Who's knocking at your door? (Proceedings)
"After all, we are a mobile society and our pets travel with us". We are all probably tired of hearing it, yet, transporting our pets around the world is one of the most significant factors in the emergence of diseases in new geographic areas. Here, we will discuss some parasites that have recently been introduced to the US, have the capability to establish should they be introduced to the US, or are present but spreading within the US.
Canine pulmonary angiostrogylosis (CPA) is caused by the nematode Angiostrongylus vasorum. The first anecdotal reports of CPA were in France in 1813 and 1833. Subsequent research on this nematode in France, coupled with endemic foci identified in southwestern France, led to this parasite's common name – the French heartworm. No longer limited to France, the distribution of this parasite is worldwide. Recent reports of CPA in Newfoundland and Labrador, Canada, as well as elsewhere, indicate this parasite continues to spread.Canine pulmonary angiostrogylosis (CPA) is caused by the nematode Angiostrongylus vasorum. The first anecdotal reports of CPA were in France in 1813 and 1833. Subsequent research on this nematode in France, coupled with endemic foci identified in southwestern France, led to this parasite's common name – the French heartworm. No longer limited to France, the distribution of this parasite is worldwide. Recent reports of CPA in Newfoundland and Labrador, Canada, as well as elsewhere, indicate this parasite continues to spread.
Compared to Dirofilaria immitis (120-300 mm), A. vasorum adults are relatively small (14-25 mm). As with D. immitis, the life cycle is indirect, but snails and slugs are the intermediate hosts rather than mosquitoes. Both male and female A. vasorum live in the right side of the canine heart and pulmonary arteries, although, with aberrant migration, they can end up in other areas (eye, kidney, brain, pancreas, femoral artery). The females lay eggs that lodge in smaller capillaries where they develop and hatch. The hatched first-stage larvae penetrate capillaries and alveoli, and migrate into the larger airways where they are eventually coughed up, swallowed and passed in the feces. They are then ingested by a suitable gastropod intermediate host where they develop to the infective third-stage larvae. It is unknown whether infective larvae can be shed in secretions or whether dogs must ingest intact molluscs to become infected. It is known that frogs and rodents may serve as paratenic hosts, but, their relative importance to the maintenance of the life cycle is unknown. Once ingested, the infective larvae penetrate the gastrointestinal tract wall, migrate to visceral lymph nodes and develop into immature adult nematodes. They then migrate to the right ventricle and pulmonary arteries by way of the portal circulation. The prepatent period is around 38-57 days. The adult nematodes are very long-lived and the dog may remain infected for life.
Reservoir hosts for A. vasorum include other canids, such as foxes, wolves, coyotes and jackals. This parasite has also been reported in ferrets, badgers and red pandas.
There does not appear to be any gender or breed disposition, although one study did show Cavalier King Charles spaniels and Staffordhisre bull terriers were overrepresented among dogs with CPA compared to the control group. CPA has been reported in dogs as young as 3-months-old and as old as 14 years; however, more than half the cases have been reported in dogs ≤1 year. Clinically, infected dogs may be asymptomatic, minimally affected or present with life-threatening disease. Classic CPA usually presents as pneumonia. Respiratory signs can include dyspnea and coughing, Crackles may be present in severe cases. Pulmonary hypertension, cor pulmonale, and subsequent systolic heart murmur may be observed in chronic infections. Other signs that may be present include depression, exercise intolerance, anorexia, weight loss, vomiting, and diarrhea. Severe coagulation disorders have also been identified in chronically infected dogs. petechial and ecchymotic hemorrhages, hematomas (both traumatic and surgically induced), epistaxis, hemoptysis, intracranial hemorrhages, hematuria, and gastrointestinal bleeding have all been reported. Thrombocytopenia, prolonged APTT and PT, presence of fibrin degradation products, hyperglobulinemia, anemia, or Factor V deficiency are associated with these cases. Thus, a consumptive coagulopathy is indicated, but, the mechanisms involved are not defined.
Larvae can be detected using the Baermann technique. However, ante-mortem diagnosis can be difficult due to the sporadic shedding of larvae in the feces. Therefore, it is recommended that feces be collected on 3 consecutive days to enhance detection. Larvae can also be found in direct fecal smears, particularly if clinical signs are moderate to severe. Larvae can also be recovered by tracheal wash or bronchoalveolar lavage. Larvae of A. vasorum are approximately 350 µm in length and are distinguished from those of other canine parasites that also pass larvae in the feces by the presence of a kinked tail with a dorsal spine and a cephalic button at the anterior end. Additional diagnostics, such as thoracic radiographs, hematological and biochemical profiles or coagulation profiles, may be required, depending on the severity of disease.
Several anthelmintics and therapeutic regimens have been used to treat CPA. Current recommendations include milbemycin oxime (0.5 mg/kg once a week for 4 weeks), moxidectin topical (2.5 mg/kg; imidacloprid/moxidectin spot-on combination product; single application) or fenbendazole (25 mg/kg daily for 20 days). No treatment is 100% efficacious; therefore, follow-up fecal exams should be conducted 3-7 days after completion of the treatment regimen. Resolution of clinical disease but not infection can occur; in these cases, retreatment is necessary.