insignis has been reported in the raccoon, mink, striped skunk, fox, muskrat, fisher, short-tailed weasel, opossum, badger, Bonaparte weasel and dog in the U.S. and Canada. Raccoons are the most favorable definitive host for D. insignis in North America. In Ontario, surveys found infections of D. insignis as high as 50% in raccoon and mink.
D. lutrae has only been reported in river otter in Ontario, New York, and Michigan. Eighty-eight percent of the river otter in Ontario surveyed in one year were infected with D. lutrae. In Michigan, dracunculosis has been diagnosed in the raccoon, mink, red fox, river otter, fisher, and pine marten.
Transmission and Development
Gravid adult female D. insignis and D. lutrae are found in the subcutaneous space of the front and hind legs, thorax, abdomen and groin. The worms are generally in the fascia in the tibial region of the hind leg. The anterior end of the viviparous female penetrates the dermis resulting in the formation of a blister. The blister soon ruptures and an ulcer forms. When the ulcerated area contacts water, the skin over the gravid female ruptures. First-stage larvae are liberated into the water and are ingested by suitable intermediate copepod hosts, the cyclops, Cyclops vernalis and C. bicuspidatus, and possibly other species. The infected cylops may contain from 1 to 23 larvae, but usually has only 4 or 5 present. After larval ingestion, the copepods may become lethargic and may live only 50 days. The first-stage larvae develop to the infective third-stage larvae in a few weeks.
A paratenic host, such as frogs (leopard frog, Rana pipiens, and green frog, R. clamitans) or fish (rainbow trout, Salmo gairdneri, and white sucker, Catostomus commersoni) may serve as an accumulator of the D. insignis and possibly D. lutrae infective stage larvae by eating the infected cyclops. The accumulation of infective larvae maintains the high prevalence of the worm in the definitive hosts. The infective third-stage larvae probably remain viable in frogs for extended periods of time, so that large numbers of larvae can be ingested by eating a single frog.
The definitive hosts become infected by eating infected reservoir hosts or by drinking water containing parasitized cyclops. The infective larvae are released in the intestinal tract. The larvae penetrate the wall of the host's intestine and migrate through the body cavity to the connective tissues of the abdomen, thorax and groin. In these preferred locations, the larvae mature, with the prepatent period usually being a year but possibly being as short as 77 days. Following maturity, the worms mate, and egg development in the female occurs.
The males and immature females remain in the above locations but the egg-bearing females migrate to the legs with larvae developing within the eggs during the females' migration. Viviparous females may be found as early as 120 days post-infection in the infected animal's legs.
After larval production, the exhausted female, in addition to the adult male and immature worms, may die and become calcified and resorbed by the host.
Maximum numbers of D. insignis in raccoon and mink from a study in Ontario were 54 and 17 respectively with averages of 5 and 3. In this same study maximum numbers of D. lutrae in river otter were 63 with an average of 7 worms.
Transmission of D. insignis in raccoons is confined to only a few weeks of the year. Adult worms are usually patent in late spring or early summer thus corresponding with changes in the definitive host's food habits. Mink infections are not as seasonal as raccoon infections due to the mink's year-round feeding on aquatic life. Raccoons may serve as a reservoir host for this parasite and there is a higher incidence of infection with D. insignis in mink when raccoons share the same area. River otter probably would not show a seasonal infection rate because of their year-round food habits.
Clinical Signs
Raccoons infected with D. insignis have been observed inactive for 30 to 60 minute periods and move slowly and only then with difficulty and distress. The animals frequently raise affected legs for short time intervals and occasionally scratch the skin overlying the viviparous females.
No clinical signs have been reported in river otters infected with D. lutrae, nor in mink infected with D. insignis.
Diagnosis
A D. insignis or D. lutrae infection can be diagnosed by finding and identifying the adult worms in the subcutaneous space. They are more likely to be found if both the pelt and carcass are examined, not just the carcass. Rarely can larvae be found in the circulating blood.
The adult worms differ from each other in appearance. The males measure 1.5 to 4 cm in length and are dark and extremely slender. The female worms are long and slender, measuring up to 28 cm in length and are white.
The long, tapering tails of D. insignis and D. lutrae larvae differentiates them from Dirofilaria
immitis and Dipetalonema reconditum microfilaria.
Pathology
Externally, there is local hair loss and skin damage to the extremities due to self-inflicted trauma (scratching). These lesions are usually on the lateral surface of the carpal and tarsal regions of the legs.
There are no gross lesions in the subcutaneous space adjacent to the adult worms. Lesions are found on the extremities where the viviparous females reside. The skin over these worms is inflamed and hemorrhagic. Small, round, shallow ulcerations form when the female worms place their heads into the dermal layer of the skin. After larvae are released from the adult female worms, the ulcerations contain a purulent exudate and bacteria. Following the production of larvae, the female worm dies. The lesions heal rapidly; 14 to 21 days after the female dies and the only visible signs of an infection are yellow patches of necrotic debris in the subcutaneous tissues of the legs.
Microscopically, areas of localized edema, hemorrhage and a connective tissue capsule surrounding the viviparous females are seen on the legs. At the site of ulcer formation there is a preponderance of eosinophils and neutrophils and a purulent exudate. The epidermal and dermal layers of the skin are often obliterated and the result is a hyperkeratosis, paraketosis and a perivasculitis.
Treatment and Control
The adult female worms may be removed through the skin opening on the legs or by surgical dissection. Removal of the worms is very difficult and usually not done. Therefore, there is essentially no treatment.
In wild mammal populations, control would be impractical and unnecessary.
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Last edited by JEFFHESTER on 01-25-2012 at 03:09 PM
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