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.

Angiostrongylus vasorum

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.

Heterobilharzia americana

Canine schistomiasis is not an exotic disease; it is caused by the digenetic trematode Helerobilharzia americana which is endemic to many parts of the southeastern US. Unlike most trematodes, H. americana have separate sexes. The mature trematodes live in the mesenteric veins where they mate and the female produces eggs. Eggs in the terminal mesenteric veins penetrate through the vessel, entering the intestinal wall. After traversing the wall, they are released into the lumen and passed with the feces. The miracidium is fully developed by the time the egg enters the external environment. If the egg contacts water, the miracidium hatches and enters a freshwater snail. Asexual reproduction occurs, producing cercariae. These emerge from the snail, beginning about 25 days after infection. Cercariae penetrate the skin of the definitive host and migrate to the liver where they mature in about 40 days and then migrate to the mesenteric veins. The prepatent period is approximately 68 days.

There are numerous reservoir hosts for H. americana, but, raccoons and nutria appear to be the primary ones. Dogs are the most important domestic definitive host but red wolves and coyotes may be important wild canid reservoirs. Experimental or natural infections with H. americana have been demonstrated in 2 species of aquatic snails; however, little information is known about whether additional species can be competent intermediate hosts. Geographic distribution of the parasite originally included the southern Atlantic coast and the Gulf coast but has been documented as far north as Kansas. Thus, the current distribution of the parasite appears to be the central and southeastern US.

Passage of the eggs through the tissues result in granuloma formation resulting in enteritis. Clinically, weight loss, diarrhea , hematochezia and wasting can occur. In severe infections, hepatic disease may also be present. CBC and chemistries are often normal, although hypercalcemia with decreased serum parathyroid hormone and/or increased serum parathyroid hormone-related protein may be present. These may be misdiagnosed as neoplasia and hypercalcemia of malignancy when it is actually hypercalcemia due to granulomatous disease.

Clinical diagnosis generally comes from demonstration of the eggs in feces or in intestinal or hepatic biopsies. Routine fecal flotations will not detect eggs as they do not readily float. Also, if placed in water, the eggs will hatch within minutes. Therefore, fecal sedimentation with 0.85% saline is the diagnostic technique of choice for demonstrating these eggs. As with other parasites, eggs are passed intermittently in feces so multiple fecal exams may be required. Both fenbendazole and praziquantel are effective against this parasite.

Trypanosoma cruzi

Trypanosoma cruzi is a protozoan parasite that causes Chagas disease or American trypanosomiasis. This zoonotic disease affects an estimated 28 million people, mostly living in Latin America. However, with increased movement of people from endemic areas, tourism, and pet travel, Chagas disease has become an important public health issue in the US. Even though human prevalence is low, the blood supply is now routinely tested for Chagas disease.

The life cycle of the parasite is indirect with mammalian definitive hosts and triatomine bugs as intermediate hosts. Reservoir hosts within the US include opossums, wood rats, raccoons, armadillos, and coyotes. Within these hosts, T. cruzi amastigotes multiply by asexual reproduction in reticuloendothelial, neural, and glial cells, and cardiac and smooth muscle cells. Amastigotes are released when the host cell ruptures and change into trypomastigotes, which appear in the circulating blood. Trypomastigotes either invade new tissues or are ingested by the triatomine bug as it takes a blood meal. The parasite multiplies and undergoes metamorphosis into a new form in the hindgut of the bug. The bug defecates as it feeds and the parasite is transmitted in the feces. It then enters the body by penetrating the oral, nasal, or conjunctival mucosae or by rubbing the infectious bug feces into abrasions, such as when the bite site is scratched. Transplacental transmission as well as transmission through blood transfusion can also occur.

Acute disease in dogs is characterized by lymphadenopathy and clinical signs associated with acute myocarditis such as pale mucous membranes, lethargy, ascites, and tachyrhythmia. Signs present in the chronic stages of the disease are related to congestive myocardial failure. In a recent report characterizing canine Chagas disease, about half of dogs <1 year of age presented with acute death. In non-acute death cases, duration of apparent illness ranged from 1 day to 6 weeks and is dependent on when the client seeks veterinary attention. Cardiac dysfunction, represented by cardiac enlargement and myocarditis, is the primary problem reported in both puppies and adults. Conduction disturbances, including premature ventricular contractions and atrial fibrillation, were reported in about one-fifth of the animals.

The age range of clinical cases has been reported to be 6 weeks to 13 years with about half the cases in animals <1 year. No sex predilection has been reported. Cases have been reported in 48 breeds of dogs, with most in the sporting group, likely as a result of the lifestyle factors. Cases have also been reported in dogs from both urban and rural areas.

Diagnosis of Chagas disease is difficult and has traditionally depended on demonstration of trypomastigotes in peripheral blood or amastigotes in tissue biopsies. Serological and molecular methods are also available. The primary problem with most serological methods is the cross-reaction with Leishmania, another protozoan parasite also endemic to the US. Current recommendations are to confirm screening tests with another diagnostic method. Generally, by the time a diagnosis is made, treatment is unrewarding.

Dogs are more competent definitive hosts than either cats or humans and are considered important reservoir hosts in South and Central America. The importance of dogs as reservoirs for human infection in the US is unclear; however, evidence of canine involvement in domestic transmission cycles in the US is supported by the presence of seropositive dogs in close proximity to two locally acquired human cases – one in Tennessee and one in California.