Strongyloides felis

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Strongyloidesfelis Chandler, 1925

(Figures 4-02 through 4-04)

ETYMOLOGY:Strongyl = round and oides = like along with felis for the cat host.

SYNONYMS: None.

HISTORY: Chandler (1925a) described a new species of Strongyloides from cats in Calcutta. Further features of this species were descrbied by Goodey (1926) and by Baylis (1936), but there were no additional findings presented on this worm until the the 1980s when Spear and Tinsley (1986 & 1987) reported that over 50% of cats examined in Townsville, Australia, were infected with this parasite.

GEOGRAPHIC LOCATION: India and Australia.

LOCATION IN HOST: The parasitic female is found in the mucosa of the anterior half of the small intestinal of its host.

PARASITE IDENTIFICATION:Strongyloidesfelis differs from Strongyloidesstercoralis in that the parasitic female of Strongyloidesfelis has a narrower tail and the free-living female of Strongyloidesfelis has a post-vulval constriction of the body which is lacking in the free-living female of Strongyloidesstercoralis. The parasitic females of Strongyloidesfelis and Strongyloidesstercoralis have ovaries that are straight, while the ovaries of the parasitic female of Strongyloidesplaniceps are spiral. Also, infections with Strongyloidesfelis and Strongyloidesstercoralis result in larvae being passed in the feces of the infected cat, while infections with Strongyloidesplaniceps produce eggs that are found in freshly deposited feces. Strongyloidestumefaciens differs from the other species of Strongyloides present in the cat by having a longer parasitic female (5 mm long) that is found in tumors in the mucosa of the large intestine.

Diagnosis of infection is best performed using the Baermann technique. Larvae can be detected using a direct smear of feces, but because most cats shed less than 50 larvae per gram of feces, the sensitivity of this method is low. To determine whether a cat is infected with Strongyloidesfelis or Strongyloidesstercoralis, it is necessary to perform fecal cultures that will generate the free-living adult stages.

LIFE CYCLE: The life cycle of this parasite has been described by Spear and Tinsley (1986). The adult parthenogenetic female lives in the mucosa of the small intestine and produces eggs that hatch in the small intestine to produce first-stage rhabditiform larvae that are passed in the feces. The larvae passed in the feces will typically develop into free-living adults, males and females. At 20ºC, the free-living adults will typically produce eggs that hatch to yield larvae that mature to the infective filariform third-stage larva in about six days (Figs 4-02 and 4-03). Occasionally, the larvae passed in the feces will develop directly to infective-stage larvae in about two days. There is only one generation of the short-lived free-living adults; most of the adults produced die within ten days after cultures are established (Fig 4-04). Infection of the cat is by the penetration of the skin by the infective-stage larva. After skin penetration, the infective larvae are carried to the lungs, break through the alveolar spaces, migrate up the trachea, and down the esophagus to the small intestine. The prepatent period is 11 (9 to 14) days. The fact that infections are found almost exclusively in older cats and that kittens of infected queens remain uninfected would suggest that transmammary infection with this species does not occur. Infections have been shown to persist for over two years in experimentally infected cats.

CLINICAL PRESENTATION AND PATHOGENESIS: There are no pathognomonic clinical signs of infection with this parasite (Speare and Tinsley, 1986). Diarrhea is not a typical feature of infection, although some cats with naturally acquired infections had acute watery diarrhea that cleared after treatment (see below). The experimental infection of cats with 500 larvae produced no signs other than a slight unthriftiness and unkempt coats. Alertness and appetite remained normal in experimentally infected cats.

There does not appear to be an inflammatory response associated with the intestinal phase of the infection, but some worms were found to be associated with an adenomatous metaplasia of the glandular epithelium of the intestinal crypts (Speare and Tinsley, 1986). There were focal granulomas, subpleural inflammatory plaques, and a vasculitis associated with the migration of the larval stages through the lungs of experimentally infected cats.

TREATMENT: Thiabendazole (25 mg/kg BID for two days) has been found to be 100% efficacious in three cats. Fenbendazole (20 mg/kg SID for three days) caused no change in the numbers of larvae shed by two cats but caused a transient disappearance of larvae in a third cat. Oxfendazole (8 to 9 mg/kg SID for two days) causes only slight larval reductions. Levamisole (10 mg/kg) in combination with niclosamide (200 mg/kg) caused a temporary drop in larvae being produced in two cats. Pyrantel emboate (12.5 mg/kg) and pyrantel pamoate (25 mg/kg), both had no effect following a single treatment. Praziquantel (25 mg/kg) was also without effect (Spear and Tinsley, 1986).

EPIZOOTIOLOGY: The infective stage larvae survive for a maximum of three weeks in the external environment and are very susceptible to dehydration. Infections are confined mainly to adult cats with cats less than 6 months of age only rarely being infected. Speare and Tinsley (1986) reported that 56% of 198 adult cats from Townsville and Ingham, Australia, were infected with this parasite while only 9% of 63 kittens and juvenile cats were infected. Most natural infection are not heavy with there typically being less than 50 larvae per gram of feces and less than 100 adult worms being present.

HAZARDS TO OTHER ANIMALS: Unknown.

HAZARD TO HUMANS: Unknown.

CONTROL/PREVENTION: Because infections are obtained by the direct penetration of the skin with larvae, it is difficult to prevent infections in cats that are allowed outside.

REFERENCES:

Chandler AC. 1925a. The helminthic parasites of cats in Calcutta and ther relationship of cats to human helminthic infections. Ind J Med Res 13:213-227.

Chandler AC. 1925b. The species of Strongyloides (Nematoda). Parasitology 17:426-433.

Goodey T. 1926. Observations on S. fulleborni von Linstow, 1905, with some remarks on the genus Strongyloides. J Helminthol 4:75-86.

Speare R, Tinsley DJ. 1986. Strongyloidesfelis: An “old” worm rediscovered in Australian cats. Aust Vet Pract 16:10-18.

Speare R, Tinsley DJ. 1987. Survey of cats for Strongyloidesfelis. Aust Vet J 64:191-192.

Figure 4-02. Strongyloides stercoralis. Third-stage infective larva. This is the stage that penetrates the skin of its host.

Figure 4-03. Strongyloides stercoralis: Tail of third-stage infective larva showing the forked appearance at the tip.

Figure 4-04. Strongyloides ratti. Free-living male and female in copulation. These are the stages that sometimes develop within the environment

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