Introduction

Classification

Taxonomy

• Superfamily: Rhabditoidea.
• Genus: Strongyloides.

Active Forms

Clinical Effects

Epidemiology

Habitat

Parasitic stages

• Parasitic females in submucosa of anterior small intestine and L1 to L3 in lumen of intestine.
• Parasitic L3 in liver, lungs and other somatic tissues.

Free living stages

• L1 to infective L3 and L1 to parasitic male and female and then infective L3 in environment.

Lifecycle

• See lifecycle diagram:
  • Parasitic females.
  • Autoinfective 3rd stage larvae.
  • Parasitic 3rd stage larvae.
  • 1st stage larvae.
  • Infective 3rd stage larvae.
  • Free living males and females.

Transmission

Transmission from bitch to puppies

• Transfer of infection from the bitch to her puppies occurs via fecal reshedding and possibly transmammary transmission, though the existence of this latter is now disputed.

Horizontal transmission

• Neonatal infection is followed by transmission between the puppies and by transmission between dogs in kennels when infective L3 in the environment penetrate the skin or are ingested to migrate and return to the intestine.

Autoinfection

• Autoinfective L3 penetrate the colon directly early in infection in puppies and immunosuppressed dogs, and then migrate to return to the intestine.

Pathological effects

• The host immune response modifies the course of infection.
• Infection of a naive animal results in an infection with a patent period of about 3 weeks to 3 months.
• Internal autoinfection occurs early in the course of infection.
• Gut level resistance (that does not involve IgA) soon occurs and an increasing proportion of larvae are now excreted as L1 in the feces.
• Low level chronic infections can persist in intestine and tissues.
• Immunosuppression during pregnancy can permit renewed fecal shedding of larvae and possibly transmammary transmission.
• Marked immunosuppression can permit reactivation and massive autoinfection.

• Most infections asymptomatic.
• Heavy infections are seen in kennel puppies in warm moist conditions or in immunosuppressed dogs.
• Parasitic females buried in the submucosa. Eruption of their L1 to the lumen causes a catarrhal enteritis in the anterior small intestine with inflammation, edema and petechial ulceration and hemorrhage.
• Malabsorption, moderate to severe diarrhea which may be hemorrhagic, weight loss and dehydration result.
• Mucosal ulcerations in the colon are probably due to penetration of autoinfective L3.
• Petecchial and more severe hemorrhages in subpleural and parenchymal lung tissues, plus interstitial pneumonia in response to large numbers of migrating larvae, may induce respiratory distress.
• Dermatitis (particularly on the feet or belly) may be possible due to skin penetration of larvae from a heavily infected, warm, moist environment.

Control

Control via animal

• Anthelmintic treatment including in-contact dogs.
• In infected kennels, anthelmintic treatment of bitch prior to pregnancy and puppies during the latter part of sucking and during weaning.

Control via chemotherapies

• All therapies are essentially experimental.
• Ivermectin Ivermectin (200 mg/kg) (not licensed for use in dogs at this dosage). May eliminate intestinal stages but not all tissue stages. Has proved useful in treatment of horses and pigs and to prevent transmammary transmission in these species.
• Albendazole Albendazole (100 mg/kg bid for 3 days) (not licensed for use in dogs). In one experiment this very high dose markedly reduced but did not completely eliminate intestinal and tissue stages.
• Nitroscanate Nitroscanate (3 doses of 200 mg/kg at 5-6 day intervals) (unlicensed use in dogs) was reported to be effective in one experiment for treatment of intestinal infections in a breeding colony.
• Fenbendazole Fenbendazole (20-50 mg/kg/day for 2-3 weeks) (unlicensed use in dogs). This regimen seems likely to have an effect in reducing numbers of intestinal and tissue stages but information is not available.

Control via environment

• Hygiene and dryness.

• A very dry environment in the kennels will kill most of the free-living stages.

Diagnosis

Further Reading

Publications

Refereed papers

• Recent references from PubMed and VetMedResource.
• Dillard K J, Saari S A, Anttila M (2007) Strongyloides stercoralis infection in a Finnish kennel. Acta Vet Scand 49, 37 PubMed.
• Schad G A, Smith G, Megyeri Z, Bhopale V M, Niamatali S & Maze R (1993) Mathematical model to explain variation in development of larvae - Strongyloides stercoralis - an initial autoinfective burst amplifies primary infection. Am J Tropical Med Hygiene 48, 716-725.
• Mansfield L S & Schad G A (1992) Strongyloides stercoralis infection in IgA-deficient dogs. Am J Tropical Med Hygiene 47 (6), 830-836 PubMed.
• Genta R M, Schad G A & Hellman M E (1986) Strongyloides stercoralis: parasitological, immunological and pathological observations in immunosuppressed dogs. Transactions of the Royal Society of Tropical Medicine and Hygiene 80 (1), 34-41 PubMed.