Tapeworms in all the wrong places: some unusual presentations of common parasites (Proceedings)
May 01, 2011
Raw food diets – when will we learn that truly raw foods are the pathway for disaster? In addition to bacterial problems, most tapeworm infections in dogs and cats are a result of eating raw food (prey) or ingesting untreated water. Pets should be fed cooked or prepared food and provided with fresh, potable water.
All tapeworms of dogs and cats have an indirect life cycle. The definitive host is the one in which the tapeworm matures, reproduces and generates eggs. The intermediate host is the host in which the metacestode (immature) form of the parasite develops. The definitive host becomes infected by eating the intermediate host while the intermediate host becomes infected by eating eggs in an environment contaminated by the definitive host. In general, dogs and cats serve as definitive hosts, although metacestodes can sometimes develop within them.
The life cycles are fairly straightforward. Gravid proglottids break free of the tapeworm and are shed in the feces. Eggs are released from the segment either as it travels through the digestive tract or as it sits on the fecal. These eggs are then ingested by the intermediate host, the embryo hatches and migrates to its developmental site, and the metacestode develops. When the intermediate host is ingested by the definitive host, the metacestode is digested free, the scolex embeds itself in the mucosa of the small intestine and the neck begins to grow, forming proglottids. The prepatent period is usually reported as 5-12 weeks, depending on species. How long untreated tapeworms will survive is not known for sure but, T. taeniaeformis has been reported to remain patent in cats for as long as 34 months.
Intestinal infections tend to not be pathogenic. Infections are generally diagnosed based on finding proglottids in the feces although eggs can be found on fecal flotation if the proper specific gravity is used. Praziquantel, epsiprantel, and fenbendazole are approved for the treatment of Taenia infections in dogs and cats.
Occasionally, dogs and cats develop cysticercosis as a result of infection with T. crassiceps. The metacestode of this species of tapeworm is unique in that it is prolferative cysticercus that develops asexually through budding. Consequently, ingestion of 1 or a few organisms can result in massive infections. Intraperitoneal, intrapleural, intracardiac, intracranial and subcutaneous cystcercosis have been documented, most with fatal results. Why these animals develop cysticercosis is uncertain; however, an impaired immune system is thought to play a key role. Route of infection is also speculative. Ingestion of eggs from the environment, autoinfection via eggs from gravid tapeworms within the small intestine and ingestion of cysticerci in intermediate hosts have all been proposed. Eggs, either ingested from the environment or autoinfection, are considered the most likely source.
Cysticercosis associated with T. crassiceps occurs in people as well. Although the source of infection (wild vs domestic canid) is usually not known, at least one case was linked to the family dog.
Dogs can also develop cysticercosis as a result of infection with T. solium. Although uncommon any more in the United States, this parasite is responsible for cerebral cysticercosis in humans in many areas of the world. In these same areas, dogs also can be infected by ingesting eggs. If the cysticercus localizes to the brain, the dog can become aggressive. In developing countries where rabies is endemic, aggressive behavior is often sufficient evidence for a diagnosis of rabies, resulting in euthansia. While canine neurocysticercosis due to T. solium has not been weel recognized in the US, it does exist in Mexico where many rescue groups travel to bring dogs back to the US.