Strongyloides stercoralis is a small, slender nematode that when fully mature is ∼2 mm long, located at the base of the villi in the anterior half of the small intestine of dogs and cats. The worms are almost transparent and all but impossible to see grossly at necropsy. Usually, infections are associated with warm, wet, crowded, unsanitary housing. The species found most often in dogs is identical to that found in people.
The parasitic worms are all females. The eggs embryonate rapidly, and most larvae hatch before being passed in the feces. Under appropriate conditions of warmth and moisture, development in the environment is rapid. The third larval stage may be reached in little more than a day. Some of these larvae develop into infective filariform larvae; others develop into free-living worms that mate and produce progeny similar to that of the parasitic female. The filariform larvae penetrate the skin but also may infect a host via the oral cavity. Transmammary transmission is possible. Progeny may be shed in the feces 7–10 days after infection. Autoinfection caused by larvae that developed to the infective stage within the GI tract can result in infections in which dogs shed larvae for lengthy periods.
The presence of clinical signs indicates that a heavy infection has been building up for some weeks. A blood-streaked, mucoid diarrhea, usually seen in young animals during hot humid weather, is characteristic. Emaciation is often prominent, and reduced growth rate may be one of the first signs. Appetite usually is good, and the dog is normally active in the earlier stages of the disease. In the absence of concurrent secondary infections, there is little or no fever. Usually in advanced stages, there is shallow, rapid breathing and fever, and the prognosis is grave. Autoinfection may be induced by the use of corticosteroids or other factors that affect immunocompetence. There may be larvae in tissues, and these dogs are more likely to die. At necropsy, there can be evidence of verminous pneumonia with large areas of consolidation in the lungs as well as marked enteritis with hemorrhage, mucosal exfoliation, and much secretion of mucus.
First-stage larvae (~380 μm long) are identified by direct microscopic evaluation of a small quantity of feces. Usually, the Baermann technique is used to separate larvae from fecal material. It is important to use fresh fecal material obtained from the infected dog so that the larvae can be easily differentiated from hookworm larvae or free-living soil nematodes. Occasionally, eggs (50–60 × 30–35 μm) may be identified by flotation of fresh feces. Adult female worms can be identified by scraping the mucosa of the small intestine. They are only ∼2 mm long, but the presence of eggs in the uterus easily differentiates them from larvae of other nematodes.
Treatment and Control
Poor sanitation and mixing of susceptible with infected dogs can lead to a rapid buildup of the infection in all dogs in a kennel or pen. Dogs with diarrhea should be promptly isolated from dogs that appear healthy. Direct sunlight, increased soil or surface temperatures, and desiccation are deleterious to all free larval stages. Thorough washing of wooden and impervious surfaces with steam or concentrated salt or lime solutions, followed by rinsing with hot water, effectively destroys the parasite. Because the disease in people can be serious, caution should be exercised in handling infected dogs. The disease in people (as in dogs) is much more likely to be severe if the person is immunosuppressed.
Infections in dogs can be treated with ivermectin (0.2 mg/kg, SC or PO, once, with a second dose 4 wk later; 0.8 mg/kg, PO, once), fenbendazole (50 mg/kg, PO, sid for 5 days, repeated 4 wk later) or thiabendazole (100–150 mg/kg, PO, sid for 3 days, repeated weekly until larvae are not detected in feces—toxicity may be observed with this regimen). In cats, fenbendazole (50 mg/kg, PO, sid for 3 days) can be used. These are not approved regimens in either cats or dogs. In all animals, feces should be examined regularly for at least 6 mo after treatment to confirm efficacy.
Last full review/revision March 2012 by Andrew S. Peregrine, BVMS, PhD, DVM, DEVPC, DACVM