Parasitic zoonoses of wildlife (Proceedings)

The major zoonotic helminth affecting people in the US is Toxocara canis. This is a well-known parasite of our canine companions and one of the driving factors behind the call for year-round use of a broad-spectrum anthelmintic. However, this parasite is also found in wild canids, including coyotes and foxes, across the country. Toxocara canis remains common in many areas of the country, primarily because of the numerous routes of infection and an incomplete immunity. Infection in canids occurs by one or more routes, including transplacental transmission, ingestion of infective eggs or ingestion of paratenic hosts. Infective eggs can remain in the environment for years and can be ingested at any time of the year. Once infected, an age-asspciated immunity does occur, which aids in the expulsion of adults from the intestinal tract but does not completely eliminate the parasite. Adult females are highly prolific, with a single female producing between 25,000 and 85,000 eggs per day. Thus, environments can become heavily contaminated even when only a few parasites are present in an individual animal.

Larval toxocariasis can cause one or more forms of larva migrans in humans. Humans become infected by ingesting infective eggs present in contaminated soils, food or other articles. Visceral larva migrans (VLM) occurs when ingestion of infective eggs results in larval migration and damage to internal organs. VLM most often occurs in children <3 years of age. Symptoms produced depend on the organ invaded, the number of larvae involved and the frequency of reinfection and is likely the result of ingesting a large number of eggs over a short period of time. Hypereosinophilia, hepatomegaly, and pneumonitis are typical manifestations. Typically, once the early migratory phase of the larvae has stopped, the symptoms also subside as long as reinfection does not occur.

In older children (3-13 years of age), the larvae tend to migrate to the posterior chamber of the eye, resulting in ocular larval migrans (OLM). Granulomatous retinitis develops, which can result in severe ocular damage with retinal detachment, loss of vision or blindness. It is thought that the age of the child and ingestion of fewer infective eggs may play a role in the preferential migration to the eye.

Fortunately, even though 14% of the US human population has antibodies to T. canis, many cases are asymptomatic. However, CDC estimates >10,000 cases of larval toxocariasis occurs each year, of which approximately 700 will result in partial or complete blindness. Most of these will occur in children. While there is little we can do to directly control the parasite population in wild canids, we can certainly control the parasite in our pet population. Up to 15% of dogs are estimated to be infected with this parasite in the US. Likewise, prevalences in some wild canid populations also approaches 15-20%. Thus, by reducing/eliminating this parasite in our pet population, we can drastically reduce the environmental contamination and exposure of both human and wild canid population.

When discussing wildlife and ascarids, most veterinarians are aware of raccoons and Baylisascaris procyonis. This is a highly prevalent parasite of raccoons. Transmission occurs through ingestion of infective eggs in contaminated soil, water or other contaminated articles or ingestion of paratenic hosts. When non-raccoon hosts ingest infective eggs, larva migrans results. Even though the larvae can parasitize any organ, including the eye, this species has a tendency to migrate to the central nervous system. The resulting symptom, neural larva migrans (NLM), is the most serious of the larva migrans syndromes that occurs in human and other animals. Other than the location in the neural tissue, the primary factor responsible for the seriousness of the infection is the rate of growth and size the larvae achieve. Fatal encephalitis have been documented in over 90 species of birds and mammals, including humans.

Baylisascaris procyonis is particularly prevalent in young raccoons, resulting in high shedding rates. These high shedding rates and the tendency of raccoons to use communal defecation sites ("latrines"), results in focal areas of extreme contamination. As long as these sites are not in the urban environment, the risk of human infection decreases. However, the presence of raccoons in the ruban landscape greatly increases the risk of human exposure. Veterinarians should discourage their clients from feeding raccoons or adopting them as pets. Clients should also be advised of potential latrine sites such as fallen trees, tree stumps, and woodpiles. In addition to raccoons, patent infections have also been documented in domestic dogs. Although not common as of yet, the indiscriminant defecation habits of dogs is a concern. Should more dogs become infected, the potential for increased human exposure greatly increases.

Toxoplasmosis is caused by the protozoan parasite Toxoplasma gondii. Most people associate this parasite with cats, While it is true that felids are the only definitive host and shed oocysts in their feces, oocysts are not the sole means by which people can get infected. Ingestion of tissue cysts in undercooked meat is probably a more important route of human infection. Estimates of up to 33% of humans worldwide have circulating antibodies to this parasite, implying either active infection or prior exposure. Within the US, the overall seroprevalence appears to be declining - 14.1% (1988 – 1994) vs 9.1% (1999 – 2004). Seroprevalence increases with age such that exposure risk increases among women of child-bearing years.

Acquired toxoplasmosis, those infections acquired after birth, can present with no symptoms or a brief flu-like illness characterized by fever, malaise and enlarged lymph nodes. The groups at greatest risk of disease, however, are congenitally infected infants, HIV-infected individuals, and individuals immunosuppressed for transplantation. If a T. gondii-naïve woman becomes infected during pregnancy, the parasite can infect the fetus. In these cases, congenitally-infected children may not show clinical signs, may be clinically apparent during the first few months of life or may become clinically affected later in childhood or adolescence. With approximately 4 million live births every year, estimates range between 400 and 4,000 infants born each year with congenital infection. As long as a woman does not become otherwise immunocompromised, infection of a mother prior to conception poses no threat of congenital transmission.

Toxoplasmosis in HIV-infected or otherwise immunocompromised individuals is usually a result of recrudescence of resting bradyzoites in tissue cysts. The bradyzoites revert to the more active tachyzoite stage and undergo repeated rounds of asexual reproduction. Unimpeded because of the compromised immune system this rapid reproduction results in toxoplasmic encephalitis, which can be fatal.

It is usually not possible to determine the source of human infection. However, ocular toxoplasmosis has been described in a group of people, apparently acquired from ingestion of undercooked and uncooked venison. Just how many other human infections occur as a result of eating improperly prepared game is unknown.

Other parasitic zoonoses for which wildlife can be reservoir hosts include heartworm (Dirofilaria immitis), Cryptosporidium parvum, trematodes in the genus Alaria and echinococcosis. The consequences of infections with these parasites varies from minor inconvenience to more serious disease with potential deadly consequences. Proper personal hygiene and common sense can prevent the vast majority of these and other parasitic infections.